Body size, what are the evolutionary trade-offs?

I don't think one can fully answer to such a broad question. It depends on the population, the environment (presence of predators for example), the genetic background (having a big stomach is good but only if the intestin is big too), the population's social relations, .. Many traits are correlated and one might want to say that a given trait is beneficial but it is not because this trait is correlated (because of genetic, physical or social constraints).
Trade-offs
Here is a list of possible advantages/disadvantages.

visibility to predators
ability to hunt bigger preys or to manipulate smaller preys
running faster
be more impressive
fighting ability
energy consumption for maintaining a body
Quantity/quality of food to be found
homothermy (heat loss)
sustaining its own weight
Rooms for the organs
Attractiveness to the other sex
being more able to move freely (in viscous environment (water))
mechansisms for bringing nutrients and air to the tissues
density of the body (water)
excretion of wastes
moving in small habitats
Hiding in small areas
bearing big and complex structures
Parental care
flying better
acceleration in each movement
etc...

Allometric relations
You might be interested in life-history traits, and in allometric relations. You might be interested by this article as well. The reason for allometric relations can be found here:

If an animal were isometrically scaled up by a considerable amount, its relative muscular strength would be severely reduced, since the cross section of its muscles would increase by the square of the scaling factor while its mass would increase by the cube of the scaling factor. As a result of this, cardiovascular and respiratory functions would be severely burdened.
In the case of flying animals, the wing loading would be increased if they were isometrically scaled up, and they would therefore have to fly faster to gain the same amount of lift. Air resistance per unit mass is also higher for smaller animals, which is why a small animal like an ant cannot be seriously injured from impact with the ground after being dropped from any height.
As was elucidated by J. B. S. Haldane, large animals do not look like small animals: an elephant cannot be mistaken for a mouse scaled up in size. This is due to allometric scaling: the bones of an elephant are necessarily proportionately much larger than the bones of a mouse, because they must carry proportionately higher weight. To quote from Haldane's seminal essay On Being the Right Size, "...consider a man 60 feet high...Giant Pope and Giant Pagan in the illustrated Pilgrim's Progress.... These monsters...weighed 1000 times as much as Christian. Every square inch of a giant bone had to support 10 times the weight borne by a square inch of human bone. As the human thigh-bone breaks under about 10 times the human weight, Pope and Pagan would have broken their thighs every time they took a step." Consequently, most animals show allometric scaling with increased size, both among species and within a species.
The giant monsters seen in horror movies (e.g., Godzilla or King Kong) are also unrealistic, as their sheer size would force them to collapse. However, the buoyancy of water negates to some extent the effects of gravity. Therefore, sea creatures can grow to very large sizes without the same musculoskeletal structures that would be required of similarly sized land creatures, and it is no coincidence that the largest animals to ever exist on earth are aquatic animals.

This post talks about the reasons for the allometric relations between animal size and speed of movements.
Concerning the relation between heat loss and size, you might be willing to have a look to the Kleiber's law. This law has been extensively debated and is today thought (or known) to be wrong.

Just a philosophical note
You might also be interested in the philosophical discussion of adaptation, optimality, cost and benefit like this book (which I haven't read!) for example.


From Bionumbers, the average transcription rate of RNA Polymerase II is about 3.8 kb/min. Other researchers measured it as 6.3 nucleotides/sec, or 378 bp/min, a 10-fold decrease. In the same paper, however, they measured the maximum rate at 71.6 nucleotides/sec, or 4.3 kb/min. To figure out the differences between the measurements, I suggest reading the paper, but since it's from Nature Publishing Group you'll have to pay for it, unless you're at a subscribing university or institution (or someone posts the paper in the comments <hint hint>).

So, the answer to your question, like most simple questions in biology, is it depends. It likely depends on the size of the gene, its structure, what transcription factors are necessary for the assembly of the polymerase complex, and, last but not least, exactly how and when you measure. Transcription likely initiates in fits and starts, then gets going faster. This is similar to (but not exactly like) measuring the speed of your car from Point A to Point B. Are you starting from a dead stop, or passing the starting marker at speed? Do you have to start the car first, or is it already running? How many turns and other slowdowns are on the road? Do you stop measuring as the car passes the finish marker, or when it comes to a complete stop? All of these things figure into the final answer, and the result given is entirely dependent on the scientists' choices of methodology.

If you are interested in a broader discussion, I got started on this page at Bionumbers.


How can I pare down a PDB file in Python to only include specific residues?

With the program RasMol, you can select, as Mad Scientist explained it for PyMol, everything in a specific distance around an atom. RasMol can be run from command line, using a script (with the -script option under UNIX).


How does the bladder transition from releasing urine at night to being able to hold urine at night?

The bladder is controlled by both the autonomic and somatic nervous systems. This means that part of the bladder activity is voluntary and another part is involuntary - more precisely, the detrusor (which is the smooth muscle in the bladder wall) is controlled involuntarily, while the external sphincter (the muscle around the bladder neck) is controlled voluntarily (see picture, this is the female bladder).

I found all kinds of references that describe the maturation process of the bladder during infancy. This paper, from Pheonix Children's Hospital, is about voiding disorders in children. It notes in the first paragraph three conditions that make up the bladder's maturation process (the rest of the paper discusses voiding disorders):

The bladder capacity must increase.
The child must develop voluntary control over the sphincter muscle in order to start and stop voiding.
the child must develop voluntary control
over the infantile voiding reflex which allows the child to stop involuntary bladder contractions.

This article discusses the topic of bladder maturation in greater detail (see the first section titled: MATURATION OF BLADDER CONTINENCE). From the article: "As bladder urine increases, a critical volume is reached (functional bladder capacity), which initiates a spontaneous reflex contraction that is mediated by the sacrospinal ganglia. As the bladder contraction ensues, the increased bladder pressure overcomes the detrusor muscles at the bladder neck and spontaneous emptying occurs. As the infant grows and matures, control centres in the pons and medulla initiate inhibitory signals that slowly dampen this reflex over a period of years ... Nighttime continence is achieved in association with the abolition of spontaneous bladder contractions, mediated by the pons and medulla; a nocturnal bladder volume less than the nocturnal functional bladder capacity (NFBC), which is ADH-dependent; and the achievement of prolonged rapid eye movement (REM) sleep and attainment of sleep arousal."


Why do animals have more heavy nitrogen and carbon than plants?

Organisms accumulate certain isotopes because their metabolic enzymes have a slight preference for molecules containing that isotope. A well-known example is ribulose-1,5-bisphosphate carboxylase (Rubisco) which is responsible for CO$_2$ fixation in photosynthetic plants: this enzyme is somewhat more efficient with $^{12}$CO$_2$ than with $^{13}$CO$_2$, causing plants to accumulate $^{12}$C.

In animals, there is an enrichment for $^{15}$N because the deaminases and transaminases that transfer nitrogen from amino acids to urea (for excretion) tend to favor $^{14}$N. So in this case, $^{14}$N tends to be removed from the body faster than $^{15}$N when breaking down dietary protein. The differences are very small though: the relative enrichment of about 0.4% per trophic level corresponds to 0.367% $^{15}$N in a herbivore, compared to 0.366% $^{15}$N in a plant.

Source: this article.


What are the ants underneath leafs in my garden doing?

From what you described, it seems to me the "fruitflies" are aphids and the ants are farming them. This is a widespread and common phenomenon known as ants-aphid mutualism.
P.S.
I elaborate a bit. Aphids feed on plant sap, rich in sugar, which they don't digest completely. The excretions (poop) are thus still rich in sugar (you may have noticed how your car windows get sticky sometimes under tress - that's aphids poop, I believe). Some ant species co-evolved with particular aphids and collect their excretions, a valuable sugary energy source. In turn, ants protect aphids from predators and they move them around to cover other good plant spots for aphids to suck sap and even move them to different plant individuals. This mutualistic interaction between aphids and ants is quite common and causes a lot of economic losses to the agriculture sector.
The behavior you observed of an ant attacking aphids was probably more the ant checking them and trying to evoke a pooping response. Sometimes they get them between their jaws and carry them around. Aphids also have quite complex social structure, with an optimal spatial organization. Hard to say if ants are moving them around to reach this optimal "farm density" or for other reasons.
TL;DR ants farm aphids as humans farm cows. When ants interact with aphids they are mostly checking them and trying to get their sugary poop.
/Emilio


Can androgen-insensitive genetic-males get pregnant?

Short answer
People with androgen insensitivity syndrome do not have a functional uterus and cannot bear a child.

Background
Androgen-insensitive genetic males may develop female genitalia and internal female reproductive organs. However, in both partial androgen insensitivity syndrome (PAIS) and complete androgen insensitivity syndrome (CAIS) the uterus is absent, or is present only in a rudimentary form.

The reason for the absence, or rudimentary form of the uterus is the fact that Mullerian inhibiting substance (MIS), produced by the Sertoli cells of the fetal testes is present. MIS controls the regression of the mullerian ducts, and in its absence in XX females, the mullerian system develops into the uterus, oviducts, and upper vagina. However, in XY individuals with CAIS (and likely also with PAIS), MIS is produced normally by the testes resulting in inhibition of the growth of the uterus and fallopian tubes (Oakes et al., 2008).

Reference
- Oakes et al., J Pediatr Adolesc Gynecol (2008); 21: 305-10


Why do people remove excess solution after they put on a coverslip?

Neither of the current answers fully answer the question.

The amount of liquid underneath a coverslip should be just sufficient to hold the coverslip and sample onto the slide. If there is too much water, the surface tension would become reduced, allowing the coverslip to fall off the slide.

Additionally, minimising the amount of water between the coverslip and the slide would ensure that the z-axis variation in your sample is minimised, therefore reducing the likelihood that your sample will have different focal points across the sample.

