Hair loss in a nuclear submarine? Biologically, how prevalent is hair loss on a nuclear submarine? How can prolonged exposure to radiation levels typically present on a nuclear sub affect a person, say over a year or even more?

If the question is related to exposure to radiation in a Nuclear submarine then the answer is valid for radiation exposure irrespective of the place.

As you are aware there are many effects of radiation. Some of them are.

  Nausea and vomiting
  Diarrhea
  Skin burns (skin reddening)
  Weakness
  Lethargy and fatigue
  Loss of appetite (anorexia)
  Fainting
  Dehydration
  Inflammation of tissues (swelling, redness or tenderness)
  Hemorrhages under the skin
  Bleeding from your nose, gums or mouth
  Anemia
  Hair loss (usually from just the scalp)
  Decrease in platelets (reference)

Of course there is no safe quantity of radiation that has been quantified (reference) and there are personal anecdotes by submarine officers about first hand problems they faced due to radiation (reference). However, since this is a career you chose, you can be happy that the amount of radiation that you would be exposed to has decreased over the years (reference). Since you are interested in the biological aspect of what happens in your body due to radiation, I quote

  When cells -- and what lies within them -- get exposed to radiation,
  components of DNA and critical proteins within the cell get all jazzed
  up (ionized), meaning that the electrons with our atoms get kicked
  out, causing the DNA strands to break and the proteins to cramp up
  (denature).

  Ionizing Radiation:

  Leads to the production of free radicals
  Breaks critical chemical bonds
  Leads to changes in cellular structure within irradiated cells
  Damages vital molecules, such as DNA, RNA, and other regulatory
  proteins

  Because our cells are mostly water, this ionizing radiation breaking
  H$_2$0 down is harmful to free radicals (H$^+$ and OH$^-$). While cells are
  damaged by free radicals all the time, they normally repair
  themselves, keeping the body healthy. However, high doses of radiation
  can damage the cell's ability to repair itself, and then all hell
  breaks loose.

  This shakes things up all over the body.

  Let's do a head-to-toe walk-through to investigate how high doses of
  radiation can damage the human body.

  BRAIN: Nerve cells (neurons) and brain blood vessels can die, leading to seizures.

  EYES: Radiation exposure increases the risk of cataracts.

  THYROID: When a nuclear reactor malfunctions, radioactive iodine (I-131) can be released into the atmosphere (this is one of the
  particles that hangs out in a "radioactive plume"). The thyroid is
  very sensitive to the effects of I-131 (in fact, I-131's affinity for
  the thyroid is used therapeutically to specifically attract radiation
  to the thyroid in order to treat thyroid cancer and overactive
  thyroid). When a healthy thyroid is exposed to I-131, it can lead to
  decreased thyroid function and, over time, thyroid cancer.

  LUNGS: When you breathe in invisible nuclear fallout particles, it can lead to lung cancer down the road.

  HEART: High doses of radiation can damage the cells in the blood vessels that feed the heart, reducing cardiac function.

  GI TRACT: Sensitive cells in the intestinal lining can be damaged, leading to nausea, bloody vomiting, and bloody diarrhea.

  REPRODUCTIVE ORGANS: Rapidly dividing cells (eggs and sperm) in the ovaries and testes can die, leading to sterility.

  SKIN: Rapidly dividing skin cells can be damaged, leading to skin lesions and burn.

  LYMPHATIC SYSTEM: Rapidly dividing lymphatic cells die and damaged bone marrow may have trouble replenishing these immune-boosting cells,
  increasing the risk of infection (reference).

Many jobs have occupational diseases connected with it so I would say don't worry about it too much, enjoy your job and keep your fingers off the firing mechanism.


How does the muscle return to its resting state after muscle contraction? I know that when ADP binds to the myosin head, it moves along and as it does so, it releases the ADP. The ATP attaches to the myosin head and releases the myosin head from the actin filament. Then the enzyme ATPase hydrolises the ATP to ADP, causing the myosin head to move to the original position.

My question is:

How does the actin filament (troponin) move to its original
position? Does it use a mechanism similar to a spring?
Is there a limit to how much the myosin head can pull the actin filament?

ad 1. : In skeletal muscle, contraction of the antagonist stretches the agonist to its original position (Fig. 1).

ad 2. : Yes, ATP generates a fixed amount of energy that limits the force generated.

Fig. 1. Agonist/antagonist pairs in the skeletal musculature have opposing actions. source: wikipedia


What plant/tree is this? Found this in a rural area next to the road last month and I wonder what is it?

From my searches I think it is a strawberry bush but I'm not sure and any help would be appreciated, thanks!

Your pictures are a bit vague, but I think recognize Euonymus europeus, the spindle tree. So I assume the picture comes from Europe? The fruits are encapsulated in pink capsule, the fruit itself is bright orange.

https://en.m.wikipedia.org/wiki/Euonymus


Does DNA replication in 5' to 3' (leading strand) need RNA primase? https://www.youtube.com/watch?v=27TxKoFU2Nw

In the above video it shows that during DNA replication, the lagging strand require RNA primase to add 3' -OH group for further addition of nucleotides. However, it hasn't been shown that the above strand ( leading strand) require it.

Besides, RNA is needed to initiate the polymerization because it has the 3'-OH.
But when I look at the structure of deoxynucleotide, it also has the 3'-OH but it does not have the 2'-OH. So why DNA cannot initiate the polymerization?

Thanks for your answer!

The DNA polymerase also needs a RNA primer on the leading strand to be able to start polymerization. Afterwards this is not needed anymore, since the replication goes on without a break. On the lagging strand polymerization replication can only work between the replication fork and the next region of double-stranded DNA. See the figure (from here):

The reason for the need for RNA primers is located in the function of the enzymes. While the DNA polymerase can only work on a double stranded template (add nucleotides to the 3'OH-end of the strand) the DNA Primase (actually an RNA polymerase) can work on single stranded targets and thus add the RNA primer there.


Which mountain range was formed first (historically) and which the pedigree is correct? Source 1:

Source  1 shows a map of a particular area. In this map you will find the  mountain ranges 1 and 2, the species P, Q and R. Two possible pedigrees of  the ancestral history of the species P, Q and R are drawn .
Which mountain range was formed first (historically) and which  pedigree is correct?

If mountain range 1 was formed first, pedigree 1 is correct.

If mountain range 2 was formed first, none of the two pedigree seem correct.

If mountain range 1 was formed first you would first have the split of the initial population into population P and the population Q+R. Then, the formation of mountain range 2 split the population Q+R into Q and R. Therefore, Q and R are more closely related than they both are to P. Therefore Pedigree 1 is correct.

You can apply the same kind of reasoning by guessing that mountain range 2 was formed first and you will realize that you would expect a pedigree different than Pedigree 1 and Pedigree 2. If mountain range 2 appeared first then, the correct Pedigree would display the population/species/lineages P and Q more closely related to each other than they both are to R.


How many molecules of ATP are actually produced in aerobic respiration? I have been through the process of aerobic respiration a few times in different text books and almost every book quotes a different value for the number of ATP molecules produced. The consensus seems to be 30–32, but why is there disagreement and why aren’t the numbers exact?

The possible reasons I can think of are:

Phosphorylation of ADP is not directly coupled to redox reactions.
The number of ATP molecules produced depends on the shuttle used to transport electrons from the NADH in the cytosol to the mitochondria, i.e.  whether it’s FADH2 which enters the ETC or NADH. (I have a silly question on that, but I need confirmation, does the electron carrier chosen depend on availability?)
The proton-motive force can be used to drive other cellular processes other than the production of ADP? (I'm guessing.)

Are these suggestions correct, or is there some other explanation?

The discrepancy between 30 and 32 molecules of ATP quoted in the question may well arise from the two possible ways in which the reducing equivalents of the two molecules of NADH generated in glycolysis may be shuttled across the inner mitochondrial membrane into the mitochondrion (suggestion 2).

If one assumes that the malate-aspartate shuttle is used, then NADH is transported into the mitochondrion as such, and the yield of ATP is the same as for those molecules of NADH generated in the mitochondrion — 2.5 ATP per NADH from the most generally accepted measurement.

However, if one assumes the glycerol phosphate shuttle is used then the reducing equivalents are transferred from NADH to FADH2, from which only 1.5 molecules ATP is produced per molecule.

In summary, using the malate–aspartate shuttle a total of 5 molecules of ATP (2 x 2.5) will be produced from the two molecules of glycolytic NADH, whereas using the glycerol phosphate shuttle there will be only 3 molecules of ATP (2 x 2.5). This gives a difference of 2 molecules of ATP, which would cover the range in the question.

As the relative proportions of the two shuttles varies between tissues, a range of values is actually possible.


Why pain caused by blunt objects vanish after some time and return at the event of touching? Background

When any bone/muscle of body is hit badly by a blunt object, it hurts pretty bad of course for some time. But, after some time the pain goes off completely or to some extent.

Then, if we touch the wounded spot, the terrible pain returns.

Why?

If the pain goes off as the healing process of severed tissues, blood capillaries, then why does it return at the event of touching?

My reasoning: I think there is a sophisticated pain mechanism responsible for this phenomenon.Firstly, pain warns our nervous system to be cautious against any new injury. As time goes on, sensory adaptation diminishes the pain. But the event of touching is a new pressure for the blunt wound.So, the pain comes back again. But, I need well-referenced answer to support my view.

Papers: The most relevant paper I've found till now: 1 which is behind paywall

BASIC REASON WHY THE PAIN DISAPPEARS FOR SOMETIME:

There are gating mechanisms involving pain both in the spinal cord and in the brain.

