Do bacteria grow on pure dry glucose? I've accidentally touched pure glucose with my bare hands (fingers to be specific), which was intended for cell-culture.

I'm worried that bacteria from my skin may start to grow on the glucose and contaminate my animal-cell cultures.

Should I be worried about this really and get another glucose packet for it or just proceed to feed cells with that one?

Bacteria or other microorganisms cannot really grow on anhydrous (totally dry) glucose because they need water.

However, they can remain there and cause contamination. Even if you haven't actually touched the glucose sample, there are many bacteria suspended in the air and they may settle down in your glucose packet. When you take the glucose out for weighing, then also bacteria that are in the air, on your gloves, on the paper that you use for weighing, can settle on the glucose sample. In fact any substance, for that matter (salts in PBS, water etc).

That's why before using solutions in cell culture, you have to sterilize them by autoclaving or filtering. Glucose solutions should not be autoclaved because the heat chars glucose. You should filter them using a 0.2 micron filter. All the materials that are to be used for cell culture purposes should be opened only inside the laminar hood.


How might IV-saline cause kidney damage that seems to be less likely with "balanced fluids" IVs instead? The ABC News article What's in the IV bag? Studies show safer option than saline includes:

Saline — salt dissolved in water — has been the most widely used fluid in the U.S. for more than a century even as evidence has emerged that it can harm kidneys, especially when used a lot.
Other IV solutions called balanced fluids include saline but also contain potassium and other things that make them more like plasma, the clear part of blood. They're widely used in Europe and Australia.
The studies involved 28,000 patients at Vanderbilt University who were given IVs of saline or a balanced fluid. For every 100 people on balanced fluids, there was one fewer death or severe kidney problem.

and refers to research "...which were discussed Tuesday at a critical care conference in San Antonio and published by the New England Journal of Medicine."
Presumably the traditional saline solution does not contain a "wrong" or dangerous concentration of salt, but it seems that it's now conclusive that a balanced combination of ingredients beyond NaCl is safer.
Is there any understanding of the particular mechanism by which saline alone lead to issues with kidneys that seems to be alleviated by the addition of other natural constituents of blood plasma?
At first I thought the issue may be connected to "...especially when used a lot." by itself, but (also presumably) the study would have accounted for this.

Short answer
There is not likely to be a single mechanism involved, but the study authors suggest that high chloride is the main issue; they refer to previous work showing a whole variety of issues that can be caused by higher-than-normal chloride levels.
Although saline contains roughly the same sodium content as blood plasma, it contains a lot more chloride than usual, because blood plasma contains several other anions such as bicarbonate.
However, please see the rest of my answer: this study shows a fairly modest effect and is certainly worth some more investigation but might not be as definitive as the news makes it seem.
The study in question
I assume the news article you reference refers to this recent paper:

Semler, M. W., Self, W. H., Wanderer, J. P., Ehrenfeld, J. M., Wang, L., Byrne, D. W., ... & Guillamondegui, O. D. (2018). Balanced crystalloids versus saline in critically ill adults. New England Journal of Medicine, 378(9), 829-839.

I am constantly befuddled by why journalism considers it appropriate to refer to a study with no citation at all of the original article, only barely noting one of the original authors and only after mentioning an interview with someone completely different. Even their link to "New England Journal of Medicine" is not a link to the journal but to other articles written by that news organization that also refer to NEJM.
Careful interpretation of the study results
First, note that this study is talking about a fairly small difference. It isn't like saline is causing people to just drop dead, and you recognize this in your question, writing:

Presumably the traditional saline solution does not contain a "wrong" or dangerous concentration of salt

Rather, the study showed that 1139/7924 (14.3%) with "balanced fluids" had an adverse kidney event versus 1211/7860 (15.4%) with saline.
They also reference two previous papers, one from the same authors:

Young P, Bailey M, Beasley R, et al. Effect of a buffered crystalloid solution vs saline on acute kidney injury among patients in the intensive care unit: the SPLIT randomized clinical trial. JAMA 2015;314:1701-1710.
Semler MW, Wanderer JP, Ehrenfeld JM, et al. Balanced crystalloids versus saline in the intensive care unit: the SALT randomized trial. Am J Respir Crit Care Med 2017;195:1362-1372.

each of which showed no difference between "balanced fluids" and saline.
Therefore, I think concluding

"...that it's now conclusive that a balanced combination of ingredients beyond NaCl is safer."

is not necessarily true. In Young, et al., 102/1067 (9.6%) versus 94/1025 (9.2%) of patients showed signs of acute kidney injury for the "balanced" versus saline groups - a difference that was not significant (i.e., there are not enough subjects in the study to know that an effect this size is unlikely due to chance), but numerically the "balanced" group was worse. In Semler, et a. 2017, major adverse kidney events were 128/520 (24.6%) "balanced" versus 112/454 (24.7%) saline - literally as close to "no difference" as possible with this number of subjects (i.e., 111/454=24.4%).
Therefore, although this latest work shows a significant result with a larger population size, if you consider the previous work in this area the results are definitely mixed. The more recent Semler et al. 2018 paper's result is based on a p-value of 0.04, which is just below a commonly used threshold of 0.05 for deciding whether a result is significant. That doesn't mean the result is wrong, but it means that it should be considered in the context of other work being done in the area.
This study is also focused specifically on kidney issues, and although they have some other general secondary measures like deaths, the study is not designed or able to tell whether certain patients may actually be harmed by use of 'balanced' IV rather than saline IV.
To your actual question,
How might IV-saline cause kidney damage that seems to be less likely with “balanced fluids” IVs instead?:
The authors refer to other work showing that high chloride levels lead to a variety of issues; saline has a higher chloride level than normal blood plasma levels, so they suggest that if there is an issue with saline, the chloride levels are a likely cause, but this study has no ability to test those mechanisms.
Relevant quotes from the article, with emphasis mine:

In preclinical models, the high chloride content of saline has been reported to cause hyperchloremia, acidosis, inflammation, renal vasoconstriction, acute kidney injury, hypotension, and death. Studies involving healthy volunteers suggest saline may decrease renal perfusion through chloride-mediated renal vasoconstriction.


What are the limiting factors of human stamina? What are the limiting factors of (human) stamina? Let's define stamina as the capacity to continue doing a physical activity. We clearly have our limits, so what aspects of physiology impose a limit on human physical exertion? How do these aspects work together and interact?

Great detail isn't necessary, but a concise overview is what I am looking for.

A few explanations at the cellular and molecular level:

First, for contraction to happen, muscles need signals from nerves. Replenishing the pool of neurotransmitters (used for each synaptic burst) takes a bit of time, and short-term exhaustion may happen at this level.

In the muscle cells, contraction is caused by a calcium release within the cell, from a cellular compartment called the sarcoplasmic reticulum. This reticulum can only contain so many ions, so if the muscle contracts a lot, it will eventually need to rest for a while to re-accumulate calcium in the sarcoplasmic reticulum to prepare for more contractions.

Muscles need molecular "fuel" (like ATP molecules) to contract/relax. After an intense or sustained effort, these molecules are partially consumed and the muscle simply runs out of energy; it needs a bit of time to resore the pool of metabolites needed to work properly. Conversely, muscle contraction also causes the accumulation of metabolites and ions like potassium, which partially inhibit muscle contraction. Fatigue occurs when these accumulate at high level, and they must be cleared before making new efforts.

For references see:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5668469/ doi:10.1038/emm.2017.194 (general review)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5033663/ doi:10.1249/MSS.0000000000000923 (focuses more on muscle-neuron relationships)
https://www.ncbi.nlm.nih.gov/pubmed/9232550 Green, J Sports Sci. 1997 Jun;15(3):247-56.  (at the cellular scale)
https://www.ncbi.nlm.nih.gov/pubmed/7715628 Williams & Klug, Muscle Nerve. 1995 Apr;18(4):421-34.(more focused on calcium)


Why did Opabinia have 5 eyes? I recently read about a fossil called Opabinia. What intrigues me is that it had five eyes. I was under the impression that most features, such as eyes, ears and legs are always even-numbered, i.e., 2, 4, 6 etc. Why did Opabinia have 5 eyes?

Short answer
The number of eyes are not always even-numbered. In fact, many present-day lower vertebrates feature an uneven number of eyes.

Background
Eyes can be generally defined as photosensitive organs. Besides the regular paired eyes, lower vertebrates such as fish, amphibians and reptiles feature an unpaired (single) brain structure called the pineal gland, or parietal eye. It is primarily a photoreceptor organ, and its electrical activity changes in response to environmental lighting (Fig. 1). The pineal does not mediate vision, and it is mainly involved in regulation of circadian rhythms (Deguchi, 1981).

Hence, many lower vertebrates can be considered to have 3 eyes. In fact, the blind cavefish Astyanax mexicanus undergoes bilateral eye degeneration during embryonic development. Despite the absence of light in the cave environment, cavefish have retained a structurally intact pineal eye. Hence, cavefish can be said to have a single eye (Yoshizawa & Jeffery, 2008).

Fig. 1. Reptilian parietal eye. Source: review of the Universe.

The mammalian pineal gland is a secretory organ only, and no longer responds to direct illumination. In mammals it is situated deep in the brain and the mammalian skull does not admit light into the brain. Instead, the mammalian pineal needs input from the eyes to regulate the circadian rhythm.

References
- Deguchi, Nature (1981); 290(5808):706-7
- Yoshizawa & Jeffery, J Exp Biol; 211:292-9


Parthenogenesis in Bees Parthenogenesis is defined as:

"A type of asexual reproduction in which egg develops without fertilization to form a new individual."

If parthenogenesis takes place in bees, a drone or male bee is produced.

My question is that parthenogenesis is the development of EGG into new individual so, how can egg be developed into male because egg won't have that "Y" chromosome required for male offspring?

Because the "Y chromosome" has nothing to do with sex determination in bees.  Instead, the number of X chromosomes determines the sex.  With only one X chromosome, the egg will develop into a male.  This is called a haplodiploid system of sex determination (the male bees are haploid, having only half the number of chromosomes).

