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Passing on Alleles
Just a basic question on alleles, I am just trying to learn the basic concepts.
So if we are to screen two parents, both with one dominant and one recessive allele for a given characteristic e.g. eye colour, does this mean that we can say for certain (given a correct screen) that the child has a 3/4 chance of having the dominant characteristic (expressed) and a 1/4 chance of having the recess characteristic?
Similarly, if both parents had 2 dominant alleles, does this mean it is certain for the child to exhibit said quality given that the screen was effective?
Also, are there only these two types of alleles? I heard something about gene driving creating 'super dominant' alleles and would appreciate if someone could explain this to me.
Finally, is it the case that all alleles have a 50% chance of being passed on?
(assume in this question there aren't any relevant mutations going on)

It can be a little confusing. A genetic allele is just a portion of the genome responsible for an observable trait or phenotype. Examples of phenotypes consist of your example (eye color) and millions of others. As @swbarnes alluded to, most phenotypes are complex phenotypes, meaning they are not described by a single genetic locus. Height, weight, hair color, pulmonary function, and eye color are all examples of complex phenotypes (or traits); meaning that more than 1 genetic locus controls the observed phenotype. Other traits like PTC tasting bitter are determined by a single genetic locus; these are referred to as simple traits.
When it comes to dominant verses recessive, this classification is usually applied to simple traits, and refers to whether it requires two copies or one copy of a causal genetic variant to observe the phenotype. For example, a single copy of the genetic variant responsible for sickle cell disease does not cause the phenotype of sickle cell anemia. It takes two copies to cause it. Thus we label this genetic variant as a recessive allele. If a single copy of the genetic variant were sufficient to cause the observed phenotype, then we would label that variant a dominant allele.
Some traits are intermediate, in that a single copy of the allele causes an intermediate phenotype, that is more exaggerated if you inherit two copies. The PTC tasting bitter above is such a trait. If you have a single variant allele, it will taste bitter, if you have two copies of the variant allele, it will taste very bitter. If you have zero copies, you will wonder why your friend with two copies just made a horrible face.
IF you are referring to a simple trait (controlled by only one genetic region) and the allele controlling the observed trait is a dominant allele, this would mean a single copy of the variant allele is sufficient to see the trait. However, this also means that both parents could be heterozygous for the allele ( each possessing 1 copy of the variant and one copy of the normal). In this case, there is a 25% chance their offspring gets both normal alleles. So your supposition was correct if the trait is simple and dominant.
With regards to 50% chance of passing any given allele, yes. However, in complex traits, the math gets complex quick with regards to odds of any given phenotype.
Lastly, some traits are influenced by both a genetic determinant and an epigenetic determinant that can be environmentally driven which provides infinite more complexity. I'll let look you look that up or ask another question :)  The same with "gene drives".
A neat listing of simple traits in humans and whether they are dominant or recessive comes from here:

does this mean that we can say for certain (given a correct screen)
  that the child has a 3/4 chance of having the dominant characteristic
  (expressed) and a 1/4 chance of having the recess characteristic?

If you are sure that the phenotype is 100% determined by that allele only, then yes, barring things like new mutations.  Biology always has some exceptions.

Also, are there only these two types of alleles?

In real life, most characteristics are not well described with simple Mendelian genetics.  Most traits are controlled by many genes, and the different alleles can interact in many potential ways.

Finally, is it the case that all alleles have a 50% chance of being
  passed on?

In general, yes.  Meiosis puts half of your alleles into half your gametes, and half of your alleles in the other half.

Thanks
I understand that most characteristics (phenotypes?) will rely on a number of different types of genes and the exact types may not be understood as of yet. However for characteristics which are only affected by a single gene i.e. eye colour (?) does this mean that such alleles can only be recessive or dominant?

Further, am I correct in saying that there are more than two possible types of each gene and that as a result of mutations there could be very large number of alleles? For each such allele, if it is say dominant or recessive, are all dominant genes 'equally dominant'?

Eye color is affected by multiple genes, though if a particular family has only brown and blue eyes, that variation is likely caused by variation in a single allele, and should mostly behave in a Mendelian manner.

We label one allele dominant to another if the heterozygous condition looks the same as the homozygous condition for the "dominant" allele. Like blood type; the AO phenotype is identical to the AA phenotype.  A is classically dominant to O.  But if a snapdragon with red flowers is bred with one with white flowers, the result is pink flowers.  Neither allele is classically dominant to the other.  People with AB blood type have a different phenotype than people with A or B blood.

