Are facial 'cleansing' products 'effective' on human skin, and if so, what is their mechanism of action? All major supermarkets and beauty stores stock some form of facial cleansing products. They come in the form of scrubs, gels, and lotions which vary in application (from in shower, to apply daily without rinsing). Many of these are not marketed towards clearing acne or other legitimate dermatological problems. The claims these products make tend to include: reduction of dry/oily skin, neutralizing skin PH levels, and clearing pores. I am unsure if any of these terms are reflective of a real problem, or if the products can even even help said issues.

Therefore, this is a three-part question:

Do facial cleansing products actually do what they claim?
If so, what is their mechanism of action (i.e., how do the ingredients work)?
If not, what do the ingredients in the product actually do to human skin?

Examples of such products and associated claims:

Deep Clean® Invigorating Foaming Scrub by Neutrogena
Dr. Alkaitis Organic Purifying Facial Cleanser
L'Occitane Aqua Reotier Gel Cleanser

Example ingredients from the Neutrogena product above:

  Water, Glycerin, Sodium Laureth Sulfate, Cellulose, Lauryl Glucoside, Acrylates/C10-30 Alkyl Acrylate Crosspolymer, Microcrystalline Cellulose, Phenoxyethanol, Fragrance, Synthetic Wax, Methylparaben, Sodium Hydroxide, Menthol, Disodium EDTA, Polyquaternium-7, Sodium Benzotriazolyl Butylphenol Sulfonate, Ultramarines, Blue 1

Do facial cleansing products actually do what they claim?

This dermatologist-tested cleansing gel formula lathers into a bubbly foam removing surface dirt, oil and makeup, while energizing exfoliators sweep away dead skin cells.

So essentially, they are claiming that it is a foaming soap.
Sodium Laureth Sulfate is a detergent, Lauryl glucoside is a surfactant, so it is a good bet that the product is effective as soap. There are a bunch of other compounds that modify how it forms films, so it probably also foams.
If so, what is their mechanism of action (i.e., how do the ingredients work)?
Similar to any other soap.  They make non-water soluble things on the surface of you skin (such as oil, make up, dead skin cells, etc) more water soluble so that it dissolves when you wash your face.
Some of the other you linked also have moisturizers, so they probably put another oil back in the place of the ones you removed to keep the skin from getting too dry.

I am unsure if any of these terms are reflective of a real problem, or if the products can even even help said issues.

Or do they work better than normal soap of comparable strength?  Probably not much, although having them labeled as use for your face is nice in that you have a reasonable idea that it won't be too harsh or irritating, whereas if you tried dish soap on your face that might not go so well.


Are there any non-mammalian species known that lactate? Are there any non-mammalian animals that produce milk to feed their young, or are mammals the only milk-producing animals?

Short answer
Technically, only mammals lactate. To lactate means to produce milk from the mammaries to feed a baby or young animal. Milk, in turn, is defined as the secretions from mammary glands. However, there are animals other than mammals that produce milk-like substances to feed their young.

Background
Both male and female pigeons (Columba livia) possess the ability to produce a nutrient substance, termed pigeon ‘milk’, to feed their young. A similar substance is produced by flamingos and male emperor penguins. The normal function of a crop is a food storage area located between the oesophagus and proventriculus where food is moistened before further break-down and digestion through the gastrointestinal tract (Fig. 1).

Fig. 1. Schematic of the location of the 'milk'-producing crop in a pigeon (left) and a pigeon feeding its chick from its crop (right). Sources: ZME Science and Bird Ecology Study Group

During the process of pigeon ‘lactation’, a curd-like substance is regurgitated from the crop to the chick. The dry-substance of pigeon ‘milk’ is 60% protein, 32-36% fat, 1-3% carbohydrate and some minerals, including calcium. It has been shown that pigeon ‘milk’ contains IgA antibodies, which provides evidence suggestive that it is more than a nutrients alone. The physiological mechanisms governing pigeon ‘milk’ production and delivery are unknown. It is well documented that the pigeon crop is responsive to the lactogenic hormone prolactin. However, the pigeon crop tissue during ‘lactation’ is structurally unrelated to the mammary glands in mammalians, because it is not glandular and secretory processes do not seem to be involved (Gillespie et al, 2011).

The similarity between this process and lactation in mammals is striking, but is a case of convergent evolution, where unrelated species independently evolve similar traits. 'Milk' production is also recorded in some fishes, where it is fed to their young in the form of a mucous secretion on the skin (Buckley, 2010). Certain amphibians shed skin cells that are fed to the young. But the 'milk' of pigeons and doves is thought to be the most highly specialized of any non-mammalian 'milk' (Australian Geographic, September 2011).

References
- Buckley et al., J Exp Biol; 213: 3787-95
- Gillespie et al., BMC Genomics (2011); 12: 452


Why don't macaws get selenium poisoning from brazil nuts Google research has indicated macaws love or eat a lot of Brazil nut. These are highly toxic to humans in somewhat small quantities due to their selenium content.

Given the mass difference between a human and macaw, lets say 80kg and 2kg, if toxicity for humans 'starts' around 900micrograms or ~9 nuts, maths would indicate toxicity for a macaw might be around 20% of a nut?

These figures are all based on google and the margin of error I expect is quite large, nonetheless it seems quite disparate if a macaw could consume even a single nut a day on average, without consequence?

One explaination is that macaws (Ara sp.) eat clay and other food item which absorb the toxins. Here is the full answer from Wikipedia:

  Like all macaws and most parrots seeds and fruit are the major part of the diet of the genus Ara. The particular species and range of diet varies from species to species. Unlike many birds macaws are seed predators not seed dispersers, and use their immensely strong beaks to open even the hardest shells. Their diet overlaps with that of some monkey species; in one study of green-winged macaws in Venezuela they shared many of the same trees as bearded sakis, although in some cases they ate the seeds at an earlier stage of ripeness than the sakis, when they contained more poison. Macaws, like other parrots, may consume clay to absorb toxic compounds produced by some poison...but with further research we now at last know it is just to eat life saving sodium that is missing. As well, the toxic compounds of some foods may be neutralized by compounds, such as tannins, found in other foods consumed at the same time...but we have found that it is untrue and really just to gain access to sodium missing otherwise in their diet because of the area they live in.

Source: Wikipedia - Ara (genus)


What type of beetle is this? I found this beetle in my yard. Wondering what type it is.

This is probably Prionus californicus, which is a coleopteran native to the American west.

Look at the serrate antennae:

Also, the abdomen looks like the one in your specimen:


Where does moss come from? I've been growing plants in pots for several years, and in some of my pots a patch of green moss appears and steadily grows to fill the whole surface area of the soil. But that doesn't happen in other pots. I've used different bags of soil for different types of plants, but moss doesn't seem to appear only in one type of soil from the same bag.

How does moss appear in the first place? Or is it present in all soil and only grows to a visible size under certain conditions?

Short answer
Moss plants form spores; minute, invisible, typically one-celled, reproductive units that are carried off by the wind and into your pots.

Background
Mosses belong to the Bryophytes. Bryophytes are embryophytes; i.e., non-vascular land plants. They are spore-producing, rather than seed-producing and they do not bear flowers.

The leafy moss plant you are describing is the sexual phase of the moss life cycle. When mature, most mosses develop sex organs. Under wet conditions, sperm cells are released from male sex organs (antheridia) and swim to the female organs (archegonia), attracted by a chemical released by the female organ. After fertilization, the egg cells that are embedded in the female organ form a spore-producing plant. This consists of a stalk with a spore capsule and stays attached to the parent moss plant. As the spore capsule matures, it releases its spores into the air, and then dies. If moss spores fall in a damp place, they germinate and grow into leafy moss plants, and the cycle is completed (Fig. 1).

Hence, to answer your question - moss appears in your pots when spores land into it and enough water is available for their outgrowth.

Fig. 1. Reproductive cycle of moss. source: Encyclopedia of New Zealand


Balancing selection vs introgression? Balancing selection can maintain polymorphisms in natural populations for extended periods of evolutionary time. However, in this paper, Dannemann et al. 2016 identify three archaic haplotypes in the modern human genome that are due to adaptive introgression. Why can we exclude that haplotypes III, IV and VII (the introgressed haplotypes) have remained in the human gene pool since the split between modern humans and Neanderthals because of balancing selection?

Balancing selection and positive selection are not mutually exclusive. Neither are balancing selection and negative selection. Sickle cell is a classic example where there is negative selection against the homozygote for the sickling mutation, and positive selection for the heterozygote. The result is that there both alleles are maintained in the population under balancing selection.


Why is contractile vacuole absent in parasitic protozoans but present in free living protozoans? I know that contractile vacuole helps in osmoregulation of protozoans and some nitrogenous wastes are also excreted through it. Since contractile vacuole plays an important role in protozoans, why is it absent in parasitic protozoans? I could not find the logic behind this.

No, you are wrong. Parasitic protozoans too have contractile vacuole, for example trypanosoma.
Also Wikipedia says:

  Not all species that possess a contractile vacuole are freshwater organisms; some marine, soil microorganisms and parasites also have a contractile vacuole


Why does muscle tissue have relatively constant AMP + ADP + AMP? I was going over slides of energy expenditure in muscle cells. It mentions that in muscle tissue, the cell's energy charge ([ATP] / [AMP]) is the principle factor controlling glycolytic activity, and also that glycolysis’ primary role here is to provide ATP for contraction.

However, the slides also mentions that "Keep in mind that [ATP] + [ADP] + [AMP] remains relatively constant in the cell over short time frames" with no further explanation. I was under the impression that ATP was actively consumed in muscle tissue during intense activity (which is why lactic acid builds up in muscles: oxidative phosphorylation can't keep up with your rate of energy expenditure).

Thus, my question is Are my slides wrong? During muscle activity, is there a general lack or constancy of ATP?

Adenosine triphosphate (ATP) is often thought of as the energy currency of cells. It is not "used up" per se, but energy is released from the conversion of ATP to ADP (adenosine diphosphate), and yet more can be obtained by removing another phosphate to make AMP (adenosine monophosphate).

Here's a chemical schematic of ATP, you can see the three phosphates to the left.