Although the pain gating pathways in the brain are multifold complex,the spinal pathway can be simplified.
The latter may be understood in a simplified manner in 2 ways:

When there is a nociceptive stimulus,the epicritic receptors are stimulated.Sensory fibres from them synapse with internuncial neurons which inturn transmits impulses via the ascending tract to the periaquiductal grey. This region is capable of inhibiting pain impulse transmission to the spinal cord or thalamus by modulating impulses via the descending tracts.
This type is called supraspinal control
Another spinal reflex-type gate control operates in which stimulus like rubbing over the pained area ,application of warmth or cold causes inhibition of pain.
This is due to the impulses by large type (myelinated)A-fibres which arises from the  rubbed areas synapse with the internuncial neurons which are already synapsed with the epicritic sensory neurons of the dorsal root.The ends of such type of fibres release neurotransmitters that inhibits transmission of pain impulses through the internuncial neurons .
This is termed as segmental suppression

WHY DOES THE PAIN RETURN AGAIN:

This is because the pain receptors are the slowest to adapt.It's exactly as you said because it keeps the body apprised of tissue damaging stimulus.
So when there is the return of the noxious stimulus we can understand the tremendous summation effect which takes precedence over the gate control.

This occurs by a greater output of neurotransmitters from the synapse of the pain sensory fibres which outdoes the inhibitory effect of the neurotransmitters favouring gate control of pain.


What's the highest glucose concentration (in mM) anywhere in the human body (tissue, capillaries, tumor microenvironment, etc.)? Glucose blood levels are around 5mM, or 10mM after meals. In capillaries these levels can rise by about 40 %. I haven't found measurements of glucose concentration in tissues, or in extracellular spaces. I'm wondering what's the highest glucose concentration, anywhere in the human body?

Glucose concentration in the blood is a highly regulated biologic variable. From personal laboratory experience, it is very difficult to raise a healthy, non-diabetic individual's blood glucose over about 6.5-7 mM (i.e. 120-130 mg/dl). My best guess at where the highest glucose concentration might be in the body is within the hepatic portal vein that drains the intestines after a high carbohydrate meal. The glucose concentration is probably highest in the prandial state or, in other words, when carbohydrates (i.e. food) is being digested and absorbed by the gastrointestinal tract. Many simple and/or complex carbohydrates are digested to glucose and absorbed through the gastrointestinal tract. Once absorbed the glucose enters the venous mesenteric circulation and then drains into the hepatic portal circulation. This allows high concentrations of glucose and other compounds like amino acids from dietary nutrients to be "buffered" by the liver.

I don't have hard evidence to demonstrate that this is the highest glucose, but I think it's probably a good guess. It is inherently difficult to measure the blood glucose concentration in the portal vein - mostly because it's so difficult to get to that place anatomically during a meal. The dog is probably the most used animal for these types of metabolic studies, because catheters can be placed in the peripheral venous and arterial circulation, as well as in the portal vein and hepatic veins, to measure nutrient uptake by the intestine and nutrient extraction by the liver.

A number of previous studies by Cherrington and colleagues, who have done some of the most comprehensive work in this field, frequently measure glucose concentration and blood flow rates across the liver. In one such paper that is freely available from the American Journal of Physiology by Abumrad et al (1982) entitled, "Absorption and disposition of a glucose load in the conscious dog" you can see from Figure 1 the average plasma glucose concentration in the portal vein from a group of dogs given an oral glucose load of ~40 grams is somewhere in the 250 mg/dl region (i.e. ~14mM). These were otherwise healthy dogs, and similar to healthy humans I would bet the glucose concentration doesn't rise too much further. As you could imagine though, in a diabetic individual who has high peripheral glucose concentrations to start, the portal vein concentration might be expected to be higher. How much higher is another educated guess - maybe 100-200 mg/dl higher on an extreme end (obviously pathologic).

In a healthy human (i.e. non-diabetic) who undergoes a 75-gram oral glucose tolerance test I can't imagine that the portal glucose would go any higher than 300-400 mg/dl (or, 16.5 to 18 mM). But again - these numbers are just educated guesses. This is probably the highest glucose concentration anywhere in the body. Additionally, in diabetic patients the glucose concentrations would be expected to be slightly higher because circulating glucose may be slightly higher, but probably not by too much (definitely not an order of magnitude).


Is the human biological clock genetically programmed or learnt? Argument favouring learning:
A newborn sleeps for 20-22 hours. But overtime (s)he learns to focus sleeping time to night time, according to his or her needs and family needs. Some sleep from 1 am to 7 am, some from 11pm to 5 am. So it is learnt.

Argument favouring a genetic origin:
Somewhere I read (I don't exactly remember the article) where it was told that the biological clock is not of 24, but of 25 hours. This means that the synchronisation is not maintained with the earth. If it would be learnt, then why is it not in synchrony with the world?

Short answer
The biological master clock is neurologically and genetically hardwired. The biological clock is not affected by learning. Instead, it is constantly entrained mainly by daylight.

Background
The biological clock is hardwired in the human body and can be traced back to the master clock in the suprachiasmatic nuclei (SCN) of the hypothalamus (Fig. 1).

Fig. 1. The SCN is entrained by environmental light captured by the retina in the eyes. Source: Neuroscience News.

The SCN is an intrinsic oscillator that governs sleep and wake timing, rhythms of temperature, hormones, mood and cognitive acuity etc. etc. These rhythms are entrained to 24 hours by the environmental light-dark cycle primarily via a subset of photosensitive retinal ganglion cells that project directly to the SCN (Fig. 1). Using hormones and neuronal signals, the SCN entrains peripheral clocks of similar molecular mechanism present in many tissues (Pagani et al., 2010).

In humans and other organisms, the timing of 24-hour behavior is governed by the period length of the circadian oscillator. This period is approximately, but not exactly, 24 hours long (circa diem), and ranges from 23.47–24.64 across people (23 hours 28 min to 24 hours 38 minutes) in laboratory conditions (Pagani et al., 2010).

Why is it circa diem and not exactly 24 hours? Note that the absolute length of a day depends on the definition used. For example, one complete rotation of the earth around its axis (the sidereal day) actually takes 23 hours, 56 minutes and 4.1 seconds. The solar day is 24 hours and is defined by the time it takes the sun to make an apparent circuit across the skies. More importantly, there is apparent solar time, sometimes called true solar time, which is determined by the daily apparent motion of the observed sun. It is based on the interval between two successive returns of the sun to the local meridian. The length of a solar day varies throughout the year, and the accumulated effect of these variations (equation of time) produces seasonal deviations of up to 16 minutes.

The length of a day can also be defined in the number or hours from sunrise to sunset, which varies where you are on earth. At the equator every day of the year is exactly 12 hours long. At 50° latitude (e.g., England & Canada) the longest day is 16.5 hours and the shortest day 7.5 hours. At 35° latitude (e.g. many US states and Greece) the longest day is 14.5 hours and the shortest day 9.5 hours. Given that light is the most effective way to entrain the circadian rhythm, it is obvious why the absolute length of the intrinsic circadian rhythm is not important. As long as it is circa diem, it will do.

Reference
- Pagani et al., PloSONE (2010); 5(10): e13376


When analyzing whether selection favors an allele that allocates indiscriminately, should the initial frequency of the allele be considered? For example, Refardt, Bergmiller & Kummerli (Proceedings Royal Society-B, 2013; http://rspb.royalsocietypublishing.org/content/royprsb/280/1759/20123035.full.pdf)
model bacteria that have been infected and that commit suicide  in order to prevent the spreading infection to the rest of the population.  They do so even though relatedness is low, approaching zero.

Two questions:

In section 3c, they write

  (A)ltruistic host suicide cannot evolve with $r=0$ because populations
  go extinct before invasion of the Abi trait is possible.  Thus, we
  predict marginal relatedness ($r < 0$) to be required for successful
  invasion.

I am assuming this is a typo and they mean $r>0$?
In a situation in which altruism is not directed toward any particular individual(s) but is rather allocated to the whole population, doesn't $r$ depend upon the frequency of the allele that is engaging in the altruism?  If it is a new mutation and there is no other allele in the population to receive the benefit, then r=0.  If the allele has gained fixation, $r=1$ and selection is much more likely to favor the altruism.

What is a way of modeling whether selection will favor fixation of a new mutation that allocates benefits to the population but not any particular individual (e.g., by committing suicide), given that the new mutation is not shared by (m)any other individuals and consequently, $r$ is initially very low?  I would think there is a way of determining the odds that genetic drift would lead the new mutation to develop a substantial enough frequency to increase the odds that the resources would benefit holders of the allele.  But I am unfamiliar.

I have not read the paper but here is my guess and a hint

  Is it a typo?

Yes, I think so

  In a situation in which altruism is not directed toward any particular individual(s) but is rather allocated to the whole population, doesn't r depend upon the frequency of the allele that is engaging in the altruism?

Yes

  f it is a new mutation and there is no other allele in the population to receive the benefit, then r=0. If the allele has gained fixation, r=1 and selection is much more likely to favor the altruism.

If the allele that is causing altruism has reached fixation, then there is no more selection as there is no genetic variance in the population.


Neurology: spinal tract I have had a few difficulties finding answers for the questions below. I have tried answering the first two myself; but, I am not sure they are correct or not. And I am not too sure about the third one.

In which structure of the brain does the axon from the spinocerebellum tract synapese? Is it the cerebellum?
Are the cell bodies of axon in the gracile tract located at the dorsal root, tectospinal tract located in cerebral cortex?
Which region  of spinal cord carries feed-forward information to help accommodate for upcoming motor movement?

Yes, the spinocerebellar tract ends in the ipsilateral cerebellum.
The gracile tract is a bundle of axon fibers in the dorsal root. The neural cell bodies are in the dorsal root ganglions. The tectospinal tract is part of extrapyramidal tract that connects midbrain (mesencephalon) with the spinal cord.
Didin't get exactly what you meant but: the lateral corticospinal tract (part of pyramidal tracts) controls fine movement of ipsilateral limbs, while the anterior corticospinal tract (part of the pyramidal tracts) conducts voluntary motor impulses from the precentral gyrus.

Source: Wikipedia: Tectospinal tract, Spinocerebellar tract, Dorsal root ganglion, Pyramidal tracts, Anterior corticospinal tract, Lateral corticospinal tract.


How does the social structure of lion prides prevent incest? I assume that lions don't have a concept of incest and they will just mate with any adult lioness in heat, daughter or not.
If so, is incest inevitable as the female cubs will grow up and remain in the pride? Their brothers will be kicked out as they reach mating age. But the females stay, so what is the mechanism that will prevent their fathers from mating with them?
I suppose that their fathers will be driven out of the pride by incoming males sooner or later. But if it doesn't happen soon enough, then what prevents them from mating with their daughters?