Just because 95% of your genetics homework involves traits that fit the Mendelian paradigm doesn't mean that anywhere near that much real biology does.  Most alleles and traits simply do not fit the classical Mendelian paradigm.  The results are more complicated to predict than "This allele always masks that allele"

I understand that the vast majority of traits can not be characterised under one gene.
Is there a more complex mechanic behind it, or would it say require information from n different genes (which would mean we could theoretically calculate it)?

I think the "gene drive" that you are talking about involves the CRISPR system, and it is an engineered run of code that deliberately makes that allele 'super dominant' (by making more CRISPR components that are loaded with the particular gene replacement instructions), like in a scenario where they are trying to replace the faulty gene for Huntington's disease or ALS in an adult.


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Do ants see, have brain?
I'm new here and I would like to know if ants can see, I mean with their eyes not with antennas: I was walking around and found an ant specy,  they were reacting when I moved my fingers towards them, as if they were seeing.
I would also to know  do they have a "brain" and what I'm the most fascinated by is how do they find their way?
PS: English is not my local language that's why my vocabulary is limited. Please feel free to correct any mistakes and or improve my words. Thanks

Related question : 1) https://biology.stackexchange.com/questions/19848/how-do-ants-know-where-they-are-going-without-eyes 2)https://biology.stackexchange.com/questions/56654/how-do-ants-follow-each-other

This question was flagged as off-topic and it doesn't really answer my question. But thanks pointing out.

I just told related questions, that if you are interested you can have a look at it :)

Yes, thank you. I found some useful informations there.

Welcome to Biology.SE! What research have you done before asking it here?

Ants do have eyes, though how well (and even whether) they see depends on the ant. They also have brains.
You aren't wrong to put quotes around "brain" since in many organisms the nervous system isn't as centralized as in vertebrates, and when they do have concentrations of neurons in various places ("ganglia") it isn't always in the head, and the one in the head isn't always significantly larger than the other ones, so it's often hard to call that having a brain. This can be true of many insects:
http://cronodon.com/BioTech/insect_nervous_systems.html
Having said that ants do have a centralized nervous system, with the neurons in the head making a larger percentage of their body than most other insects, i.e. they have brains. It appears social insects tend to have larger brains for their body size, which includes bees and ants.
http://guides.library.harvard.edu/fas/Brains/ants
Ants also have eyes; they're just often too small to see clearly, especially when the ant itself is small and the eyes are the same color as the ant's head. Ants descended from wasp-like ancestors that probably had quite good eyes, like modern wasps and bees do. But ants mostly live on and underground and don't need eyes as much as flying, pollinating insects do, and how well ants can see varies a lot between the species.
Or I'll just quote Wikipedia:

Like most insects, ants have compound eyes made from numerous tiny lenses attached together. Ant eyes are good for acute movement detection, but do not offer a high resolution image. They also have three small ocelli (simple eyes) on the top of the head that detect light levels and polarization. Compared to vertebrates, most ants have poor-to-mediocre eyesight and a few subterranean species are completely blind. However, some ants, such as Australia's bulldog ant, have excellent vision and are capable of discriminating the distance and size of objects moving nearly a metre away.

And the cite for that latter example:
ATTACK  BEHAVIOUR  AND  DISTANCE  PERCEPTION
IN THE  AUSTRALIAN  BULLDOG  ANT
  MYRMECIA
NIGRICEPS
Those same ants even have color vision it seems. Conversely, African army ants appear to be blind, although even that depends on the caste. From Sociobiology of the hypogaeic army ant Dorylus:

On workers:

Eyes are either reduced or absent.

On males:

Army ant males do indeed resemble wasps, having large and robust bodies and well developed eyes and wings

So it's very possible the ants you ran into could see your fingers.

This is good answer. I am curious that ants use pheromones to know who is who or who is the queen?

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Mold identification
I poured some agar plates and tried inoculating them with mushroom spores (I don't think they germinated bc of low humidity), but noticed what looks like mold with crystals on the surface of the agar.
My question is, what are these "dew-like" structures?