Your slides state that the amount of (ATP + ADP + AMP) remains constant in the muscle, which makes sense because ATP is not used up, but converted to ADP. So as cells use energy, they do not actually reduce the total concentration of (ATP + ADP + AMP). Energy is required to add the phosphates back onto an ADP or AMP molecule - the process is called oxidative phosphorylation in cellular respiration (although this is not the only way).

I hope I didn't misunderstand your question.


Any food crops that could grow in a desert provided that they get fertilizer and water I am working on an idea to provide nearly unlimited amounts of water in desert regions. To make this commercially viable. I would use the water to irrigate desert sand and grow crops. Given my extremely limited understanding of biology, I cannot find an answer to the following question:
Are there any food crops (preferably high valuable/low maintenance ones), that can grow in a desert, given that I can just provide the seed, water and fertilizer and stop sandstorms.
My motivation for investigating this is the following map showing regions that are either already deserts or at risk of becoming deserts:

Source: http://en.wikipedia.org/wiki/Desertification

Even if you have unlimited water available to the plants you'd still have to worry about the high temperatures and light levels of these areas. In the hot periods I would look into any plant that uses c4 carbon fixation like millet, sorghum, corn, sugar cane... In the cooler periods maybe look into rotating to a cool season legume crop like the cowpea that would help fix nitrogen. Another really important thing to do would be to find cover crops that will hold down the soil and build up some life in the otherwise sterile sands of the desert.


Are we capable to generate sounds of animals to the point that they mistakenly recognize it as members of their species? From Animal language (Wikipedia), there are many evidences that we can communicate with animals, at least to baboons and dolphins. There is a case that fish moving away when hearing a record of whale sounds, however no examples mentions about the sound we actually make to communicate with them. We can even dog whistle, but this doesn't mean the dogs thinks that there is another dog. In my opinion, the answer is yes, since once we can capture the sound with spectrograms we can ultimately generate it. Is there any research on this?

The most clear and indisputable case of a human being generating a sound (using his own voice) that was mistakenly recognised by an animal as a sound made by a member of its own species is the case of Konrad Lorenz and the imprinting on birds.

Lorenz needs no introduction. However, in the case you don't know him, he is the father of modern ethology, together with Niko Tinbergen.

Among several other things, Lorenz studied and explained imprinting, specifically filial imprinting. According the Wikipedia link above:

  Lorenz demonstrated how incubator-hatched geese would imprint on the first suitable moving stimulus they saw within what he called a "critical period" between 13–16 hours shortly after hatching. For example, the goslings would imprint on Lorenz himself (to be more specific, on his wading boots), and he is often depicted being followed by a gaggle of geese who had imprinted on him.

For imprinting in an object (the mother), some species depend on movement that object makes, some depend on the sound it makes and some depend on a mix of movement and sound. From Brittanica:

  Lorenz demonstrated the phenomenon by appearing before newly hatched mallard ducklings and imitating a mother duck's quacking sounds, upon which the young birds regarded him as their mother and followed him accordingly. (emphasis mine)

During his life, Lorenz had several bird children, making several different youglings imprinting on him. As you can see in pictures like this one below, those animals will follow Lorenz (for the rest of their lives) as if Lorenz were their mother.

The funny thing is that, during some time after his early publications (but way before his Nobel Prize in 1973), some people had problems accepting Lorenz's discoveries, because they could not reproduce them.

It turned out that Lorenz was very effective in imprinting a lot of different bird species because of his uncanny ability of mimicking that bird species' sound, be it a goose, a chicken or a duck.

Of course, raising so many children has its problems:


How to bind antibodies to study their properties? I want to experimentally look at the behavior of antibodies. To do so, I need to be able to bind these antibodies to a substrate.
Eventually, I want to study the specificity of antibodies to know to what substrates they bind. After that, I want to study the biological activity of the antibody over time.
But my question is more basic, namely: to what material do antibodies bind non-specifically? It's not about antigens at this stage, it's just about non-specific binding of antibodies to a carrier material. Also of interest would be howw to get the antibodies of that carrier again.

Like any other protein, antibodies will aspecifically bind nitrocellulose or PVDF membranes, but any other protein present in your antibody preparation will also do.

Depending on the antibody class, more specific binding can be obtained with protein A or protein G, that recognize the Fc domain. It's usual to have protein A/G immobilized on a stationary phase like agarose.

If you know the antigen used to develop the antibody, you can also use the immunizing peptide crosslinked to CnBr activated sepharose as a probe to bind your antibodies.

Knowing something more about your antibody preparation and what exactly is the 'behavior' your want to study could help obtain better answers.


Do ants also use the Earth magnetic field? A lot of animals, specially birds use the Earth magnetic field to orientate on their flight across the Earth. Now some scientist suggest that ants has on their antenna a kind of magnetite crystals by which they also can use the magnetic field. But for what would and could an ant use this huge magnetic field, while they just walk for only meters a day?

Hard to say, but for at least one ant species (see below) it seems to be an orientation cue for (relatively short-distance) migration (even if you're only going a few meters, it can be important to walk in a straight line!). At present it seems we know something about the proximal mechanisms of magnetoreception, and a little bit about the observed behavioural patterns, but don't have much more than informed speculation about the ecological/evolutionary advantages of this form of spatial orientation.

Searching "ant magnetotaxis" gets to this article on magnetotaxis in the migratory ant Pachycondyla marginata:

  The influence of geomagnetic field changes on the behavior of ants has been studied in the species Solenopsis invicta (Anderson and Vander Meer, 1993), Formica rufa (Çamlitepe and Stradling, 1995), and Oecophylla smaragdina (Jander and Jander, 1998) ... Another migratory insect species is the ant Pachycondyla marginata, which has very peculiar habits: a diet of living termites and migration in a preferential direction (Leal and Oliveira, 1995). These habits make such a migratory ant very attractive for the study of biomineralized magnetic materials.

From Leal and Oliveira 1995 ref above:

  Migration by P. marginata colonies lasted over 2 days and covered distances of
  2-97 m (n=48).

Selections from Acosta-Avalos et al. 2001 Naturwissenschaften:

  abstract: Migrations during the dry/cold season are significantly oriented 13 degrees with the magnetic North-South axis, while rainy/hot migrations do not exhibit a preferred direction. This result is discussed considering the hypothesis that P. marginata ants may use the geomagnetic field as an orientation cue for migrations in the dry/cold season.

  Given that colonies resume nest relocation late
  in the afternoon of the second day, most of the migratory
  process takes place under darkness conditions.

  On  the  other  hand,  nest  relocations  in  the  dry/cold
  season can be considered as typical migrations.

  The  use  of  geomagnetic  cues  is  more  commonly  associated with darkness conditions, as reported for mole rats
  (Marhold et al. 1997) and also proposed for bumblebees
  (Chittka  et  al.  1999).  As
  P.  marginata
  ants  start  the
  migratory  process  in  the  afternoon,  they  can  use  any  of
  those  cues  in  their  orientation  during  the  migratory
  journey. However, it is intriguing that they prefer an axis
  around the North–South axis to migrate. The only possible
  cue  to  give  this  information  under  all  conditions  is  the
  one  provided  by  the  geomagnetic  field.


How can we know which alleles are together on a chromosome? This illustration says that if the two homozygotes pr+ pr+ vg+ vg+ and pr pr vg vg are crossed to produce a heterozygous offspring (pr+ pr vg+ vg), then:

this cross gives us exactly what we need to observe recombination: a
fly that's heterozygous for the purple and vestigial genes, in which
we know clearly which alleles are together on a single chromosome.

(My emphasis.)
Source: Khan Academy - Genetic Linkage & Mapping

I can't see the logic of this: surely if there were four chromosomes involved instead of two, wouldn't we get the same result via independent assortment?
In this scenario, the red-eyed, long-winged fly would have pr+ on chromosome 1, pr+ on chromosome 2, vg+ on chromosome 3 and vg+ on chromosome 4.
Conversely, the purple-eyed, vestigial-winged fly would have pr on chromosome 1, pr on chromosome 2, vg on chromosome 3 and vg on chromosome 4.
As the mother and father are both homozygotes (the mother for the dominant alleles and the father for the recessive alleles) the offspring couldn't fail to inherit pr+ and vg+ from the mother and pr and vg from the father, and the offspring would be the same as in the illustration.
I can't see how we can get any information as to whether genes are on the same chromosome or not from this crossing (unless we know they are on the same chromosome before we do the cross!).
I'm sure I've got my own logic wrong - can anyone enlighten me?

Your headline question:

How can we know which alleles are together on a chromosome?

is not quite the same as the question at the bottom of the body of your post:

how we can get any information as to whether genes are on the same chromosome or not from this crossing

These questions are different in two ways that matter: (1) the second question is asking about a single crossing, the one shown in the diagram, and (2) the second question asks about knowing if the genes are on the same chromosome or not, whereas the first asks if the genes (I presume, it says "alleles") are "together on a chromosome" (depending on how you take that phrase).
On difference (1): the single crossing in the diagram does not give information about distinguishing gene locations, but the Khan Academy page you got this from goes on to describe further crossings using the flies created in the first crossing, and those crossings can show information about gene locations.
On difference (2): I would take the genes being "together on a chromosome" to mean "linked to each other", that is close enough to each other on a single type of chromosome to tend to stay together during recombination events.  Maybe you meant "on the same chromosome", but that is, importantly, a different thing.  Recombination testing cannot tell you if genes are on the same or different chromosomes; it can only tell you if they are on the same chromosomes and are close enough together that recombination will not sort them randomly, but rather tend to sort them together.  If they are far apart, the genes will stay together or be separated by recombination with equal probability, which is the result that also happens when genes are on different chromosomes.
So, the full procedure that is described on the Khan Academy page will show how much recombination you get in the fly grand-offspring.  If you get few recombinant forms compared to the number of parental forms, then the genes are close together on the same chromosome.  If you get equal numbers of recombinant and parental forms, it indicates that is not the case, and therefore the genes are either on separate chromosomes or so far away on one chromosome that recombination has full effect and randomly separates them.