This UCLA guide on microscopy slide mounting explains it (emphasis mine):

  Small pieces of filter paper (Whatman #1) are placed around the edge of the coverslip to absorb excess mounting medium. If your specimen is tissue culture cells or frozen tissue sections, this should not harm them. This does two things: a) it allows the coverslip to come as close to the specimen as possible and reduces the depth of the field. You will get less focus aberration if you do this judiciously. b) the coverslip will be a lot less likely to float around on the slide and move which could specimen damage. The surface tension between the coverslip and slide will be much higher. You will also be much better able to seal your coverslip to the slide.


When gene editing are both chromosomes in a pair changed?

Gene editing using CRISPR-Cas9 can result in both heterozygous and homozygous conditions. It is just the event of probability. But even if u get heterozygous line, making it homozygous is not very difficult. You just have to cross two heterozygous line and screen for homozygous line through markers.


What's the mixture of plasma and haemoglobin called

You and Dr. James must be friends ;)

There is no specific name for the mixture of plasma and haemoglobin, however, when hemoglobin is found in the plasma (i.e. not in blood cells) it is usually referred to as "free hemoglobin." This is a term you are most likely to encounter when dealing with plasma/ serum hemoglobin testing.

Additionally, when haemoglobin is broken down, it forms bilirubin, which contributes to the color of plasma (there is no specific name for the mixture of bilirubin and plasma either, except perhaps "plasma bilirubin").


You can tell that the structures labelled At are axons, or rather axon terminals, due to the presence of the synaptic vesicles.

I think this is a fine photo that's a bit more a clear representation:

Source

PSDs are really just protein aggregates that are thought to facilitate neurotransmitter trafficking. So the structures here make sense. At least, they make sense if you know the tissue you're running in TEM, and you understand that how you cut the samples for microscopy affect the way they end up looking. My only assumption that Den is a dendrite is knowing that axon terminals synapse with other dendrites: they're receiving structures. I'm also somewhat sure the cell body from which the dendrites extend have that characteristically large nucleus.

The other understanding is that these pictures are just snippets of a larger image and you only get used to identifying structures through practice and experience. Rather, the author wants you to see this section and for lack of context has identified the structures for you.


How do I clean phenol contaminated RNA without losing any of the sample?

You can clean up phenol by washing with choloroform, and then doing an isopropanol precipitation followed by a 75% EtOH wash (let me know if you'd like an exact protocol).

To avoid contamination (and sample loss), you have to be meticulous in your pipetting (which you'll get better with practice). You can always use those phase-lock tubes which basically jams a solid gel between the aqueous and organic phases so it's a lot easier to pipette.


Question regarding the number of alleles

The two-allele scenario is often used in genetics teaching because of its simplicity. However, quite a few genes have more than two alleles. Some examples that readily come to mind are:

The ABO gene in humans: This determines ABO blood group, and has six common alleles. Many more rare alleles have been described [1].
The human leukocyte antigen (HLA) genes: These are well-known for their allelic diversity. One of them, HLA-A, alone has over 6,000 alleles [2].

Reference

Seltsam A, Hallensleben M, Kollmann A, Blasczyk R. The nature of diversity and diversification at the ABO locus. Blood 2003; 102(8):3035–3042. https://doi.org/10.1182/blood-2003-03-0955
Robinson J, Halliwell JA, Hayhurst JD, et al. The IPD and IMGT/HLA database: allele variant databases. Nucleic Acids Research 2015; 43:D423-431. http://hla.alleles.org/nomenclature/stats.html


What types of plants are Gibberellin used on?

I don't know what you mean with 'used on' but gibberellins are plant hormones in ferns, monocots and dicots. All of these plants will react to the application of gibberellin but the effect will depend on the dose, type of molecule and tissue where it is applied. All plant hormones have multiple effects but the classic one for gibberellic acid is stem elongation.

Too much of this can kill the plant though as is the case with Bakanae fungus infection which forces the plant to overproduce gibberellic acid which kills it (reference).

One common agricultural use is boosting the growth of seedless grapes as the seed is an important site of gibberellin production for maturing fruits.

This pdf gives you a reasonable overview of what gibberellins do


Is there a term to quantify how spread a character is on a phylogenetic tree?

I agree with Terdon's terminology in the comment ("ubiquitous" or "widespread").

You can use clade-specific or species-specific for a restricted character.

For the characters that appear in all species of a branch and in a quantitative way you can also provide the estimated age of the last common ancestor to the branch featuring that character. This tool might help you: http://www.timetree.org/


Can people with paralyzed eye muscles see?

Short answer
Visual perception persists in the absence of functional eye movement.

Background
An example case would be retinal implants wearers. Retinal implants like the Argus II consist of a set of electrodes placed onto the degenerate retina of blind folks. Electrical stimulation of the electrode array elicits flashes of light (phosphenes). Visual input is provided via a head-mounted camera, and the device translates the camera images into patterned electrode stimuli. Hence, because the camera is head worn, Argus II wearers cannot use eye movements to scan the world. They have to use head-scanning techniques. Still they are able to perceive flashes of light (phosphenes) and can recognize simple shapes and perceive motion.

In fact, eye movements such as saccades are detrimental in Argus II wearers, because the oculomotor system feedbacks muscle movements to the brain when a saccade is made to stabilize the perceptual field of view. In normally sighted people the oculomotor feedback system is important, as it tells the brain to compensate the retinal image position shift when a saccade is made. Compensation occurs through a shift in the brain representation of the retinal image to the opposite direction, thereby stabilizing the image representation. However, this is detrimental in Argus II wearers, because the position of the electrode array and hence retinal position of the image is unaffected by eye position. Hence, when subjects use their implant, any saccades will disrupt visual processing, because the oculomotor system will abberantly compensate the perceived location of the object being viewed.

More importantly, perhaps, are micro-saccades. Micro- saccades are small, involuntary eye movements. When images are present stably to the retina the images fade very quickly due to adaptive processes in retinal neurons. Micro-saccades are thought to prevent fading, as they constantly produce small, involuntary fluctuations in gaze, thereby shifting the image quickly over the retina, and thereby refreshing the retinal image and preventing adaptation (Stingl, 2013). When Argus II wearers stop scanning the image, images indeed fade within seconds (Stronks, 2013).

To get back to your question and summarize:

Title question: No, eye muscles are not needed for sight, given that Argus II wearers have sight (though artificial, crude vision). However, a functional saccade system in normally sighted folks improves scanning, and anecdotally micro-saccades prevent image fading by constantly refreshing the retinal image.

Body question: Argus II implant wearers are an example of vision without oculomotor control. Although they cannot use their eye muscles for scanning, they still have functional vision.
 However image fading is a problem in Argus II users and folks without functional eye muscles alike, so head scanning techniques will be needed.

PS: Other implant systems, such as the Alpha-IMS use light-capturing methods inside the eye. Hence these subjects can use normal eye scanning and saccades for scanning. Also, albeit anecdotally, fading is reduced in Alpha-IMS wearers, because of the micro-saccades preventing adaptation (Stingl, 2013).

References
- Stingl et al., Proc Royal Soc B (2013); 280(1757)
- Stronks et al., IOVS (2013); 54(6): 3891–901.


What is meant by "opposing plasma membrane" with respect to cell adhesion molecules?

Opposing means facing each other, so the two outer surfaces can interact. Like two opposing armies.
I found an article:
"Pharmacology of cell adhesion molecules of the nervous system"
at
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2644493/
doi: 10.2174/157015907782793658
"...CAM-induced intracellular signalling is triggered via homophilic (CAM-CAM) and heterophilic (CAM - other counter-receptors) interactions..."


Firstly I'll clarify that you are talking about simultaneous hermaphrodites rather than sequential hermaphrodites (1st one sex, then the other e.g. the limpet Patella vulgata).

It is perhaps easiest to address the question by countering it and asking why dioecy (2 sex systems/2 gonochoric types e.g. male and female) is better? As you have pointed out there are obvious advantages to being a hermaphroditic species such as more chance of mating - more likely to provide an advantage at very low population densities where interactions are infrequent.

There are two key disadvantages of hermaphroditism which I will briefly cover but have been discussed in this paper and probably other costs.

The first is energy costs. Maintaining the capacity to produce male and female gametes will be more costly than maintaining one. This gives the hermaphrodite a fitness disadvantage because energy is rarely an infinite resource. Therefore at higher population densities, when mating opportunities are not rare, the gonochoric individuals will have a higher fitness because they have more energy. Monogamy is also analogous to rare encounters but true monogamy is rare (1 partner for life).

The second disadvantage of hermaphroditism is self fertilisation. This will cause an increase in homozygosity and lead to inbreeding depression (reduced fitness).

So you are right to some extent...

  the hermaphrodite way of reproduction is more successful than the
  "normal" way.

...but the conditions which give rise to an hermaphroditic advantage are restricting. Overall, the above costs, combined with the obvious complexity of evolving the ability to produce male and female gametes, the ability to both fertilise and be fertilised, pregnancy and birth, and mating systems, mean that it is often more beneficial to be a dioecious species. Thus dioecy evolves.

EDIT: Question Raised by @Single_Digit

  I have been pondering this question for a while and I get what RG255
  is saying. I'm just not sure I entirely buy it. Take earthworms, for
  example. They are simultaneous true hermaphrodites (as far as I
  understand). The anatomy doesn't have to be that complex*. They simply
  have two genital openings (one for eggs and one for sperm) and they
  line up in a "69" (excuse the vulgarity) position. This should, in
  theory, minimize the inbreeding depression. However, it doesn't
  eliminate the maintenance of two sets of reproductive systems. But
  most organisms are not internally fertilized mammals with wildly
  complicated systems of internalized embryonic care. Most species lay a
  pile of eggs that a male squirts sperm on or squirt eggs while the
  male squirt sperm and then they hope for the best.

  I would think the advantages of simultaneous parenting (after all,
  many MANY species' males don't provide much in the way of child care)
  and its fitness advantage would vastly outweigh the burden of a second
  set of reproductive organs.