Location: Near Columbus, Georgia
Incubation conditions: Indoors (room temp), covered

I initially figured it was condensation from the agar.  But it is not on your lid and you said you suspected humidity was low.
I found this here http://www.gettyimages.ca/detail/photo/mold-penicillium-vermiculatum-growing-on-high-res-stock-photography/128606087.

with this caption

Mold, Penicillium vermiculatum, growing on agar. The water droplets on
  the mold are part of the respiration process of the mold.

Those droplets do look like pure water.  And oxidative metabolism does produce water: CHOH+O2 -> CO2 + H2O.  It is interesting that the top of the mold is so hydrophobic that the water forms little balls.  Why might that be?  If you know, comment please.
Other fungi might put stuff in the exudates that collect atop them.  I read that some aspergillum species collect droplets of purple exudate on old colonies but I could not find good images.  Here is another penicillium with amber looking exudate.  These exudates can contain metabolic products.

from http://thunderhouse4-yuri.blogspot.com/2015/08/penicillium-citrinum.html

Exudates (or Extrolites): Some fungi can produce exudates as a
  by-product of their growth, many of which can be collected for
  commercial use.  Mycotoxins are by-products (secondary metabolites)
  which are potent poisons.  Penicillium citrinum produces Citrinin, a
  nephrotoxic mycotoxin which derives its name from the fungus.  It may
  also produce other extrolites such as tanzowaic acid A,
  quinolactacins, quinocitrinines, asteric acid and compactin.

If these fungi were spreading out in their natural habitat of rotten stuff, the secreted mycotoxins would be clearing a path for them, wiping out those organisms that dare compete for that rotten stuff.

thanks Will! The droplets looked a little yellow (not captured well in the pic) to be just water, and I was actually going to take a closer look under a microscope once I finished building my flowhood, but now that I know the droplets are likely to occur again, I'll take a closer look without worrying about contamination! If they are waste products, it makes sense that the mold would excrete them onto a hydrophobic surface to avoid poisoning itself! Fascinating. I will share microscopic photos of the surface structure soon.

I like that scheme about the hydrophobicity providing a dumping ground for wastes.  That would make sense.

It makes sense that the surface of the mold is hydrophobic if it needs to release spores in the air to get a good dispersion. Just my adaptive interpretation.

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Blue light in a fridge. Is it really beneficial or just marketing?
Recently while visiting a shop with electronics I saw a fridge with a huge advertisment sticker going more or less like this:

There's blue light source in this fridge so there will be less bacteria inside and your fruits will have larger quantities of vitamins.

Can it be true? How can dead (picked, transported and refrigerated) fruit produce more vitamins? How does blue light affect this?
Furthermore I thought that only UV light kills bacteria.
Therefore my question is: how much truth was on that sticker?

Until proven by the manufacturer, I would see this as an unsubstanciated marketing claim.

Fruits and vegetables are generally not dead.  Most fruit contains seeds, which will grow if planted.  (Aside from those bred to be seedless or sterile.)  Many vegetables, e.g. potatos & onions will likewise grow, and sometimes will sprout even in the refrigerator.

Maybe a little bit?
There are two claims here, so let's talk about them individually. I'm not sure how this light is being produced (probably LED), but it'll have a wavelength somewhere between 400 and 500 nanometers.
Reduced bacterial presence:
The intrinsic antimicrobial activity of blue light is well documented. Although the mechanism is not entirely understood and widely debated, the commonly accepted hypothesis is that the blue light triggers the production of reactive oxygen species like singlet oxygen that are highly toxic. However, this has only been observed under high-power light sources, and low levels of light may actually increase bacterial activity. What counts as a high-power source, you ask? The number from this article is $\frac{10mW}{cm^2}$. For a fridge with an internal surface area of >1 meter, such a power source should draw at least 100 W. Given that normal refrigerators use draw 100-200 watts, you'd essentially be doubling your electrical bill for the fridge.
It should also be noted that the above is a best-case scenario. As soon as you add anything to the fridge, you'll reduce the intensity and thus the effectiveness of the light source. Also, the light is unlikely to be on all the time- it probably turns on when you open the door and turns off when you close it. While this helps a lot with power use, it minimizes the effect of the blue light, which is constantly on in experiments.
Larger quantities of vitamins
There's no (reliable) evidence of light of any kind actually creating vitamins, so what the sticker suggests is that it doesn't degrade the vitamins already present as quickly as other kinds of light.
There's a good article here that discusses the stability of various vitamins. It's worth noting that most of these vitamins and essential amino acids are much more likely to be destroyed by cooking than light, which is probably why the fridge focuses its claim on fruits, which are less likely to be cooked.
There's very little research that I was able to find about the effect of different wavelengths of light on the stability of various vitamins, but as a whole I remain fairly skeptical that there's any notable difference. Most experiments that do study degradation of vitamins under light subject pure vitamins to high-intensity light for several days- unlikely to happen in your fridge.
TL;DR:
A claim like this shouldn't be a major factor in your buying decision. The effects of the blue light are probably negligible given the conditions in your fridge, but if you've got two very similar choices this feature could act as a nice tiebreaker. Besides, there's a lot to be said about how cool blue light looks and the confirmation bias present in your purchase.