It is true that African lions have recently become more prone to inbreeding, largely due to human actions (reasons include limited dispersal and at least temporarily reduced pride sizes). see here
Generally though, lions likely avoid mating with close relatives innately as most animal species do. see e.g. here
A few things about the social structures of lions (ref.):

First, many prides are not controlled by a single male. Although the males might often be related to one another.

A single male might often not be in control for long enough to mate with his grown daughters.

Females do not only mate with the leader of their pride, but mate sometimes with males from outside of the pride.


Predicting progeny of recessive mutations using recombination I was asked this question on a test and got it wrong, but I'd like to know how to do it.  The answers are shown in the blanks below:

  You are studying two recessive mutations in the fruit fly D.
  melanogaster. The red_ mutation causes flies to have red bristles
  (wild-type flies have black bristles) and the shiny- mutation causes
  flies to have shiny eyes (wild-type flies have eyes that are pebbly).
  You mate females from a true-breeding strain with red bristles and
  pebbly (wild-type) eyes to males from a true-breeding strain with
  black (wild-type) bristles and shiny eyes. F1 females are then mated
  to males that have red bristles and shiny eyes to produce F2 progeny.

  If you analyzed 1000 male progeny in the F2 generation, how many flies
  of each possible phenotypic class would you expect, if:

  The two traits are determined by two autosomal genes that are 15 cM
  apart:

Red bristles, pebbly eyes:_____ 425_______
Red bristles, shiny eyes: ______75____
Black bristles, pebbly eyes:____ 75_____
Black bristles, shiny eyes:____ 425______

My attempt:

So I know the 15cm=recombinants/parentals * 100 but I don't see how that formula can help.

First, the recombination equation is:

cM = recombinants/(recombinants AND parentals) * 100

Let's assign the following genotypes for clarity's sake:

RR = black bristles
Rr = black bristles
rr = red bristles
SS = pebbly eyes
Ss = pebbly eyes
ss = shiny eyes

F1 cross: rrSS x RRss = RrSs (all progeny)
F2 cross: RrSs (F1) x rrss = ?

You would have the following gametes:

Parent 1, RrSs = RS, Rs, rS, rs
Parent 2, rrss = rs, rs, rs, rs

Draw your punnet square and you get the following genotypes of the offspring.

So your GENOTYPES of your F2 cross will be RrSs, Rrss, rrSs, rrss

Let's translate those to phenotypes.

RrSs: black pebbly (parental)
Rrss: black shiny (recombinant)
rrSs: red pebbly (recombinant)
rrss: red shiny (parental)

Now let's look at recombination frequency.

15cM = (recombinants/(recombinants+parentals)*100
recombinants/(parentals+recombinants) = 15/100

This tells you for every 15 recombinants, you have 85 parentals. If you scale this up to 1000, that's 150 recombinants for every 850 parentals.

Your 150 recombinants comes from 75 black/shiny and 75 red/pebbly.

Your 850 parentals ceoms from 425 black/pebbly and 425 red/shiny.

Anyways that was my attempt which appears to be directly opposite to what your answer key says. Did you copy it down correctly?


Why are dogs so selective about choosing a spot to defecate? Anybody who walks a dog knows that dogs are normally selective about choosing a spot to defecate. They sniff around for a long time, while I just want to be on my way.

I understand about marking territory with urine. Is it the same with feces?

Marking territory with faeces

Despite urine being the most common way for dogs to mark territory, they also can use faeces to do so. Not only the faeces have a unique scent for the dogs, but, most importantly, it contains secretions from the anal glands, which are very important in dog communication. In fact, when you see two dogs sniffing each other "behinds", they are smelling the other dog's anal glands secretion.

So, being selective about the place to defecate is indeed an expected behaviour in dogs.

Magnetic sensitivity in dogs

However, if you are specifically talking about the dog spinning around after it — more or less — decided where to defecate (which makes the dog seem like it had not yet decided if it is going to defecate or not) one factor that plays an important role is that dogs like to eliminate with their bodies aligned to the North-South axis.

According to Hart et al. (2013):

  Dogs preferred to excrete (sic) with the body being aligned along the North–South axis under calm Earth's Magnetic Field (MF) conditions. This directional behavior was abolished under unstable MF. The best predictor of the behavioral switch was the rate of change in declination, i.e., polar orientation of the MF.

So, the dog has to spin some times until it finds the desirable orientation, which explains the behaviour.

It's worth mentioning that the interesting aspect of this research is not the fact that it explains why dogs spin around before eliminating, but the fact that it shows that dogs have magnetoreception!

Still according to Hart et al. (2013):

  It is for the first time that (a) magnetic sensitivity was proved in dogs, (b) a measurable, predictable behavioral reaction upon natural MF fluctuations could be unambiguously proven in a mammal, and (c) high sensitivity to small changes in polarity, rather than in intensity, of MF was identified as biologically meaningful.

Source: Hart, V., Nováková, P., Malkemper, E., Begall, S., Hanzal, V., Ježek, M., Kušta, T., Němcová, V., Adámková, J., Benediktová, K., Červený, J. and Burda, H. (2013). Dogs are sensitive to small variations of the Earth’s magnetic field. Frontiers in Zoology, 10(1), p.80.


Leaves not liked by herbivores I at times have many goats grazing in our locality. Recently a few cows were seen too. I just offered one of the cows a few leaves from Jasminum sambac plant growing in our garden. The cow smelled and left those leaves untouched. However on being given mango leaves, not a bit of it remained. The same situation did I observe with goats.I have the following questions:

What is the difference between leaves of others and leaves of Jasminum sambac?
Why do herbivores avoid consumption of these leaves?
Does it happen with other leaves too?

Cattles actually hate shrubs which are very tough to break and tasteless(for a cow). Some plants they won't touch are:

Lantana urticoides (West Indian shrub verbena),
Malvaviscus arboreus var.drummondii (wax mallow)
Rhus copallinum (winged sumac)
Viburnum acerifolium (mapleleaf viburnum).
Morella cerifera (wax myrtle)
Ilex vomitoria (yaupon).

Source:

https://www.wildflower.org/expert/show.php?id=2108

Lantana urticoides

http://www.wellgrowhorti.com/Pictures/Landscape%20Plants/Shrubs/Web%20Pictures1/M/Malvaviscus%20Arboreus.jpg

Malvaviscus Arboreus

http://www.floridata.com/wallpaper/jpg/Rhus_copallinum_frt800.jpg

Rhus copallinum

(source: naturallandscapesnursery.com)

Viburnum acerifolium

Morella cerifera

Ilex vomitoria


Question about radiation and how it affects biological systems I'm doing research on the effects of radiation, and specifically UV, X-Ray and Gamma radiation, on biological systems at the cellular level and beyond. I understand that radiation types can be classified by their wavelength, with the gamma radiation being of the shortest wavelength and thus highest energy.

How does this measure of wavelength relate to the unit rads, or radiation dosage? And how do they both affect the survivability of cells? I can understand that the lower the wavelength, the higher the energy and it will affect the cells more adversely at those levels, but how does rads relate to that?

The absorbed dose describes the amount of radiation absorbed by an object or person, i.e., the amount of energy that radioactive sources deposit in materials through which they pass. The units for absorbed dose are the radiation absorbed dose (rad), or better: the gray (Gy) unit.

One gray dose is equivalent to one joule radiation energy absorbed per kilogram of organ or tissue weight. Rad is the old and still used unit of absorbed dose. One gray is equivalent to 100 rads.

1 Gy = 100 rads

Equal doses of all types of ionizing radiation are not equally harmful. Alpha particles, for example, produce greater harm than do beta particles, gamma rays and X rays for a given absorbed dose. Alpha radiation is the most dangerous because it is easily absorbed by cells. Beta, gamma an X radiation are not as dangerous because they are less likely to be absorbed by a cell and will usually just pass right through it (source: BBC).

To account for this difference, radiation dose is expressed as equivalent dose in units of sievert (Sv). The dose in Sv is equal to absorbed dose" multiplied by a radiation weighting factor (WR - see Table 1 below). Prior to 1990, this weighting factor was referred to as Quality Factor (QF).

Note that the heaviness of the alpha particle makes its penetration rates very low. Hence, it will not easily penetrate through the outer layers of the skin.

Table 1. Recommended Radiation Weighting Factors. source: Canadian Centre for Occupational Health and Safety

Now to your question:
Ionizing radiation has more energy than non-ionizing radiation. Ionizing radiation can cause chemical changes by breaking chemical bonds and damage living tissues.

Shorter wavelength UV begins to have enough energy to break chemical bonds. X-ray and gamma ray radiation, which are at the upper end of the EM spectrum, have high frequencies (~100 billion billion hertz). Radiation in this range has high energy and it can strip electrons from an atom or even break up the nucleus of the atom.

The process in which an electron is given enough energy to break away from an atom is called ionization. It results in the formation of two ions: the molecule with a net positive charge, and the free electron with a negative charge. Each ionization releases a large amount of energy which is absorbed by the surrounding tissues.

There are three main kinds of ionizing radiation:

Alpha particles, which include two protons and two neutrons; beta particles, which are essentially electrons; and gamma rays and x-rays are photons. Alpha particles, beta particles and neurons are not part of the EM as they are energetic particles as opposed to pure energy bundles (photons) (source: ARPANSA Australia).

So in the EM realm, frequency is proportional to energy and hence to tissue damage (Fig. 2) and hence to rads.

Fig. 2. EM spectrum. source: ARPANSA


Why do cats' claws retract? Humans have nails, horses have hooves - but they are always exposed. Why are cats' claws retractable rather than always exposed? Is it related to "Why are there nail growth differences  between humans and other mammals?"?

Retraction of claws is a feature of the cat family, Felidae along with some civets that helps them keep those sharp by preventing unwanted wear.These claws are important for the members of cat family, including domestic cats that hunt preys by grasp attack rather than bite.

However cheetah among the big cats that usually hunt through bite-attack, has evolved to have semi-retractable claws that help it generate traction.

In pet cats it has offered another advantage:
Retraction keeps them from getting tangled in fabrics.