Why are some neurones unmyelinated? As far as I am aware, most of the central nervous system consists of myelinated axons and most of the peripheral consists of unmyelinated.

What is the reason for this?

Would it not be more efficient to have them all myelinated?

In this answer I'm building off of @Fizz's pointer to the nice paper by Laurence Knowles, "The Evolution of Myelin: Theories and Application to Human Disease" [1].

First -- I just want to point out that your question is adaptationist, which means that it assumes that myelin is on some axons and not on others for a reason. Whereas maybe evolution just hasn't gotten around to it yet, even though myelinating all axons would actually be beneficial.

That said, here are two of the main downsides of myelination:

It might cost energy. This one is a bit controversial, but at least one study has found [2] that while myelin decreases the energetic cost of firing an individual action potential, the whole apparatus involved in myelin (e.g., in the CNS, the oligodendrocyte, its processes, and the sheath itself) actually costs more energy than it would cost to just open all of those ion channels without saltatory conduction.
Myelin and its associated oligodendrocytes/Schwann cells take up space. This is likely to be especially important in areas of the nervous system where there are a lot of neurons packed into a small area.

So from the adaptationist perspective, the question is whether the benefits of myelinating an axon, such as increased conduction velocity, increased conduction fidelity, axon protection, and supplying the axon with nutrients, are worth the downsides of taking up space and possibly increasing net energy use.

http://www.ashdin.com/journals/JEM/235996
http://www.jneurosci.org/content/32/1/356


Does a blood transfusion cure disease? Does transferring blood between two people also transfer all the white blood cells?

Why can't AIDS victims with low t-cell count just get blood transfusions till they have more t-cells? Why can't someone who's over a cold give blood to someone with a cold to cure them? I know this is silly, but I really want to know why this won't work.

Not really no.  Most blood transfusions we think about are red blood cells or platelets, which don't have the immune function you're asking for.  That's a good thing.  Usually, if there are white blood cells in the transfused blood, the host's immune system will recognize them as foreign and destroy them.  Remember, your cells all look like foreign invaders to my cells; blood transfusions of red blood cells are carefully matched to limit negative reactions.  There is also a process called transfusion-associated graft versus host disease in which the donor white blood cells will attack the host cells; this mainly occurs in immune-compromised individuals, but GvHD is definitely something to avoid.  Blood transfusions are usually filtered and irradiated to remove, among other things, white blood cells.

That being said, people are beginning to use white blood cells as treatment.  A new therapy being studied heavily for all sorts of diseases, from cancer to HIV, is to take the hosts own white blood cells and grow them up in the lab to select for the strongest and most effective cells.  The researchers then wipe out the individual's immune system and give them a dose of their own, super-powered white blood cells, hoping that works.

Sometimes it kind of does.  They've also been trying a new system, similar to what you propose, using bone marrow.  They had a huge success with an HIV-positive individual now referred to as "the Berlin patient."  They gave him a marrow transfusion which would produce HIV-immune white blood cells and replaced his immune system.  He was and is effectively cured of HIV/AIDS.


Linear and Circular DNA So school has taught us that eukaryotes have DNA that is linear and inside of a membrane - called the nucleus. And that prokaryotes have circular DNA that is free floating inside of the cell.

We also know the pros and cons of both linear and circular DNA.

Are there organisms with circular DNA that also have a cell nucleus?
Are there organisms with linear DNA that is also free-floating within the cell?

Strictly speaking, all nucleated (eukaryotic) cells contain linear DNA. In addition to the nucleus, the mitochondria (which break down food molecules and create chemical energy) and chloroplasts (which facilitate photosynthesis) also have small stores of their own DNA and this DNA is circular. This adds weight to the hypothesis that these organelles were once prokaryotic cells that came to exist in symbiosis with early eukaryotes.

There is also cytoplasmic DNA free-floating in eukaryotic cells. These are also circular and normally contain short copies of chromosomal DNA sequences. Their function is not well understood.

In prokaryotes, some species of spirochaetes and bacteria have been found with linear chromosomes. In addition, prokayrotes contain extra-chromosomal DNA called plasmids. Bacteria are able to pass plasmids from one to another and express the genes on them: this is an important source of the spread of antibiotic resistance genes through bacterial populations. Plasmids are also normally circular, but linear structures also exist.

References:

Cohen, Sarit; Andreas Houben; Daniel Segal (2008). "Extrachromosomal circular DNA derived from tandemly repeated genomic sequences in plants". The Plant Journal 53 (6): 1027–1034.
Hinnebusch J; Tilly K (1993). "Linear plasmids and chromosomes in bacteria". Molecular Microbiology. 10(5):917-22
Finbarr Hayes (2003). "Chapter 1 - The Function and Organization of Plasmids".


What is the evolutionary reason behind the fragility of teeth? Almost all organs in the human body have a rather large threshold within which the organ or tissue is capable of repairing itself using materials supplied by the body, whether it's made from organic tissue or structural proteins. Wounds and minor damage to the skin or flesh for example heal by themselves, skin, nails and body hair can grow back if damaged or removed, even most bones can be repaired autonomously by a biological body. Cutting off a significant chunk from the human flesh or removing over 90% of a hair or a nail would cause no permanent injury, and the body is capable of repairing the damage over time with ease. The vast majority of the human body (not counting critical organs such as the heart or the brain) can be "grown back" to an extent by itself, because such parts have a rather large damage threshold.

On the contrary, teeth do not. There is a certain threshold in which tooth enamel can be supplied and "repaired" by the body to an minimal degree, but past that point virtually any damage caused to teeth are permanently irreparable by natural means. Which is quite strange, given how fragile a set of human teeth is, be it chemical or physical damage. Especially if you take more "artificial" causes into account. A moderately heavy object aimed towards a human mouth, for example, can easily render ten to fifteen teeth permanently damaged past the point of recovery within a heartbeat, also causing the said person's digestive process to be heavily impaired.

Another strange fact worth noting, is that the human body is capable of producing two separate set of teeth due to biological growth and size differences, but not more than that. Wouldn't it be beneficial for a biological body to be able to supply new teeth in the place of ones that have been damaged or removed? One could argue that such an action would be too complex and impossible, similarly to growing back an entire limb or a spare heart, but given the material that makes up teeth and its fragile nature, it would be safe to assume that it is biologically possible, especially given the fact that the human body DOES produce two separate set of teeth over its lifespan.

However, even stranger still, is that the only element capable of damaging or deteriorating  teeth by natural means, is the consumed food itself, and the acidic bacteria found within. Several types of edible food consumable by human means are capable of damaging the enamel to critical levels within relatively short periods of time, even non-artificial ones. What happened before the invention of the toothbrush and various dental cleaning methods? Why haven't humans evolved in the past tens of thousands of years to the point where repairing or regrowing teeth by natural means is feasible? Simply put, why don't teeth grow back contrary to hair, nails or skin?

What is the biological and evolutionary reason behind teeth being so fragile and indisposable?

The evolutionary biologist in me would argue that, on average, teeth are exactly as strong as they need to be. In other words, the fitness cost of producing and maintaining teeth is balanced with the the fitness benefits of having teeth.

To address your questions from an evolutionary lens:

Why haven't humans evolved in the past tens of thousands of years to the point where repairing or regrowing teeth by natural means is feasible? Simply put, why don't teeth grow back contrary to hair, nails or skin?

The short answer is that we have evolved the ability to regrow teeth. That's why you lost your baby teeth and a new set grew in their place. And why most folks have wisdom teeth that grow in later in life.
Essentially, we only need enough functional teeth to get us to the point of reproduction. After that, the effects of selection for stronger, more, better teeth wanes.

You may find this review article1 helpful wherein the authors explore the evolution of teeth, and specifically health issues related to teeth from an evolutionary perspective.

[1] Koussoulakou et al. (2009) A curriculum vitae of teeth: evolution, generation, regeneration. Int J Biol Sci; 5(3): 266-243.


What is it that creates that wonderful smell after a fresh rain? I've heard that the wonderful smell of a fresh rain is actually chemicals  released from the trees and grass and other plants.

What is the process that allows these chemicals to be released?
What are the chemicals that create that smell?
How is it advantageous for the plant to release the chemicals rather than hold onto them?

That molecule is called Geosmin. It is mainly produced 1 by Actinomycetes such as Streptomyces which are filamentous bacteria that live in soil. Other organisms also produce geosmin:

Cyanobacteria
Certain fungi
An amoeba called Vanella
A liverwort

It is an intracellular metabolite and cell damage is the primary reason attributed to its release. However oxidant exposure and transmembrane pressure also causes geosmin release in cyanobacteria. It seems that the release is triggered by some kind of stress.

I am not quite sure about their advantage to the host species.

1 or perhaps the most well-studied in


How can two biological sequences be anything but homologous? If we consider homology between two nucleotide sequences as a yes/no answer to whether they have shared a common ancestral sequence, then given that all life share common ancestry and sequences are carried by living things, then how can two biological sequences be anything but homologous?

One possibility I can think of is perhaps natural transformation in bacterial---but even so, the DNA sequences picked up must have come from a biological source.

(I assume that it must be possible that there are sequences that are non-homologous, because otherwise there wouldn't be a need to point out which things are homologous, i.e. I assume that the concept of sequence homology would not be as widely used as it is right now)

There has been some discussion on my claim that homology should take a Boolean value. As I have stated in the comments, for this I refer to Inkpen, S.A. & Doolittle, W.F. J's "Molecular Phylogenetics and the Perennial Problem of Homology" in Mol Evol (2016), pp. 187.

  Nevertheless, there is a general understanding that conflating the extent of similarity and the inference of common descent is always a misuse of the concept—that there can be no such thing as ‘‘percent homology.’

Homology in this context is always a matter of degree exactly because of shared ancestry. Measures of homology are often in terms of "percent homology" (or more often "percent similarity" as evidence of homology) or some other measure that allows representation of that degree.

To emphasize why this makes sense, think about a receptor family. In an extant organism, you might have 3 receptors that all are homologous. However, if receptors 2 and 3 are more similar to each other than to receptor 1, then you can make some better assumptions about the history of the evolution of receptors 1 to 3, that there is likely a "common ancestor receptor" to both 2 and 3. There is more "information" if you consider the degree of homology rather than just its existence.