EDIT: I should add that there are many systems of sex determination, not just XY or the haplodiploid system.  See the Z-W system (males are ZZ and females are ZW), the X0 system (the males are diploid for all but the sex chromosome), and temperature-dependent system of sex determination.


Can ncRNA convert to coding RNA/mRNA by mutations? DNA has transcribed into RNA (Non-coding). Can this RNA mutate and become a Protein-Coding one/mRNA? Have there been any such instances reported by scientists?

Answers

Possibly, but with such a low frequency as to be unimportant and undetectable. (Monkeys with typewriters producing Shakespeare’s Hamlet comes to mind.)
No. Because it would be extremely difficult to detect, it would seem to be of no importance if it did occur at a very low frequency (you make no suggestion of why it would be of interest) and therefore there would be no reason for anyone to try.

Why would it be difficult to detect?

The difference between mutations that occur in DNA and any that might occur in RNA, is that a mutation in DNA can give rise to a population (e.g. of bacteria, or offspring) all of which carry the mutation. Thus, even though the chance of the particular mutation may be very low (say 1 in a million or less), a situation can arise in which the whole population is producing the RNA transcribed from the mutated gene and the protein encoded by the RNA. If RNA mutation occurs with the same frequency and managed to change a non-coding RNA (perhaps a pseudogene with a frameshift) to a coding RNA, only 1 in a million transcripts would be changed. Therefore if one sequenced the RNA the incidence of such changed RNA would be too low to detect, or if detected would be below the error margin in such experimental work.

Why has nobody looked for it?

Experimental science costs time and money. Scientists explore theories that have an importance and probability of success that attracts competitive funding. If there is no particular reason to look for something and the chances of seeing it are minute, nobody will waste their time on it, and they would certainly not get funded to do so.


What do you call mRNAs that translate to the same protein? For example AUAACC and AUCACG in distinct mRNAs may both be translated to the same dipeptide Ile-Thr.

This is by no means a consensus, but this paper from 2000 proposes a new term: Isotranscript.

According to the authors:

  Duplicated genes often encode distinct proteins that differ by only a few amino acids, such as the two mammalian S27 isoforms, S271 and S272, documented here and the yeast and Arabidopsis S27 isoforms identified previously. On the other hand, we have found that different S27 transcripts encode 100% identical proteins. This phenomenon has also been described previously for the histone subtype, H3.3, in which two different transcripts encode the same H3.3 amino acid sequence . We have chosen the terminology “isotranscripts” to describe such mRNAs. (emphasis mine)

Source: Thomas, E., Alvarez, C. and Sutcliffe, J. (2000). Evolutionarily Distinct Classes of S27 Ribosomal Proteins with Differential mRNA Expression in Rat Hypothalamus. Journal of Neurochemistry, 74(6), pp.2259-2267.


Do Japanese have a different pelvis position than Europeans? I was watching a show that made the claim that European women's pelvis is tilted more forward compared to Japanese women's which places their butts higher up.

Is this information accurate?

According to this study there are significant pelvic position differences between Caucasian and Asian populations. However the biggest difference is lumbar lordosis (the curve at the small of the back) where Caucasians have almost 10 degrees more curve. The study doesn't explicitly say it but that would suggest Caucasians butts are higher.


What would "N" and "V" stand for in DNA barcoding? I'm currently looking protocol for PAT-seq, and when it talks about the barcoding that's utilized, the documentation mentions there being an "N" and "NN" in the sequence, as well as a "V". For example:

...CCGATCTNNxxxTTT...TTTVN

where the "..." is an abbreviation of the the sequence and the "xxx" is the location of the barcode sequence.

As you can see, there's an "NN" just before the barcode sequence, and then, at the end of the T sequence there's a "VN". It says that the "NN" serves to affirm that the reads obtained are derived from different RT reactions and not all from a single RT product that's been excessively amplified.

So, I'm guessing that the "N" just stands for an undetermined nucleotide. Is that right? But then, what about the "V"?

It is standard IUPAC nomenclature to write bases that are not uniquely defined.

For example, "N" means "any base", but "V" means "A, C or G, but not T".

See the full list here


Do B/T cells form from lymphoid tissue or bone marrow? This website says lymphocytes are produced in bone marrow https://courses.washington.edu/conj/immune/lymphoid.htm

But if that's true, then what cells do lymphoid tissues produce? It could make sense if bone marrow is a lymphoid tissue, but red blood cells are also produced from bone marrow.

This is a good question and I can see where some confusion can arise. Lymphocytes are a class of cells that include both B and T cells among others. They both have the same precursor cell that being a small lymphocyte [1,2]. The small lymphocyte will grow into a large lymphocyte then differentiate into a pro-B-cell or a pro-T-cell [3]. After differentiation the pro-B-cells are "trained" in the bone marrow and the pro-T-cells are "trained" in the thymus [4,5]. The processes of training for both B and T cells are active areas of research and are quite interesting if a bit confusing.

from [6]
"Lymphoid tissue has several different structural organizations related to its particular function in the immune response. The most highly organized lymphoid tissues are in the thymus and lymph nodes, which are well-defined encapsulated organs with easily identifiable architectures. In the spleen (a soft, purplish organ lying high in the abdomen), the lymphoid tissue is a cylinder of loosely organized cells surrounding small arteries. In the bone marrow this tissue is mixed with the blood-forming cells, and no organization is apparent."

It is true that red blood cells are produced in the bone marrow and are somewhat related to lymphocytes. They are cousins to each other in some way [7].

I hope this helped show the differences in the maturation of T and B cells and cleared up some confusion for you. If you would like to know more I would recommend picking up an immunology book. I used this one [8] and quite liked it when I was taking immunology.

[1] https://en.wikipedia.org/wiki/Lymphocyte

[2] https://medical-dictionary.thefreedictionary.com/small+lymphocyte

[3] https://www.researchgate.net/figure/Life-and-death-decisions-during-B-and-T-cell-developmenta-This-panel-is-a_fig2_8014354

[4] https://www2.nau.edu/~fpm/immunology/Exams/Tcelldevelopment-401.html

[5] https://www.researchgate.net/publication/6196234_B-cell_anergy_From_transgenic_models_to_naturally_occurring_anergic_B_cells

[6] https://www.britannica.com/science/lymphoid-tissue

[7] https://www.ncbi.nlm.nih.gov/pubmedhealth/PMHT0022042/?figure=1

[8]https://www.amazon.com/Basic-Immunology-Functions-Disorders-Immune/dp/032339082X/ref=sr_1_7?ie=UTF8&qid=1524514359&sr=8-7&keywords=immunology


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

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

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

Some theories:

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

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


Why do mammalian red blood cells lack a nucleus? How did the red blood cell in humans get to lose its nucleus (and other organelles)? Does the bone marrow just not put the nucleus in, or is it stripped out at some stage in the construction of the cell?

Red blood cells are initially produced in the bone marrow with a nucleus. They then undergo a process known as enucleation in which their nucleus is removed. Enucleation occurs roughly when the cell has reached maturity. According to one research (Ji, et al., 2008), the way this occurs in mice is that a ring of actin filaments surrounds the cell, and then contracts. This cuts off a segment of the cell containing the nucleus, which is then swallowed by a macrophage. Enucleation in humans most likely follows a very similar mechanism.

The absence of a nucleus is an adaptation of the red blood cell for its role. It allows the red blood cell to contain more hemoglobin and, therefore, carry more oxygen molecules. It also allows the cell to have its distinctive bi-concave shape which aids diffusion. This shape would not be possible if the cell had a nucleus in the way. Because of the advantages it gives, it is easy to see why evolution would cause this to occur. However, since little is known about the genes the control enucleation, it is still not a fully understood process.


Functioning of BCG vaccine I  read (from Nature Volume507, S4–S7 (06 March 2014) :

  For reasons that are poorly understood, BCG protects only infants; it
  is ineffective in older children and adults. Its efficacy also depends
  on latitude. BCG works better, and protects people at later ages,
  farther from the equator. Both effects may result from interfering
  exposure to noninfectious mycobacteria that are closely related to
  both BCG and TB. These bacteria are more abundant closer to the
  equator, and while infants are unlikely to have encountered them,
  children and adults have more exposure over time.

I am unable to understand the relation between exposure to noninfectious mycobacteria and lessening of efficacy of BCG vacccine. What exactly is the "interference" caused by the noninfectious mycobacteria ?

The exposure to environentally occurring Mycobacteria causes a immune response to these (mostly unspecific, since no real infections occur). It seems that immunizations with BCG in these individuals is causing either no, or only a very attenuated immune response
This is shown in this ("BCG-induced increase in interferon-gamma response to mycobacterial antigens and efficacy of BCG vaccination in Malawi and the UK: two randomised controlled studies.") in which individuals with a high environmental exposure to mycobycteria showed only a very small response to this vaccination. If this natural level of immunity is enough to produce immunity to tuberculosis is unknown (and can not be tested for obvious reasons).

Another possibility is that the natural occurring immunity blocks the vaccine strains so they get eliminated before they induce an immune response. See here.
This is called the masking theory,if you want to read further, have a look at this three reviews, they give a good overview over the field:

TB vaccines: progress and problems.
A novel TB vaccine; towards a strategy based on our understanding of
BCG failure.
The success and failure of BCG - implications for a novel
tuberculosis vaccine.


How quicky does dental pH change after eating? I would like to know how quickly after eating I can expect the pH do change in my mouth, and how quickly this will cause dental damage.

Obviously any answer to this will have plenty of caveats (diet, composition of oral bacteria, etc) but I would like some numbers for some scenarios please.

Dental damage is mainly caused by the demineralization of the tooth enamel. Demineralization can happen due to a low pH caused either by acidic food/drinks like fruits or carbonated beverages or by bacteria producing acid while breaking down sugars.

Measurements (1, 2) have shown that food intake changes the pH (increasing or decreasing, depending on the food source), returning back to baseline after 15-30 min due to the buffering capacity of the saliva via bicarbonate and phosphate.