Sources:

Wikipedia
Russell AP, Bryant HN. 2001. Claw retraction and protraction in Carnivora: the cheetah (Acinonyx jubatus)
as an atypical felid. J Zool ,Lond 254:67-76.


What are non-heritable changes to genomes? I am told that mutations are heritable changes to the genome.

So this begs the question - what are non-heritable changes to genome?

I don't know what you really mean by "heritable changes to the genome". I think you will understand why this sentence makes no sense after reading what follows. I start with some background and then try to address directly what confuses you.

Short introduction to the concept of heritability

The concept of heritability may have two meanings.

Heritability is a concept defined at the population level for one given trait. The heritability ($h_B^2$) (in the broad sense) is the ratio of the genetic variance $V_p$ over the phenotypic variance $V_p$, where the phenotypic variance can itself be decomposed into environmental $V_e$ and genetic variance $V_g$ (and their covariance that we will neglect for the purpose of this question).

$$h_B^2 = \frac{V_{g}}{V_{p}} = \frac{V_{g}}{V_{e} + V_{g}}$$

When saying environmental variance $V_e$, we don't refer to the total variance in the environment (such as the variance in temperature for example) but we refer to the phenotypic variance (in a given population of a given trait of interest) that is caused by environmental variance. The same logic is true for the genetic variance.

Inheritence

While the concept of heritability applies to phenotypic traits, the concept of inheritence can apply to DNA material. A mutation is inherited if the offspring receives the sequence from his/her mother or from his/her father (assuming we are talking about a species that have sexual reproduction with 2 genders).

Somatic versus germline mutations

As pointed by @Chris in the comments. In multicellular organisms, not all mutations can be transmitted to the multicellular offspring. Most of the cells do not give rise to any other multicellular organisms. For example, imagine that while the biceps is under development at very low age, a mutation occurs that will be inherited by the daughter cells but not to the multicellular offspring. we call the line of cells that do not give rise to gametes (sperm and ovules), the soma line, by opposition to the germ line which gives rise to the gametes.

To answer your question

As soon as a given locus (position on the DNA) has some variance and that this variance explains some phenotypic variance, then the phenotypic trait it influences has a heritability greater than zero. If the variance at this locus has no effect on the phenotype, then it's heritability is zero (because $V_g = 0$, although there is some variance in the actual sequence). If the phenotypic trait of interest does not show any variance (in the population considered), then the concept of heritability is undefined for this trait!

I think you may have a confusion between "inherited trait" and "heritable trait". A mutation will necessarily be transmissible to the offspring (except if it happen to be in the somatic line in such case it will only be transmitted to daughter cells but not to the multicellular offspring) but it doesn't mean that this mutation will necessarily explain some variance in a phenotypic trait. A new much is necessarily heritable (pay attention to the soma vs germ line) but does not mean that a phenotypic will have higher heritability thanks to this mutation.


Can genetically engineering the DNA of a human zygote, make it a twin of another human in entirety? My question is simple. If I wanted to make an exact twin of an individual, will genetically engineering the DNA of the zygote to match with the individual suffice?

The answer is no, and it is because sequence of the genome is not all information that is required for gene expression and development, there are also epigenetic factors.

A lot of patterns of epigenetic marks, such as most of DNA methylation and some histone modification patterns, are set during parental germline development, and these marks are transmitted to the zygote by gamets (except paternal histones, those are not transmitted because they are temporarily substituted for protamines in sperm for greater compaction). Therefore, the naked DNA inserted into zygotic nucleus will not have access to the machinery that established epigenome during development of the gametes.

And even though nucleosomes may assemble in the zygote on the naked DNA and histones may acquire post-translational modifications, and cytosines may get methylated, but most definitely the zygote is going to have no means to correctly set distinct patterns of epigenetic marks at alleles that are normally imprinted, i.e. those alleles whose epigenetic state depends on the gender of the organism that produced the gamete.

Therefore, the twin created in this way will have the same DNA sequence, but it will be a  subject to disorders associated with imprinting


Coronavirus capsid missing? According to several sources, Coronavirus is a helical virus, i.e. it should have a helical capsid. Although most sources did not labelled or pointed any kind of capsid. It was mysterious to watch diagrams of spherical envelops with no underneath capsids.

Cutaway view of coronavirus from Wikipedia

David Goodsell painting on PDB

No mention of capsid.

Initially I guessed the proteins around the RNA fibre formed the capsid, not labelled otherwise. Alternatively I was speculating whether coronavirus is lacking the capsid.

However a researchgate paper picture (heavily diagrammatic) shows a polygonal capsid, the picture is captioned as coronavirus.

It makes me think of whether the capsid is like a hollow spherical or polygonal thing spirally wrapped.

Now my questions are .

What is the actual/ realistic shape of coronavirus capsid?
Does it really contain a capsid?
(Just speculating) Is it SARS-CoV2 lacking a capsid, and thus special exception from g eneral description of coronavirus?

Does it really contain a capsid?

Yes. Coronaviruses have a capsid, but it's not reminiscent of the polygonal (icosahedral) capsid depicted in the Research Gate picture you referenced. Icosahedral capsids form a sort of shell around the viral genome, where helical capsids actually bind the viral nucleic acids, holding them in a more rigid shape.

  Is it SARS-CoV2 lacking a capsid, and thus special exception from general description of coronavirus?

SARS-CoV-2 is not an exception. In fact, its nucleocapsid is a target for diagnostic tests.

  What is the actual/ realistic shape of coronavirus capsid?

It is actually depicted in Goodsell animation you referenced. The nucleocapsid proteins are the squigly bits in and around the genomic RNA (labeled "N", for Nucleocapsid). The actual capsid is the complete complex of N proteins bound to genomic RNA, so it doesn't have that polygonal outline that maybe we're used to when we see depictions of viruses. If you want a more detailed look at the actual capsid protein structure, there's a depiction of its crystal structure in this New York Times piece co-authored by Carl Zimmer.


I need some forearm bone motion pictures I would like to know how my forearm bones move inside my forearm when I'm twisting my hand. (Also, it would help to see the hand bones action too). "twisting hand" means to me the motion in which the rest of the body is in place except the hand which turns from upside up to downside.

I have the intuition that the bones inside my forearm move between themselves to make my hand twist, but am not sure if that is true.

I would like pictures of the forearm bones before and after twisting. Animations would also be great of course.

Here is a basic image. Palm up is called supination and is the resting (anatomical) position. The radius and ulna sit parallel. When the forearm is in pronation, the radius crosses the ulna.

You can feel this yourself. Put your fingers on the ulna and move the palm into pronation and supination. You will not feel the ulna rotate. Only the radius pivots during this movement. The wrist is not involved in this movement.

The ulna is unable to rotate at all, because its olecranon process is locked into a groove on the distal end of the humerus. If you put you fingers on your bony "elbow" (olecranon process) and pronate/supinate your hand (without flexing/extending your elbow), you will not feel you ulna moving.


What is a focal copy number variation? Often, genetics studies, especially genome wide ones, talk about "focal copy number variations" in genes or regions of the chromosome. I know what a copy number variation is. What does "focal" mean, exactly?

Are there non-focal CNVs? What are they? Where did the term "focal" originate? Is there a specific paper that coined (and hopefully unambiguously defined) the term?

A search for "focal copy number variation" on Google Scholar should turn up plenty of papers about it. The GISTIC algorithm is a popular computational method for finding putative CNVs- so information about this algorithm may have some clues.

A documentation text for one GISTIC implementation on the Broad Institute's website states the following:

  (8) Broad or Focal: Identifies whether the region reaches significance due
  primarily to broad events (called “broad”), focal events (called “focal”), or
  independently significant broad and focal events (called “both”).

A copy number variation (CNV) is when the number of copies of a particular gene varies from one individual to the next.
From: the NIH Glossary

Focal CNVs are regions of repeated genetic information that only span a small proportion  (<25%) of the chromosome arm (although this does not seem to be a consistent rule), and can contain few genes. CNVs greater than this are termed either 'large-scale' or 'broad'.

Here are some relevant papers I came across (no doubt there are more);
This paper is about a program (VarScan2) the authors have made to robustly detect somatic mutations and CNVs;

To identify SCNAs [somatic copy number alterations], VarScan 2 compares Q20 (base quality >=20) read depths between tumor and normal samples for contiguous regions of coverage ... Therefore, we apply a circular binary segmentation (CBS) algorithm (Seshan and Olshen 2010) to delineate segments by copy number and identify significant change-points. A subsequent joining procedure merged adjacent segments of similar copy number and classified them as either large-scale (>25% of chromosome arm) or focal events.
From: Koboldt D, et al, 2012.

I continued searching, as I wondered whether this was a standard definition, or just one used by the authors.
This paper is reporting bacterial genes that drive focal chromosomal aberrations, but do not give a great definition (as it seem quite arbitrary to me);

Many of these [chromosomal] aberrations concern large chromosomal regions, which makes it difficult to identify actual driver genes. Increased resolution has led to the detection of focal chromosomal aberrations, defined as 3 Mb or smaller in size [5–8]. Inherent to their size, focal aberrations contain a small number of genes, facilitating driver gene identification
From: Brosens R, et al, 2010.

This extract is from one of the studies referenced by the previous paper (when they mention their definition of focal CNVs). This paper is about CNVs in different tumour cells;

Primary tumors contain varying proportions of nonneoplastic cells thereby obscuring focal amplifications, defined by the increased copy number of a small region of the genome, from simple gains of whole chromosome arms.
From: Leary RJ, et al, 2008.


Plants without bacteria? is it theoretically possible? I know from school, that all live on the Earth need bacteria as low-level "machines" that break down/extract/convert/produce chemical elements and combinations, other high-level organisms needed. But it is a natural way.

But is it possible to have a world with plants (without mammals or microorganisms and without bacteria) that could exist in the long term. Saying the atmosphere of these world has already enough nitrogen, oxygen and CO2, and of course there is water.

What could break this artificially created world with such conditions (say the world created not from low-level living structures)?
Could bacteria emerge in the world?

This is the sort of question that should be considered from more than one perspective.  Since this is speculation, take it as a given that there is a lot of 'what if' here.