At some extremes, sequences could be so different that even if they share a lineage they may have now diverged to the point that they are not distinguishable from independent sequences. However, selective pressures prevent such complete reorganization in key sequences and so at least some homology can be maintained across very distantly related organisms.

As far as deciding what is "homologous" versus "not homologous", that is somewhat of an arbitrary threshold that depends on levels of evidence and the purpose for recognizing the homology.


Lizard species identification I managed to photograph a lizard in Haruvit Forest, Israel. I would like to know - what lizard species is this? Size appr. 20-25cm

This lizard is likely a Roughtail Rock Agama (Stellagama stellio or Laudakia stellio). They are colloquially referred to as hardon (or hardun) lizards.

According to Wikipedia:

  Like many agamids, stellions can change color to express their moods. They bask on stone walls, rocks, and trees. They are usually found in rocky habitats, and are quite shy, being very ready to dive into cracks to hide from potential predators.

More from natureisreal:

  The most commonly seen local lizard where I live in central Israel is probably the roughtail rock agama (laudakia stellio stellio), known locally as a hardon or hardun. They are rather sinister looking with rough dark armoured skin, but perfectly harmless. If frightened they run away and hide in the crevice of a rock or tree, inflating their skin and opening their mouth wide to wedge themsevles into the space, making it impossible to dislodge them. Sometimes I see a large dark male surveying his territory from the top of the nearby water tower.More usually they are to be seen during the warmest times of day sunning themselves on rocks, to the extent that it seems that each rocks has its own resident hardon, and believe me, this country is full of rocks, and that makes for a lot of these lizards...


How does a tiny spider interpret/cope with gravity? The Question:

Does a tiny spider know that it is walking on a wall or a ceiling as opposed to the (horizontal) ground? Does gravity play a role in this knowledge?

Further thoughts:

I am interested in how other organisms sense gravity, and how they are affected by it. I have read how gravity played an important role in the physical evolution of all animals, but am interested in how the animals perceive gravity, and to what extent they are aware of/affected by it.

Can you point me to any research in this area?

The following is an excerpt from work of the German Aerospace Center, showing how the orientation of a fish is guided via a mixture of gravity and light:

Your question's title ("Sense of gravity felt by other organisms" - edited since it was originally posted) is quite broad, since "other animals" is all Animalia except Homo sapiens, which gives us at least 1 million species...

Therefore, I'm going to answer only your "The Question", regarding spiders:

  How does a tiny spider senses gravity?

First, it's worth noticing that while the gravitational acceleration is a constant (at sea level), the weight of the organism depends on its mass. Thus, for tiny animals, the effects of the gravitational force can be extremely small, and because of that those animals require very precise sensitive structures in order to measure the gravity.

Aquatic invertebrates have statocysts and statoliths, which are well known. However, spiders use another method to perceive gravity: they use their sensorial "hairs". According to Bender and Frye (2009):

  In the absence of wind, an animal standing at rest is acted upon only by the force of gravity. An animal might not explicitly calculate the global gravitational vector per se, but rather may actively modulate local joint angles and torques to implicitly compensate for gravity's pull. In many instances, insects and crustaceans measure the angles of their appendages' joints using clusters of mechanosensitive hairs, called hair plates.

According to Seyfarth, Gnatzy and Hammer (1990), one of these organs is the coxal hair plate:

  Natural stimulus situation and the spike response to maintained deflection suggest that these hairs are used in proprioception and graviception.

Here is an image:

However, the same authors say:

  Yet behavioral changes following selective hair-plate ablations are not very pronounced. Unilateral removal of hair-plates produced significant increases in average body height in 7 of 10 animals, while the angular orientation of the long body axis with respect to gravity remained unchanged after hair-plate removal.

That means that another sensors may play a role in graviception, such as proprioceptors. Still according to Bender and Frye (2009):

  In addition to measuring joint position, invertebrates also have specializations for measuring joint load. Whereas our bones have no active sensory capacity and instead our sensors are imbedded in surrounding, soft tissues, many invertebrates are equipped with sensory arrays embedded in the exoskeleton at strategic points and with specific orientations. Called campaniform sensilla in insects, lyriform organs in arachnids and centipedes. (emphasis mine)

Sources:

Bender, J. and Frye, M. (2009). Invertebrate solutions for sensing gravity. Current Biology, 19(5), pp.R186-R190.
Seyfarth, E., Gnatzy, W. and Hammer, K. (1990). Coxal hair plates in spiders: physiology, fine structure, and specific central projections. Journal of Comparative Physiology A, 166(5).


Protein binds to DNA and just stays there, what will happen next? If I hypothetically make an inactive version of Cas9 or ZFN (that will bind to the DNA but does not apply the cleavage reaction). What will happen after the protein bound to DNA? Will it be stuck in there forever and disrupt the transcription/translation process? Or will it be self-unbound after a while?

All binding reactions are reversible. The binding and unbinding (association and dissociation) are usually in equilibrium. How much of the protein is bound to the DNA and how much time a single molecule spends in the bound state depends on the kinetic parameters. In case of the non-catalytic Cas, the protein may inhibit transcription if it is bound at the promoter. In fact, such inactive variants have been developed and used for targeted inhibition of transcription (Himeda et al., 2015).

If the CRISPR-Cas is blocking a binding site for a transcriptional activator, then the degree of inhibition would depend on the competition between the activator and the CRISPR-Cas-inhibitor for the binding sites. This competition would be dependent on the kinetic parameters as well as the concentration of the competing species.

Similarly, you can design proteins/RNAs that can bind to mRNAs (at RBS in prokaryotes or Kozak sequences in eukaryotes) and inhibit translation.

Another interesting fact: CRISPR-Cas system has been engineered to work like transcriptional activator, as well (Didovyk et al., 2016).


Is it true to say that the more an organism is smaller, the faster it's going through evolution? As someone who never formally learned biology, I assume that currently;

The number of species of (non Archaea) Bacteria
The number of species of Algae
The number of species of Plankton
The number of species of Bivalvia
The number of species of Poaceae
The number of species of flowers
The number of species of mushrooms
and of many other sets of species

Are all vast (from hundreds to tens)

Is it true to say that the more an organism is smaller, the faster it's going through evolution (hence, is generally more genetically varied)?

I think that you are talking about what are sometimes called "rates of evolution", see also https://www.thenakedscientists.com/articles/questions/do-smaller-organisms-evolve-faster. That wiki is a collection of info of interest mostly to specialists, but the blog post may be helpful.

The short answer is that there is a strong negative correlation between mass of an individual organism and rate of evolution, in terms of years or whatever. But there is not necessarily a causal relationship there.

People can argue that there is such a causal relationship, because the life cycles of small organisms are shorter, and more generations means more mutations, which means more evolution is possible. In the classic example, E. coli reproduces every 30 minutes under good conditions, whereas humans reproduce every 30 years. This is sometimes true but not always.

Alternately, there are bacteria such as Micrococcus that are smaller than E. coli but divide more slowly, and by this same logic must therefore be evolving more slowly than the larger bacteria. So there's a lot of variation.

As another counterexample, bacterial cells can form spores that undergo stasis for tens of thousands of years, then wake up under better conditions and go about their life. During that time, elephants are evolving much faster than the bacterial spores- even though outside of that time the bacteria are dramatically faster.

Another confounding issue is that the different groups you name are of dramatically different ages. Bacteria are probably ~4 billion years old, and have had tons of time to diversify. Even if they had the same evolutionary rate as elephants, you would still expect more species in bacteria than you would in flowering plants, which are ~200 million years old. So measuring evolutionary rate in terms of "number of species" is quite misleading.

Yet another issue is that evolution may not happen at a constant rate. This is a normal assumption people make because it makes life simpler, but there is a certain amount of data that suggests that a lot of large evolutionary changes happen very quickly, and then there are periods of relative stasis; this is sometimes called "punctuated equilibrium" or "saltation". An example of this is the so-called Cambrian Explosion. So even though one group A may have gone through 1/2 the generations of group B in a unit of time, it may have gone through 10X the "evolution" in terms of changes to body shape/other characters.

So, it's complicated, and there's a large field of research in evolutionary biology that is trying to answer these kinds of questions. Your assumption is broadly correct in terms of agreement with the data, but it's not clear that smallness per se is what makes evolution happen more quickly.


Maximum biologically possible age for a human being? Today, most of people die because of some kind of illness that we do not yet have a cure for. However, if that was not the case, how long can human body possibly live for? Is there a theoretical maximum at which our brain will simply refuse to function due to age alone, or can we remain conscious forever if we could simply swap our brains into new bodies without any risk?

Even in perfect environmental conditions we would age. Living is associated with a myriad of deleterious processes, both random and deterministic, which are caused by imperfectness, exhibit cumulative properties, and represent the indirect effects of biological functions at all levels, from simple molecules to systems. Here is a good read on this topic https://www.ncbi.nlm.nih.gov/pubmed/27060562

Even if nothing else was wrong (which is not the case) the accumulation of intracellular and extracellular junk which our systems are unable to dispose of (lipofuscin, amyloid beta, etc) would eventually kill us. https://en.wikipedia.org/wiki/Senile_plaques

As for the maximum age - nobody we know of made it past 125 years yet. https://en.wikipedia.org/wiki/List_of_the_verified_oldest_people


Do repetitive movements on EEGs show up as discernible patterns? Here is a typical EEG reading:

(source: frontalcortex.com)
If I am connected to an EEG, and am sitting perfectly still, and then begin doing some repetitive motion, say, 10,000 times, will we see discernible patterns emerge in the output?
In other words, would it be possible to categorize a particular pattern in the output and say "Waves with this signature correspond to the subject wiggling his left pinky"?
I would imagine that, over time (and many trials) wave patterns converge to predictable signatures for a given movement.