The drop in pH happens immediately after food intake. If teeth are not cleaned, the acid producing bacteria can have a longer-lasting effect on the pH for more than an hour. In these studies, participants are asked not to clean their teeth, so bacteria will populate the mouth. Removing bacteria or their food source as well helping the remineralization with fluoride toothpaste can counter the effects.


Where does all the food go? Food goes in, excrement come out. This seems obvious.
But it seems like the mass of the excrement is less than the one of the food.

Most people I asked answered: "There's a difference because it's transformed into energy, like heat...". I think that's bull-excrement.
There's still the law of conservation of mass: our body does no nuclear reactions, or does it?

Example:
Someone's on a "high protein / low carb" diet, he may ingest like 1kg of food, he isn't really productive on the toilet (it's difficult to find any fibers in those diets), he loses 500g in a day... My question is: where does the 1.5kg of matter go?

Whatever the diet, the food intake contains macronutrients: carbohydrate, fat and protein. When they are metabolised all of these molecules will end up, for the most part, as carbon dioxide, water, and ammonia, unless they are incorporated into components of the body.

These waste products are, of course, lost via breathing, and via the urine. That's where the "missing mass" goes.

A related question is here.


Can proteins structure change depending of alimentation of an organism? In my understanding protein are built using information caring by RNA. So a given protein should always have the same structure in a given organism has the DNA of this organism does not change.

I'm asking this question because peoples told me that "cow milk protein become longer because how we feed them today". But I don't understand how a protein can become longer or shorter.

Info: I have no background in biology.

While it is theoretically possible for a protein to change size (based on length) because of nutrition, I don't think that's happening here.

You are right-- DNA encodes information that is transcribed to RNA which is translated into proteins. Proteins are made of a finite number of amino acids, which are the building blocks of proteins. Proteins can be modified (and can be cleaved to make the protein shorter), but I think this claim of "cow milk protein becomes longer" is a misunderstanding because there is not a single "cow milk protein", but rather many.

There are many different proteins in cow milk, and most of them are casein proteins. source

The milk protein likely at the root of this claim is beta-casein. It was a hot topic in the 1990s, because there are a dozen different variants of this beta-casein protein. Two of these variants are the most common in milk have been studied a lot: variant A1 and A2. The only way these are different is a single amino acid change at amino acid position 67 (remember that proteins are made of amino acids). Variant A1 has a histidine amino acid but variant A2 has a proline. What does that mean? That means that A1 can be cut (in your body) to produce a smaller protein bit (called a peptide). Because of the proline in the A2 variant, it cannot be cut like the A1 variant. The peptide resulting from the A1 getting cut is called BCM7.

In short:
beta-casein variant A1: can be cut to produce BCM7
beta-caesin variant A2: gets cut way less than A1 so way less BCM7 is produced.

So, what is BCM7? It had been reported to been linked to some different diseases but the European Food Safety Authority (EFSA) published this report which concludes that there is no link between BCM7 and non-communicable diseases. Despite this, there is still a lot of talk about A1 vs A2 in the dairy community. While websites such as this appear compelling, remember the EFSA report!

this paper is open source and has the information about these variants that is summarized above.

So what does all this have to do with "cow milk protein" changing size? Maybe more cows used as dairy cows have the A2 variant, which would not produce as much BCM7 (the small peptide). Since A2 is not cleaved to produce BCM7, it could be thought of as "longer"... at least relative to only a few thousand years ago.
The beta-casein A2 variant is thought to be the original version of beta-casein from undomesticated cows.

So, if this claim was originally about beta-casein, you can respond that "yes, the beta-casein protein can be thought of longer because it is not cut to produce the BCM7 peptide as much as the A1 variant is, but it is also the original beta-casein size." Whether it was 10,000 years ago or just now, the A2 beta-casein variant is the same size.

tl;dr / Good reading from the California Dairy Research Foundation.


What in the brain has gone awry during sleep paralysis? I experience episodes of what I assume is sleep paralysis (lasting ~ 10-30 seconds) a few times a year, where I'm conscious of being somewhat awake but unable to move.  I can hear, but not see, and am quite focused on my breathing which feels labored and uncomfortable (can be accompanied by a feeling my face is covered by a sheet).  Sometimes, I've even been able to "jolt" myself awake if somehow muscle control is regained. Otherwise, I assume I drift off back to sleep.

Do we know yet what has gone wrong (if it can be assumed to be aberrant) and which neural circuits are involved? What i'm looking for is a specific explanation at the neural circuit level of how it can occur.

Is anyone aware of anyone conducting research into this or how it could be studied as it doesn't occur frequently and likely difficult to induce on demand?

Body paralysis occurs during REM sleep to keep your body from acting out your dreams.  You experience sleep paralysis when the mind awakens from REM sleep before the body paralysis has subsided.  I've had this happen before also, along with the "jolting" out of it you describe.  It usually happens when I'm very tired and trying to stay awake.  I try to stay calm but it's not easy as you know.  There is a good description at WebMD.


Need for proper air filter for bioreactor? I am going to build a simple bioreactor for microalgae growth.

I already have fluid filters pore size: 0.2um, diameter: 25mm
https://nl.vwr.com/app/catalog/Product?article_number=514-4039

I wonder if I can use them for air filtration to avoid the bacteria when pumping in the air.
Or do I necessarily need air filters?

Well then you need to get a filter specific for air filtering.  I recommend Polytetrafluorethylene PTFE membrane filter.  Now the only issues are size and "how sterile."

There are a lot of vendors out there that supply these.  If your institution has an agreement with VWR, they certainly have them.  If not, I have used Sartorius in the past, but I don't have any particular brand loyalty to them.

Let me know if you need any more help.


How much are phase-contrast and dark-field microscopy used in biological research? How much are phase-contrast and dark-field microscopy used in biological research today? It seems these were invented a long time ago, so I am thinking would it be a good idea to learn these techniques. (I will start an undergraduate program in biology next spring.. but I am still mostly interest how much the researchers use these technologies: if little, I should use my time better)

I use phase contrast very often, as it is only a matter of switching a lens group from bright field. Instead of spending hours with staining, or, worse, immunostaining, I get the big picture (cell diameter) in a few seconds. I can even go back to the same cells next day. Switching to dark-field is also a matter of turning a dial or pushing a switch.

If you already use brightfield, there is not much to learn about them in terms of actually useful physics, or sample preparation. The things you could learn - say, that colors are altered in darkfield - will rarely be needed in practice. These methods are the sort of things you don't really need to know in depth unless your experiments require them. Even then, practice and elbow grease would be more helpful than advanced optics. Remember that in most cases, the scientific hypothesis is more important than the tools you can use to solve it.


5,6-dihydrouracil and 5,6-dihydroxyuracil - how they arise in DNA? 5,6-dihydrouracil can be formed from cytosine after exposure of DNA to ionizing radiation under anoxic conditions [Ref]. What are other ways by which 5,6-dihydrouracil is formed in DNA? What about 5,6-dihydroxyuracil?

Dihydrouracil oxidase can catalyse the reduction of uracil to dihydrouracil in the presence of hydrogen peroxide. The reduction of uracil to dihydrouracil can also be catalysed by dihydrouracil dehydrogenase using NADH.

According to this paper, 5,6-dihydroxycytosine can be formed by treating cytosine or DNA with osmium tetroxide, an extremely strong oxidising agent. Since they are both pyrimidines (and in fact cytosine often spontaneously hydrolyses to uracil), uracil will also be affected by the same oxidation. 5,6-dihydroxyuracil was also detected within the oxidised DNA sample as a result of oxidation and demethylation of thymine.

  The presence of 5,6-dihydroxyuracil (peak 11 in
  Fig. 1) can be explained analogously to the formation
  of 5-hydroxy-5-methylbarbituric acid from thymine on
  permanganate oxidation (lida & Hayatsu, 1970, 1971)
  (Scheme 2). The actual oxidation products ofcytosine, i.e.
  structures (I) and (II), were not observed in DNA. As the
  calf thymus DNA used in this work did not contain uracil,
  the uracil derivatives discussed above could not have been
  formed from uracil in DNA.


Ideal lab glassware cleaner for molecular biologist I'm using Alconox powder detergent to clean my laboratory glassware, the powder is a pain to store near the sink and to use. Would like to make a   concentrated liquid to use in its stead.

I have tried a few things, obviously just water and mixing, even up to overnight. It really doesn't go into solution very well, even at seemingly low concentrations. Ive got it up to about 20% w/v but I've tried heat, glycerin, adjusting pH to ~8.8, adding EDTA. I have not added these things in any scientific way, just kind of pouring glycerol or EDTA in.

Wondering if anyone in here has experience with detergents like this , or has done something like this before. Thanks in advance!

If you're just using it for hand washing, you probably don't need an ultra-concentrated solution. A very small amount of detergent goes a long way. (Think about it - what would you do with an ultra-concentrated solution? Probably squirt a small amount on the glassware and then add water.)

What I've seen done is to make your "dilute" solution of Alconox, put it in a squirt bottle, and then use a healthy squirt of it when washing. In fact, you probably find you don't even need a healthy squirt of it. A small amount of even the dilute solution is fine.

The approaches I've seen have been rather cavalier - basically just throwing a bunch of the powder in the squirt bottle and filling it with water. You quickly get a sense of how much will dissolve, and if you use a squirt bottle with a drop tube that doesn't go all the way to the bottom, you don't need to worry if not all of it dissolves.

Alternatively, as you you seem the fastidious type, you can fill another (non-squirt) bottle partway with Alconox, the rest of the way with water and let that sit (perhaps with occasional mixing). This should give you a saturated Alconox solution, which you can use to fill the squirt bottle, being careful not to transfer residual powder from the bottle. Then you can add more Alconox powder and water to the stock bottle, let dissolve, and you should be ready for the next time.

Again, this may only give you a 10-20% solution of Alconox in water, but that should be more than sufficiently concentrated for most usages.


Can rapid eye blinking induce epileptic seizures? Photosensitive epilepsies are characterized by visually-induced seizures. Flashing-light stimuli are known to induce seizures in some (but not all) patients. My question is whether people with this type of epilepsy can self-induce seizures by rapid eye blinking?