  With that said, I don't have a better explanation, but I find the
  question a very interesting one. The linked article is pay-walled,
  aside from the abstract, but I still disagree with some of its tenets.
  To me true hermaphroditism should be very common (I realize it isn't)
  in species that don't need two parents to raise offspring, but do
  benefit from some (as in one parent's) parental care. I recognize that
  it would do little to help species that merely dump gametes and leave
  because specialization of one reproductive system would likely do the
  job better and both genders equally contribute under that type of
  system.

  So, RG255 convince me! Clearly there are good reasons, since gender
  (or asexual repr) is the norm, but I need more/better evidence.

  Yes I realize they would need separate internal anatomies for each type of gamete, but still...

My response:

  You have presented one example of hermaphroditism and used that as
  evidence that all species should be hermaphrodites. Earthworms are
  small slow creatures living in soil, I don't imagine they have high
  rates of encounter, and therefore low rates of encountering the
  opposite sex, therefore hermaphroditism would be favoured as discussed
  above.

  Further, you say most species are external fertilisers (do you
  have a reference for this?) and therefore it is not costly be a
  hermaphrodite. I don't see your logic there, the cost is not
  necessarily to do with the cost of bearing child, producing &
  maintaining the gonads and gametes is also a costly process. I would
  argue that this is extremely complex. This is not just on a
  morphological level but also physiological: in non-hermaphroditic
  species the sexes have very different, and often, conflicting gene
  expression and hormone production patterns. Hermaphrodites would not
  be able to optimize to the fulfilling both the male and female roles.

  Finally, you pointed out that the worms do not inbreed. Inbreeding
  avoidance does not have to be the cause of the hermaphroditism
  persisting, if the environment/other factors favour hermaphroditism. I
  never said that both were simultaneously necessary.

  I hope this
  clarifies it for you, if not please expand as to why, I am on here
  because I want to help people understand biology properly!

Further response from @single_digit:

  Well fair enough about my external fertilizers comment. I don't have a
  reference, but I was thinking all multicellular life and I'd have to
  imagine that when you factor in plants, that external fertilization is
  relatively the norm (as is hermaphrodism (dioecy) for the plants). As
  to earthworms, I disagree about your description of them. Their
  densities are actually pretty high, so I'd wager they encounter each
  other frequently, so I'm not sure where that leaves them in terms of
  pressures for hermaphroditism. Your point on the physiologic/hormonal
  issues of maintaining the systems is one I haven't previously
  considered. I honestly don't have any clue as to how daunting (or
  simple) that is, but I'd imagine that the sophistication of the
  systems would play a pretty key role. Makes me wonder how much this
  has been researched in true hermaprhodites. I suppose the main thing I
  keep coming back to is the overwhelming disadvantage gender has in
  terms of potential to create offspring. Males in many (most?) species
  essentially act as little more than sperm donors, thus half the
  individuals have effectively zero fitness. That just seems like an
  overwhelming advantage for hermaphrodites.

My Response

  Why do you consider half of the individuals to have zero fitness?
  Fitness is widely accepted as the number of offspring a parent
  produces because this is directly related to number of copies of their
  genes passed to the next generation. Sperm donor type males achieve
  increased fitness by mating as do females - with out the male they
  would never be fertilized. The key disadvantage of dioecy is the
  halved (assuming equal sex ratio) frequency of potential encounters
  that could lead to mating. The general disadvantages of
  hermaphroditism are inbreeding depression and high cost & complexity.

Single_digit:

  Zero fitness isn't exactly correct, but if we look at parental care as
  conveying a survival advantage for K selected species, and huge
  numbers of offspring conveying an advantage for r-selected species
  (obviously the type of env affects this) does a deadbeat dad really
  optimize for either of these? Passing on genes is fine, but if
  offspring survival is low, does it matter? Does it simply boil down to
  the maintenance of two repr systems plus decreased fitness from
  inbreeding vs the increased reproductive success from extra child
  care? Or is there more?

My response:

  r/K selection theory has generally been disregarded in the
  evolutionary biology community due to the substantial evidence against
  it so it is unhelpful to think of selection in this way. As long as
  the 2 sexes strategy is more successful at passing on genes than a
  hermaphroditic strategy it will (should) prevail. Dioecy will be more
  successful if the hermaphroditism introduces to much cost through
  production and maintenance of sexual organs/gamete and inbreeding
  whilst not attaining substantial gains from higher potential mating
  frequency.

@Single_Digit

  Interesting about r/K selection. I hadn't heard that. Do you have any
  links? I'd be curious to learn more there. I incorrectly earlier made
  a comment about dioecy where I meant monecy. But this seems to beg the
  question, why is monecy/hermaphroditism so much more prevalent in
  plants? Obviously there are different survival pressures, but I'd
  think the same basic principles would apply as in animals, but the
  condition seems to be far more common than in animals.

My Response

  I seem to remeber there being a reason in plants, don't
  have time to look it up right now. The work about r/K selection was
  Reznick/Stearns/Charlesworth. Reznicks is the most recent and more
  overview type paper - best place to start:
  http://www2.hawaii.edu/~taylor/z652/Reznicketal.pdf


How can prokaryotes repair double strand breaks by homologous recombination if they're haploids?

Several answers to this question:

Much of the time what bacteria are doing to repair DSBs is actually non-homologous end-joining, which does not require strict homology. This is the more likely mechanism earlier in the cell cycle when copy number is more likely to be ~1.
If cells have completed DNA replication (later in the cell cycle), there are at minimum 2 copies of all DNAs present in the cell. These can be used for homologous recombination.
Bacterial chromosome copy number can be overreplicated in some situations, such that DNA replication is not synchronized to the cell cycle and is more than normal for a cell. In these situations copy number can be >2.


What is the role of Homocysteine in cognitive function?

I'm not sure if this answers your question, but I'll give it a try anyway. Here's a diagram of homocysteine metabolism. Vitamin B12 is a cofactor for homocysteine methyltransferase, and folic acid is required for tetrahydrofolate (THF). As both vitamins are involved in homocysteine metabolism, the symptoms of folate and vitamin B12 deficiency are similar. Vitamin B12 deficiency can result in neurological symptoms due to abnormal myelin, but folate deficiency does not. Vitamin B12 also metabolizes methylmalonyl-CoA to succinyl-CoA as seem here, so the methylmalonic acid level is often measured to test for vitamin B12 deficiency.

Hyperhomocysteinemia is the condition of high levels of homocysteine, but it is usually due to low vitamin B12 or folate.


The CDC has made available online its nCoV test kit. Briefly,the kit contains primers and probes for real-time reverse-transcriptase PCR, as well as instructions for appropriate use and (critically) controls and guidelines to avoid false positives and negatives. Kits from different countries may use slightly different primers and probes, though since they are all working from the same sequences and the same principles they should be broadly quite similar.

Explaining how quantitative PCR works and the details of the primers and probes is out of the scope of this SE. A layman's introduction was written by John Timmer at Ars Technica.


Why is exclusive breastfeeding recommended for 6 months only?

I guess this is the review (ISBN: 92 4 156211 0) that they are referring to.

  We found no objective evidence of a “weanling’s dilemma.” Infants who
  are exclusively breastfed for 6 months experience less morbidity from
  gastrointestinal infection than those who are mixed breastfed as of 3
  or 4 months, and no deficits have been demonstrated in growth among
  infants from either developing or developed countries who are
  exclusively breastfed for 6 months. Moreover, the mothers of such
  infants have more prolonged lactational amenorrhea. Although infants
  should still be managed individually so that insufficient growth or
  other adverse outcomes are not ignored and appropriate interventions
  are provided, the available evidence demonstrates no apparent risks in
  recommending, as public health policy, exclusive breastfeeding for the
  first6 months of life in both developing and developed country
  settings. Large randomized trials are recommended in both types of
  setting to rule out small adverse effects on growth and to confirm the
  reported health benefits of exclusive breastfeeding for 6 months.

However, another report suggests that exclusive breastfeeding for a long time may lead to deficiency of some nutrients which cannot be supplemented via maternal diet.

  The dual dependency on exogenous dietary sources and endogenous stores
  to meet requirements needs to be borne in mind particularly when
  assessing the adequacy of iron and zinc in human milk. Human milk,
  which is a poor source of iron and zinc, cannot be altered by maternal
  supplementation with these two nutrients. It is clear that the
  estimated iron requirements of infants cannot be met by human milk
  alone at any stage of infancy. The iron endowment at birth meets the
  iron needs of the breastfed infant in the first half of infancy,i.e. 0
  to 6 months. If an exogenous source of iron is not provided,
  exclusively breastfed infants are at risk of becoming iron deficient
  during the second half of infancy. Net zinc absorption from human milk
  falls short of zinc needs, which appear to be subsidized by prenatal
  stores.

Both these reviews are from WHO website; you can search for different WHO research materials on the site.

Note: WHO does not say that breastfeeding should not be continued till a later stage. As noted in the review, exclusive breastfeeding for more than six months can cause some nutritional deficiencies. However, reducing exclusive breastfeeding to 3-4 months can reduce the immunity of the infant.


When did bison exchange smartness for larger skeletal muscles or a digestive system that can ferment grass?

Patricia Churchland is wrong there.

Bison are very big deer/goats, and they are not dumber than deer and goats, you know how clever sheep are! There is a theory that they are related to a rabbit sized early ruminant about 40 million years ago.

Bison and deer have common ancestors about 17 million years ago.

Goats and deer have common ancestors about 22 million years ago, they have a similar digestive system to bison, your book is being vague there.