Specific events, e.g. finger flexions, generate synchronized neuronal responses in the brain that can be measured on the scalp with EEG. However, a voltage response to a single event typically generates a low-amplitude response relative to the background EEG. One way to enhance the signal-to-noise ratio is to repeatedly record the EEG in response to the same event. By time-locking the event with the EEG and averaging the individual event-related EEGs, the random background noise will be reduced (stochastic noise) and the event-related potential (or ERP) can be extracted from the EEG (Woodman, 2010). An example of an ERP to repeated index finger flexions is shown in Fig. 1. Such a wave doesn't need 10,000 repeats. 25 may be sufficient.

If you characterize this ERP and determine specific features of it (duration, amplitude, latency after event etc.) you can generate algorithms that detect these features in the raw EEG, without the need to do repeated measures. In fact, thinking of a motor movement (e.g. grasp that coffee mug) generates very similar EEG activity as the factual act of grasping that mug. By recording the ERPs using events like think of grasping that coffee mug from a person missing a hand, and subsequently designing the necessary algorithms to detect that waveform near-realtime in the person's EEG, one can design brain-computer interfaces to control prosthetic limbs (Guger & Pfurtscheller, 2016).

Fig. 1. ERP to voluntary index finger flexions. Motor activity was recorded from the motor area. Source: Ball et al. (1999)

References
- Ball et al. NeuroImage (1999); 10: 682–94
- Guger & Pfurtscheller, AAATE 5th European Conference Advancement of Assistive Technology (2016)
- Woodman, Atten Percept Psychophys (2010); 72(8): 10.3758


Why is there low hepcidin levels in hemochromatosis? If hemochromatosis is iron overload and there is excess iron in the blood, why does the liver reduce hepcidin secretion (which increases the iron uptake) furthering the worsening of hemochromatosis?

From what I remember it all depends on which type of hemochromatosis we are talking about. There are several types depending on the cause and some of those like the hemojuvelin gene mutation-related have low levels of hepcidin as the CAUSE of the hemochromatosis (since like you mentioned, seeing it as a consequence wouldn't make much sense)
The first 4 pages of this paper should clear things up a little bit https://www.aasld.org/sites/default/files/guideline_documents/Hemochromatosis2011.pdf


The reason why researchers usually use cell lines from "blast cells"? What's the reason why researchers usually use cell lines from "blast cells" (so, immature, like lymphoblastoid cells) for measuring gene expression data? Is that they are growing up, which would make their expression data higher and more significant?

Some of the reasons why immature blast cells are studied:

They have self renewal ability
Can be differentiated to different types of cells
Serve as model for studying development: this is quite pertinent to the gene expression studies. Because it is important to know what changes take place during differentiation and simply looking at the differentiated state won't explain that process.


Clarification regarding a statement in "The Selfish Gene" by Richard Dawkins In the third chapter of The Selfish Gene: Immortal coils, Dr.Dawkins makes the following statement while arguing for the case that ultimately "the gene" as he defines it is the unit of natural selection.

  Natural selection in its most general form means the differential
  survival of entities. Some entities live and others die but, in order for
  this selective death to have any impact on the world, an additional
  condition must be met. Each entity must exist in the form of lots of
  copies, and at least some of the entities must be potentially capable of
  surviving—in the form of copies—for a significant period of evolutionary time. Small genetic units have these properties: individuals,
  groups, and species do not.

I am not sure what "impact on the world" he is talking about. Could someone explain this? He then goes on to say..

  An individual body seems discrete enough while it lasts, but alas,
  how long is that? Each individual is unique. You cannot get evolution
  by selecting between entities when there is only one copy of each entity!

Whereas in his other book, The Blind Watchmaker, he describes a computer drawing program EVOLUTION where he does precisely that, i.e, select between entities (here, computer drawn insect-like figures) of which there is only one copy and allows them to evolve. This seems contradictory to his above statement in The Selfish Gene. Could somebody explain?

tl,dr: Why must there be many copies of entities that are being selected for evolution to be possible?

"Impact on the world" is just his writing style.  Dawkins means "evolutionary significance".  For example, all the intermediate forms leading up to the modern horse have been evolutionarily significant because they contributed to survival of the lines of descent that are still present.  Any tiny evolutionary branch that dies out would have little significance or impact.

In the first part of your second question, the answer is again Dawkins' writing style plus the fact that he's writing for popular consumption.  And, his own thoughts have a way of evolving just as they should; so we shouldn't expect perfect consistency between what is said between sequentially written books.  The Blind Watchmaker was written to convince people that evolution can produce complex organisms without any pre-existing goal to do so, using a relatively simple process.  The Selfish Gene was written to promote his idea that the unit of evolution is the gene. (Note that his idea is not necessarily correct.)

In the second part of your second question you ask:Why must there be many copies of entities that are being selected for evolution to be possible?.  The answer to this is that it is NOT necessary.  It's simply a much more easily implemented - and generally better- evolutionary strategy.  If there is only one organism, and selection means killing it if it is unable to adapt to a given environmental change, then failure to adapt puts an end to it and all its possibilities.  If, on the other hand, that one organism produces a series of single copies (offspring) and each of them has some random genetic variation that's subjected to selection, there's a chance that some will make it past the selection process.  That's equivalent to the one organism producing a lot of offspring at the same time, each with its own genetic differences.

This is a slightly SiFi perspective on the above, but: In general, it's a lot safer to test a disposable copy of oneself against a new danger, than to test oneself directly.  If the copy passes the test, it's safe to face the danger directly.  If the copy fails, then you can test a slightly modified version of yourself against the danger.  If that modified copy passes, then if you're able to do so, you could make the same modifications to yourself and go face the danger.  However, there are now two identical new modified copies of you.  One of you is superfluous, so you flip a coin to decide which survives.

In the SiFi scenario, we have one organism evolving safely up one possible branch of an evolutionary tree.  But if that organism reaches a dead end from which there is no escape, its branch dies.  On the other hand if all the other branches are allowed to continue (that is, if you let both copies survive and evolve independently), there's a far better chance at least one branch will still be growing and branching far in the future.

I personally think Dawkins "Selfish Gene" idea fails when we try to fit it into that picture.


Can a human being live without any carbohydrates? Nowadays low-carb is in fashion, but what I recently wondered is whether a human can live without any carbohydrates at all?

Of course this would be hard to do in reality, as most food will contain proteins as well as carbohydrates, but let's assume it would be possible to circumvent any carbohydrates.

The Atkins diet is based on that. Without carb intake, however, the citric acid cycle (CAC) eventually basically stops and proteins will be utilized to be converted to carb intermediates to feed the CAC. Progressive and strict use of the Atkins diet will eventually kill you as the CAC is essential to life.

The idea behind Atkins is that fats will be used to feed the CAC, and that will happen until the carbohydrates that keep the cycle running are depleted. At that point one will develop ketosis and the CAC stops, and with it the production of ATP. Note that fatty acids can be fed into the CAC, but are not sufficient to keep it running; fats burn on a fire of carbs.


What is head of a bone? For most of the long bones head is the proximal end, but for metacarpals and Ulna, head is the distal end. Why are their distal ends called as heads?

What's the criteria for calling an end as head end?

Here is a head and a neck:

Anatomy is fairly straightforward. regarding individual long bones, "heads" are curved ends of bones distal to a narrowing called a neck of a bone. Take the radius:

See how the radial head (curved) is just distal to a narrowing (neck)?

The ulnar head, though, is at the opposite end, because the proximal end isn't rounded, but the distal end is.

Metacarpal heads are distal (see blue area):

The humeral head is probably most obvious:

So, the head of a long bone is not determined by the position (it can be proximal or distal) but by the contiguous shapes.


Is there a maximum size for an insect? I have read in biology text-books that one of the most important constraints on the size of an insect happens to be the importance of the surface-volume ratio. It simply states that
if we assume constant oxygen levels and increase the size of an insect there would be a point where the insect's exoskeleton would no longer be able to support its weight.

Some textbooks go on to say that this is why we don't have insects the size of elephants. But, if this is true...is there a least upper-bound on the maximal body mass of an insect?

I assume there must be a maximum size for insects, and I atmospheric oxygen probably has something to do with it. Insects do not breath like vertebrates, they have a series of tubes call trachea that run through their bodies and open to the surface at spiracles. Air passes through these tubes and oxygen and CO2 passively diffuse through the tissues. Insects can force air through the trachea to increase the diffusion rate, but they just aren't as efficient as vertebrates with lungs and hemoglobin to carry oxygen around the body.

In the past, oxygen levels were much higher. Higher amounts of oxygen could allow for larger invertebrates, and there were 6 foot long millipedes and giant dragonflies. Their size probably was not entirely caused by the extra oxygen, this was before they faced competition from vertebrates, so increased competition probably had more to do with their size reduction than loss of oxygen.

I don't know what the maximum size for an insect is at modern oxygen levels, but you'd have to eliminate the other selective pressures such as competition and limits on food before an insect could reach that size.


Sewall Wright for dunces [This is one more post in my growing "X for dummies/idiots/morons/etc." series.]

I've been enjoying Provine's The origins of theoretical population genetics for the last couple of days, but I must confess that I find his description (on pp 127-8) of the logic behind Sewall Wright's (and W. Castle's) selection experiments with "hooded rats" about as clear as if it had been chiseled in Linear A...

Which is really bumming me out, because I'd love to understand these experiments.

Does anyone know where I can find a description of these experiments aimed at those with only a very limited grasp of classical genetics?  (I took a graduate-level genetics class a billion years ago, and I did not find it easy.)

I don't have access to Provine's book, and I can't describe the details of the hooded rat experiments, but here is an attempt to explain the importance of the work.

Darwin published “Origin of Species” in 1859. He proposed that modern species were all descended from ancestral species, and that evolution proceeded by natural selection. He believed that evolution proceeded gradually by an accretion of small changes (gradualism). The origins of hereditary change were, of course, unknown to Darwin.

Mendel’s work (published in 1865) was rediscovered in 1900, and gave rise to a school of thought referred to as mutationism.  Mutationist theories emphasised the importance of single factor changes with large effects, and placed these “leaps forward” at the centre of the mechanism for the generation of new species. This was in contrast to the biometricians who argued, in the Darwinian tradition, that natural selection acted on populations in which there was continuous variation. Extreme mutationists believed that continuous variation within a species had no relevance to the evolution of new species. Their view was that within a species most genes were fixed (100% wild-type allele), and that only mutations could create new species (‘hopeful monsters’). T.H. Morgan, for example, was a strong proponent of the mutationist theory, so this wasn't some minor controversy.