wooooooowwwwww :O

Good question. Asian fridge moguls want to shine blue light on your chopped fruit, mostly, rather than save your life from a hazardous food.
Some research by National University of Singapore studied the effect of visible blue light diodes on some bacteria although not fungi which makes the fruit go moldy (mould propagation in apples is a common bio practical study).
The bacteria studied are not fruit surface bacteria. they are gut and skin bacteria.
The study did not test if fruit last longer in blue light. it just exposed gut and necrotizing bacteria to blue light.
You may get less E-Coli and salmonella, which is weird because you would have a very unwholesome fridge to have a E-Coli danger from it. fruit is not only consumed by bacteria. Salmonella dangers exist inside certain eggs, which is a dark environment. Fruit practically can't transmit major illnesses like S.Aureus, they live in different environments than fruit and are endemic to humans, but fruit do contain a lot of microorganisms necessary for their fermentation and to break them down.
Blue light perhaps increases your appetite too. https://www.sciencedaily.com/releases/2014/06/140602115916.htm
The raw scientific research for it from 2015 is not for funghi or yeasts, and it doesn't penetrate a steak properly, so it's fairly misleading marketing.

And how would the blue light help the salad or make people less greedy?

I found more qualified research which states that blue light can increase your appetite. previously I had read the opposite statement. good comment.  https://www.sciencedaily.com/releases/2014/06/140602115916.htm

That is actually something that makes a little sense to me, as in general, I have always heard that blue makes people "more comfortable". Some people eat more when they are comfortable, while others eat less, though.

"fruit is not consumed by bacteria" Can you support this with a source?

I'll rephrase it.. fruit is not ONLY consumed by bacteria. ask your local fungicide toting farmer. can you support a motion that suggests that fruit treated with antibiotics will not develop fungal and yeast decomposition? if not, the result is the same. The science does not protect fruit from funghi. let's just say that no one puts antibiotics on their fruit to prevent rotting. They industrially use fungicides.


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Why are chromatophore in phaeyophycae chloroplasts integrated within the endoplasmic reticulum?
Why are chromatophore in phaeyophycae chloroplast integrated within the endoplasmic reticulum? While reading about phaeyophycae I came across this point, but couldn't figure out why and what could be the evolutionary basis for this?

@ always confused can u give an elaborate answer please


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why on hydrolysis ATP bond releases energy?
While studying respiration all i came across was that ultimately all that cell does is for the energy currency the ATP and some useful intermediates used in the cell building but i could not figure out how contrary to the notion of supplying energy to break a bond is energy released when the phosphate bonds in ATP are broken .

There are many many chemical reactions where breaking a bond releases energy, so this notion in your question is not correct; note that releasing energy isn't the same thing as having no activation energy, you still need to put a little in but you get a lot more out.


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Are cells electrically neutral or charged to setup the membrane potential across them?
While studying about membrane potential I usually come across the Na K pump . But I can't understand does it cause any generation of net charge in the cell If yes then how do charged cells stay together with other similarly charged ones ,  if not why and how not .

It isn't neurons that are charged, it is their membranes. From the distance of other cells, they "see" both the charges inside and outside the membrane, so there isn't any substantial repulsion on that scale.
The charge across a membrane comes mostly not from the Na+/K+ pump directly, but due to differential permeability of the membrane to different ions. Ions normally tend to flow down their concentration gradients, but that flow can be influenced by an electrical potential. From the perspective of just Na+ and K+, there is more K+ inside the cell and more Na+ outside, and more permeability of the membrane to K+ than Na+. Therefore, the inside of the cell will be negatively charged at equilibrium where the net flow of ion charges is equal. At a negative resting potential, the negativity of the inside of the cell equalizes the net flow of potassium out with the net flow of sodium in. However, the actual concentration changes involved are miniscule. From the perspective of ion counts, there are basically as many positive ions inside as there are negative ions inside a cell; it's the very minute imbalance (fractions of a %) that gives a potential of ~-70mV.