I doubt most animals and plants can do entirely without bacteria - as you say most of the essential nutrients come from bacteria, who fix nitrogen.  If only plants were left on earth, eventually the plants would use up all the nitrogen and they would have to find a way to fix more.

Can bacteria emerge from just a world of plants?  I don't think viruses arise spontaneously, but since genomes often have viruses embedded in them, over the course of a billion years or so, its possible since bacteria and viruses continue to be impressed upon our genomes.  Would it happen in time?  Most would be skeptical whether that timing could work out.

In practice it would be hard to create a world like this.  I would be interested to see whether you could sterilize the microorganisms off of seeds without killing the plant for instance.  If you're asking about a small sterile environment with only plants, you could do it by adding the nutrients the plants need and giving them sunlight.  Such self sustaining systems have been made with cyanobacteria and i'd be surprised if plants could not be included.  But these are closed systems and judged by limited amounts of time, so whether this is an answer to your question is not clear.  Here it looks like some water plants and fish have been done.  If there was a plant that created CO₂ at an adequate rate its possible.

At one time there were no animals at all.  Its thought that for a while there might have only been photosynthetic structures that lay in the water and soaked up the rays.  Its not clear whether as some say there were colony formations of cyanobacteria as we see today, or whether there may have been larger pre-cellular or proto-cellular structures.  But recovering the pre-cambrian configurations of genes from just plant genomes seems like a gambler's bet to me.


Evolution theory - roses spikes - being more bulgy doesn't give you advantage I've seen spike, huge spike. And I thought that development of such spikes could be contrary to the evolution theory.

Being „little more” spiky doesn’t give you any advantage... So those individuals having one won't have smaller mortality rate than those with smooth stem.
Even more, the individuals with bulgy (more spiky) waste resources their ruggedness and have more things to feed, which should mean that they would have higher mortality rate.

So I can see no way to develop spikes on the stems of roses according to the evolution theory which embrace "small improvement". Spike is only efficient (to deter aggressor) when it's very sharp, it's either sharp or it isn't - there is little in between.

Could anybody tell me that this is bullshit (and why it is bullshit), and that I should us believe in Darwin competence?;)

I think that the most important point has been given by CactusWoman, when (s)he says "Just because you cannot forsee a use for more "bulgy" spikes doesn't mean there isn't a use for them."

In addition to that, I would like to say that several plants evolved traits that were beneficial at a time where other herbivores existed and that are now useless. Those lineages did not lose their traits (yet?) just because there is a relatively low cost to making the trait in question.

Your post shows several of the very common misconception about evolutionary processes. Evolution is not all about Natural Selection. It is more interesting than that.

  "small improvement"

The conception that evolution proceed through "small improvements" is either partially wrong or totally wrong.

First, because of the loaded term "improvement". Evolution can yield a population to have a lower mean reproductive success or a lower complexity, things that you could eventually see as deterioration.

Second, because changes not need to necessarily be small. Some mutations have a very big effect.

Third, because even small deleterious mutations can spread in the population and reach fixation (=and all individuals carry this mutation), just because of the joint effect of other evolutionary processes such as genetic drift. This post may help you to get a quick grasp of what genetic drift is. There are already multiple posts that emphasize the importance of other processes than natural selection in evolution to layman. Here is one of them.

  believe in Darwin competence

Evolutionary biology is not anymore Darwin's evolution theory. It is way more than that. We've been working on the subject a lot since Darwin and today we have a much much better understanding of evolutionary processes than Darwin at its time. Everything is not fully understood yet and therefore there are still many people researching to better understand evolution. Of course, not to better test if evolution is true as this has been known for a long time now.


How to determine if a plant is autotrophic or heterotrophic? How do you determine if a plant is autotrophic or heterotrophic, and are there any traits in particular that can be used to classify species?

As two examples, how should Melampyrum pratense and Orobanche be classified?

This in part depends on how you define heterotrophic. The most common definition is the inability to synthesise energy-containing molecules, most commonly by fixing carbon through photosynthesis (but dont forget chemotrophs). However, I've sometimes seen definitions that also include dependency on external sources for nutrition (e.g. nitrogen) but also to supplement carbon sources.

Using the first, main definition a lack of chlorophyll is a sufficient trait to define heterotrophic plants, which clearly places Orobanche (lacks chlorophyll) in the heterotroph category. If you use the second definition you will include more species, but it also becomes much more tricky to draw the line between autotrophs and heterotrophs. I know that Melampyrum pratense is a hemiparasite, but don't know exactly to what extent, and therefore cannot say if it is accurate to label it as heterotrophic (using the second looser definition - it has fully functional photosynthesis). Checking whether a hemiparasitic plant can establish, survive and reproduce without its host should be a useful way to establish if it is a obligate or facultative hemiparasite (I suspect that Melampyrum pratense will be found in the latter category). Myco-heterotrophy can also be obligate and facultative, and can involve transfer of both carbon sources and nutrients, see Merckx et al (2009) for a review. Insect-eating plants such as the Venus flytrap are however sometimes called partial heterotrophs, based on the fact that they get part/most of their nitrogen from insect trapping, while still obtaining their energy from photosynthesis.


Low migration rate in Papadopoulou et al. (2008) In the paper "Speciation and DNA barcodes: testing the effects of dispersal on the formation of discrete sequence clusters" by Papadopoulou et al. (2008), is there an explanation as to why the authors simulated very low migration rates ($m$ between $10^{-8}-5\times 10^{-5}$)? The population size was 160,000, which produces $Nm$ between 0.0001-0.5. This is much less that a single migrant per generation.

Any insight would be most appreciated.

After a quick look-up, they don't seem to comment much on this choice of parameter unfortunately. Here are my quick thoughts.

They are dealing with quasi isolated species. They explored a range of values and I would like to assume that made sure that more extreme values won't yield to drastically different results.

These simulations can be pretty computationally intensive, it is possible that they considered $Nm$ to be the important statistic but they would assume that the results could scale up and down for different $N$ and $m$ values. In fact, they almost systematically refer to their migration rate as $Nm$.


Binucleate cells of transitional epithelium (bladder)? Working through Histology slides of the transitional epithelium (urothelium) of the urinary bladder, I noticed that the dome-shaped cells at the top of the transitional epithelium are frequently binucleate.
In doing research, I found that the top cells of the transitional epithelium are 'often binucleate and usually polyploid'

  Why is this?
  What purpose does this serve?
  Is the binucleate feature consistent enough across slides to be used as a common identifying feature to recognise transitional epithelium from the urinary tract? Is the absence/over-abundance of binucleate cells characteristic of certain diseases?

I also see prominent granules (of glycogen, I presume?) in these cells.

  Is this glycogen? & What purpose does this serve?

Also, I'm having difficulties recognising transitional epithelium in slides. Does anyone have any tips to share on how to easily recognise transitional epithelium as such (common features to look out for, etc.), especially in distinction to pseudo-stratified epithelium, which often looks similar?

In other stratified epithelium, it is the basal cells that replicate to replace the cells lost in the top layers.  In transitional epithelium, which is also a stratified epithelium, the most superficial layer of cells are replaced or  turnover occurs because of mitosis of the superficial facet cells themselves.  In this case it is not unusual to see dividing cells in its last stage of division as a large cell containing two nuclei, which soon that cell will be 2 cells.


How can a species switch from r to K - reproductive strategy in a single generation? I ask because it seems as though humanity is in the midst of doing exactly this. Only a few decades ago, human population was growing exponentially, and it seemed destined to keep growing until hitting constraints of food supply, at which point we would devolve into resource wars and famine. But then it didn't happen -- over the last few decades, fertility rates in the developed and developing world have plummeted and the world population is expected to stabilize in the second half of this century around 10-11 billion people. Demographers list a number of reasons for this -- education and empowerment of women, urbanization, decreased child mortality and increased life expectancy, availability of safe and effective contraception, etc. The common thread is that these trends encourage people to invest more into fewer offspring. It's as though our entire species is spontaneously deciding to switch from an r-strategy of reproduction to a K-strategy.

My question is whether this is unprecedented or not. I had the impression that r or K strategy was typically a function of species, but here we have a case where humans seem to be switching between the two strategies in a single generation. Are there other species which can change their entire reproductive strategy when the population approaches its carrying capacity? If so, what kinds of environmental cues or epigenetic factors trigger the switch? How do they manifest themselves in the case of humanity's current switch?

The issue in your reasoning is to associate a $r$ or $K$ as being a property intrinsic of the species which, while not entirely wrong, is rather misleading.

The classical and simplistic model of population growth is the model of logistic growth

$$n(t+1) = n(t) + rn(t)\left(1-\frac{n(t)}{K}\right)$$

, where $n(t)$ is the population size (number of individuals in the population) at time $t$, $r$ is the growth rate and $K$ is the carrying capacity. Of course, there exist also continuous time equivalent of this discrete time recursion equation. Here is a quick and dirty R code to compute this recursion equation

r = 0.0004
K = 1e4
f = function(n) {return(n + r * n * (1-(n/K)))}

nbGenerations = 1e5
n = numeric(nbGenerations)
n[1] = 1
for (t in 2:nbGenerations)
{
    n[t] = f(n[t-1])
}

plot(y=n,x=1:nbGenerations)

If you want to compute such function fast you can look for the general solution of the recursion equation (it is a good exercice if you are a little uneasy with recursion equations).

As you can see, the population grows exponentially until some point and then the growth is slower and slower until reaching the carrying capacity. If you look at this species at $t=2000$, then you will deduce that it is a r-strategy species because its growth is dictated by the parameter $r$ (the growth rate). If you look at the same species at generation $t=6000$, then you will deduce that it is a K-strategy species as the population dynamic is dictated by the parameter $K$. Yet, the species has not changed so much.

Being r or K strategic is not a intrinsic characteristic of the species as much as it is a characteristic of the species population size in a given environment.

Now, in my example I chose $r=0.0004$, just pick some greater $r$ value and you'll see that such change from being a r- to being a K- strategy species can change very quickly. Consider for example

r = 0.02 # growth rate
K = 1e10 # carrying capacity
f = function(n) {return(n + r * n * (1-(n/K)))} # recursion function

nbGenerations = 1e3    # number of generations to computer
n = numeric(nbGenerations)
n[1] = 1e7             # starting population size
for (t in 2:nbGenerations)
{
    n[t] = f(n[t-1])
}

plot(y=n,x=1:nbGenerations)

You can now look for realistic estimates of $r$ and $K$ for humans (data from after the industrial revolution), plug them in this equation and see what you get! You can also try to estimate $r$ and $K$ from data (from after the industrial revolution only) of population size over time.