Sewall Wright joined the laboratory of W.E.Castle as an assistant in 1912, when he was 23. Starting with black and white hooded rats (white rats with black ‘hoods’) they instigated breeding programmes and showed that they could progress gradually, through a number of generations, towards all white or all black rats. The importance of this work was that it demonstrated that there was underlying genetic variation within this strain of rats that could be acted upon by selection (selective breeding) resulting in  gradual changes in coat colour. This provided strong evidence for the gradualist school.

By the 1930s the modern synthesis began to emerge, which combined mutationist and gradualist ideas: natural selection acts upon populations (gene frequencies etc.) but mutation provides the raw material that creates new variations in the population. Key to the acceptance of the modern synthesis was the development of a mathematical treatment of population genetics. This led to the current view of phenotypic  traits influenced by multiple loci, with natural populations harbouring genetic variability which can be acted upon by selective forces. We have all accepted this and so of course it is difficult to think ourselves into the controversies that existed in genetics at the beginning of the twentieth century.

Here is an article in which Sewall Wright refers briefly to his work with Castle, placing it in historical context. It also describes subsequent work with guinea pigs. This is a quotation from the article which underscores what I have written:

  From assisting Prof. Castle, I learned at firsthand the efficacy of mass selection in changing permanently a character subject merely to quantitative variability. Because of this and a distaste for miracles in science, I started with full acceptance of Darwin's contention that evolution depends mainly on quantitative variability rather than on favorable major mutations. Thus, I have assumed that species are typically heteroallelic in tens of thousands of loci in which the leading alleles differ only slightly in effect, a situation that is maintained in a continually shifting state of near-equilibrium by the opposing pressures of recurrent mutation, diffusion and weak selection. Only a few loci at any time can show fairly rapid changes in allelic frequencies from strong selection.


Non-Salticidae with °oo° Eye Arrangements Since childhood, I've always thought of the °oo° pattern of four frontmost eyes as iconic for spiders (note: the pattern does not account for any additional eyes or lack thereof further to the sides or back; also, title font seems to make the °'s relatively smaller than the main text's font does - this was not intentional). And yet taking a look at a couple of eye-based family identification tables, it seems that the above pattern is the go-to sign of a jumping spider.

Is this pattern unique to salticidae, or are there other groups of spiders with the four foremost eyes matching such a pattern (either four equal-sized eyes, or the secondary ones slightly smaller)? If the latter, what groups sport a similar look?

It is pretty much unique to salticidae, although I did find some similar eye arrangements in sicariids and scytodids.

Salticidae:

Sicariidae:

Scytodidae:

Image source


How do fairy rings propagate? It was somewhat new to me that mushrooms usually aren't individual organisms, but are merely the visible bodies of a bunch of fungi living in the soil. I know that mushrooms emit spores to reproduce, but what has been bizarre to me is how fairy rings form. Why do the fruiting bodies arrange themselves in a more or less circular shape, as opposed to the random scattering one would expect from wind-borne spores?

When a fungal spore germinates in a suitable location, the growing mycelium will spread underground in all directions. In the ideal situation, the result is that the mycelium will become circular. Over time, the center of the mycelium will die out whereas the newly formed mycelium (underground) will develop the familiar mushrooms above ground and this will result in a fairy ring.


Can a color-blind person see color with filter glasses? Why does color vision improve in color-blind persons using these filter glasses from Enchroma? Will a color blind person be able to see the same colors on a television? I'm asking, because the colors for every point on a TV screen are combinations of red, blue and green.

Short answer
Optical filters can optimize color contrast, but never restore color blindness. Filters remove colors, they can never add something. However, glasses like this can prove helpful for certain sub-populations of people that are partially color blind.

Background
First, the term color blindness is deceptive. It is better to talk about colour vision deficiency (CVD). This, because many people labeled as color blind in fact have all the red, green and blue cones like the normally-sighted. These people have protanomaly (abnormal, but still functional red cone photopigment), or deuteranomaly (abnormal green cone photopigment). These two conditions are mild and don't affect daily life too much (source: NEI / NIH).

The other two most common forms of CVD are protanopia and deuteranopia. Protanopes have no working red cone cells and deuteranopes have no green cones. These conditions are more severe and do affect daily life as color perception is compromised. These conditions can be coined color-blindness, as these folks miss one type of cone altogether (source: NEI / NIH).

The glasses of Enchroma target the first two conditions, namely the anomalies and not protanopia or deuteronopia. The Technology page of Enchroma explains why. Basically, protanomaly and deuteranomaly are characterized by the red and green pigments having a shifted spectral maxima. The end result is the same, namely more overlap between the spectral absorbance curves (shown for deuteranopia in Fig. 1). In normal vision, the overlap is already pretty extensive, meaning that green light activates a large portion of red cones and vice versa. In protanopia or deuteronopia this effect is further increased, resulting in a degraded capability to separate reds and grees. For example, protanopes perceive reds, oranges, and yellows as greener, and colors are not as bright. Deuteranopes perceive yellows and greens as more red and they have difficulty telling violet from blue (source: NEI / NIH).

Fig. 1. Left: normal cone spectral distribution vision, right: cone distribution in Deuteranopes. source: Enchroma

What Enchroma has come up with is actually really clever (!) - they've put a spectral notch filter in place and wedge it in-between the red and green spectral optima, thereby removing the large area of overlap. This reduces brightness, but it will enhance contrast when the glasses are worn (Fig. 2).

Fig. 2. Spectral notch filter to enhance green-red color contrast. source: Enchroma

And yes, above considerations hold for any colored object, including monitor pixels.


Defining dominance and selection in these formulae This paper uses two equations to explain the different conditions under which sexually antagonistic genetic variance is maintained in a population, while allowing for unequal dominance, for autosomally linked loci:

$h_f / 1-h_m + h_fs_f   <$ $ $ $   s_m/s_f   <  1-h_f/h_m(1-s_f)$

And X-chromosome linked (X-linked) loci:

$2 h_f / 1+h_f s_f < $ $ $ $ s_m/s_f < $ $ $ $2(1-h_f)/1-h_f s_f$

where $s_m$ and $s_f$ are the selection coffecients against the less fit homozygote (or hemizygote) in males and females respectively where the most fit genotype has a relative fitness of 1. Similarly $h_m$ and $h_f$ represent the dominance of the less fit allele in males and females, and $h_m$ is not applicable in the X-linked equation because there is no dominance (due to hemizygosity it can only be homozygote).

I'm having a little trouble understanding how $s$ and $h$ are defined here.

For $s$, is it the fitness of the deleterious homozygote or the difference in relative fitness between the two homozygotes? Such that either $s$ = the relative fitness of the homozygote, or, $s$ = 1 - relative fitness of deleterious homozygote, where one represents the fitness of the fittest homozygote thus giving the fitness differential.

For $h$, is the dominance defined as the fitness difference between the less-fit homozygote and the heterozygote, or the most-fit homozygote and the heterozygote? Or is it the deviation from the average fitness of the two homozygotes?

Going from the graph (see below for values of fitnesses), what are the values of $s_m$, $s_f$, $h_m$, and $h_f$ where the dashed line is Females and solid line is Males. I see possible values of either $s_m$ = 0.2 or 0.8 (fittest genotype - fitness of weakest), likewise $s_f$ is either 0.3 or 0.7, $h_m$ is either 0.1 (deviation from most-fit genotype), 0.7 (deviation from least-fit) , or 0.3 (deviation from average) and $h_f$ is either 0.3, 0.4, or 0.05.

The values here are, as fitnesses for genotypes A1A1, A1A2, and A2A2, for males, 1.0, 0.9, 0.2, and for females 0.3, 0.7, 1.0.

Fry (2010) borrowed his variables from Kidwell et al. (1977).  Kidwell defines the fitness of each genotype as,

$w_{m1}$, $w_{f1}$ = male and female fitness of the A$_1$A$_1$ genotype.

$w_{m2}$, $w_{f2}$ = male and female fitness of the A$_1$A$_2$ genotype.

$w_{m3}$, $w_{f3}$ = male and female fitness of the A$_2$A$_2$ genotype.

Kidwell then establishes the following parameters for each fitness variable for opposing additive selection,

$w_{m1} = w_{f3} = 1$,

$w_{m2} = 1-.5s_m$,

$w_{f2} = 1-.5s_f$,

$w_{m3} = 1-s_m$, and

$w_{f1} = 1-s_f$.

Therefore,

$s_m = 1-w_{m3}$, and

$s_f = 1-w_{f1}$.

$s_m$ and $s_f$ are the relative fitness differences between the two homozygous genotypes of each gender. The heterozygotes are assumed to have half of that differential. This is what Fry refers to on page 2 (page 1511 of the publication):

  In Kidwell et al.’s notation ... the most fit genotype in a given sex has a relative fitness of 1, and $s_m$ and $s_f$ are the selection coefficients against the less-fit homozygote (or hemizygote) in males and females, respectively.

For opposing selection with arbitrary dominance, Kidwell parameterizes the heterozygous fitness components as

$w_{m2} = 1-h_ms_m$, and

$w_{f2} = 1-h_fs_f$.

Notice that $h$ is modifying the fitness difference $s$ in the heterozygotes. This is due to incomplete dominance of one allele over the other. If both alleles in a heterozygote contribute equally to the phenotype, then $h = 0.5$, and you have the additive fitness described above ($w = 1-.5s$).

If one allele is incompletely dominant over the other, the selective difference $s$ will be modified by some amount, $h$. If A$_1$ is only slightly dominant over A$_2$, (say, $h=0.6$), the effect on $w$ won't be much different than if $h=0.5$. Both alleles will affect fitness but the more dominant allele will have a slightly greater affect on fitness than the other allele. If one allele is much more dominant, then $h$ becomes larger and the more dominant allele contributes more to the overall fitness than the other allele.