“Self-induction” in photosensitive epilepsy is a well-described and fascinating  phenomenon. Photosensitivity itself is rare, occurring in only ~5% of patients with epilepsy.1 Among this group it has been estimated2 that 25% self-induce epileptiform activity. The most common methods appear to be passing a hand with open fingers repeatedly across the visual field and, as you query, blinking.

Quoting from a classical paper on the topic by Andermann et al:3

  The method of inducing seizures varies
  both in detail and in principle. Light contrasts are always brought about, but they may either be applied to and alternate for the whole visual field—an effect produced by blinking or batting the eyelids and induced by any flickering light—or else the attack is elicited by the spatial displacement of brightness and darkness  over the retina.

This phenomenon is most common in epileptics with established photic triggers, and the scenario triggering an attack is often in the context of bright sunlight. However, this has also been described in epileptics who are not otherwise photosensitive. See, for example, “Seizures triggered by blinking in a non-photosensitive epileptic.”4
Notably, some authors have questioned whether blinking and other “triggers” are actually themselves ictal phenomena (i.e. representing the initial phase of an epileptic event) rather than a form of voluntary self-induction. For more on that hypothesis, see Ames, 1971.5

Presuming that this is, in fact, self-induction as has been traditionally postulated, the question of why such patients repeatedly self-induce seizures is perhaps the most interesting aspect of this. There has been some research2 considering the psychiatric factors underlying the behavior. Quoting Andermann3 again:

  The reward a patient seeks by self-stimulation may lie in escape from unwanted situations, in attracting attention, in punishing those around him, or, indeed, in deriving pleasure from the attack.

References

Kasteleijn-Nolst Trenité DG. Photosensitivity in epilepsy. Electrophysiological and clinical correlates. Acta Neurol Scand Suppl. 1989;125:3-149.
Ng BY. Psychiatric aspects of self-induced epileptic seizures. Aust N Z J Psychiatry. 2002 Aug;36(4):534-43.
Andermann K, et al. Self-induced epilepsy. A collection of self-induced epilepsy cases compared with some other photoconvulsive cases. Arch Neurol. 1962 Jan;6:49-65.
Rafal RD, Laxer KD, Janowsky JS. Seizures triggered by blinking in a non-photosensitive epileptic. J Neurol Neurosurg Psychiatry. 1986 Apr;49(4):445-7.
Ames FR. "Self-induction" in photosensitive epilepsy. Brain. 1971;94(4):781-98.


How to predict future generations from heritability The heritability of human intelligence is estimated to be around 0.5. There are of course various estimates, some lower, some higher. But let's work with this value of 0.5 for the moment.

I wanted to know how this relates to the trait value of future generations and read a bit about it. For example, in some related posts:
how should one interpret heritability is it related to r2
why is a heritability coefficient not an index of how genetic something is
how to interpret the breeders equation

Turns out the breeders equation gives us an idea about that. But we need a second variable: Selection.  I read that selection is based on the reproductive success of individuals with a certain trait value.  But how would I calculate this value?  Let's assume that the reproductive success is higher, for humans with higher intelligence. Let's simplify and say, the fertiliy rate of above average indivdiduals is 2.10 and the same value for below average individuals is 1.90. How would I plug those numbers into the breeders equation?

I tried the other way around. We know that intelligence is increasing over generations in western civilizations (see Flynn effect). Again, estimates vary (and can actually be negative) but we can work with an increase of 2 IQ points per decade. So lets say 5 IQ points increase from one generation to the next in a western civilization population. That would mean:

S = R/h²
S = 5/0.5 = 10

What would this value of 10 mean? How does this boil down to the reproductive success of individuals with certain trait values?

"How would I plug those numbers into the breeders equation?"  You would use those fertility rates in calculating the selection differential (S), which would essentially be a weighted intelligence average of the reproducers minus the population average (reproducers+non-reproducers).  So, if the population starts wih 100 IQ and those with 125 IQ produce 2.1 and those with 75 IQ produce 1.9 and those two groups are equally populated, the weighted intelligence avg of reproducers becomes (125*2.1+75*1.9)/4=101.25.  The selection differential is then 101.25-100=1.25.  Response is 1.25*.5=.625.  IQ moves to 100.625.  In your example, S=10.  That is, (x*2.1+y*1.9)/4-100=10, where x is the avg IQ of the above average group and y is the avg IQ of the below average group, assuming the two groups are equally populated.


Do Vaccinium membranaceum plants need a minimum amount of darkness per 24 hours? I have Vaccinium membranaceum (black huckleberry) seedlings growing in a greenhouse. I have the option of providing fluorescent light to the plants 24 hours a day.

However, it has occurred to me that plants like Vaccinium membranaceum might require a minimum amount of darkness per 24 hours.

What darkness requirements do Vaccinium membranaceum plants have?

Some plants are long day plants -- they require a certain number of days longer than a certain number of hours.

Some plants are long night plants -- they need nights that are longer than a certain number of hours.

See this for more details: http://www.biology-pages.info/P/Photoperiodism.html

Other plants are day neutral.  They bloom when triggered by other stimuli such as it being warm enough.

If you don't care if they bloom or not, then you can give them 24 hour light.  They should grow somewhat faster.

However, you may need to check what triggers them into dormancy.  E.g. Spruce start going into dormancy when days get shorter than about 10 hours (Varies by species, and provenance)  Reforestation growers trick them into going dormant in August with black tarps in mid afternoon.  They can then plant them with minimal stress, and they take off in the spring.


How could a species be engineered to go extinct? Non-biology background here.

I read this very interesting article: https://www.wired.com/story/crispr-eradicate-invasive-species/

However I am having a hard time wrapping my head around something:

From my basic understanding of natural selection, a gene/trait will spread if it gives the group a relatively higher chance of having children, who will pass on the trait, etc.

However in this example, the trait is infertility! Doesn't it go completely against natural selection? How could this spread??

Short answer

The article in particular that you reference is discussing the possibility of using a mechanism called gene drive. The concept of gene drive breaks the normal "rules" of inheritance and allows a gene to spread much more rapidly than normal in a population.

Longer answer

Gene drive depends on the idea of a selfish gene. There are naturally occurring genes that make copies of themselves to other parts of the genome. Selection pressures can operate at the level of these genes: a gene that can copy itself is going to end up in more offspring than would be expected due to random assortment.

For example, imagine a gene present in one chromosome of one parent. Typically, only half of that parent's offspring will have that gene. However, if the gene is able to copy itself to the parent's other chromosome, now all offspring of that parent will have that gene. The prevalence of the gene just doubled. It's possible that the gene will also confer some negative traits, but as long as those negative traits aren't sufficient to cause a >50% reduction in later reproduction of the offspring, they are going to do just fine and go on and mate, spreading the gene further, potentially to an entire population fairly rapidly.

The new technology CRISPR makes it easier to create synthetic genes that selfishly copy themselves within the genome (note: this is definitely not the only application of CRISPR) and could confer positive traits that are helpful to humans, like mosquitoes resistant to being carriers of malaria, or to introduce deleterious mutations into a population.

As you point out, introducing a mutation that causes sterility and having it spread is still not easy. There are a few clever approaches, though, that can make it possible. Note that the strategy does not to have 100% effectiveness to wipe out a population: once below a certain level, members of the population may have trouble finding mates and face greater predation pressures and the population can collapse.

One technique is to boost the proportion of males. If you can force all the offspring of one male to be male, the proportion of males in the next generation will be higher. Those males-that-only-produce-males don't have any immediate reproductive disadvantage versus normal males. If they survive and mate normally, they will continue to compete with normal males (they may also compete with females for food resources during their lifetimes). Any time a normal male mates, sure, it will create a new generation of some females, but every time a transfected male mates it will effectively double the number of transfected males. Even as the total number of individuals in the species drops, the proportion of transfected males remains high. Eventually there are too few normal males to mate, the number of females drop to unsustainable levels, and the population crashes.

This approach is similar to the technique of releasing sterile males which has been used successfully for population control. The difference is that the gene drive technique raises future generations of the (sort-of) sterile males by itself, which might mean it can be used in population control when it is not possible to lab-raise large numbers of sterile males.

Note that use of these technologies is very controversial. There are concerns that such a gene could accidentally move from one species to another, for example. Future use of the technique will require combined research into safety and efficacy.

References

Burt, A. (2003). Site-specific selfish genes as tools for the control and genetic engineering of natural populations. Proceedings of the Royal Society of London B: Biological Sciences, 270(1518), 921-928.


A good textbook on GMO I am interested in learning about GMO. The topic is so wrapped in controversy, that it's hard to find a good book that introduces the basic concepts involved. I went through various university websites, but couldn't find any lecture notes on the topic. I don't know, is it too broad a topic? Is there even a book called Introduction to GMO? Maybe that's the problem.
I am interested in a book that tells you about how gene manipulation is done. How do biology students get introduced to this concept? I hope the question is not too general.

I too had difficulty finding any textbooks or notes that focused solely on genetic engineering. However, after some rather intense looking, I did come across several textbooks that may be helpful. I wasn't sure how basic of a text you were looking for but I'm hoping college level is okay because that is all I have been able to find.

The first book was An Introduction to Genetic Engineering by Dr. Desmond S.T. Nicholl.

Another was Principals of Gene Manipulation and Genomics by Sandy B. Primrose.

If you need a more basic biology text for reference, I would recommend Miller & Levine Biology by Prentice Hall (Pearson Prentice Hall). Also, you could do a quick-study on genetics on Khan Academy - Crash Course: Biology and Ecology.

I hope this information was helpful for you!


How many species of mites live on the human body? How many known species of mites regularly live on the human body?

I've always heard that most people have eyebrow mites. This source  mentions 2 species of face mites, Demodex folliculorum and D. brevis,  that also regularly live on humans, but I'm wondering if there are in fact other species of mites that also call human bodies home. If so, how many? And where do they live?

Note: I'm not talking about disruptive mites such as scabies,  but mites that go less detected.

The answer is 2-3 human mites.