Oligocene epoch:
The formation of the Himalayas and the Alps brought about significant geographic changes. This was the chief reason behind the extensive diversification of deer-like forms and the emergence of cervids from the Oligocene to the early Pliocene.[50] The latter half of the Oligocene (28–34 Mya) saw the appearance of the European Eumeryx and the North American Leptomeryx. The latter resembled modern-day bovids and cervids in dental morphology (for instance, it had brachyodont molars), while the former was more advanced.[51] Other deer-like forms included the North American Blastomeryx and the European Dremotherium; these sabre-toothed animals are believed to have been the direct ancestors of all modern antlered deer, though they themselves lacked antlers.[52] Another contemporaneous form was the four-horned protoceratid Protoceras, that was replaced by Syndyoceras in the Miocene; these animals were unique in having a horn on the nose.[45] Late Eocene fossils dated approximately 35 million years ago, which were found in North America, show that Syndyoceras had bony skull outgrowths that resembled non-deciduous antlers.[53]

https://en.wikipedia.org/wiki/Deer#Eocene_epoch

This science mag study contradicts with the wiki references by about 20 million years:

https://science.sciencemag.org/content/364/6446/eaav6202

Here's a giant book on the topic of ungulate radiation based on their teeth, it doesn't give an easy answer to your questions though, it implies that there have been many genera of ungulates the size of cats and dogs and larger in the paleocene: https://www.researchgate.net/publication/36248483_Adaptive_radiation_of_early_Paleocene_ungulates/link/0c96051683bae86a84000000/download

Bison are at the top of the ruminants, after the cervus (deer):

That book is sociology and neuroscience, and it lacks depth for evolution. Evolution is fabulous at providing evidence and physical details, so she should demonstrate some examples ( bat digits, hand structure of primates, resemblances of sea mammals).


What is the germ layer origin of human lung fibroblasts?

All normal fibroblasts are mesenchymal in origin, including lung fibroblasts. In certain situations, usually injury related, epithelial cells can undergo an epithelial to mesenchymal transition (EMT).


Sources for common laboratory Saccharomyces strains?

ATCC is the place I would go to, just like purchasing cell lines or bacterial lines. The reference ATCC catalog numbers are also listed with each of the common strains you have linked. Depending on the purpose, you could just go to your local grocery store for baker's yeast.


How much of what we eat ends up in the toilet?

It very much depends on what specific kind of food you are taking.
Say, if we eat more green vegetables then we are supposed to excrete more compared to a highly meat-rich diet.
Also, it depends on the food-intervals, more the interval more the absorption by body so less amount going out(but giving extreme interval is not good either).
All depends on the need of body, if body needs more than what you are giving to your body it gonna obviously excrete more.
And always keep in mind to take sufficient water, because without it all things go malfunctioning in our body.


Why HIV patients have greater virulence of M.tuberculosis?

If you read this article, you will find that CD4+ and CD8+ T-cells are probably the major mediators of the immune response against M. tuberculosis. Since HIV severely depletes the number of CD4+ T-cells (and to a lesser extent other kinds of lymphocytes), it stands to reason that the frequency of infection and virulence will be substantially increased in such patients.


It is good thinking you're doing here!

Only mutations happening in the germ line can be passed on

Mutations that happen in an individual hand (or any other soma line) will not be passed on the the offspring. Only those happening in the soma line can.

Mutations are random

What I mean here is that it is not because someone is old that all of sudden the mutations that would happen in this person would be beneficial for old people.

Age dependent "quality" of genome being passed on

You are asking

  Do older parents pass on a different, perhaps more learned "quality" of DNA?

You seem to misunderstand how natural selection works. An individual alone does not get selected over its lifetime to become better (at least not in the sense of what is meant by "natural selection"). You need a population for selection to happen.

In the females as the pool of ovules is being set early in life. In males the spermatozoids keep replicating during the whole lifetime of the individual. Hence, in males, but not in females, the number of new mutations being passed on to their offspring should increase with age and it does.

In humans the mother transmit on average 15 new mutations and the father transmit on average $25+2(g−20)$ new mutations, where $g$ is the age of the father (Cochrane and Harpending, 2013; this approximation holds only for men older than 20 years of course).

As the vast majority of mutations are neutral or deleterious, the "quality" of the genome being passed on should decrease with age unlike you expected.

Efficiency of selection decreases with age

The fact that after a given age, one does not reproduce anymore (among mammals, this is particularly true for women) does affect the selection pressures on the genetic variants that affect age specific fitness. e.g. A mutation that will reduce health at young age will be quite strongly selected against while a mutation that affect health at old will not.

When talking about this discrepancy between selection pressures at different ages, the concept of antagonist pleiotropy often comes into the discussion. Pleiotropy is the phenomenon where one locus affect several traits.

The idea of age-specific antagonist pleiotropy is that a mutation that will increase health at a young age by a factor $s$ but decrease it at an old age by the same factor $s$ will be selected for. Such process can cause a population to evolve toward lower lifespan. The antagonistic pleiotropy hypothesis is one of the most important hypothesis that we have for the evolution of senescence.

Evolution of senescence

You might want to have a look at the posts:

Why does evolution not make our life longer?
Why do we age? or Do we have a theory of senescence?


How does the OD correlate with the number of algae cells?

As with bacterial cells, number of cell and OD are correlated. I am not a specialist, but it seems that you can use microscope to visually count number of cells, then correlate it with optical density of the solution you have. This will allow you to first establish how many cell correspond to 1 unit of OD, then use OD to estimate number of cells quicker than by counting.

Just a few details: counting of cell number is done by dropping given volume of culture on a special slide with grid, then manual counting using microscope.

If we assume that 100 cells/mL (or whatever) solution gives you OD of 1, then OD of 2 will correspond to 1000cells/mL concentration. That us due to logarithmic relationship between OD and light absorption by the cell culture.


Does the location of the double bond in chlorins yield a distinct biological function?

I only found a hint that this might be the case in this publication by Singh et al., stating

  Porphyrins, chlorins, bacteriochlorins, and isobacteriochlorins each have unique photophysical properties that are exploited by nature and can be used for diverse applications (1, 2).

I don't have access to "The Porphyrin Handbook" (The first citation in the quote above), but I suspect it would be your best guess in finding more information.


It looks to be a Clivia; The English common names are Natal lily or bush lily.

It's a plant that comes originally from Africa but it now commonly sold as house plants.

The Wikipedia article give a good information about that plant.

Example:

Picture taken from this site.

You have also to notice this is a toxic plant and to keep away from small children or pets.


Can't ORFS be of any size?

I think the point being made is that in a random sequence of 64 amino acids, on average 3 out of 64 should be stop codons, because there are three possible nucleotide sequences for stop codons (UAA, UAG, UGA). ORFs could theoretically be any size but the longer the sequence the more likely you are to come across a stop codon purely due to probability.

What is overlapping frames here?

An example of overlapping frames is shown in the slide:

For instance, you can see that the first "CU" in the first frame produces an alanine (as GCU), while the "CU" in the second frame produces a leucine (as CUU).

They have the same nucleotide sequence, but are offset to produce different amino acids. Viruses have very "condensed" genomes and often can use the same nucleotide sequence for different genes, just starting at different points in that nucleotide sequence. This means they have functional overlapping frames.


What kind of weird little insect is this?

This is probably a nymphal stage of a stink bug (aka shield bug).

Based on the roundness of your specimens, I'd suspect that they represent possibly the 1st or 2nd instar development stage.

I am unsure of the species currently, though I suspect this is an image of the adult (wrongfully labeled as a "bed bug" at its source):

 Source: Shutterstock

I will dig into the Brazilian fauna to see if I can get you a species...


Those are collembolans. Common name, springtails. Do you have a potted plant nearby? They are completely harmless.

Here is an example:

(picture from bugguide.net


Approximately, 250000-440000 neurons in Humans (Rice et al., 2016).

  The substantia nigra/ventral tegmental area (SN/VTA) complex is a
  heterogeneous collection of dopaminergic cell groups that extends from
  diencephalic to mesencephalic territories in many vertebrates,
  including rodents, non-human primates, and humans (Puelles and Verney
  1998; see as reviews Smits et al. 2006; Smidt and Burbach 2007; Smits
  et al. 2013). The SN/VTA contains the largest number of dopaminergic
  neurons in the brain (see as reviews van Domburg and ten Donkelaar
  1991; Haber and Fudge 1997; Nieuwenhuys et al. 2008), with average
  estimates ranging in most studies from approximately 250,000 –
  440,000 dopaminergic neurons within the complex (Bogerts et al.
  1983; Hirsch et al. 1988; van Domburg and ten Donkelaar 1991; Damier
  et al. 1999a; Kubis et al. 2000).


How to search NCBI in bulk for a list of accession numbers?

After some trial and error in an interactive python shell and some documentation checking, I found that the relevant information is present in the genbank-formatted output (rettype="gb"), and this can be parsed using Entrez.read provided it is returned in "xml" mode (retmode="xml").

The following code that seems to work:

#!/usr/bin/env python3

from Bio import Entrez

Entrez.email = "Your.Name.Here@example.org"
id_list = ["KJ841938.1", "FJ911852.1"] # real list is about 500 elements

for accession in id_list:
    handle = Entrez.efetch(
        db="nucleotide", id=accession, rettype="gb", retmode="xml")
    gb_record = Entrez.read(handle)
    handle.close()
    organism = gb_record[0]['GBSeq_organism']
    print("{}\t{}".format(accession, organism))

(You don't need a while loop here, by the way: python has the more convenient forsyntax to loop over the elements of a list.)

Output:

KJ841938.1  Setoptus koraiensis
FJ911852.1  Gaeolaelaps aculeifer


What is the biological reason that some viruses cause sore joints (eg flu)?

Almost certainly what is causing the joint pain isn't the virus, but rather its the body's response to the infection.   Cells that are infected with viruses can release proteins called interferons. Interferons can act on surrounding cells and cause them to become less susceptible to viral infection.  Other cells, including your immune cells respond to a virus by releasing other proteins into the blood called cytokines.  Cytokines activate other immune cells and can stimulate the body to generate a fever and 'lock up' molecules of iron so they are not available to invading bacteria.

Some cytokines act on the bone marrow and cause the pool of 'reserve' neutrophils (a type of white blood cell) to move into the bloodstream.  Other cytokines shut down the lymphatic vessels, causing lymph nodes to swell up.   And other molecules such as histamine and prostaglandins are released and also play a role.