Finally, if $h=1$ then one allele is completely dominant so the other allele will not contribute at all to fitness. When $h=1$, the equations reduce to $w = 1 - s$ (for the respective genders), remembering that $h$ is based on the dominance of the allele with maximum fitness in the other gender.

Consider a female. Her maximum fitness is the A$_2$A$_2$ genotype.  If A$_1$ is completely dominant over A$_2$, then a heterozygous female would have fitness equal to the A$_1$A$_1$ genotype which, for females is defined as $w = 1-s_f$. On the other hand, if A$_1$ is not completely dominant over A$_2$, then the heterozygote will have some reduction in fitness but not as much as for complete dominance.

To answer your final question about your figure, given the following values for A$_1$A$_1$, A$_1$A$_2$, and $_2$A$_2$, respectively:

$w_m = 1, 0.9, 0.2$, and

$w_f = 0.3, 0.7, 1$, then

$s_m = 1 - 0.2 = 0.8$, and

$s_f = 1 - 0.7 = 0.7$.

For the heterozygosity effect ($h$), given that

$w = 1 - hs$, then

$h = \frac{1-w}{s}$, therefore

$h_{m2} = \frac{1 - 0.9}{0.8} = 0.125$.

A$_1$ is nearly completely dominant over A$_2$ in males, so the presence of A$_2$ is the male is not reducing his fitness by very much. For females,

$h_{f2} = \frac{1-0.7}{0.7} = 0.429$.

The presence of the dominant A$_1$ allele in females has stronger heterozygous effect so her fitness is reduced more, compared to heterozygous males.

Citations

Fry, J.D. 2010. The genomic location of sexually antagonistic variation: some cautionary comments. Evolution 64: 1510-1516.

Kidwell, J.F. et al. 1977. Regions of stable equilibria for models of differential selection in the two sexes under random mating. Genetics 85: 171-183.


Why are smaller mammals more prone to cancer and tumors especially rats and mice usually develop cancer and tumors very fast, reducing their life expectancy.
From an evolutionary point of view, how come that these mammals are so prone to cancer and tumors even though they reproduce at a very fast pace?
Shouldn't they develop a resistance towards these illnesses through natural selection?

Source: https://www.thesprucepets.com/rat-tumors-1238498

The topic is called Peto's paradox, you can find references to studies on the wiki page, here's a summary:

A rat cell is more likely to get cancer than an elephant cell in the same time span. Mice have cancers in 2 years as often as humans have in 60 years.

Studies find that 4 ton elephants have only 4 times more blood cells than a 12 gram shrew. They have big mammal cells that divide at a slower rate. Rats can double their body weight every 10 days when they are teenagers, as if a puppy with a lot of appetite could become an adult dog in 30 days.

It is thought that the genetic safeguards that have evolved to protect large mammals against cancer would slow the growth and reproduction rates of small mammals. For example, an elephant has 14 copies of the cancer suppression gene TP53, humans have three copies, hyraxes and manatees have one copy.

Evidence for the paradox began to emerge in the 1970's. Studies from zoos on many mammal species have confirmed that big animals are protected from higher cancer rates.

https://en.wikipedia.org/wiki/Peto%27s_paradox


Two state exponential growth model I want to write an expression to model exponential growth of a microbe that scholastically and irreversibly acquires a mutation at a fixed rate that slows growth.

I can do it iteratively, but am curious whether a simple expression can be written.

I started with:

$P_{total} = P_{wt}e^{r_{wt}t} + P_{mutant}e^{r_{mutant}t} $

How do I factor in the mutation rate that converts $P_{wt}$ to $P_{mutant}$?

In general

Analytic solutions only exist for special cases. Therefore a good way of approaching these problems is to first act like they don’t and be happy if you can see how to derive one. It’s also more straightforward than wild guessing.

Your problem

Notation:

$P_\text{w}$ denotes the original population and $g_\text{w}$ its growth rate.
$P_\text{m}$ denotes the mutant population and $g_\text{m}$ its growth rate.
$r$ denotes the mutation rate.

The differential equations that describe your problem are:
$$
\dot{P}_\text{w} = g_\text{w} P_\text{w} - rP_\text{w},\\
\dot{P}_\text{m} = g_\text{w} P_\text{m} + rP_\text{w}.
$$
This system of differential equations is linear as it can be written in the form $\dot{\vec{P}} = A·\vec{P}$ with $\vec{P} = (P_\text{w},P_\text{m})$ and:
$$A = \pmatrix{g_\text{w}-r & 0 \\ r & g_\text{m}}.$$
Linear systems in turn can be solved by finding the eigenvalues and eigenvectors of the matrix $A$, which are:

$\vec{v}_1 = (0,\frac{r}{g_\text{w}-g_\text{m}-r})$ for the eigenvalue $λ_1 = g_\text{m}$.
$\vec{v}_2 = \left( 1, \frac{r}{g_\text{w}-g_\text{m}-r} \right)$ for the eigenvalue $λ_2 = g_\text{w}-r$.

This means that the solution can be written as:
$$\vec{P} = c_1 e^{λ_1 t} \vec{v}_1 + c_2 e^{λ_2 t} \vec{v}_2,$$
where $c_1$ and $c_2$ are constants determined by the initial condition:
$\vec{P}(0) = c_1 \vec{v}_1 + c_2 \vec{v}_2.$
If you assume that you have no mutants at the beginning and you initial wild-type population is $1$, you have $c_1=-1$ and $c_2=1$.
With this you get:
$$
P_\text{w} = e^{ (g_\text{w}-r) t},\\
P_\text{m} = \frac{r}{g_\text{w}-g_\text{m}-r} \Big(e^{(g_\text{w}-r) t} -e^{g_\text{m} t} \Big).
$$


Why must a planet be in a star's "habitable zone" to have life? I have seen many articles that talk about a star's "habitable zone" as the ring around it which is just the right temperature for planets to have liquid water, which is necessary for life. My question is, why does a planet need to have liquid water in order to sustain life? Who says that extraterrestrial life can't live off of some other kind of sustenance?

Your question is not complete. I would suggest to slightly change the title to something like:

"Why must a planet be in a star's “habitable zone” to have life as we know it from our experience?"

You are right, when you are assuming that there could be another than carbon based life as we know it from our planet Earth.

There are many hypotheses that life could be based on Si or other elements.

But carbon is still the easiest element to create bounds with other
elements and carbon too. Why? Here is the answer from wikipedia Carbon-based life:

  There are not many
  other elements which even appear to be promising candidates for
  supporting life - for example, processes such as metabolism - but the
  most frequently suggested alternative is silicon.3 This is in the
  same group in the Periodic Table of elements and therefore also has
  four valence bonds. It also bonds to itself, but generally in the form
  of crystal lattices rather than long chains. Silicon compounds are
  generally stable but do not support the ability readily to re-combine
  in different permutations in a manner that would plausibly support
  lifelike processes.

There is a great documentary from a physicist Brian Cox published by BBC this year called Wonders Of Life which deals with the basic questions how carbon based creatures were "born" on this planet ;) + other interesting things about life.

Brian talks there why the first organisms were created probably in water and how it could be.

Why water?
http://www.pbs.org/wgbh/nova/evolution/liquid-of-life.html

  And why is water the best liquid to do the job? For one thing, it
  dissolves just about anything. "Water is probably the best solvent in
  the universe," says Jeffrey Bada, a planetary scientist at the Scripps
  Institution of Oceanography in La Jolla, Calif. "Everything is soluble
  in water to some degree." Even gold is somewhat soluble in seawater.
  (Before you get any ideas about extracting gold from the oceans, I
  should add that, according to Bada, the value of dissolved gold in a
  metric ton of seawater comes to about $0.0000004).

If you take a route that there could be a different form of life outside of habitable zone, then many things are possible. E.g. life on asteroids, ouside of solar systems, life in other dimensions, life based on silicon or some other elements, energy based life? Or even dark matter and dark energy based life or gods/God-like creatures and all kinds of sci-fi ideas ;).


Do chickens always lay eggs? http://de.wikipedia.org/wiki/Hühnerei says it takes up to 24 h for a chicken to produce an egg.

Is that dependent on the chickens nutrition, i.e., if it does not get enough food or the wrong kind, meaning it can survive on the food but it does not have everything to produce an egg?

Do we have data on this?

In short; yes. It depends on the breed (not all lay up to 1 egg/day), the age of the bird and on nutrition. High yielding breeds of chicken are e.g. dependent on supplements of calcium to be able to produce new shells rapidly (e.g. in the form of ground-up shells). Some information on the nutrient requirements of chicken can be found at Feeding the Laying Hen. Egg production will also fluctuate over the year, and will generally decrease e.g. during molting, since energy and nutrients are then diverted to the production of feathers (see info at e.g. The Poultry site).


Microalgae without cell walls? Most microalgae have rigid cell walls.

Dunaliella Salina is a pretty famous example of an algae with no cell wall, but just a plasma membrane.

Are there any other microalgae without a cell wall?. I have researched but I can only find Dunaliella being mentioned.

Cyanidioschyzon merolae seems to be an example of such algae. Cryptomonad, aka Cryptophyceae also lacks cell wall.

I think, problem you encounter is that most studies are concerned with structure and function of cell walls, as such knowledge can be used in biotech industry. Hence, you will not find answer by looking for "algae without cell wall".

As a suggestion, I would point to this evolutionary study on development of plants: Evolution and Diversity of Plant Cell Walls: From Algae to Flowering Plants. Seems like trying to look through evolutionary trees might give you more examples.


What is the context in which a species gets the name "elegans" Quite a lot of Latin binomials from different genera contain the same species name. For example, there are a number that reflect the physical properties of the species (Tables have the latin name, a translation, and the number of European species according to the European Nature Information System).

nigr[a|o|um]    black        545
minim[us|a]     small        325
alb[us|um|a]    white        264
maxim[us|a]     big          166

and some which reflect the way in which they become apparent to us humans

vulgar[is|e]    common       691
sativa          cultivated   70
domesticus      domesticated 19

as well as reduplication for particularly salient/familiar species (e.g. Gallus gallus, Mephitis mephitis)

So, I'm wondering why there are so many elegans (471 European species on the database). It's particularly widespread, but meaning "elegant" or "refined", it's a rather nondescript name to give. Maybe someone might describe a species like this if they were really running thin on defining characteristics, but if this is the reason, why would the name occur so often?