This page says that 2 mites specialize on humans:
http://www.bbc.com/earth/story/20150508-these-mites-live-on-your-face
https://link.springer.com/article/10.1007/s10493-009-9272-0

Another page I found said there are 3 common human mites, adding scabies to the list.

This page talks about bites from a variety of dust and house mites:
https://link.springer.com/article/10.1007/s10493-009-9272-0

My biology lecturer from university of Edinburgh told us that we have hundreds of species of detrital nematodes living on and inside us and that nematodes can be a few microns long. About 800 million humans have a 30cm large nematode inside them according to the WHO.


Book recommendations for algorithms used in evolutionary biology Do you have recommendations for a book that presents the different algorithm used in theoretical evolutionary biology?

I don't mean evolutionary or genetic algorithms (otherwise this question would not be a good fit for Biology.SE) but algorithms applied to evolutionary biology. I am not interested in statistical procedures and algorithms to reconstruct phylogenetic trees, to annotate DNA sequences or to find out synonymous changes by comparing sequences of closely related species. I am not interested in introductory book on programming.

I am interested to computational modeling applied population genetics, kin selection, game theory, population range expansion, simulating sexual reproduction, selection for different sex determination system, evolution for robustness/evolvability, evolution of codon usage, evolution of genetic code, evolution of cognition, evolution of multicellularity, …

I don't quite know if one book that encompass all these subjects exist. If not, I wold welcome suggestions of book that present the algorithmic used in some but not all of these subjects.

Searching a bit in amazon, I easily found tons of book but don't quite know if they fit my expectations. Below are some examples

Evolution as computation

Individual based modeling and ecology

Models and algorithm for genome evolution

modelling for field biologists

Practical computing for biologist

Evolution as computation

Genetic and evolutionary computation

Genetic algorithms+ data structures = evolution programs

The missing algorith

Cellular Model: Mathematical and theoretical biology, Algorithm, Data structure, Bioinformatics, Computational biology, Artificial life, Computer simulation

Natural-Artificial-Models-Computation-Biology

An-Introduction-Genetic-Algorithms-Paper

What you are describing usually falls under the category of computational biology or just mathematical biology. Unfortunately, the biggest part of this field is bioinformatics, or the application of statistical and/or dynamical programming techniques to sequence data. You exclude this in your question, and I would agree with you that it is a "boring" topic from a theoretical biologist's perspective, because it mostly uses computer science in a very standard way as a tool for experimental biologists.
As you noticed, it is also standard to use computational models in theory papers as a way of simulating things. I think this is the sort of resources you are asking for. Unfortunately, specific algorithms are seldom standardized or reused in this area. Typically, each paper (or sequence of related papers) uses their own models.[1] As you read a lot of papers, you will find some common themes, but these are just standard ideas of theoretical biology expressed as simulation. I doubt that comprehensive books exist, and even if some do their utility is not clear to me due to a lack of specific algorithm (re)use.[2] However, the most commonly used techniques are to either to solve differential equations numerically (which most would classify as mathematical modeling) or run agent-based or population-based models. General resources on these exist, and here are some discussions for the latter other SEs:

Simulation modeling of diseases.
Sources for Algorithmic Evolutionary Game Theory.
Canonical reference on agent-based computing.

Finally, do not confuse 'computational modeling in theoretical biology' with 'algorithmic biology'. Algorithmic biology is a new field that views ecological and evolutionary dynamics as computatioanl proccesses. Instead of using mathematical tools borrowed from physics (as is standard with the dynamic systems approaches to mathematical biology), it uses the tool of theoretical computer science (note that this is a type of math that has very little to do with programming the laptop infront of you). I know of only two books in this field:

Gregory Chaitin "Proving Darwin: Making biology mathematical" - Although Chaitin had contributed significant and original thoughts to computer science in the past, I would strongly advice against this book because it misses the point from both the biological and computer science point of view.

Leslie Valiant "Probably Approximately Correct: Nature's algorithms for learning and prospering in a complex World" - in this book (based on earlier papers), Valiant recasts evolution as a type of machine learning. This is very interesting from a mathematical point of view, although it might not connect directly enough to biologically relevant questions (see also some of the discussion in Kaznatcheev (2013) and Kaznatcheev (2019)) and misses the computational power of frequency-dependent selection (see Kaznatcheev (2020)). But I would recommend reading this book.

Notes

In general, I consider these sort of models as heuristics and I am skeptical of their usefulleness beyond rhetorical devices/examples.
I think that literature reviews would be interesting computational modeling in specific subfields. In fact some colleagues and I have wanted to do this for the smaller area of evolutionary game theory (This answer can serve as a starting point for some algorithmic considerations of EGT).


What does this mutation notation mean: MAP2K41161fs*12 I received a report that had a mutation notated as: "MAP2K41161fs*12". I'm used to seeing this sort of thing: BRAF(V600E) or BRAF(T1799TA). Can someone tell me how to interpret "MAP2K41161fs*12" ?? Is it a deletion? An insertion? A translocation? Or What?

fs means frame shift and *12 gives the length of the new reading frame (ie the number of codons up to and including new stop codon). Usually before fs they give the first mutated amino acid, so I'm not sure what the number 41161 means (but apparently the OP does).


Is there variation in which olfactory receptor genes are functional in humans? According to wikipedia humans have around 400 functional olfactory receptor genes and 600 pseudo genes. Most mammals have higher numbers of functional OR genes.

My question is whether it has been studied how the number or subset of these functional ORs varies between humans.

Perhaps the most dramatic example of variation in olfactory abilities in humans is anosmia, or the inability to smell. However, this isn't always due to broken olfactory receptors -- some total anosmias are due to cilia (small hairs) that don't function properly. (This paper mentions that.)

Specific anosmias, or insensitivities to particular smells, are probably closer to what you're asking about. The textbook chapter I linked to below talks about how proportions of the population lack the ability to smell certain odorants -- for example, about 1/10 people cannot detect ethyl mercaptan, which is the scent given to natural gas leaks. These specific anosmias are generally restricted to just one odorant (smell), which suggests that it is likely a receptor deficit. (EDIT: The comments below have even more examples of scents that vary from person to person.)

Interestingly, many conditions are associated with a decline in smelling ability and range, like Alzheimers, diabetes, and taking certain medications. These declines can be because of fewer olfactory receptors or because of deficits further along in sensory processing.

I couldn't find any papers assessing smell variation across all humans -- doctors rarely think to assess smell, so there isn't much data on "normal" populations. Also, it doesn't seem like the genes controlling olfactory receptors in humans have been characterized well, so it would be extremely difficult to do a comparison on the genotypic level.

In sum, there are definitely differences in the ability to smell a wide range of scents. To my knowledge, this hasn't been characterized in an especially systematic way. (If it has, I hope somebody on here knows otherwise!)

This chapter of Purves' Neuroscience gives a basic run-down of olfaction and some possible variations in it.
https://www.ncbi.nlm.nih.gov/books/NBK11032/


Why are beta-galactosidase proteins overexpressed in senescent cells? Wikipedia explains that it's a hypothetical hydrolase enzyme that catalyzes the hydrolysis of β-galactosides into monosaccharides only in senescent cells.

I'm just wondering - what causes it to be overexpressed in senescent cells - to the point that it often becomes a biomarker of senescence? And what exactly happens to the particular cell when you catalyze the hydrolysis of more β-galactosides (like lactose) into monosaccharides?

Looking at the articles referenced in the Wikipedia article, there's probably no direct physiological link between senescence and beta-galactosides. Lee et al (2006) and others before them have shown that the "hypothetical" protein is just regular lysosomal beta-galactosidase, which is present in higher concentrations in aging and stressed cells because the number of lysosomes increase under those conditions. There's a collection of references in the Discussion section of the Lee paper that delves deeper into the aging-lysosome connection.

I'm well out of my depth by this point, but if I were going to take a wild guess I'd suggest that lysosomal upregulation could be part of a stress response involving autophagy (i.e. the cell breaking down and recycling intracellular materials to meet critical demands), though I don't know the specific connection to aging. As far as beta-galactosides go: if you have any hanging around, you get to eat them, is all, I bet. I bet the references in Lee would tell you if I'm on track or not.


All-trans-retinal being converted back to 11-cis-retinal or vitamin A There are two pathways all-trans-retinal can take after detaching from the scotopsin: (1) it can convert back to 11-cis-retinal, or (2) it can convert to all-trans-retinol (form of vitamin A), which then converts to 11-cis-retinol and then 11-cis-retinal. My question is what factors determine which pathway will occur?

The first sounds like it doesn’t involve vitamin A at all and just recycles the retinal. Hence it wouldn’t be affected by any vitamin A deficiency, yet we know vitamin A deficiency affects the stock of retinal in the eye. Yet I don’t see any disadvantages in simply recycling our retinal; why would we go through the process of converting it to vitamin A and then back to 11-cis-retinal?

Short answer
A complex visual cycle in vertebrates involving vitamin A is useful for storage, re-distribution of retinoids to both rods and cones, to improve photosensitivity and reduce noise in the visual system.

Background
The visual cycle in mammalian rods is depicted in Fig. 1.

Fig. 1. Visual rod cycle. Source: Palczewski (2010)

11-cis-retinal isomerizes to all-trans retinal by absorption of a photon.  Your notion that this pathway can involve direct re-isomerization back to 11-cis-retinal is only true for invertebrates. They simply absorb another photon to back-isomerize all-trans to 11-cis (Saari, 2012).

In vertebrates, however, this bi-stable configuration is replaced by a complex visual cycle (or retinoid cycle, Fig. 1). The reason is that the bi-stable invertebrate system is less sensitive, as photons used for regeneration cannot be used to initiate phototransduction. Moreover, the invertebrate system is more prone to noise, as photons can both start the phototransduction or recycle all-trans retinal (Saari, 2012).

In vertebrates it is thought that the visual cycle only emerged after appearance of the cone system (Saari, 2012). Notably, the visual cycle depends on the retinal pigment epithelum (RPE), as shown if Fig.2.