SO what you are feeling when you get ill from a virus (or a bacteria or parasite) is the effect of this 'soup' of cytokines, interferons and other 'mediators'.  You may have some combination of fever, muscle/joint pain, runny nose, malaise, fatigue etc.

In the US you'll see TV adverts for drugs used to treat Rheumatoid Arthritis.  These drugs include synthetic proteins that bind to a cytokine called TNF-alpha and  block its role in inflammation.


Is there a known or quantifiable correlation between capsaicin and its effect on the body's metabolism?

Capsaicin do affect your metabolism. It affects your Capsacin receptors ( scientifically TRPV1 receptors). These receptor starts calcium influx into various types of tissues. In endothelial cells because of this it mimics stress response (McCarty et al 2015). Quoting from McCarty et al,

  Clinically, ingestion of capsaicin-or its less stable non-pungent analogue capsiate-has been shown to boost metabolic rate modestly. opical application of capsaicin via patch was found to increase exercise time to ischaemic threshold in patients with angina

Coming to your question, there are scientific studies which suggest that capsaicin helps in maintaining weight by limiting weight regain after weight loss. Not just this, capsaicin has also shown potential in treatment of obesity. However you should remember that it will required specific amount of dose (you can check details in papers I cited ) to help maintaining your weight. Do not eat pound of jalapenos a day :P


What are the distinctive structural features of single- or double-stranded xRNA, or where can I find them?

The only paper I found that examined the question is "Structural, Dynamical, and Electronic Transport Properties of Modified DNA Duplexes Containing Size-Expanded Nucleobases". They state

  The results confirm that the structural and flexibility properties of
  the canonical DNA are globally little affected by the presence of
  benzo-fused bases. The most relevant differences are found in the
  enhanced size of the grooves, and the reduction in the twist.

They also have a picture comparing the structures of conventional DNA and xDNA:

So while the basic structure seems similar, the difference in diameter and twist look rather large to me.

This is for xDNA, I would assume that xRNA behaves comparably if double-stranded. It would have to somehow fit the larger nucleobases into the helix like xDNA. And the structure of single-stranded RNA is variable, helical parts would probably look similar to xDNA, hard to say how the modified nucleobases would affect tertiary structure.


After how many hours water drunk is expelled from the body?

The time from drinking to urination depends mainly on your hydration status and the presence of food in the stomach.

Scenario: You have drunk enough fluid in the previous days, so you are normally hydrated. In the morning, you get up from the bed, urinate, drink 1 liter of water in 5 minutes and eat nothing.

Some water can come through the stomach and can be absorbed in the small intestine in about 5 minutes; the entire liter may need more than 2 hours (sweatscience.com).

When some water is absorbed into the blood it can immediately trigger diuresis - the excretion of the urine through the kidneys into the bladder. It may take about 3 hours for the entire amount of water drunk to be excreted. So, the approximate time span (from start to end of water excretion) could be 5 - 180 minutes. But not likely the entire liter of water will be excreted, because, in the morning, you are in a slightly negative water balance, so some water will stay in your body.

If you are dehydrated before starting drinking, much less urine will be excreted in the first few hours.

If you drink after eating, the food in the stomach can delay water absorption and excretion by more than an hour. This also happens when you drink nutritional fluids, such as milk or juice.

This is from my experience and understanding basic physiology. I'll try to find some references.


Does Yerba Mate contain Beta carbolines like harman and norharman?

After a bit of research I can say that Yerba mate does not contain beta-carbolines. Now, I don't know if this makes you happy or sad but the tea has many antioxidant properties which makes it good for health. You can find a list of the components in Yerba mate in paper 1 and this article.


You are correct that brachydactyly is a dominantly inherited disorder and is usually caused by mutations in the BMPR1B gene.

However, not everyone who has the mutation, will have clubbed thumbs (the phenotype). This is due to a phenomenon known as penetrance and expressivity.

Penetrance essentially is an all-or-none phenomenon whereby certain individuals who have a mutation express the phenotype (in this case, clubbed thumbs) and some do not express it at all.

Expressivity is when individuals who have the mutation, will express the phenotype to varying extents. For example, only one thumb may be clubbed.

I hope this helped.


Possible to Gain More Weight than the Food You Eat

No it is not possible.  Humans are heterotrophic organisms, which means that we use organic molecules (i.e., food) as a source of nutrients and energy.  We use the nutrients to add mass to our bodies.  These nutrients are the familiar carbohydrates, proteins, lipids (fats), etc...  During digestion food is broken down into simpler organic nutrient molecules that are then used to make our body tissues.

So even if we only used food for nutrients we could not gain more weight than the food we consume but note that the food is also used for energy. This means that some of the mass of the food that we eat is not used to add mass to the body but is "burned" as metabolic fuel.  The mass of the food used for energy is expelled from the body as waste in the $CO_2$ that we exhale and in the metabolic waste in the urine.

The carbon in the air is mainly $CO_2$, which is an inorganic molecule.  Only autotrophic organisms like plants can use inorganic molecules as a source of nutrients.  Since inorganic molecules usually contain less potential energy than organic molecules autotrophic organisms need a different source of energy.  Plants use sunlight.

Finally, fat contains about 9 Calories per gram whereas a Big Mac has about 2.4 Calories per gram so fat has almost 4 times the energy of a Big Mac.

(Calories are the amount of heat that is released if all of the energy in the organic molecules is released so it is an estimate of how much energy the body can get from food)


Why don't macaws get selenium poisoning from brazil nuts

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

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

Source: Wikipedia - Ara (genus)


What is the difference between "genetic" and "hereditary"?

From dictionnary.com

  Genetic:
  pertaining or according to genetics

  Hereditary:
  passing, or capable of passing, naturally from parent to offspring through the genes:

Note: I selected the pieces of definitions that I found most relevant to the current discussion.

Genetic information can be passed on to offspring. As such, I understand the confusion you may have.

When the adjective "hereditary" does not apply

By its definition the adjective "genetic" can be used in multiple situations where the adjective "hereditary" could not. It is specifically obvious when the term "genetic" is used in the context of a whole population. Indeed, not all genetic patterns are inherited especially when referring to population-wide patterns. Also, the adjective "genetic" focuses on genetics and not necessarily on its characteristic of being inherited.

Example

Consider for example the concept of "Genetic signature of selection". A genetic signature of selection is any pattern in the genetics of a population that can be used to infer past selection invent. These patterns include
 - high population divergence around the specific site
 - loss of heterozygosity (and polymorphism) around the selected site
 - modification of the site-frequency spectrum
 - genetic - environment covariance

Further information

Please note that the concept of heritability might have an unexpected definition for some layman. You might want to read Why is a heritability coefficient not an index of “how genetic” something is?.

When the adjective "genetic" does not apply

There are non-genetic information that can be transmitted from parents to offspring (or even between unrelated individuals).

Examples

Niche construction inheritance or epigenetic (esp. in the broad sense) modifications are examples of non-genetic inheritance.

Further information

You will get more information about non-genetic inheritance (and its role in evolution) in this answer.


Answer

The mechanism for salmon natal homing isn't exactly known, but there are really two good hypotheses out there.

Salmon have an extremely good sense of smell. One hypothesis is that they retain an imprint of their birthplace's odor, and manage to recognize it again at a later time (as explained by this article).
Another hypothesis: the Earth's magnetic field guides the salmon to their birthplace via geomagnetic navigation. They then use chemical cues to recognize the stream in which they were born (supported by this scientific article).

These hypotheses were mentioned in this Wikipedia article. Note that there was a third pheromone-related hypothesis which was disproved (as shown here).

I would say that both memory and "genetic conditioning" could potentially be factors in how these animals perform this natal homing, among other things. However, it is difficult to pinpoint which one if any, because neither hypothesis has yet to be confirmed, and both function on completely different mechanisms. Not to mention that we can't tell what exactly a fish is thinking, and also what chemical we're looking for, if there is one.

Finally, for your personal information, salmon aren't the only animals to do this: sea turtles return to their birthplace as well.

TLDR: If a salmon was displaced right before birth, or birthed in a pool, I would imagine it returning to that particular location at sexual maturity.

References

Lohmann, K. J., N. F. Putman, and C. M. F. Lohmann. “Movement Ecology Special Feature: Geomagnetic Imprinting: A Unifying Hypothesis of Long-distance Natal Homing in Salmon and Sea Turtles.” Proceedings of the National Academy of Sciences 105, no. 49 (December 5, 2008): 19096–19101.
Dittman, A., and T. Quinn. “Homing in Pacific Salmon: Mechanisms and Ecological Basis.” Journal of Experimental Biology 199, no. 1 (January 1, 1996): 83–91.
Black, Geoff, and J. Dempson. “A Test of the Hypothesis of Pheromone Attraction in Salmonid Migration.” Environmental Biology of Fishes 15, no. 3 (1986): 229–235.


Do our ears or brains gradually adapt to noise pollution?

This is a fascinating case of sensory adaptation and neural adaptation. Another example of this would be when you stop smelling something after being exposed to it for long periods of time (as you probably know, this "long period of time" happens to only be a few minutes). A great representation of this happening with the nerves in the skin was done by Georg Meissner:

This image is from https://www.boundless.com/psychology/textbooks/boundless-psychology-textbook/sensation-and-perception-5/sensation-37/sensory-adaptation-160-12695/

When stimulus is applied, these nerves begin rapidly sending messages to the brain in the alarm period. The rate of these signals slowly start to decrease over time in the resistance period until they finally reach exhaustion and stop completely in, of course, the exhaustion period. Keep in mind that the time it takes for all this to happen varies greatly upon what type of cell it is (obviously olfactory cells have a much shorter exhaustion time than, say, hair cells (hearing cells)). After these cells have had a chance to recover (more like recalibrate actually), we can begin to hear/smell/feel/taste again.

I hope this helps.


Why do proteins targeted for chloroplasts require two signal peptides?