Look via the Na K pump we are pumping out net positive charge however miniscule it be how does it get balanced Or does it get balanced at all.

The imbalance of charges from the Na/K pump doesn't actually matter much because ions can flow across the membrane through channels. You should just think about the Na/K pump as establishing a concentration gradient and ignore the 2 versus 3 ion imbalance. It just doesn't matter. The channels are a lot more important. The Na/K pump by itself can provide a couple mV but not the ~60-80mV that is typical.

But i still can't gauge whether cell turns out to be neutral or not


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do game animals have poor eyesight?
I have been watching some bow hunting videos on youtube. When hunting with a bow, the hunter needs to get really close to the animal, sometimes less than 10 meters.
It seems to me implicitly, and some hunters even say explicitly, that the animals (deer/elk/moose/buffalo) only see the hunters when they move. As long as the hunter has reasonably camouflaged clothes and is not smelled by the animal, they can stand in plain sight and the animal does notice them.
Do these game animals (deer/elk/moose/buffalo) really have such poor eyesight?
here are some videos as examples:
https://youtu.be/OqGSaGXHXgY?t=654
https://youtu.be/9tx_l9Jco_M?t=213
https://youtu.be/bP38tYhyhW0?t=303
https://youtu.be/xP9L885noEI?t=58

Their eyesight is not poor, it is just adapted to seeing moving predators. It is actually incredibly keen in that respect.

@MattDMo - if deer have acute eyesight, why don't they notice the hunter then (and the even more conspicuous cameraman). Besides, if deer are only capable of seeing moving predators, would not the predators evolve to take advantage of it ?

You are comparing deer to humans, which is a bad idea. Deer (and many other prey animals) evolved this type of eyesight as it protects them from their natural predators. Wolves don't have guns or bows, and so need to move to attack their prey, and deer can detect this type of movement very easily. Humans have not been using projectile weapons for that long, evolutionarily speaking, and deer have not evolved to address this new threat. Camouflage also helps the hunter blend into the surroundings.

These species likely don't see you as a predator, or if they do they don't know if you've seen them yet.
A study indicated that the vision of the White-tailed deer was good;

As expected for a crepuscularly active prey species, the visual system of white-tailed deer is specialized for sensitivity in low-light conditions and detection of predators.

The observation that many prey species only notice movement may relate to behavioural adaptations that increase their chances against natural predator species. Staying still while monitoring your surrounds decreases the chance of the predator seeing you.
I'll quote D'Angelo et al again;

The visual streak of deer in combination with
  their wide-set eyes likely provides them with enhanced ability
  to monitor the horizon and to detect movement with a
  wide field of view while keeping their head stationary.

Visual specialization of an herbivore prey species, the white-tailed deer.
G. J. D’Angelo, A. Glasser, M. Wendt, G. A. Williams, D. A. Osborn, G. R. Gallagher, R. J. Warren, K. V. Miller, M. T. Pardue
Canadian Journal of Zoology, 2008, 86:735-743, 10.1139/Z08-050


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What is in Mosquito bites?
I was wondering what is in the mosquito bites, which causes the swelling of the skin at the bite and also the itching. I know that the mosquito injects some stuff, but what is it?

a study on the major allergens in mosquito saliva... http://www.ncbi.nlm.nih.gov/pubmed/21038786

When female mosquitos bite to suck blood, they need to overcome the body reaction against it. So when they found a bood vessel, they inject their saliva into the wound. This saliva contains substances which affect blood clotting and platelet aggregation (so the blood will stay liquid which is essential for sucking) and a vasodilatory substance (which widens the blood vessel and prevents contraction of it). The exact composition depends on the exact mosquito species.
These "foreign" substances cause a local immune reaction which results in the release of histamine in the skin. The itching and also the red skin and the swelling are a result of the histamine release. See the Wikipedia article on mosquitos for more information.
If you are interested in a deeper look on the composition of the mosquito saliva have a look at these two articles and their references (if there is help needed in getting the articles, let me know):

Role of arthropod saliva in blood feeding: sialome and post-sialome
perspectives.
Toward a description of the sialome of the adult female mosquito
Aedes aegypti.