Fig. 2. Rod and cone visual cycle. Source: Saari (2012)

Fig. 2 shows that vitamin A (all-trans-retinol) is present in the RPE. RPE cells are able to store vitamin A by converting it to fatty acids and store it in oil droplets. Moreover, RPE cells can funnel this stored vitamin A to both rods and cones, another reason why the complex visual cycle and vitamin A conversion makes sense (Palczewski, 2010)

References
- Palczewski Trends Pharmacol Sci (2010); 31(6): 284-95
- Saari, Annu Rev Nutr (2012); 32: 125–45


Do Termites and Silverfish metabolize cellulose the same way? I am fascinated with silverfish and would like to understand more about their metabolism.
I learned that they can survive on a diet of cotton which is nearly pure cellulose. Do they metabolize cellulose in the same way as termites?  Or do some insects have different metabolic pathways for cellulose?

It has been known for 40 years or more that some insects such as termites digest cellulose by synthesizing their own cellulases, whereas others have a symbiotic relationship with gut micro-organisms that perform this digestion (see Martin, Comp. Biochem. Physiol. (1983) 75A 313-324  — requires subscription — or this short popular science article).
What is the situation for silverfish — Lepisma saccharina? Today the evidence that generally determines whether an insect can digest cellulose itself is the presence of the genes for the cellulase enzymes in its genome. There is a relatively recent review of this in Annu. Rev. Entomol. (2010) 55 609–32 — again requiring subscription for access — in which the species in which these genes have been detected are listed. I know nothing about organismal biology or taxonomy, and can only summarize the species represented there for others to comment on:

Orthoptera
Blattaria
Phthiraptera
Hemiptera
Coleoptera
Hymenoptera

This doesn’t seem to me to include Lepismatidae (which Wikipedia tells me is the family), but what do I know. (I only know the genes aren’t present in fruit flies.) However some earlier indirect experiments studying the effects of antibiotics on insect cellulase levels suggest that Lepismatidae may have their own cellulase.


What is rotational diffusion and lateral diffusion in plasma membrane? There are no good reads on internet. The idea that I have formed so far of these topics, is that lateral diffusion is translational movement of protein in a leaflet.

From this paper, rotational diffusion describes the movement of a membrane lipid around its axis that is perpendicular to the plane of the bilayer, analogous to a person spinning around while standing up.

Lateral diffusion describes the movement of membrane lipids exchanging places with each other across a face of the bilayer, rather like two dancers spinning about their mutual center of gravity.


How does the placement of it's motor domain affect the directionality of a motor protein? I'm going over some of my notes, and I have written down that motor proteins with + cytoskeletal directionality have a reversed schematic representation relative to - directed motor proteins. Then I have this sort of image drawn. I just want to clarify it, since I don't remember this part of lecture at all.

Schematic representations

Kinesin: N terminal - |Head||Coils||Tail| - C terminal
Dynein: N terminal - |Tail||Coils||Head|| - C terminal

Does this look right?

No. DNA, and RNA have a polarity in the orientation of their sugar-phosphate backbones, based on the numbering of the carbon atoms in the sugar rings. So, for example, we say that the sequence of this RNA is being read from the 5' to the 3' end, which indicates that the first nucleotide is exposing the hydroxyl at the 5’ carbon on its sugar ring.  At the other end of the linear polynucleotide the sugar is exposing the hydroxyl on its 3’ carbon of the sugar ring.

All mRNAs are translated in the 5’ to 3’ direction and all proteins are synthesized from the amino terminus to the carboxylate terminus, because the peptide bonds in the protein also have a directional polarity.

You appear to have mislabeled the N and C termini of Dynein in your diagram. Perhaps the  lecture was about the domain structure of these two motor proteins? And the point might have been that they each have three equivalent domains but in one case the part we call the head is synthesized first and in the other case the tail is synthesized first(?).


How do ants follow each other? I was observing ants in my house.They all were going in a straight line and also some of the ants were coming back through the the same line.

I took some water and rubbed the line with my finger, then the ants were not able to follow each other. Looks like they were confused.

My assumption is that they may had secreted some chemical .

Am I right ?
If yes, then which chemical is that and how it is secreted?

The chemical we are talking about here is called pheromone, trail pheromone to be specific.

  A pheromone is a secreted or excreted chemical factor that triggers a social response in members of the same species. Pheromones are chemicals capable of acting outside the body of the secreting individual to impact the behavior of the receiving individuals.1

Pheromones are of mainly 9 types (13 exactly, but 4 not so common) which are:

Aggregation pheromones
Alarm pheromones
Epideictic pheromones
Releaser pheromones
Signal pheromones
Primer pheromones
Territorial pheromones
Trail pheromones
Sex pheromones
Nasonov pheromones
Royal pheromones
Calming pheromones
Necromones2

Ants, and many other animals, use trail pheromones to mark their trail as a guide for others in their gang. Other ants, catching the signal of trail pheromone, follow the way it goes and reach their gang leader. Trail pheromones are volatile compounds, so it is not very likely that you would see ants following the exactly same path tomorrow or a week later. All ants release trail pheromones, so as long as ants are going through that path, the trail signal will keep getting stronger and will also tell lost ants "Hey, bro! We are going this way. Don't you want to join us?" See, for example, here3:

In the beginning, different ants follow different paths, but as soon as an ant finds the shortest path, all ants join it on that path, due to which pheromones on other paths evaporates and finally, they all walk in straight line.

Of course, trail pheromones are very useful for organisms who have lost their way home, but you know, other organisms, like their predators, are not just sitting and watching them. Some predators can also catch pheromones and find out where the whole team is going, to attack them all at once. Such chemicals are known as kairomones. See this4:

  A kairomone is a semiochemical, emitted by an organism, which mediates interspecific interactions in a way that benefits an individual of another species which receives it, and harms the emitter.

Semiochemical is just a type of pheromone which a species X releases, but a species Y can also respond to its presence. Its just like when you walk on road and say "Whoa! Seems like a pizza delivery van just passed by" (obviously, smell of pizza is not by a pheromone ;)

The trail pheromones released by army ants can also be detected by a blind snake or a forest beetle, leading it right inside their nest. Obviously, all semiochemicals are not bad. Chemicals like synomones (helping both species) and allomones (just the opposite of kairomones) are also present5, but they are beyond this question's scope.

References:

 Medical Definition of Pheromone
Types of Pheromones - Wikipedia
Life in Wireframe - Ant Algoithms
Kairomones - Wikipedia
These Pheromones Get The Animals That Secrete Them Killed


Can yeast ferment maltose directly? I have been taught that yeast can act only on simple sugars (monosaccharides) and breaks them down into ethanol and CO2

I also know that yeast can break down maltose (disaccharide) and maltotriose (trisaccharide) using maltase from its enzyme complex (zymase) into monosaccharides of glucose and then ferments the same.

My question is whether yeast can directly ferment maltose and maltriose WITHOUT first breaking them down into glucose?  If so how is it done - enzymatically and what is the chemical equation

The statement in your first paragraph is correct: for yeast to ferment a carbohydrate it must be fed into the glycolytic pathway which, in the case of oligomers of glucose (e.g. mannose) simply means breaking the oligomer into its constituent glucose monomers using a single enzyme. This is similar to how yeast processes sucrose: the disaccharide is hydrolysed by invertase to release glucose (fed directly into glycolysis) and fructose (fed into glycolysis via fructokinase).

A separate mannose pathway would require a completely new set of enzymes that somehow processed mannose in a stepwise fashion without breaking the glycosidic bond linking the two monomers - I'm sure that you can see that this is a much less likely option in terms of the evolution of yeast metabolism.


How do we explain the white feathers of an albino peacock? Peacock feathers are supposed to produce colours by surface structures modulating the light (in addition to the usual absorption/reflection mechanism)... https://en.wikipedia.org/wiki/Structural_coloration

But how does that explain the existence of an albino peacock? https://www.favrify.com/wp-content/uploads/2015/02/peacock1.jpg

Does albino mutation change the physical structure of feathers in addition to the lack of colour pigments?

Does anyone have a close comparison of the physical difference of the albino vs coloured peacock feathers?

The surface structuresa that are responsible for the structural coloration of peacock feathers are actually barbules and rods made of the very same biopolymer that is responsible for pigmentation in many other animal species, namely melanin. Just as in other animals, melanin is produced in the melanocyte cells which reside in the skin's epidermis. The conditions of albinism or leucism are due to mutations to genes responsible for melanin expression in those cells, or their absence. So although structural coloration is resposible for the colorful peacock feather, it is the same mechanism that leads to colorless feathers as in other animals.

Reference

a Zi, Jian, et al. "Coloration strategies in peacock feathers." Proceedings of the National Academy of Sciences 100.22 (2003): 12576-12578. https://dx.doi.org/10.1073/pnas.2133313100


How does evolution produce complex organs I've been wondering lately how evolution manages to produce complex organs. It is pretty obvious to me how evolution would select some minor traits like size, resistnce to illness or climate. There is a mutation where some organisms are slightly different and better traits are selected. However I cannot imagine how an organism will mutate to have lets say lungs at once and unless organism has a functional organ there is no reason for the trait to be selected. So how does evolution produce complx organs?

The best introduction to evolution of complex phenotypes via master control genes is Endless Forms Most Beautiful: The New Science of Evo Devo and the Making of the Animal Kingdom by Sean B. Carroll. You might also want to have a look at a more recent Evolutional developmental biology (Evo Devo) book like those you get when searching for "Evo Devo" in Google Books.

In summary, it is possible for a mutation to change a shape by changing the spatial distribution of a transcription factor during embryo development. What's more, by changing the distribution of two mutually dependent factors, formation of any shape is possible if the distributions overlap. Such transcription factors are highly conserved in evolution and the most important cause of the endless forms we see.


What is "enzymatic activity"? I should be grateful if anyone would send me a link to an article or an encyclopedia/handbook contaning an explanation of the concept of enzymatic activity. Surprisingly, I did not manage to find anything else but a brief definition.

An Introduction to Enzymes (pdf) can be found here.

  Excerpted from a very popular Worthington publication which was
  originally published in 1972 as the Manual of Clinical Enzyme Measurements. While some of the presentation may seem somewhat dated, the basic concepts are still helpful for researchers who must use enzymes but who have little background in enzymology.