Protein import to chloroplasts (and also mitochondria) can still have multiple destinations, because these structures themselves have sub-compartments:

both have an inter-membrane space as well as an 'inner space' (the stroma in chloroplasts, matrix in mitochondria).
proteins can also be targeted towards either of the two membranes
additionally chloroplasts have the Thylakoid stacks in the stroma which are separated by another membrane layer.

Due to this complex structure you need multiple signal peptides to properly target proteins to their destination.

I don't remember (or can find) all the details now but basically you (can) have:

a 'main' signal peptide that targets proteins directly towards the stroma (which will be removed there by the stromal processing peptidase (SPP)).
an additional signal peptide for import to the the thylakoid stacks (which will be 'made avaibalble' by cleavage of the first peptide)
there should be other signal peptides or at least variants that allow import to the intermembrande space and the inner membrane (via the TIC23 complex). [I couldn't find any sources for this right now]

Sources I could find:

TIC/TOC complex in wikipedia
in-depth scientific review


Are single-celled organisms capable of learning?

I'd like to know what is the reference for amoebic learning. I cannot comment directly on this, but there is some evidence for  "adaptive anticipation" in both prokaryotes and single-celled Eukaryotes which do not have a nervous system.

In the case of E. coli, it has been shown that the bacteria can anticipate the environment it is about to enter.  E. coli in the digestive tracts of mammals will typically be exposed to initially a lactose, and then later to a maltose environment as the bacteria pass down through the animal tract. This suggests that upon encountering a lactose environment, maltose operons are induced. I.e., upon encountering lactose, maltose is anticipated. This suggests a "genetic memory" of the sequence of sugar types where lactose is always encountered before maltose.

Further cultures (500 generations) of E. coli in the absence of maltose but in the presence of lactose reduced the maltose operon activity to negligible levels, suggesting that this is an adaptive prediction of environmental changes.

Mitchell, A et al., Adaptive Prediction of environmental changes by microorganisms, 2009, 460, 1038


It's hard to tell from your photo, but you should check whether Macroglossum stellatarum (German: Taubenschwänzchen/ English: hummingbird hawk-moth) looks similar to what you've seen.

This moth is living in Germany (and other regions) and due to it's way of flying (hovering and audible humming) it's sometimes confused with a hummingbird.


Can this theory on the evolution of human appearance be flawed?

Quantitative genetics is one reason why this doesn't happen. For example height is affected by many genetic loci, not just 1 gene, and we can for the sake of the following illustration call them Locus A through Locus J - 10 Loci.

Now this is purely illustrative and hypothetical - in actuality there are some differences between this example and the real world, but nevertheless I shall plough on. Imagine everyone carries a basic set of genes which makes them 150cm tall. Loci A-J each have two alleles, either T or t, with one inherited from each parent. Each T allele adds 2.5cm to the basic height per copy (each parent has two copies, one goes to the offspring) and t has no effect. The parents are both heterozygous at each loci, that is they have one T and one t at each pair of loci. Therefore both parents are 175cm tall.

When these parents mate the offspring inherit one copy of each parent at random. As such the most likely single outcome is that the offspring will inherit 10 T's and 10 t's - roughly five of each from each parent. However, purely by chance they could receive 10 T alleles from each parent, giving them a height of 150+(20*2.5) = 200cm. Likewise, a sibling could also inherit only t alleles thus giving them a height of 150+(0*2.5)= 150cm. Thus variation can actually increase from one generation to the next.

There are other reasons why we do not regress to the mean as well, but I am writing a quick answer over breakfast, but I will be in the office soon where I can get some more thorough explanations from text books. E.g. (Dis)assortative mating, Mutation, Recombination, Environmental variance, Selection. However, with the increase in global movement it has become easier for dominant alleles to spread which is why the number of blue eyed people in the US is decreasing.

Here is an interesting article which backs up what I said about quantitative genetics, called "Will humans eventually all look like brazilians?" Also for good quantitative genetics texts take this as a basic intro and this for further reading.


All nucleated cell (cells with defined nucleus) are able to present MHC-1 on their surface.  Since red blood cells do not have nucleus, they are not able to represent antigins in MHC-1 molecule.

Hope that helps check wikipedia for reference


What were the main discoveries in Biology?

Here are a few things coming to my mind

Discovery of cells by Robert Hook
Discovery of bacteria by Antonie Philips van Leeuwenhoek
Discovery of antibiotics by Alexander Flemming
The basis of heredity by Gregor Mendel
Evolution (On the origin of species by C. Darwin)
Watson and Crick discovery of DNA structure
Vaccination
The concept of ecosystem


What causes the localization of myoglobin in turkey to regions of muscle tissue?

"Localization" is probably the wrong term, but I think I know what you mean... It more has to do with "expression."  While the exact mechanism to my knowledge is not elucidated, it has to do with the type of motor neuron innvervating the fiber.
This has been demonstrated by studies where they cross-inervated; that is, they took the neurons which usually innervate Type I muscle fibers and innervated Type II muscle fibers with them and vice versa.  The Type I fibers took on fast glycolytic properties, whereas the Type II took on the slow oxidative features (such as higher levels of mitochondria and myoglobin that you're talking about).

Source:
Sherwood L, Kell R. Human Physiology, First Canadian Edition. pp. 282-283.


What effect does a bat's echolocation have on other bats?

Bat echolocation is an incredible and complex process. Bats can emit two kinds of ultrasonic signals. One is a short pulse (less than 5 ms long) that sweeps a wide range of frequencies (100 Hz to 25 kHz) and is referred to as a FM sweep, or a broadband signal. The second kind in a constant frequency (CF) and is much longer in duration (5-30 ms) and held at a specific frequency. In addition to the fundamental frequency there are first and second harmonics. This important for depth perception, pursuit of prey, and location of other bats!

Specifically, bats measure distance by comparing the time between emitted sound pulses and its returning echo. Rapid FM sweeps are especially well suited for target distance so the bat can adjust easily and locate the target. Bats can determine angle, size, elevation, azimuth, and velocity/movement of object from these time and frequency differences as well. Now, bats calculate their own velocity using the Doppler shift concept of their own echos. Meaning, when their signals comes back to them, they compare the amplitude of what their ultrasonic sound wave would be if they weren't moving to the received sound and calculate actual velocity off that (it is a very complicated process and I'm trying to simplify it to get to your question).

Ok, now that is the basics of echo location, but back to your question: What happens when there are multiple bats? Well, when you have many ultrasonic waves going at once, it might get confusing about which is your signal. At least that what you would think. Since the bats have such a wide range of frequencies they can vocally create (100 Hz to 25 k Hz), bats usually simply change the range they are vocalizing to prevent wave disruption. If you do get an overlap of waves from bats using the same frequency, you get something similar to Doppler effect where amplitudes are not what expected. Since they are pretty drastic changes (sometimes even canceling out the wave entirely), and a bat can sense if another bat is around them by calculating the size of the objects producing noise, a bat will know this distortion is due to another bat and not the prey. As a result one bat will have to change their frequency range. This has become sort of a dominance game for them as a result. The bats heightens (I think, might be lower) the frequency of their signals until one cannot go any farther. The one with the wider range is considered dominant and rules that frequency range. Neat right! Hope that answered your question!

Sources: http://scitation.aip.org/content/asa/journal/jasa/54/1/10.1121/1.1913559

Behavioral Neurobiology by Thomas Crew copyright 2000 (most of info from this source, great read if interested)


If you have or can get access to it, you might try looking in the Incidence and Prevalence database: http://thomsonreuters.com/incidence-and-prevalence-database/

Another possibility is the GIDEON database: http://www.gideononline.com/. It is possible to sign up for a 15-day trial.

For Europe, statistics are available from the WHO CISID at http://data.euro.who.int/cisid/ (select "all infectious diseases", then "Giardiasis").

The WHO does not have any global statistics available on their website, so otherwise you might have to piece together data from individual publications. Some examples:

Thailand, 2005: http://www.ncbi.nlm.nih.gov/pubmed/16438174

Germany, 2006: http://www.ncbi.nlm.nih.gov/pubmed?term=19404678

United States, 2006-2008: http://www.cdc.gov/mmwr/preview/mmwrhtml/ss5906a2.htm

Portugal, 2002-2008: http://www.parasitesandvectors.com/content/5/1/22

Quatar, 2008: http://www.parasitesandvectors.com/content/4/1/211

Tajikistan, 2009: http://www.parasitesandvectors.com/content/4/1/195

Ivory Coast, 2009: http://www.parasitesandvectors.com/content/4/1/96

Tanzania, 2011: http://www.parasitesandvectors.com/content/6/1/3

Ghana, 2006-2009: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3170632/?report=classic

Canada, 1999/2002: http://www.biomedcentral.com/1471-2334/5/72

Canada, 1990-1998: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC194172/

China, 2012-2013: http://www.biomedcentral.com/1471-2334/14/25

Ethiopia, 2009: http://www.biomedcentral.com/1471-2334/13/419

Kenya, 2010-2011: http://www.biomedcentral.com/1471-2334/13/243


What is the most primitive organism that can die of aging?

The adjective primitive is undefined, at least when comparing extant species. We have all gone through almost 4 billions years of evolution.

I would suspect you would consider a bacteria quite primitive though, so note that bacteria appears to age (see Do bacteria die of old age?).


How does an animal having toes create more friction than not?

I would say that the premise that "the surface area of contact with the ground increases in case of solid foot" is incorrect.

In practice, the ground is very far from being even and flat, and the animals need to navigate themselves throughout different terrains that include very uneven ground, stones, growing & lying plants, etc. In that case, having toes, in general, offer an advantage of gripping to the ground (and increasing contact area in multiple directions) in a large set of terrains. Then, different animals will develop their toes in different shape/form tailored to the dominating usage (including, but not limited to gripping the ground).


How much energy does a cell expend maintaining its contents?

I'm going to take a stab at this.  Its a difficult question to get right, just to put is in the right mood here.

Lets leave energy out of this as the proper term is structure.  The cell is designed to compartmentalize itself to differentiate its own living tissue from other cells.