If you play with high values of $r$, you can get overshooting and you can even get chaotic population dynamic.

  Are there other species which can change their entire reproductive strategy when the population approaches its carrying capacity?

Of course, this change in a conscious. It is not a decision of the species. It is not either so much an evolutionary process. It is just a consequence of their environment. Yes, all species follow some kind of model of population growth. The famous example of logistic population growth comes from daphnia which growth dynamic has been highly studied. Daphnia can have quite a high $r$ value (depending on the environment) and they can typically show overshooting behaviour of the carrying capacity before settling down back to the carrying capacity.


Neuroscience of temperature regulation and perception The hypothalamus is known to be important in the regulation of body temperature, but I'm curious whether anyone knows about the neurocircuitry of perceived temperature. It seems like there could be a difference between how warm/cold someone feels and the temperature to which their body is trying to adjust. Intuitively, I'd imagine that any apparent difference in these  has to do with some sort of delayed feedback that is experienced before the autonomic nervous system can kick in. Does anyone know something more about this?

I've found a good resource for this--an open-access review by Nakamura, "Central Circuitries for Body Temperature Regulation and Fever." In it, the author provides a nice summary figure of the circuitry involved in temperature regulation (see below). As I suspected, the hypothalmus is pretty central to temperature regulation. I had forgotten about the involvement of the peripheral nervous system in responding to environmental temperatures, which, now that I think about it, makes some amount of sense, but is still pretty interesting. It appears that there's a difference in the specific circuitry and neurotransmitters used in responding to warm and cold temperature (especially GABA v. 5-HT), so I think a reasonable hypothesis regarding the basis of individual differences in the perceived temperature of an external environment might be differences in peripheral 5-HT systems (in addition to differences in body composition). Perhaps someone with a background in the peripheral nervous system could speak to this better than I can, but single nucleotide polymorphisms (SNPs) leading to differences in central 5-HT systems has been an active area of research in the neuroscience community of late (e.g., Nordquist & Oreland, 2010, Gonda et al., 2010), which I think lends some face validity to this idea.


What's seen when stress echocardiography shows ischaemia? Can this happen without angina? What can be seen on the screen when stress echocardiography (a pair of heart ultrasounds before and after exercise) suggests ischaemia? Can this happen without chest pain?

Illustration from Wikipedia:

A number of things can be seen. Ischaemia is typically caused by the narrowing of blood vessels that prevents perfusion (blood flow) to the heart or other organs. When the heart muscle doesn't get enough oxygen, the walls of the heart might not "beat" (i.e. contract) properly. We observe this and thus can tell if a coronary artery is reduced or blocked or fine. It doesn't give absolute numbers of how blocked it is, although observation of the way the muscle moves can give some indication. Contrast can further allow us to visualise the wall with more detail, giving a clearer indication of coronary artery disease in the vessels that supply this part of the heart.

Pain is caused when the heart muscle is really suffering, which doesn't occur unless the vessels are seriously blocked. They're so great that even if about 70% of the artery is blocked there is almost no effect including chest pain. In fact it is silent, which is quite worrying also. However, when the heart is most stressed, we can potentially detect decrease in perfusion from small changes in the contraction of the heart.


How does a plant cutting develop roots? Please correct me if my understanding is incorrect; I understand branch/stem, and root are composed of different types of cells. Yet in some plants (e.g. rose, bougainvillea) a cutting from the stem is capable of developing and taking root.

How does this transformation from stem to root come about?

As an aside - I believe such root-generation happens only in plant cuttings, and not in a tree branch. Why? Is it a matter of the volume of nutrition required?

Plants grow only from regions at the tips of the roots and shoots called meristems.

Within the meristem areas there are stem cells ("blank" unspecialised cells).  Unlike animal stem cells, plant stem cells are totipotent - meaning that they can differentiate into any type of cell.  Therefore when the cutting is taken from the end of the shoot, the stem cells can differentiate into root cells or shoot cells depending on their conditions.

Because the meristems (therefore the unspecialised stem cells) are only located at the tips of shoots, you cant grow a cutting from the middle of a branch.


What are the types of interactions in biological network (protein networks)? In the KGML files, the types of relations between genes or proteins are precisely activation, inhibition, expression, repression, indirect effect, state change, binding/association, dissociation, phosphorylation, dephosphorylation, glycosylation, ubiquitination, and methylation. I want to know more about these interactions. Is there a particular source from where I would understand what these interactions mean in depth?

Most of them are pretty self-explanatory. KEGG pathways are often vague, as a lot of the specific biology for some proteins has yet to be properly investigated - sometimes you only know that two proteins associate, not what they actually do.

The relationship between the two is easier to predict when you know the function of one, e.g. a protein interacting with a kinase is likely phosphorylated by said kinase. A lot of those relationships correlate to post-translational modifications (glycosylation, phosphorylation, ubiquitination, acetylation, methylation, etc) made to one protein by another. Wikipedia actually has a decent overview of these with lots of examples.

Several of the other relationships have to do with regulating protein activity or expression. This goes somewhat hand in hand with what I stated above. Some proteins are only activated once phosphorylated or demethylated, etc. Other enzymes may remove phospho groups, leading to repression. Others still may interact directly with a protein, inhibiting it from binding its substrate or target. Maybe the binding induces a conformational change in one protein that allows it to bind its substrate when it can't normally. Some proteins function as transcription factors that activate or repress the expression of certain genes, indirectly affecting protein levels.

There are all sorts of possibilities - the KGML files try to represent them in a way that at least gives some indication of how the interactions between two proteins may affect each. I hope that provides some insight.


Why does the affinity of haemoglobin for oxygen increase at higher elevations? Why does the affinity of haemoglobin for oxygen increase if an organism lives at a higher elevation where the oxygen pressure is lower?

Wouldn’t its affinity for oxygen decrease because the acidity of the body would increase with the lack of oxygen? The textbook said otherwise though and I don't understand.

The question seems to be based on the idea that there would be physiological adaptation to low oxygen, possibly through the Bohr effect. In fact the usual mechanism of adaptation is through genetic change.

There are a lot of examples of animals which live (or fly) at high altitude and which have a haemoglobin with a higher oxygen affinity. Examples which spring to mind are the bar-headed goose and the camelids of South America (llamas, alpacas etc.)

Haemoglobin has evolved as an efficient oxygen-delivery protein by having a variable affinity for oxygen: low affinity at low oxygen concentration, high affinity at high oxygen concentration. This is achieved through co-operative binding (allostery), and it ensures that the protein loads up with oxygen in the pulmonary circulation but releases oxygen in the peripheral tissues.

At high altitude, where the partial pressure of oxygen is lower, the haemoglobin of humans, for example, will not be fully saturated, impairing the delivery of oxygen to the body. Haemoglobin variants with an increase in the overall affinity for oxygen can achieve full loading at the expense of slightly less release in the tissues - overall a better oxygen delivery function. This is what happens in the camelids, but there is no such adaptation in humans living at high altitudes.


What kind of insect eggs are these (found in Malaysia)? What kind of eggs are these?

Found outside on a window, when I removed them via scraping, whitish oozy fluid came out. I've seen this before but they've been appearing more frequently, always appear in a straight line and are brown.

This is in Malaysia, in South East Asia. More specifically Johor. The entire line measured about 1 inch, and in terms of individual egg size, 0.3 inches.

This eggs belong to Mictis profana which is a species of insect in the family Coreidae known by the common names crusader bug and holy cross bug. It is distributed in Australia, Indonesia, and the Indo-Pacific.


Fruit identification On the way from school to home, I came across this strange looking fruit that looks similar to a potato and it grows on a tree. Can you identify it?

it looks like medlar. Medlar is a fruit sized about 4cm (1 1/2 inch). it must be common medlar.

You can find out more about this interesting fruit here at Wikipedia.

  The medlar was already being cultivated about three thousand years ago in the Caspian Sea region of northern Iran and Azerbaijan. It was introduced to Greece around 700 BC, and to Rome about 200 BC. It was an important fruit plant during Roman and medieval times. By the 17th and 18th centuries, however, it had been superseded by other fruits, and is little cultivated today.


RNAs arising from intergenic regions Which type of RNA molecule is coded for in intergenic regions? I think it must be a non-coding RNA but I'm unsure which type.

The term intergenic is more or less obsolete now. In fact it is ironical to say that a gene, which can give rise to a functional protein or an RNA, is expressed from an intergenic region. However the usage continues for both lncRNAs and miRNAs (other major type of ncRNA in metazoans1 - piRNAs have different classification). lncRNAs are vaguely classified as sense-overlapping (expressed in the same direction as a known gene but not completely overlapping), antisense (expressed from the antisense strand of a known gene) or intergenic; similarly miRNAs are classified as intronic or intergenic.

It is not necessary that the intergenic RNA has to be strictly non-coding, it can be coding as well; a novel protein.

In all these cases the term intergenic means - not overlapping with a known gene. Better nomenclature is necessary as the field of genomics makes more progress.

See this article.

1 Most metazoans.


Do camels have nucleated RBCs or enucleated RBCs? Most mammals have enucleated RBCs as an adaptation to facilitate the transport of oxygen. My text says that camels and llamas are exceptions to these.

I was wondering why they are exceptions, and the Google search results are confusing. Some sites say that camels have nucleated RBCs to facilitate cell division. Some others state that camels, like all other mammals possess enucleated but different shaped RBCs. So, which is correct?

The links:https://www.quora.com/Why-do-camels-have-nucleated-red-blood-cells
https://in.answers.yahoo.com/question/index?qid=20070702070352AAkfspZ

Camel RBCs are anucleate [1, 2]. The dark structure seen in microscopic images is not nuclei but a network of microtubules called the marginal bands. Marginal bands cause these RBCs to adopt an ellipsoid shape. The unique shape of these RBCs possibly allows them to survive osmotic stress and is probably advantageous to a camel under extreme dehydration.