Source: Worthington Biochemical Corporation.

The quantity or concentration of an enzyme can be expressed in terms of activity in enzyme units. See Wikipedia:

  Enzyme activity = moles of substrate converted per unit time = rate × reaction volume. Enzyme activity is a measure of the quantity of active enzyme present and is thus dependent on conditions, which should be specified. The SI unit is the katal, 1 katal = 1 mol s−1, but this is an excessively large unit. A more practical and commonly used value is enzyme unit (U) = 1 μmol min−1. 1 U corresponds to 16.67 nanokatals.

Here are some additional useful, simple videos explaining enzyme activity:

How Enzymes Work
Explain factors affecting enzyme activity


If a gene is located on the X chromosome, does that mean males are never heterozygous for these genes? As said in the title I am a little confused on the idea of traits located on the sex chromosomes. The example we worked on in class was haemophilia, a recessive trait located on the X chromosome. Does this mean males only have one allele to choose from while females have two? Does this mean that only females have the ability to be heterozygous in sex linked traits?

There is a specific term for this called hemizygous / hemizygote - meaning that only one allele of the gene is present. Therefore males cannot be heterozygous for genes on the X or Y chromosome (not counting for gene duplication or other chromosome disorders) since they naturally carry only one copy of these chromosomes.


Can bats echolocation discern what insects they are preying on? Insectivorous bats feed on many different types of insects such as mosquitoes, moths, beetles, and bees.  According to the Bat Conservation Trust, bats can discern insects from other objects but I'm having trouble finding any research saying whether bats can discern between the insects they are chasing?

Yes, some bat species can distinguish the species of insects by echolocation. One of the better studied species is the greater horseshoe bat (Rhinolophus ferrumequinum).

Echolocating greater horseshoe bats (Rhinolophus ferrumequinum) detect insects by concentrating on the characteristic amplitude- and frequency modulation pattern fluttering insects impose on the returning echoes. This study shows that horseshoe bats can also further analyse insect echoes and thus recognize and categorize the kind of insect they are echolocating.
von der Emde, G. & Schnitzler, HU. J Comp Physiol A (1990) 167: 423. https://doi.org/10.1007/BF00192577

Further reading:

Hans-Ulrich Schnitzler, Elisabeth K. V. Kalko; Echolocation by Insect-Eating Bats: We define four distinct functional groups of bats and find differences in signal structure that correlate with the typical echolocation tasks faced by each group, BioScience, Volume 51, Issue 7, 1 July 2001, Pages 557–569, https://doi.org/10.1641/0006-3568(2001)051[0557:EBIEB]2.0.CO;2

Ulanovsky, N., & Moss, C. F. (2008). What the bat’s voice tells the bat’s brain. Proceedings of the National Academy of Sciences of the United States of America, 105(25), 8491–8498. http://doi.org/10.1073/pnas.0703550105

Roverud, R.C., Nitsche, V. & Neuweiler, G. J Comp Physiol A (1991) 168: 259. Discrimination of wingbeat motion by bats, correlated with echolocation sound pattern https://doi.org/10.1007/BF00218418

Hearing by Bats (edited by Richard R. Fay)


Why does contracting the iris allow less intense light to go in? The iris contracts automatically in the presence of bright light. This makes a flashlight appear bright in darkness, but outside in daylight you can't even see it's light.

The iris is changing your sensitivity to the intenseness of light. But physically all is happening is the iris is getting smaller or larger. I can see how this allows less light to go in if it gets smaller, because it's less surface area. However, I would imagine this would change the field of view though if I didn't know any better. Why does it change the intenseness of light instead?

Imagine the iris like a shutter in front of a focussing lens (which, in fact, it is; see the diagram).

This means that any light going through the iris will be focussed on a very small point on the retina, and your eye is wonderfully developed in a way that this exact spot is the fovea, the only spot in the retina that allows you to see colour and high-resolution.

The iris does not modify the focussing function, it merely changes the amount of light going through into the lens to then be focussed onto the fovea. Imagine that every single object in your field of view reflects/radiates light in every possible direction - narrowing the shutter won't exclude parts of the field of vision, it will only exclude some of the rays coming in at very flat angles and thereby reduce intensity.

Only if your lens is deformed, focussing (adaptation) will malfunction (directing the gathered light to the wrong spot; or focussing the incoming light in front of or behind the retina) and blur your vision.


Chloroplasts in an animal cell What would happen if we inject a chloroplast organelle into an animal cell?

Will the animal cell destroy it? Or is it possible that the chloroplast will somehow survive, and even replicate? Could there be photosynthesis in such a cell, or will some of the necessary mechanisms be missing?

To answer your bigger question:

Yes, most of this is possible - under some conditions -, and animals and animal cells can acquire chloroplasts, and use them.

E.g.: see Elysia chlorotica whose cells actively take up chloroplasts and use them, and keep them alive (though not replicating). - Though some genes of algae are also contained in the Elysia chlorotica genome - which may be considered as partial replication.

Also there are salamanders that have replicating algae within them (since embryogenesis) - even algae (with chloroplasts) within animal cells - though here the algae might be rather understood as symbionts or "cell types", and the animal cells don't have the chloroplasts by themselves.


What kind of beetle has fuzzy orange antennae and can flip its head down for digging? Some years ago I found this beetle while hoeing potatoes in Iowa in the United States. It had something like branches on its legs and could bury itself out of sight in five seconds! If I recall the beetle itself was mostly black.  It had the ability to flip the front part of his body up to reveal the face which was normally down facing the ground. I suppose because it usually lives underground. But when it flipped its head up, it's antennae came out and were bright orange, fuzzy ,and had round ends similar to an old-fashion side mirror on a car. When it's head was down it had a horn almost like a rhinoceros beetle.  But when it flipped its head up it had buggy eyes - the cutest little face.  I have never been able to find out what this little critter was. I just ran across my description of it in my journal today and tried to look it up online, finding your website.  Sorry, I didn't own a camera back in 2000 to take a picture of him.

I'd guess that the beetle you found was of the genus Nicrophorus ,family Silphidae . They are commonly known as Burying beetles and are true to their name

was this the beetle you saw?


Aseptic technique: a single technique, or any technique fulfilling criteria, or collection of said techniques? My friend just used the following sentence in her lab report:

  Aseptic technique is used in this step:

I immediately felt something was wrong. She used the term as if it were a specific technique. Is her usage correct, and if so is "aseptic technique" indeed a specific technique with a specific procedure?

Rather, I thought "aseptic technique" referred to any technique that involves complete sterilization of a certain environment or apparatus/instrument. If this were right, then perhaps "an aseptic technique" should be used instead?

Further still, if "aseptic technique" refers to the collection of all techniques that involve sterilization as described above, the perhaps it should have been "the aseptic technique" instead?

Which one(s) is/are correct, grammatically and semantically (hence conveying the concept accurately)?

This is primarily a linguistic question and I am answering it on the basis that it will be migrated to Stack Exchange, English Language and Usage.

The question is whether, in the context of a report describing (otherwise unspecified) student work, the phrase “aseptic technique” can be used without an article, or whether it requires the definite or indefinite article. This is a question of meaning and usage, and, without using any technical grammatical terms, can be answered by anlysis of scientific publications and by analogy.

“The aseptic technique” (definite article)?

The definite article would normally be used in this type of situation if reference was to one specific clearly defined technique. As an anlogy I would take ‘The Heimlich manoeuvre’ (where ‘manoeuvre’ occupies an analagous position to ‘technique’. Clearly the phrase does not refer to a standard defined procedure like the Heimlich manoeuvre, but merely that the work was performed asceptically (i.e. under sterile conditions). So in this context the definite article is certainly not necesary. In some circumstances employing sterile conditions requires satisfying certain enumerated criteria (example below), in which case the definite article may be used.

“An aseptic technique” (indefinite article)?

I think that this is possible but not obligatory. The use of the indefinite article indicates that the asceptic technique used was one of several possible. Although sometimes this would be used in the context of a limited number of items, this is not a necessary requirement. Analogies with a different adjective would be “she executed the dive with a graceful technique”. Here, the article is (almost) obligatory, but less so in the case of “she showed superb technique in executing the dive”.

“Aseptic technique” (no article)?

As the last example shows (“she showed superb technique in executing the dive”), omitting the article is perfectly acceptable in analagous phrases. I would say it is perfectly acceptable in this case.

The arguments above are only useful to the extent that they reflect actual practice. A quick internet search brought up an interesting example in which both no article and the indefinite article were used in the same text. This is the entry for Asceptic Technique on a website called Healthline.

The second paragraph omits the article:

  Aseptic technique is a method designed to prevent contamination from microorganisms.

But when it gets down to specifics:

  According to The Joint Commission, there are four chief aspects of the aseptic technique

So unless your friend was referring to ‘The Joint Commission’ (which I doubt) there is nothing wrong with that sentence of her lab report.

Other Professional Examples

ThermoFisher Scientific — no article

  Aseptic technique, designed to provide a barrier between the microrganisms in the environment and the sterile cell culture, depends upon a set of procedures to reduce the probability of contamination from these sources

Nuffield Foundation — indefinite article (implied by use of ‘any’)

  There are some general rules to follow for any aseptic technique.

ANTT — definite article used in reference to a specific named technique

  Aseptic technique is the most commonly performed infection prevention procedure in healthcare; it is also probably the most critical. This article looks at the Aseptic Non Touch Technique (ANTT) model for reducing healthcare-associated infections

(You could argue that the definite article refers to the model, rather than the technique, although I think if you omitted ‘model’ you would be left with an example like the Haemlich manoeuvre. In any case the English in this article is appalling — “infection prevention procedure” gives a foretaste of the stylistic horrors that follow.)


Standard Process Identification of New Disease outbreak Causing Pathogen Is the any standard procedure or protocol followed for the identification of cause of new disease outbreak(or new pathogen)? Is it different for different countries?

I was first thinking of voting to close the question because it was too broad, but in reconsideration I think the answer of showing why it is too broad would constitute a proper answer in this case.