In this regard Alan Kay's analogy is pretty good.  In multicellular organisms, individual cells (mostly) each maintain their own DNA and energy storage, though they get their nutrients and energy from outside.  They create the organism as a whole by differentiation; each cell changes to take on a specialized role and depends on other cells to support it. E.g. in animals some cells/organs digest the food and distribute nutrients to the rest, others form the lung and help distribute oxygen and others scrub the blood of waste.

This is somewhat like good code design where functions are partitioned out into specialized parts of the software for the sake of maintainability and organization.

Somewhere after this point I think the analogy breaks down since after all the point of good coding practice is to organize the code for understanding within reasonable human conceptual limits.  The cells and how they organize themselves are still plenty mysterious to us as they have their own definition of roles and function much of which is still being discovered today.  For instance the many kinds of neurons in the brain and the sorts of structures they form are extremely diverse.  We have few organizing principles for predicting how many cell types would exist in a system and these only create partial answers.

After all its just an analogy...

getting close to an answer?


A mammalian cell takes about 8 hours to replicate all of its DNA in its S phase; a yeast cell would take about 40 minutes.
Some other information that you seem to not have quite the right information about:

The DNA polymerase does not unwind/split the DNA—that is the job of DNA helicase. The DNA polymerase cannot bind to the single-stranded DNA until the helicase unwinds the double-stranded DNA ("melts"), or the dsDNA is artificially melted in a test tube via high temperature.

The dsDNA is not fully separated before it is copied. There are tens of thousands of sites—origins of replication—across the genome that unwind and begin replicating every time the cell replicates its genome.

"...DNA replication in most eukaryotic cells occurs only during a specific part of the cell-division cycle, called the DNA synthesis phase or S phase. In a mammalian cell, the S phase typically lasts for about 8 hours; in simpler eukaryotic cells such as yeasts, the S phase can be as short as 40 minutes."
"An average-size human chromosome contains a single linear DNA molecule of about 150 million nucleotide pairs. It would take (0.02 seconds/nucleotide) x (150e6 nucleotides) = 3e6 seconds (about 35 days) to replicate such a DNA molecule from end to end with a single replication fork."
"...Approximately 30,000–50,000 origins of replication are used each time a human cell divides."

–Molecular Biology of the Cell, 6e, Alberts, et al.


Alternatives to CFU plating for measuring number of viable cells?

I've only used it for mammalian work, but the Cedex HiRes Analyzer from Roche is pretty sweet. From their docs you can analyze particles from 1-90 μm in size (the cells I work with are about 20 μm), and there are a ton of configuration options depending on your needs. As long as your cells can be stained with Trypan Blue (it's been a long time since I've done bacterial work, pardon my ignorance) to look at viability, then this machine should work quite well. When set to Maximum (i.e., the analysis takes as long as possible), I get results in less than 4 minutes per sample - and this includes about a minute for the sample to settle in the flow cell. If you lower the sensitivity, you can get results faster.

Basically the way it works is you take 300 μl of your liquid culture (diluted if you think the concentration is too high), and add it to a sample cup. Put all your cups in the tray, fill out the sample info and analysis options in the MultiRun screen, and hit Start. The machine includes all the reagents onboard, so it mixes the Trypan Blue with your samples, then injects the proper amount into a flow cell. The sample is allowed to settle, then a high-resolution image is taken of the entire length of the flow cell. Then, depending on your sensitivity settings, a certain number of frames are taken from the full-length image and analyzed. An average count is then generated based on all the images, and your final numbers are spit out. You can then print or save a report of the cell counts and viability.

The software comes with some analysis tools as well, so if you keep multiple cultures going over time with different growth conditions, you can aggregate the data for each one and generate graphs of cell counts, viability, cell size, etc. - there are at least 10 or 20 parameters to choose from. All the image analysis options are configurable, so if you look at the results and think the machine is picking too many dead cells, or not enough, you can change the parameters to your liking, and save the options as a custom analysis type.

One option I like that would beat the pants off CFU-based counting (besides the drastically-reduced time) is the fact that the machine can detect aggregation of the cells. One issue with CFUs is that it's hard sometimes to know that a certain colony really arose from just one parent cell - if you let the colonies grow long enough you may be able to tell based on size, but it's a tough call. Since the Cedex is looking at the cells themselves, it doesn't matter if they're aggregated or not, as they'll all get counted (assuming the aggregation particle doesn't contain a huge amount of cells, like 50+, that can't be resolved by the software due to occlusion of the image).

I don't know how much these guys cost, so depending on your budget you may not be in the market for one, but if you're going to be doing a lot of counting then one of these is invaluable. I'm sure other companies make similar instruments, but I haven't used them, so I don't know how they compare to the HiRes. I do know that the person at my company that was responsible for buying the HiRes is very good about researching possible alternatives, so this one is probably as close to the top of the line as we could find, for the needs that we have.

Good luck with your counting!


Why do we need to amplify DNA sequences?

This is a question I also remember wondering about when I was younger in school. Now as a professional it's way too obvious to even explain. But i think it's an important and common question, which warrants an example or two from common daily lab practice.

Preface

You have to understand that DNA is a molecule. It's really tiny. It's not trivial to work precisely with it, nor detect it or discriminate two different pieces of DNA from each other, let along sequencing them. We make a lot of DNA through amplification so that we can prepare a sufficient amount to make reactions with.

Visualization

We usually make DNA visible by using chemical dyes that emit light (fluorophores) or incorporated radioactive pieces to make the DNA visible.

Here's a common case in the lab: we need to get enough DNA to use in subsequent reactions. When we work with DNA it is very rare that we obtain exactly what we want 100% of the time, or perfect yield. For example, we want to cut a piece of DNA once. But we have scissors (i.e. restriction enzymes) that will chop up the DNA multiple times, especially when we leave the reaction going too long. What we do is take 100 units of DNA, subject them to the reaction, and then view the results using electrophoresis using an agarose gel, for instance. We can then see 40 units of uncut DNA, 30 units of single cut DNA, and some 30 units of DNA cut multiple times (2+ times, so they are small fragments). We need enough single cut DNA to proceed with the next reaction, with full knowledge that there are no contaminating chunks of DNA. Typically there are many reactions in a row that we do to achieve anything in the lab. Cloning, in vitro amplification, sequencing, gene editing, preparing genes for transgenesis, creating RNAi probes, what have you.

More is better

Another case: if you want to know the sequence of DNA, you must sequence it. However, sequencing is imperfect and errors occur. To be sure, we re-sequence the same DNA many times to get a confident picture of what the sequence is like, beyond reasonable doubt. Sequencing DNA ten times is really more reliable than sequencing it once. This could be because of how the molecules behave in solution, or because of degradation, or tens of other things. You must understand this is also not specific to sequencing; a lot of reactions follow the same logic.

Amplification as a specification tool

By using primers in PCR, we can make sure we are obtaining what we want. In principle, this means that we can make a gajillion copies of something we are interested in (e.g. a gene), even from a single strand of DNA which may contain things we are uninterested in (e.g. the rest of the genome).

Some thoughts

This answer is certainly not extensive, but I hope it's a primer for you to understand that DNA work is just really smart nanotechnology, and we are not yet at the level of performing nanotechnology on single molecules, with full confidence, precision or efficacy. On the daily, we need enough to see it with our eyes so we amplify and react it with intercalating dyes to make them visible to the naked eye!


Answer to the question
How much DNA is there in our cell nuclei?
In humans, there are about 6 billion base pairs in the nucleus of each cell. Why 6 billions and not 3? There are 3 billions base pairs per haploid genome (see ploidy) and therefore 6 billions base pairs for the whole genome. This number may actually further double during specific phases of the cell cycle. Each single cell contains a copy of the whole genome (with a few exception such as red blood cells for example).
So the total number of base pairs in a 10 trillion cells individuals is about $6\cdot 10^9 \cdot 10^{13} = 6\cdot 10^{22}$ base pairs.
Further information for fun
How much DNA in our cells outside of nuclei
Now, in cells there is DNA outside of nuclei. In animals (incl. humans), we have DNA in mitochondria as well. there is of the order of 104104 base pairs per mitochondria (16,569 sites to be accurate) and there are of the order of 104104 mitochondria per cell, that is 108108 base pairs total per cell which is only one order of magnitude below the number of base pairs in the nucleus per cell.
There is therefore an extra $3\cdot 10^8 \cdot 10^{13} = 3\cdot 10^{21}$ base pairs in cells outside the nucleus.
How much DNA in bacteria living in the human body?
Note that by "in the human body", I also include "in the gut" even though the inside of the guts are typically considered as being the outside our body.
There are about 100 trillions of bacteria in every one of us (this number is a vague approximation; see wiki > Human microbiota). Yes, most of the cells living in us are not our cells but are bacterial cells!
Bacterial genome vary widely but as a gross and almost insulting approximation, let's consider that the average bacterial genome from our microbiome has a genome size of $10^6$ base pairs (note bacteria don't have nuclei or mitochondria).
That means that in our body we have to add to the above numbers $10^6 \cdot 10^{14} = 10^{20}$ base pairs (which is only a hundredth of $10^{22}$).
How much DNA in the viruses in our body?
Let's not forget our virome. Unfortunately, I could not find estimates of the number of viruses (and viroids) in our body.
How much DNA is outside cells and viruses in our body?
Of course, there's plenty of DNA in our body. There's DNA in everything we eat and this DNA end up in our blood stream and in our cells. I failed to find an estimate of how much DNA does that represent.


Why all particles have same influence on osmosis

When you dissolve something in water, you build a solvation shell around this - so each ion (in the case of salts) gets surrounded by a number of water molecules. For more details read this Wikipedia article.
The concentration change in free water molecules is usually not taken into account since it can be neglected due to the vast number of "unbound" molecules. So if you have one litre of water, it contains approximately 56 moles of water molecules. If you dissolve 1 mole of sodium chloride in this water, and take in account that this takes quite some water to get solvated, there is ways more water available. So the water concentration is almost constant (especially when you work at physiological osmosis condition).