References:
[1] Cohen, William D., and N. Barclay Terwilliger. "Marginal bands in camel erythrocytes." Journal of cell science 36.1 (1979): 97-107.
[2] Long, Charles A. "Evolution of function and form in camelid erythrocytes." Actas de The 2007 WSEAS International Conference on Cellular & Molecular Biology, Biophysics & Bioengineering. 2007.


Why don't we find animal corpses and skeletons all throughout the woods? Where in the forest do wild animals die?  I rarely (occasionally, but rarely) come across animal bodies.

Where are the large skeletons of bears and deer?

Detectives often investigate human bodies that were dumped months earlier.  They've partially decomposed, but are still mostly there.  Why?

Large predators can break up the bones to get at the marrow. This disperses the skeletons. But for the most part, bones are a good source of calcium, and are eaten by rodents. You can see evidence of this when you come across the gnaw marks that rodents make on the plastic boards made from recycled milk cartons. As for the reason that human skeletons are particularly resistant to this destruction, I have only a guess. Perhaps the first stage of destruction, the dispersal by large predators, is less common because these predators have been trained to avoid humans. I would also guess that many murder victims are concealed by the murderer.


What determines the duration of larval stage? Why do insects have very long pre reproductive periods and very short reproductive periods? Is there a common characteristic that can indicate the duration of these stages or offer an explanation for the same?

I actually see two different questions in your question. The first is "what determines the duration of the larval stage ?", the second is "why is this duration longer that the adult stage ?"

A) What determines the duration of developmental stages?

First, you must note that not all insects follow the same development process. Holometabolous insects (e.g. butterflies) have four life stages: egg, larva (with several instars), pupa and adult (or imago). On the other hand, hemimetabolous (e.g. bugs) only have three life stages, and some insects are ametabolous, i.e. no metamorphosis. Development time thus greatly depends on the mode of development. Of course, there can also be a huge variation within insects that have the same mode of development.
What else determines the duration of developmental stages ? (i.e. eggs/larva/pupa) A large combination of factors. Before they reach the adult stage, insects need to accumulate enough energy to undergo every developmental step and become mature. Resource quality and availability of course influence developmental "speed", but abiotic parameters such as temperature or humidity are also of prime importance. Actually, development time of many insects can be measured in degree days, which corresponds to the accumulation of temperature over time. For instance, larval-pupal development of the codling moth Cydia pomonella can go from 1 to about 6 months, according to temperature conditions.

B) Do insects have longer pre-reproductive periods that reproductive periods ?

It depends. There is a huge variation a) in the lifespan of all insect species, b) in the relative length of their developmental stages.
Some insects indeed have a very short adult life stage, relatively to their developmental stages. Mayflies are a classical example, but it's also true for many butterflies and moths of for mosquitoes, for instance.
On the other hand, it's not true for many other insects. Many Coleoptera (e.g. beetles, cockroaches) can have several-month long adult lives, sometimes way longer that their life as a larva. Bees are a more extreme example: bee queens need three weeks to become fertile, and can then reproduce during several years (same for ants).

C) Why do s̲o̲m̲e̲ insects have short reproductive periods ?

To my knowledge, the reasons are mainly ecological. Insects that have short adult lives are often fragile, flying insects that disperse a lot. They face an increased risk of predation as well as environmental fluctuations (weather, etc.) against which they are poorly protected. Besides their resources (e.g. sugar) may be scarce or poor-quality - some even do not have the ability to feed, e.g. mayflies.
What about evolutionary reasons? Developmental stages need some time because, as I said earlier, insects need to acquire a lot of energy to pass all developmental steps. I didn't even talk about metamorphosis, which is a complete cellular re-organization -that takes some time. On the other hand, adults just need to mate and/or lay all their eggs before they die. They don't need to live too long as they'll probably die soon anyway. Think about mayflies: they are less protected as free flying adults that as underwater-protected nymphae. And they'd better try to maximize egg laying in a reduced time.
Besides, note that there is a difference between potential lifespan and realized lifespan. For instance, parasitoid wasps can live up to 30 days in safe, food-abundant conditions - in the wild however, they often live just a few days.

References

https://www.terminix.com/blog/bug-facts/how-long-do-bugs-live/

Harvey, J. A., Cloutier, J., Visser, B., Ellers, J., Wäckers, F. L., & Gols, R. (2012). The effect of different dietary sugars and honey on longevity and fecundity in two hyperparasitoid wasps. Journal of insect physiology, 58(6), 816-823.

Müller, T., & Müller, C. (2015). Behavioural phenotypes over the lifetime of a holometabolous insect. Frontiers in Zoology, 12(1), S8.

Rafoss T, Saethre M-G (2003) Spatial and temporal distribution of bioclimatic potential for the codling moth and the Colorado potato beetle in Norway: model predictions versus climate and field data from the 1990s. Agric Forest Entomol 5:75–85


Colorblindness in females and random X chromosome inactivation From Annenberg Learner:

  Because the X is inactivated randomly in cells, one cell could have the maternal X inactivated, while the adjacent cell could have the paternal
  X inactivated. This causes a pattern of gene expression called mosaicism, which occurs when different alleles of X-linked genes are expressed in different cells.

However, this seems at odds with colorblindness being more likely in males.  From Wikipedia:

  The genes that produce photopigments are carried on the X chromosome; if some of these genes are missing or damaged, color blindness will be expressed in males with a higher probability than in females because males only have one X chromosome, whereas females have two and a functional gene on only one of the X chromosomes is sufficient to yield the necessary photopigments.

Question: If X chromosomes are randomly inactivated cell by cell, shouldn't the fully functional photopigment-producing gene be inactivated approximately half the time?  In which case, wouldn't we instead see females with colorblindness with higher frequency as males, but experiencing colorblindness to a lesser extent?  (After all, two X chromosomes means two chances for a dysfunctional gene.)

I'm guessing I'm missing a piece of the puzzle here, e.g., perhaps the relevant cells "know" to inactivate the dysfunctional X chromosome, or perhaps it's to do with X chromosomes only being incompletely inactivated.

In heterozygote females with colour defect genes on the X-chromosome, even if approximately half of their photoreceptors are dysfunctional they usually have enough functional cone photoreceptors to have normal colour vision.

From Molecular genetics of colour vision deficiencies:

  Due to X-chromosome inactivation during early development,
  heterozygotes are mosaics for two populations of cones, one expressing
  visual pigment genes encoded by an X-chromosome that would cause
  colour vision defects in males, and the other expressing genes that
  would confer normal colour vision on a male. In support of this,
  patches of defective colour perception were detected by shining a very
  narrow beam of red or green light into the retinas of female
  heterozygotes for X-linked colour vision defects. The majority of
  heterozygote women (carriers of colour vision defects) have normal
  colour vision.

This means that  – in most cases – for a female to be colourblind, her father must be colourblind and her mother must be either a heterozygote (carrier) or homozygote colourblind. In a male, only the mother's X-chromosome determines whether he inherits the defective genes, so he is more likely to have the colourblind trait.


Can Biting Insects Detect Specific Places On A Host Body? I'm gonna make a presumptive statement: It -seems- as though I get bitten by mosquitos and other biting insects in -exactly- the same places over and over. I mean within a few mm. Is that true?

If true, that implies that insects have a mechanism to detect certain preferred spots in order to get blood or whatever they want. (Location of blood vessels? Sweat glands?)

And if that is so, what -is- that mechanism? What are they going for? And how does this detection work?

IOW: How do they know to bite me exactly on the side of my right knee over and over and over... but never on other spots?

There are at least two sources that influence patterns of behavior: the individual that is doing the biting, and the individual that is being bitten.

The example of lice in one of the comments is a good example.  Three categories of lice that get on humans are: head lice, body lice, and pubic lice.  They are related species (possibly the same species in some cases - https://www.insidescience.org/content/are-head-and-body-lice-same-species/550), but each type has their own preference for habitat and feeding.  There are all kinds of reasons for a species to have a preference, and some stick to those preferences quite strongly.

As for your mosquitoes, their absolute preferences are still not known but blood seeking insects do have their senses attuned to clues such as carbon dioxide and heat (that help identify potential hosts) as well smells and other influences on their senses.  There might be something special about the side of your right knee as far as mosquito senses go, but not every individual in a species sees, smells, hears, etc. the same way.  My brother has a gene that makes broccoli taste very bitter, but I am fortunate to not have those taste buds.  Color blindness is another example of differences in perception, but even without being color blind, what you see as red is probably not how someone else sees red due to natural variations in the patterns of sensory cells in the eye.  For a consistent pattern of behavior from the mosquitoes, in spite of individual differences we still need to consider another source of variation that might lead to this mosquito preference: the host.

If the variation of individual mosquitoes is trumped by a consistent pattern of predation, perhaps the mediating factor is the host.  Your knee could have a special smell, or other sensory flag that attracts mosquitoes.  There are efforts to understand how a mosquito's perception directs who gets bitten: http://www.scientificamerican.com/video/future-repellents-mess-with-mosquit2013-12-23/ .  Not enough is known yet about the preferences of mosquitoes to say for sure what makes your knee so good.  There is also a chance that your knee is not special to the mosquito because it appears the most appetizing.

Host behavior is another possible influence.  The knee is just far enough away from the reach of your hands.  Conscious or absentminded grooming would both be limited at that distance.  The knee may also be better than an ankle or a foot, because of what is worn or because the knee moves less than the lower leg during walking and other movements.  If you are bitten on the lateral (outside) side of your knee, this would add evidence to this hypothesis of your movement influencing mosquito behavior, because the inside of your knee more frequently brushes against the other leg.  The frequency of the inside of the knee being a safe place for a meal is much lower.

As for why it's the right knee rather than the left, there is  possibility that that is also a reflection of you, rather than the pests.  Humans display preferences in dominance for both hands and feet.  One side of your body may be selected more often than another because of you being right- or left-handed, or right- or left-footed.  This could affect grooming habits (how you swat at the bugs), how your cross your legs, which side you carry items or lean against other objects which might brush against the body, influence how well you spray yourself with bug repellent or who knows what else.  (Just for curiosity's sake, ¿are you right-handed or are you left-handed?)