Since the substances affect the blood coagulation cascade, there is some research going on if and how this can be used clinically. See this article for an overview or have a look at the original publication here ("Unique thrombin
inhibition mechanism by anophelin, an anticoagulant from the malaria vector")

So this is comparable to what is used in medicine? Can this be used in medicine?

It is comparable in the way that it keeps the blood from coagulating. Regarding the reasearch, I updated the article.


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Is the tomato a very very close relative of the pepper?
I ask because if you look at a tomato, the way it grows on a vine, its color, the texture, and make up of its skin and internal structure it seems very much like a pepper.  The only thing I can think it lacks that a pepper has is any amount of spice.  I wouldn't be surprised to learn that it has trace amounts of capsaicin.

There are different unrelated plants called "pepper" in English. Black pepper (species of the Piper genus), as indicated by Chris, is not related to tomato and doesn't "look alike".
I guess the OP meant actually a different plant (Capsicum genus), to which the common bell pepper (Capsicum annuum) belongs. This one is similar to tomato and they both belong to Solanaceae, the same subfamily Solanoideae, but different tribes: tomato is classified in Solaneae and Capsicum in Capsiceae.
In this study you can see, how distant phylogenetically the two genera are. Currently accepted classification generally reflects phylogeny, and there are three more tribes that are closer to Capsiceae, to which Solaneae is nevertheless a close relative.
The most striking morphological difference between Capsicum and Solanum is that the first one is characterized by hollow fruits, while tomato and other Solanum species have fleshy berry-like fruits.
EDIT: It's actually not a difficult task for one's imagination to see that the two types of fruit are structurally very similar. In reality a pepper-structured tomato cultivar is known, and even quantitative trait loci underlying this morphological trait were already found.

They are not related, both plants belong to different taxonomic orders:
Pepper belongs to:

Order: Piperales
Family: Piperaceae
Genus: Piper

Tomatoes belong to the

Order: Solanales
Family: Solanaceae
Genus: Solanum

If you look at Capsicum (as MattDmo suggested) then this is different. These peppers belong to the same order (solanales) and family (solanaceae) as tomatoes. They form a different tribe (Capsiceae).
Wikipedia states on this:

The name "pepper" came into use because of their similar flavour to the condiment black >pepper, Piper nigrum, although there is no botanical relationship with this plant, or >with Sichuan pepper.

I think OP is referring to Capsicum sp., not black pepper...


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Which bird of Upper Michigan is it?
While doing morning-walk in Keweenaw Penisula, Michigan; I found this juvenile bird wandering around looking for her mother !
Can someone spot which bird is it?

I suspect that it is a nuthatcher.

A shorebird, perhaps some kind of sandpiper - it's often difficult to ID between species in chicks because they look very similar. (Personally I also don't think you should have touched it, could have taken a photo with out interfering with it).

Hard to identify a juvenile.

Based on the location and picture I believe this a Spotted Sandpiper (Actitis macularis) chick. Once they hatch, they are out of the nest, the one you are holding looks fairly small still, must have hatched recently.
You can find more information about them here.


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How do primers anneal to ssDNA?
In a PCR type protocol, the high temperature stage of the cycle will cause dsDNA to denature, as well as any annealed primers. At the lower temperature the denatured dsDNA will remain denatured. As far as I understand, though, the primers are re-annealed.
My question is this: are there any enzymes that catalyses this re-annealing, or does this happen by chance?

No enzyme is involved in base-pairing (annealing).
This does happens by chance, but the chances are governed by stoichiometric considerations.
The main such consideration is that the (low molecular weight) primers are added at a high concentration (greater than that of the DNA) and therefore have a greater chance of encountering the appropriate region of the DNA than its complementary strand does. (Reannealing of the denatured DNA strands can occur, but not over the time period of PCR.)

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Is it possible for a sex chromosome to be homologous?
I am following a great introductory biology course online, MITx: 7.00x on edX.
A question in the course assumes a cross between a pure-breeding male fly and a pure-breeding female fly:

You are studying genetics in a hypothetical fly and you find a fly
  that has purple eyes. Assume that the purple eye phenotype is due to a
  mutation at a single locus. Use the notation E and e, where the upper
  case letter is used for the allele associated with the dominant
  phenotype and the lower case letter for the allele associated with the
  recessive phenotype.
You cross a pure-breeding male fly with purple eyes to a pure-breeding
  female fly with normal eyes. All of the F1 offspring have normal eyes.
  From this experiment you determine that the purple eye phenotype is
  ______________ to the normal eye phenotype.