So I'm fairly sure I'm missing something important about how species get named. What is/was the reason for naming so many species "elegans"? Does it have perhaps have something to do with type species?

Since "meaningfulness" is not listed among the requirements for new names, any author is free in his choice of name derivation. [There are nevertheless some natural restrictions, such that new names are to be treated as Latin irrespective of the etymology and should follow Latin grammar (with botanical nomenclature being much more meticulous in this respect).]
There are indeed some cases when the name of the species may be meaningful for the purpose of the choice of type species (the "typicus/a/um" names and tautonomous names like "Glis glis"), but "elegans" doesn't belong here.

So, the high frequency of "elegans" has nothing to do with typification and reflects nothing else than the will of authors to reflect their emotions. One recurrent cause of "elegans"-names among paleontologists, for example, is good preservation of the respective fossil material. [By the way, there are even more emotionally loaded (but less frequent) names like "mirabilis/e" or "enigmatica/us/um".]

Since providing etymologies for names alongside formal descriptions of new species at a certain moment became an official recommendation, you can make your own collection of causes people provide to justify their choice of "elegans" as species names.

EDIT: I've just found this revelation: (Oxytomoides elegans, fossil bivalve) "Etymology. Elegans, Latin for choice or select, referring to what we regard as esthetically pleasing appearance of the species".


Where can I find large datasets of protein-interaction networks? Where do I find large datasets of protein interaction networks for cancer or alzheimer diseases?  So far, I found String but it is does not have enough proteins for my purposes. Are there such databases with more entries?
I'm still open to any proposition of the disease to choose from .
the most important part is the volume of data .
And how can I get the annotation of each protein  of the extracted network from Uniprot ?

There is a bunch of decent protein-protein interaction databases: Biocarta, BioGrid, DIP, InnateDB, IntAct, MINT, PPID.
Some of them aren't available now, but you can download datasets from the Expression2Kinases download page because they are integrated into X2K pipeline as part of Genes2Networks analysis. If you need more proteins, you can submit your list of proteins to X2K and use G2N analysis to connect enriched transcription factors through known protein-protein interactions.

Also, the new dataset called hu.MAP was published recently. It is a dataset of human protein-protein interactions determined by over 9,000 mass spectrometry experiments performed by the Marcotte Lab from UT Austin. A paper that describes the hu.MAP project is available on Biorxiv.

BioPlex (biophysical interactions of ORFeome-based complexes) is another database with experimental verification. Authors describe it as a network that is

  the result of creating thousands of cell lines with each expressing a
  tagged version of a protein from the ORFeome collection.
  Immunopurification of the tagged protein and detection of associated
  proteins by mass spectrometry are the building blocks of the network.
  The overarching project goal is to determine protein interactions for
  every member of the collection.


Why do viruses cause different symptoms? If the sole purpose of a virus is to hijack the nucleus of a cell to replicate, why do we have different symptoms for different viruses?

I can think of the following comming into play:

immune response of the body
destroying tissue of type A is different than destroying tissue of type B
the rate of the destruction --- some (virus, cell) combination are causing more harm than others

Reference:

Why Do Viruses Cause Different Symptoms In Different People? --- talks about how we can have different symptoms for the same virus.

every virus having differ differ spike proteins so they make infection  a particular type of cell ( just like HIV that only bind with CD4 type of receptor) and make effect. another fact is that every virus have different genomic marital so that have different codon and these different codon make different protein and that different proteins make different effect on host cell metabolism that's why different virus having different symptoms.


Calculating fraction of protein unfolded from spectroscopy data This is a question from a homework pset of previous year. We are given the absorbance at 222nm of both a wild type and mutant protein at different temperatures. We are then asked to calculate various thermodynamic quantities from these data. The first thing it asked for is the Tm of both wt and mutant. To get the Tm, I need the fraction of protein unfolded, since Tm is defined as the temperature at which fraction unfolded is 0.5. However, I am confused as to how to calculate fraction unfolded. In the answer key, the professor used a equation, f=2*(A222-0.5), without any explanation. Can anyone explain to me where does this equation come from?

Edit: Sorry, I forgot to tell you that f stands for fraction unfolded.

Thank you very much
Zeyuan

I've plotted the data for ease of answering, though it is not necessary if you know what to look for in the data.

As expected, the melting curves are sigmoidal with horizontal asymptotes at approximately 0.5 and 1. You should be able to see this in the raw data as well: the absorbances hover around 0.5 before rising rapidly and then plateauing around 1.

You want the fraction of unfolded protein as a function of absorbance, so you need to normalize this data to the range of [0,1]. There's a straightforward formula for this which, put into the terms of your question, would be:

$f = \frac{A_{222} - min(A_{222})}{max(A_{222}) - min(A_{222})}$

$f = \frac{A_{222} - 0.5}{1 - 0.5}$

$f = \frac{A_{222} - 0.5}{0.5} = 2(A_{222} - 0.5)$

Intuitively, you might think about it as follows: at low temperatures, when the protein is folded, absorbance is 0.5. Consider this a blank or baseline measurement which gives the absorbance of the solution when no protein is unfolded. Since you are only interested in the signal from unfolded protein, you can subtract this value (0.5) from the rest of the data.


Methods for varying insert size in E. coli clones I'm writing my master's thesis proposal, and I need to improve the solution-behavior of some truncated protein domains which have previously shown poor solubility when expressed in E. coli.

To prevent this unwanted aggregation, one experiment I will perform will be to alter the domain boundaries.  I will create gene constructs where each clone will have an A domain of a certain length and domain border (see below).

My question: Is Gateway cloning better than restriction/ligase methods for this?  If i use restriction/ligase methods to construct vectors for transformation, then my choice for domain boundaries will be determined by restriction sites. Howevever, with a system like Gateway cloning, I can define boundary limits to bp resolution by simply desining an appropriate primer.

Is my reasoning here correct? I need to justify my choises for experimental design to researchers, so want to make sure I'm being efficient and logical.

Yes.  In principle you will have a vastly increased ability to customize the boundaries of each protein domain with a primer and PCR based approach.  It is not obvious to me that the Gateway Cloning System is required, or necessarily the best choice for this approach, but that is likely subjective.

Are you familiar with, or aware of, the efforts of the SGC (Structural Genomics Consortium)?  My understanding (now somewhat outdated) is that they were going to design/use a semi-automated way of implementing the strategy you discuss (domain trimming) so that they could us a high-throughput approach to define crystallization conditions for their targets.  Perhaps you could adapt their method(s) to your protein of interest?


What are the binding sites (or receptors) of cortisol? I am in the process of a OCR GCSE Case Study, and my question is "Do the benefits of anabolic steroids outweigh the risks, which has an obvious conclusion.
I need to know the scientific name, or a scientific analysis of why it causes an increase in protein synthesis,  for the binding of cortisol to understand this quote:"Anabolic steroids may block the binding of cortisol to its receptor sites, which would prevent muscle breakdown and enhances recovery.". For without enough understanding i can't explain it.

The intracellular receptor for cortisol is called NR3C1.
http://www.uniprot.org/uniprot/P04150

To my knowledge, a direct (competitive) effect of anabolic steroids on the binding of cortisol to NR3C1 has never been proven. The anabolic effects can easily be explained by other targets. A good starting point for further reading might be this review:
https://www.ncbi.nlm.nih.gov/pubmed/22101547


What happens when we dream? When a human dreams does the brain activate the cones and rods in the eyes creating the images we see in dreams?

The cones and rods would not contain the images from our dreams. Visual scenes get transferred from the eye to the thalamus (which serves as a relay to the cortex) by optical fibers that are overwhelmingly uni-directional (information is carried from the eyes to the thalamus and not vice-versa).

Dreams do, however, activate the thalamus, the visual cortex, and the visual regions that control eye movements (see refs 1,2). I don't believe there has been successful attempts to decode the activation, mainly, I think, because fMRI would be the best that we could use for humans and it does not have good temporal or spatial resolution.

Hong, Charles Chong‐Hwa, et al. "fMRI evidence for multisensory recruitment associated with rapid eye movements during sleep." Human brain mapping 30.5 (2009): 1705-1722.
Dresler, Martin, et al. "Neural correlates of dream lucidity obtained from contrasting lucid versus non-lucid REM sleep: a combined EEG/fMRI case study." Sleep 35.7 (2012): 1017.


How to reduce edge effects in cell-based high-throughput experiments? In high-throughput experiments where cells are cultured, treated, stained, and imaged in 384-well microplates, I frequently see significant edge effects. For instance, the following plot shows cell count (as measured by CellProfiler from images) for each well on such a plate:

How can I reduce these effects? I can try to correct for them statistically, but it would be so much nicer to reduce them at the wet-work stage.

Lundholt et al. describe a very simple trick: let the plates settle in air at room temperature for a couple of hours before placing it in the incubator. We tried it out, and although the color scales are different in the following plots, it is easy to see that it really does help:

(Thanks to Sigrun Gustafsdottir and Kate Madden for testing this.)

I have seen some people "pad" the plate by using only the 308 interior wells and filling the  76 edge wells with only liquid, but I have no data for how well that works.

Allison Tanner from Corning has collected a compendium of techniques to reduce the occurrence of irregular patterns of cell adhesion or “edge effect” in microplates. Brifly summarized:

Avoid bubble formation in the media when seeding cells.
Use cell harvesting methods that foster adequate mixing of the cells in the media and complete dissociation of the monolayer into single cells.
Seed cells at a density that will support attachment and growth.
Allow cell attachment to occur in media of the proper formulation for the particular cell type.
Dispense cells in an appropriate volume of media.
Follow strict aseptic techniques according to respected microbiological practices.
Cultures should be routinely monitored for mycoplasmal contamination.
Minimize entrance to incubators to help reduce fluctuations in the internal environment.
Allow cells to settle in the microplates while the microplates are on the benchtop.
Culture cells in an environment that reduces the formation of static electrical charges.