In short: There's a lot of evidence to collect before we could come to a definitive answer.  There are a lot of possibilities, including that your knee may not be the tastiest spot, but rather a relatively safe spot for dinner.

For more unempirical thoughts on the relationship of insects to the lower limbs, please see: http://fishboyridesagain.blogspot.com/2005/11/bugs-and-trousers.html


A diagram of a crossover How can one draw a crossover between ABK and aBk where genes A and B follow the Mendel's law of independent assortment and gene K does not i.e. K is linked to B?

I'm not sure if this is what you're asking for, but in the following image, allele K (or k) is linked to B while A (or a) and B are independent.

Again, this is just a guess because your question seems a bit unclear to me.


Spider found in bathroom can’t identify Found this spider in my bathroom on the wall by the door. Near Houston, TX.

Almost certainly a spider belonging to the genus Scytodes. It largely resembles the species S. thoracica with very similar markings to the picture above. It is a common spider in the United States, and is often found in houses.


Why have humans evolved much more quickly than other animals? Humans have, in a relatively short amount of time, evolved from apes on the African plains to upright brainiacs with nukes, computers, and space travel.

Meanwhile, a lion is still a lion and a beetle is still a beetle.

Is there a specific reason for this?  Do we have a particular part of brain that no other animal has?

This question appears to address at least two distinct concepts:

the "speed" of evolution
whether there is some "end goal" that evolution seeks

I will provide an explanation of each separately below:
The Speed of Evolution
The speed at which a species evolves—that is, the speed at which it acquires new heritable characteristics—can be affected by numerous factors. Among the most obvious which come to mind are:

existing population size
reproductive cycle rate
number of offspring
offspring survival rate
environmental demands

That said, have humans evolved faster than other species?
On the whole, I do not feel that I could say without a doubt that humans have evolved significantly faster than other organisms. Considering the above factors (we have a slow reproductive cycle, few offspring, etc.), it seems unlikely but this is where a zoologist would know better. The answer provided by bobthejoe may provide insight as well.
I would just raise a word of caution before leaping to the conclusion that we have evolved rapidly without looking into it, because while we often study human evolution quite extensively in biology classes and thus are more aware of changes like upright walking and opposable thumbs and increased brain size, that doesn't mean other animals didn't evolve that much as well (we just don't learn about them in as much detail). Being a psychologist and not a zoologist, I do not have the knowledge to say with any surety that other species did not evolve in their own ways to the same magnitude as we have in the last 3-4 million years, so perhaps someone else can help you there.
But you ask whether we have a particular part of our brain that no other animal has; the answer to this is no, but the parts of our brains which we do share with animals are often much larger than as seen in those other species.
The "Goal" of evolution
I would like to point out here that human technology has nothing to do with evolution. Not only have all of our notable technological achievements occurred in the last couple hundreds years when human evolution was at its slowest (early human evolution as we know it today dates back at least 5-7 million years, and it was during this several million year period when all the genetic evolution you speak of happened), I would argue that human spaceships and computers are no more sophisticated to us than a mushroom garden and ventilation system are to a termite. I could be wrong here but it seems as if you are under the impression that evolution is striving towards something... That humans are somehow intrinsically better than lions or sharks or beetles. On the contrary, each of these creatures is not significantly more or less adapted to their environments as we are to our own, and in many ways these creatures possess features which are beyond our own.
I shall leave you with one of my favorite quotes:

"We need a wiser and perhaps a more mystical concept of animals. We
patronize them for their incompleteness, for their tragic fate having
taken form so far below ourselves. And therein we err, and greatly
err. For the animal shall not be measured by man. In a world older and
more complete than ours, they move finished and complete, gifted with
extensions of the senses we have lost or never attained, living by
voices we shall never hear. They are not brethren, they are not
underlings. They are other nations caught with ourselves in the net of
life and time, fellow prisoners of the splendor and travail of the
earth."

–Henry Beston, in The Outermost House
I don't have a dog in this fight, and I could very well be falsely assuming that you think this particular way when you in fact don't (you only wrote 4 lines after all, it's hard to glean much from that), but I wanted to make sure that these concepts were clear either way, particularly for any future visitors who might get the wrong impression. :)


What is the number of DNA strands per cell? I wonder if each cell possess only one strand of DNA which according to my book is more than "7 feet" long(if uncoiled), then why does human has 46 chromosomes which are actually coiled chromatin (DNA wrapped around histone proteins)? Does DNA break into parts and form 46 chromosomes during cell division (I am just guessing I am not sure about it)?

Human cells contain 23 pairs of chromosomes (46 chromosomes in total).
Each chromosome is formed by 2 strands of DNA tied by hydrogen-bonds to each other making the classic  DNA double helix (double-stranded DNA). So, in total there are 46*2=92 strands of DNA in each diploid human cell! Gametes contain half of the chromosomes, so half of the strands as well.


Finding specific genotype occurrences given allele frequency So let's say I have a tetraploid species and I have 4 possible alleles for a particular locus. I have found that I can have 35 total possible genotypes and I know the allele frequencies for each of the 4 alleles, that I will randomly set as $$F_a = 0.2, F_b = 0.3, F_c = 0.4, F_d=0.1$$ for the sake of the example.

However, I am having a hard time wrapping my mind around how to calculate the number of occurrences of a particular genotype, $abc$, in a population of 1000 people.

I understand the allele frequencies, for instance, in the population of 1000 people, given all 1000 observed genotypes, 40% of them had allele $c$. But these are individual values and I have no information on how likely they are to be linked. (I am supposed to assume HW principle holds, but not sure how this helps).

How do I calculate the number of occurrences of the genotype $abc$ in the population?

Under Hardy-Weinberg conditions, the frequency of the genotype abcd (in this particular order) is simply $F_a \cdot F_b \cdot F_c \cdot F_d = 0.24\%$.

If we don't consider the order, then we must ultiply the previous probability by 24. There are indeed 24 (=4*3*2*1) ways you can get this particular combination. The probability of abcd in any particular order is therefore $24 \cdot F_a \cdot F_b \cdot F_c \cdot F_d = 5.76\%$.

You might want to have a look at the post Solving Hardy Weinberg problems


Looking for study/genome data for HIV in different organs I am looking for a research study or data base that has HIV genome data available in fasta or similar format. Specifically I need genome data of HIV taken from different organs in the same subject. I am interested in studying the way HIV diversifies and changes to infect different organs and in comparing the process across different patients.
If you are familiar with such a study, or if you have general pointers as to where I may find similar data, I would appreciate it very much. I have done a few hours of searching on NCBI GeneBank, but have had no luck.
Thanks!

This website comes to my mind
https://www.hiv.lanl.gov/content/index
It is a HIV databases containing HIV sequence data and related immunologic information


If human proteins are synthesized from only 20 different amino acids, then how can there be such variety of proteins in human cells? I know that human proteins are synthesized using only 20 different amino acids. However, how can there be thousands of different proteins in human cells, if we only use 20 amino acids to make them?

There are only 26 letters in the English language, and more than 80% of words are under 10 letters. Yet there are over a million English words. Nonsense words don't count.

Now imagine the possibilities of a 20 letter alphabet, where the average "word" length is about 375 letters, and where words of up to 800 letters are possible. And that also does not include "nonsense words".

That should give you an idea of the possibilities, and why "thousands of different proteins in human cells" can exist.

How big is the “average” protein?


Why are there different gene expressions that are refered to the same gene in microarray experiments results? I am studying gene expression profiling considering a dataset available on NCBI website. I do not understand the following: why are there some genes that have different profile and different ID numbers but they refer to the same indentical gene ?
The dataset that I am analysing is here .
For instance, we have that ID-8938, ID-1870, ID-7323 and ID-15 refer to the same gene called RadA but the gene expression profiling is different for each ID. So I ask which is the difference between these ID if they represent the same gene ? Moreover, how can I understand which is the one that has to be chosen for the analysis ?

What you are looking at there is a microarray dataset (see the description here).
Microarrays are chips that have many sequence specific probes on them and sometimes they have multiple probes for the same gene.
Readout differences between the probes of the same gene could be caused by either noise in the data or biological effects like expression differences between transcript isoforms - other reasons could be possible as well.


Is bad tasting food more likely to cause harm? Taste is often referred to as subjective. For example certain foods taste bad to me, such as oranges, grapefruit, grapes, raisins, and sweet potatoes. However the wiki article on taste explains that from an evolutionary perspective, it's important that bad taste might indicate poison in the food; taste isn't an arbitrary matter of subjectivity.

With that in mind I pose the question if a food tastes bad to a particular person, is it more likely to be causing harm to that person than someone who finds the food pleasant? In other words, is the bad taste a sign that my body is not suited for some components in the food?

tl;dr; If someone likes a food item, then even if it taste not so great to you, it will probably not harm you. If a food item taste awful to everybody (in particular bitter), then it would probably be best to avoid it.

Taste perception per se is not subjective, you either can detect or not a defined compound at a defined concentration. Food preference however is of course much more subjective.

The most established theory in the field is that we evolved both bitterness and sourness as a warning signal for poisonous compounds and inedible food. Bitterness is often the most referenced as most poisonous substances taste bitter to humans (e.g. strychnine, nicotine, ...) and are detected at very low concentrations (in the nM to $\mu$M range) (Meyerhof W, 2005). In comparison, the threshold for sweet taste perception is well above > 100mM (Park DC, 2015), or put otherwise, humans are at least 1000x more sensitive to bitterness compared to sweetness. As a result, we evolved to detect small quantities of bitter compounds and to dislike food items that are bitter as they could be poisonous.

Now for your question, you are probably misusing the word taste when you meant flavor, which is a combination of both taste and aroma (i.e. taste perception and olfaction combined, for example the "taste" of a banana). Food preference varies from people to people based on both genetic, physiological and more importantly environmental factors, in particular food habits. Typical examples are spiciness and saltiness where you can slowly adapt to tolerate higher and higher concentrations, meaning that your own food preferences can shift over your lifetime. Another illustration is the common shift in food preferences between childhood and adulthood. In other words, food preference is not an excellent predictor of a harmful food item.