My question is this: how can a male fly be pure-breeding? The reason I wonder is that as far as I understand, pure-breeding implies a homozygote gene, yet the sex chromosome can not be homozygote because the Y chromosome is not homologous to the X chromosome. In other words, does it make sense to speak of homologous sex chromosomes?

How can a male fly be pure-breeding?

A fly or any organism can only be pure-breeding for a certain trait, not all traits at once. If the trait-determinant allele is found on an autosomal chromosome, this is not a problem. If it's on a sex-chromosome (chr1 in flies), it is sex-linked, and therefore cannot be pure-breeding because it may depend on the sex of the offspring whether the trait is expressed. For instance, you may have a male carrying an allele on its X chromosome; its female offspring will inherit the X, but male offspring will not (those inherit the Y chromosome), i.e. it is not pure-breeding. Male flies cannot be pure-breeding for traits determined by loci on their sex chromosomes. Similarly, you may have a heterozygous female carrying an allele on one of its X chromosomes (A/a); its female offspring will only inherit one allele, either A or a, so it is not pure-breeding either. A female fly must be homozygous for an allele on its sex chromosomes to be pure-breeding for that trait.
Male flies can be pure-breeds for traits determined by alleles on autosomes.
Also, cool and useful funfact, Drosophila sp. male flies do not experience homologous recombination during meiosis. This is called achiasmy! This is useful to know when designing complicated crosses when there is a difficulty in balancing a genotype.

Does it make sense to speak of homologous sex chromosomes?

The X chromosomes in females (X + X) are homologous, but the male Y chromosome is not homologous to the X. They are vastly different, just like the X and Y sex chromosomes in humans.

Pure-breeding implies a homozygote gene

Correct. Pure-breeds are allele homozygous so that all offspring, regardless of recombination, inherit the allele.

Thank you so much! It all makes more sense now.

To add to @S Pr's answer and provide another cool and useful fact, in some organisms, like birds, the males are the  homomorphic sex (their sex chromosomes are the same size and haven't decayed like the Y has in human males), not the females (who are ZW, with the W being the analogue of the mammalian Y chromosome).
So more generally, sex chromosomes can be homologous only in those organisms which are members of the homomorphic sex, which otherwise phrased means they're homogametic organisms. This sex is female (for mammals).


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Confusion regarding seedless grape and the normal process of germination
In general, does seedless grape by definition contains seed or is the seed small enough that the process of ingestion creates the illusion that there is no seed?
If the latter is true, is the seedless grape capable of germination?
Lastly does the fruit part of the seeded grape function as an incentive for animals to ingest it and provide nutrients for seeds in the form of feces, or can it function as nutrient itself?
Thanks

The seedless grape technically has a seed, but the seed has no hard outer shell and is microscopic/invisible. These seeds aren't viable. Technically you could isolate out the seed tissue from the grape and grow it in specialized germination medium, but that process also works for any other part of the grape plant. Hooray cuttings! Certainly the seedless grape would not grow if you put it in the ground.
The fruit part of the seeded grape is 'bait' to get animals to ingest the grape and carry the seeds within inside their digestive tracts. The goal is distance, but the surrounding feces provides bonus nutrients. The fruit is not designed to feed the seedling grape, but instead to act as bait for herbivores. The grape is mostly sugars and water, which makes them excellent bait but not amazing plant food. Plants can make sugar from the sun and pull water from the ground, but nitrogen and phosphorus are harder to come by.
Contrast fruit (which are for animals) with coconuts, which are examples of large fruit storing lots of calories for the seedling itself. The coconut flesh isn't as sweet as fruit, and it's much harder to get at.


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Thrombus and Embolii
Can treatment of thrombus cause embolism, in case of very high blood pressure, that may even lead to a heart attack ?
As the very high Blood pressure may cause some of the enzymes not act completely on the thrombus and release emboli in the blood stream ?

Which treatment of thrombus are you talking about? Angioplasty or thrombolytics?

Yes, treatment of thrombus can cause embolism. Hypertension favors hemorrhagic complications.
Thrombolytics:
Yes, they can cause paradoxical embolism, although it is a rare complication [1]. The most fearful complication of thrombolytic medication is major hemorrhage. And hypertension favors bleeding [2].
Catheter-directed thrombolysis:
Hypertension (more than 180 mmHg and associated with congestive heart failure) was found to increase hemorrhagic complications [3].
Angioplasty:
Angioplasty produces some embolic particles [4]. However, using embolic protection is disputed [4, 5].