There are various databases of homologs, for example:

eggNOG
Ensembl Compara (accessible via BioMart, I think)
Homologene
OMA
TreeFam

The advantage of using an existing database is that more sophisticated methods for detecting orthologs than simple BLAST searches have been used (see "Computational methods for Gene Orthology inference" for a review), and everything is already precomputed, so it's much faster. The downside is that all precomputed methods need to use a snapshot of the genomes from the past, so not all currently available genomes will be there.


An answer I got from Jan Kolář of Charles University:

  I'm not sure that people prefer fluffy things just from the fact that
  they are fluffy. They like things that are soft to touch such like
  pillows. The popularity of fluffy things might have a simple
  explanation: There's no danger of getting cut.

So the fact we like to cuddle with dogs and cats has probably nothing to do with our furry past.


Short answer
Water of 180 oF (82 oC) causes immediate scalding (thermal burn wounds).

Background
The severity of a scald injury depends on the temperature to which the skin is exposed, and for how long. Residential water heaters warm up tap water typically to 120 oF (48 oC). At this temperature, the skin of adults requires an average of five minutes of exposure for a full thickness burn to occur. When the temperature of a hot liquid is increased to 140 oF (60 oC)) it takes only five seconds or less for a serious burn to occur. Coffee, tea, hot chocolate and other hot beverages are usually served at 160 to 180 oF (71 - 82 oC), resulting in almost instantaneous burns that will require surgery (American Burn Association).

How these numbers apply to steam I am not sure, but I think they will be comparable, given that steam is essentially made up of a dense mass of water droplets. Further, the amount of steam obviously matters. Consider these numbers: The temperature in a sauna typically ranges from 160-200 oF (71 - 93 oC) with a low level of humidity (ranging from 5 - 30%). Steam rooms provide moist heat from a water-filled generator pumping steam into the enclosed room. The temperature in a steam room typically ranges from 110-114 degrees Fahrenheit (43 - 46 oC) with a humidity level of 100%.

There is anecdotal evidence of the Russia-born Ivan Ivanitz Chabert (1792-1859), who supposedly entered an iron oven in Paris (Times telescope, 1831) with a few trays of meat, and stayed there unscathed for 5 minutes at a temperature of 380 degrees F (193 oC). When he re-emerged from the oven the meat was cooked, while the only noticeable effect on him were profuse sweating and a dramatic increase in heart rate (from 98 to 168 bpm).

This experiment shows the remarkable capacity of the human body to reduce overheating by means of evaporative cooling (sweating). However, the effects of steam are far more devastating to the human body than dry heat. Not only does it carry much more energy than hot air, it also prevents perspiration by saturating the air with water vapor.

References
- American Burn Association Educator's Guide
- Times Telescope, 1831


What are Antihistamines doing in a baby?

This song most likely refers to an off-label (and usually inappropriate) use for certain antihistamines like Benadryl. They are sometimes used by parents to sedate their children, functioning through the exact physiological mechanisms @Chris describes.  Parents use it inappropriately as a means of behavioral control for active or upset children to make them more docile or sleepy, such as for airplane rides, etc.  It's not recommended by most pediatricians, because even though adverse (bad) side effects are usually rare, it is an actual medication with another primary mechanism of action having effects on many body functions, not a medication designed as a sedative.


How do inward rectifier potassium channels work in the heart?

According to Boron's medical physiology textbook:

  "Although inward rectifying potassium channels pass current better in
  the inward than the outward direction, the membrane potential (Vm) is
  typically never more negative than Ek (equilibrium potential of potassium across the membrane). Thus,net inward K+ current does
  not occur physiologically. As a result, the activation of GIRK
  channels (G protein coupled inwardly rectifying potassium channel)
  hyperpolarizes cardiac cells by increasing K+ conductance or outward
  K+ current."


Career progression through biosafety levels?

My short answer would be no, careers of people who study pathogens requiring biosafety training are not focused biosafety level.

More broadly, the people I know who study infections diseases are not motivated by the biosafety levels of their infections organisms. Rather, they are motivated by biological questions and their research that often require higher biosafty for their labs.

For example, the researchers featured in a recent (July 2015) National Geographic do not study Ebola because they want to work on a BSL-4 level virus. Rather they want to about learn about the disease from both a basic science and applied human heath perspective.

Your hypothetical Dr. Kliener would not work his way up the biosafety chain as a conscious. Let's say a young Mr. Kliener always wanted to study human health. He probably would have started doing research in a BSL-2 facility as an undergrad research assistant (See BSL-2 requirements here. As a grad student, he might have worked at a BSL-3 lab if he choose a good program while spending years focusing on a specific pathogen or system. By the time he became because a PI, he would have needed to find a BSL-3 facility for his research. He worked his way up, but not because he wanted to study dangerous pathogens. Rather his research question guided his path.

Other career tracks could end up using a BSL-3 facility, but not necessarily need the stop at a BSL-2 facility. For example, a hypothetical Dr. Fish may have started off loving the outdoors. She studied limnology as an undergrad and grad student and did not step foot inside a lab. However, when she began working as biologists for a state conservation agency, a novel fish virus emerged. She now is tasked with studying it. Her agency trained her to work in a BSL-3 lab so she could culture fish with their virologists.


Because both of those produce single-cells able to viably survive and grow on your own. For example, take a fungal spore and it can grow into a full fungus given enough food. I assume algae cells are the same way. In a single-cell form, fungi and algae qualify as self-sufficient microbes.

Animal cells are typically specialized and dependent on a support framework. Usually, a single animal cell left out on its own is largely doomed.


Why can we use mouse-produced antibodies on mice tissues?

The reason why the secondary antibody only recognizes the primary antibody is relatively simple: It is directed against the Fc-part of the primary antibody. As this part is species specific (but constant between all antibodies from one species, hence the name constant) a secondary anti-mouse antibody is directed against all mouse antibodies.

The general principle can be seen in the figure (although this is from immunolabelling, the principle stays the same, Image from the Wikipedia):

The anti-mouse secondary does recognize the antibodies which are present in the tissue. These are usually present at low levels (unless you work with immune tissues as spleens) and only cause a relatively low background. If it causes a problem, you can treat your sample before you add the primary with an Fc block which blocks the antibodies present in the tissue so that the secondary antibody will not recognize anymore later.


Examples of genes involved in plastic responses

I assume that you mean gene expression regulation when you say genetic processes. The best example for your question would be that of synaptic plasticity in neurons.

The immediate responses are obviously that of protein modifications (cell signaling). These are fast responses that have immediate effects but are also quite short-lived. During the long term potentiation (LTP) some stable changes happen via gene regulatory mechanisms.

It is to be noted that in a polarized cell such as neuron the distance between the nucleus and the point of action i.e. the synapses (at dendritic spines), is huge. Any event leading to transcription regulation would take a long time to act. Therefore there are post-transcriptional regulatory mechanisms in place. The mRNAs are localized at the spines and are kept in a repressed state; poised for translation when the signal is received. Finally, if the signal is sufficient enough, transcriptional regulation (sometimes stable due to epigenetic changes) takes place.

You can look for the genes involved in this pathway which also include ncRNAs (lncRNA and miRNAs).

Other examples:

Acute stress response (such as Unfolded Protein Response [UPR])
Acute inflammation
Chemotaxis


What causes zygotic termination in aneuploidy often isn't an issue with proteins or other gene products i.e. being "too sick" to live. It's that the zygote is basically "self error checking" and if it encounters a serious genetic error (e.g. aneuploidy) it self-terminates, as it would likely not survive anyway. Sometimes this self-termination fails, and the zygote develops. Depending on the specific aneuploidy, it may not make it to term, or perhaps it will, and you will have a child born, albeit the child will usually have a decreased quality of life/life-span.

A similar mechanism works in your somatic (non-reproductive) cells everyday when they replicate and divide - if they detect and error in their DNA that cannot be repaired, the cells SHOULD kill themselves. Sometimes this fails, and can give rise to cancer.


Honey bees rely on the position of the sun (and the ephemeris function) to navigate and communicate (i.e. the waggle dance). If they are out too late in the day to return to the hive (occasional), or if they are disturbed at night in the hive, they will fly towards a light.

Beekeepers and bee renters have learned that if you are going to disturb a hive at night, do so with minimal light so as not to lose bees. Also, they avoid lights in the vicinity of the hive in general.

There are a number of parasites and insecticides that cause bees to behave erratically. Colony Collapse Disorder is a major threat to the honeybee's survival.

Why are bees attracted to light? I don't know if anyone knows that.

Dinner and Dancing: Bee Navigation
The Cause Of Colony Collapse Disorder, Disappearing Bees Becoming More Clear


How to identify the genes that distal enhancers pair?

Check this technique called Chromosome Conformation Capture (3C). Its variants exist such as 4C, Hi-C etc.

Basically, the principle of this technique is based on the physical interaction between the enhancer and promoter that is bridged by a transcriptional modulator(protein).

The chromatin is crosslinked
DNA is sheared
The protein is pulled down (Optional)
The fragments of the promoter and enhancer are ligated together and then sequencing/qRTPCR is done.

Sequencing (low throughput- sanger) can be used to identify enhancers of a given promoter. qRTPCR can be used to quantify the strength of the association.

What I just said is not a high throughput technique. Hi-C is high throughput variant of 3C. See the protocol here.


Short answer: yes.

Floral parts, as petals and sepals, have stomata, and transpire just like a normal leaf or a primary stem (that is, a stem covered by epidermis, not periderm). And, besides stomatal transpiration, flowers have cuticular transpiration, like most of structures covered by epidermis.

This is a SE micrography of a petal's stoma:

(source: http://www.sciencephoto.com/media/32403/view)

There is a very famous experiment that we make with the kids in primary school: take a white flower and put it in a vase with coloured water. The petals will become coloured. This experiment shows that there is an ascendent flux of water, and this flux depends on transpiration. You can see it here: https://youtu.be/y9hprlmck44