First of all, the term disease is one of the most general terms for a problem in medicine.  The only term that could be higher up is "medical condition."  It could be an infectious disease, genetic disease, induced disease (think chemicals, tobacco, etc), or [insert organ here, ie heart] disease (which are not necessarily genetic).  There are attempts to distinguish between "diseases" and "disorders," but the difference is not always clear.  The term "disorder" is growing in usage and scope because it is seen as having fewer negative connotations than disease (think disease of the mind vs. disorder of the mind).

Thus each field has it's own ways of identifying new diseases.  As a general trend new diseases are found now by identifying greater specificity within a previously general disease.  For example, a person could be said to have an "adrenal cancer," but now we would want to know if they have an adrenocortical carcinoma.  In an infectious setting, we could think of all the particular pneumonia being specified out of interstitial lung diseases.

Diseases caused by external agents (pathogens, toxins, etc) can sometimes be more uniquely novel, in that they can change into something unpredicted (new compound or virus made by man for example).  Perhaps you meant to ask if there were standard ways for identifying new viruses or microbes?


What are the frequency ranges of most marine mammal vocalizations? I am trying to determine a list of frequency ranges into which marine mammal vocalizations fall.
Ideally, I would like a list showing where the most popular marine mammal vocalizations fall, followed by the species name. That being said, I only really care about frequencies above 20 kHz, should they exist.

Example: (Numbers fabricated)

Orcas       : 30-40 kHz
Dolphins    : 100 kHz
Blue Whales : 60-88 kHz

etc.

Even if the list is 'quick and dirty', thats ok. The list will essentially point me to which species' songs/sounds I need to study.

Some additional context, this wikipedia link as well as this one have some nice sound files of many marine mammals' songs/sounds. I am trying to avoid having to download each one and analyze their spectral content. (I could, but would rather not).

Here there are spectrograms from Bottlenose dolphins (Tursiops truncatus), Killer whales (Orcinus orca) and False killer whales (Pseudorca crassidens).

Here there are spectrograms for Humpback whale (Megaptera novaeangliae) and from Sperm whales (Physeter catodon or Physeter marcocephalus)

Here there are spectrograms from Blue whale, Fin whale and Minke whale.

Some other google search for "spectrogram + your preferred cetaceans" should make your list. Enjoy.


What is a "scutella of reindeer"? In the film "The Perfect Human Diet" at 32:36, a scientist points to animal remains and states "we've got a scutella of reindeer there."  What is scutella in this context?

Scutella refers to shield or plate-like structure on animals (dictionary.com), such as the scutes of a turtle shell.  I have never seen reference to scutes or scutella or anything similar on any type of deer, including reindeer.

I have not seen the movie so I do not know the context of usage. My gut reaction is the person was trying to make something sound important or "scientific" when a much simpler (and perhaps more accurate) word would have sufficed.


Trying to identify a baby bird seen in Palermo, Sicily I'm trying to identify a baby bird that i saw in a pond in Palermo, Sicily, Italy. Unfortunately i did not see any parents!
Any help is appreciated.
Thanks,
Robert

It looks like the chick of a Moorhen (Gallinula chloropus) or Coot (Fulica atra), probably the former. Both species are common on ponds.


unknown bird in Long Lake Michigan......chocolate brown head and neck, charcoal body and tail, ivory wings, top and bottom light chocolate head and neck w/ charcoal body and tail. the wings are ivory white, top and bottom from the body outwards. the colors are clear.....not mixed with other colors. no stripes or spots, etc. slightly smaller than a robin.

That's a very interesting set of colors.  Unfortunately nothing springs out at me, although I can think of a couple of birds that might sort of (maybe) match.
First, common pigeons come in all sorts of colors and patterns, and it's possible that yours is one.  On the other hand, common pigeons tend to be very familiar to most of us, so I don't think you'd be asking about that.
Second, there is a tern that is moving through the area about this time of year, that might fit:  Black Terns can have a lighter wing.
Here's a link and a representative photo:
 https://www.allaboutbirds.org/guide/Black_Tern/overview

There is another, even better possibility, if your bird is ternish:
The White-winged Tern (formerly White-winged Black Tern) is an uncommon late-summer wanderer through much of the region.  Here is a link and a representative photo:
https://avibirds.com/white-winged-tern/


Looking for book or article that derives formula for estimating the "average heterozygosity" An online lecture I need to watch on population genetics describes a formula for the "average heterozygosity" as follows:

  ...we can theoretically predict that the average heterozygosity in the population will simply be four times N, the size of the population,
  multiplied by the mutation rate.

The formula that appears on the screen as the lecturer says this does not match what he says (but it's hard to say; the typesetting is terrible).  Furthermore, I find this description too vague (I have a million questions about each of the words in it).  Also, I would like to see how this estimate is derived.  Finally, judging by the number of egregious typos I've found in this series of lectures so far, I'd like to get a second independent rendition of these ideas.

I thought that Google would make quick work of this question, but to my surprise, when I search for "heterozygosity" or "average heterozygosity" none of the hits I get mention this formula.

I imagine that this is textbook-level stuff (i.e. not something that I'd have to go to the current research literature to find).  Can someone point to a textbook that derives this estimate?  (I am interested only in textbooks that discuss the formula alluded to in the quote above, as opposed to general textbooks on population genetics.  I've already consulted several of the latter, and not been able to locate the formula in question.)

$H=4N\mu$ is the formula you're trying to derive.

It is an approximation coming from an infinite site model and applies to diploid populations only. For haploids, it becomes $H=2N\mu$. The value $4N\mu$ or $2N\mu$ is often also called $\theta$ as it is a value that appears in many places in the field.

There are a number of ways to derive it. It can be derived from coalescent theory or from classical fixation index stuff from Wright.

Any good intro book to population genetics should derive this formula. (see for example in Gillespie's book). You will find more book recommendation at Books on population or evolutionary genetics?.


How does LDL leave the circulatory system and enter the interstitial fluid to deliver cholesterol to cells? I have read that small molecules like oxygen and carbon dioxide diffuse through the capillaries, but larger structures can't fit through.

This answer indicates that some proteins go through via transcytosis.

The wikipedia article on capillaries shows that there are 3 types of capillaries, and it looks like LDL could fit through fenestrated or sinusoid, but sinusoid seem to only be found in certain organs, and if it did go through the holes in fenestrated capillaries, how would the LDL get to cells that are nearby only continuous capillaries? Would fenestrated capillaries be regularly dispersed so one is always nearby, or would the LDL just diffuse through the interstitial fluid originating wherever the fenestrations are?

Many biologists had the same question for a number of years. In the 1950s, Nobel Laureate George Palade identified small vesicles in endothelial cells and postulated a mechanism whereby these vesicles would take in macromolecules from the luminal side of the endothelial membrane and transport them across the cell to release them to the tissues. His hypothesis has been tested, confirmed, and is now well documented.

Endothelial cells have LDL receptors that bind LDL in the capillary lumen, cause the cell to form a vesicle, and then transport it across to the membrane facing the tissues. There, the vesicle fuses with the tissue facing membrane, and LDL is released for uptake by peripheral tissue.

This process is called transcytosis. Endothelial cells use receptor mediated transcytosis to deliver many different large molecules to peripheral tissues in a regulated manner. You can read about this in some detail here (also the source of the figure), and more generally here.


Solid mouse (C57BL/6) WT primers I am trying to get a good pair (or better yet, library of pairs) of primers that give me one band in WT mice (C57BL/6). Do you know where I could find such a thing?

Alternatively, I thought of just designing a few sets of primers myself for highly-conserved regions. But that's quite a bit of guessing work (what regions, what pairs from what eprimer3 will calculate for me etc.).

So:

Do you know where such a database could be found?
If not, could you help me get started with creating it myself? What specific regions would in your opinion be particularly good for this purpose?

I have settled for two GAPDH primers with a short amplicon (~50bp):

>gapdh_rv3 <unknown description>
GAGACCTGAATGCTGCTTCC

>gapdh_fw3 <unknown description>
CTCCATTTCCCCTGTTCTCC

They provide consistent and good controls, as seen here (lower bands):


How do animals avoid the problem of inbreeding? In humans, there are various cultural rules to avoid inbreeding (to the level of paternal cousins, nieces/nephews and uncles/aunts etc)

How do animals such as dogs avoid the problem of inbreeding? They do not have a record of their relatives and there seem to be many siblings in each batch for some animals. How does it work in the wild or among stray animals? Is their DNA somewhat resilient to these genetic disorders?

Likewise, how do birds handle this issue?

EDIT: I am not trying to breed animals, want to understand how it works in the uncontrolled wild when the young leave home early and are scattered.

The question is interesting. However, it will be impossible to answer accurately for all birds as the mechanisms actually used vary from species to species. So I will give you some information in the general sense.
Recurrent inbreeding reduces inbreeding depression
Inbreeding depression is caused by both

Recessive deleterious alleles that are brought to homozygosity
Some epistatic interaction

In any case, in a population where inbreeding is common, those recessive deleterious alleles and alleles involves in these deleterious epistatic combinations will be washed out (or at least brought to lower frequency) of the population via selection and the population will end up suffering less from inbreeding than a typical outbreeding population. In the extreme, a population of exclusively selfer individuals, such deleterious recessive alleles are brought to extremely low frequency within lineages.
How to avoid inbreeding?
Now, sure animals and plants typically don't have a big book that allow them to tell how related they are to another individual. However, there are other mechanisms of kin detection
Self-incompatibility
For example, in plants self-incompatibility is thought to be relatively uncommon. There exist many mechanism, so I-ll just consider a simple example. Consider a self-incompatibility locus as a specific loci for which if the same allele is shared by both the pollen and the ovule, then no fertilization occurs. This prevents selfing and prevents mating with many of the closely related mechanisms.
Body odour and sexual attraction
Also, there are mechanism that can mediate sexual attraction toward individuals that differ. The classical example is Major histocompatibility complex (MHC) and sexual attraction (vertebrates), where individuals tend to be attracted to individuals that have a different MHC.