References:

Liu YF, Bayliss M. Paradoxical embolism: a rare complication of thrombolysis. Emerg Med J. 2008 Mar;25(3):180-1. doi: 10.1136/emj.2007.053934. PubMed PMID: 18299379.
Meneveau N, Vuillemenot A, Bassand JP. [Complications of thrombolytic therapy in pulmonary embolism]. Arch Mal Coeur Vaiss. 1995 Nov;88(11 Suppl):1769-76. PubMed PMID: 8815838.
Agle SC, McNally MM, Powell CS, Bogey WM, Parker FM, Stoner MC. The association of periprocedural hypertension and adverse outcomes in patients undergoing catheter-directed thrombolysis. Ann Vasc Surg. 2010 Jul;24(5):609-14. doi: 10.1016/j.avsg.2009.12.011. PubMed PMID: 20413257.
Malik RK, Landis GS, Sundick S, Cayne N, Marin M, Faries PL. Predicting embolic potential during carotid angioplasty and stenting: analysis of captured particulate debris, ultrasound characteristics, and prior carotid endarterectomy. J. Vasc. Surg. 2010 Feb;51(2):317-22. doi: 10.1016/j.jvs.2009.08.063. PubMed PMID: 20006918.
Divani AA, Berezina TL, Zhou J, Pakdaman R, Suri MF, Qureshi AI. Microscopic and macroscopic evaluation of emboli captured during angioplasty and stent procedures in extracranial vertebral and internal carotid arteries. J. Endovasc. Ther. 2008 Jun;15(3):263-9. doi: 10.1583/07-2326.1. PubMed PMID: 18540698.

Those complications which the above mentions is not necessarily talking about due to embolic events, the tPA interferes with clotting and as such can lead to events such as haemorrhagic stroke. But yes thrombolitics can cause emboli. Using the treatment is weighing up the effects of ischaemia due to the thrombus vs risk of the treatment.


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What do Wild Silverfish Eat?
Silverfish are famous for eating wallpaper paste.

The paste is made of starch mixed with water.  Wikipedia says silverfish love starch

They consume matter that contains polysaccharides, such as starches and dextrin in adhesives.[4] These include book bindings, carpet, clothing, coffee, dandruff, glue, hair, some paints, paper, photos, plaster, and sugar.

But all of these are artificial substances. I wonder what do they eat in the wild?
I suspected they eat wood but a cursory search suggests they do not. Or maybe the articles I found are talking about them not eating wooden furniture. Perhaps they prefer to eat damp wood such as rotting logs in the wild.
Most of the obvious info on Silverfish is about what they do inside your house, rather than in the wild. Does anyone know what they eat in the wild?

Related Bio.SE posts: Do Termites and Silverfish metabolize cellulose the same way?, What is this tiny bug,

Silverfish are shredders. Shredders are...

...responsible for processing coarse particulate organic
matter (CPOM). CPOM is greater than 1 mm in size and typically derived
from allochthonous sources, such as woody debris, leaves, and other
vegetation [..].

Their diet includes sources of starch and protein, including grains, vegetables, fibers, sugars and fabrics. Silverfish can actually digest cellulose, a feat not shared by many animals. They are able to do so thanks to cellulase activity in microorganisms that live in their gut (Lasker & Giese, 1957).
Reference
- Lasker & Giese, J Exp Biol (1957) 33(3): 54–553

Good info's, nearly all animals that bore into wood or use wood to build a nest can digest cellulose, some beetles, termites, moths, barnacles, grasshoppers, leaf cutter ants, worms, wood mollusks, sea cucumbers, wood crabs, leafhoppers, gnats, weevils, aquatic insects, something like 15% of invertebrates can.

The answer to this is in their habitat some points to note are:

They inhabit moist areas, requiring a relative humidity between 75% and 95%

It avoids light

Silverfish are a cosmopolitan species

Silverfish can live for a year or more without eating if water is available

They are agile runners

Citation:
(1) https://en.m.wikipedia.org/wiki/Silverfish
(2) https://animaldiversity.org/accounts/Lepisma_saccharina/
This concludes that they dwell (in wild) on the lowest strata of forest (i.e forest floor - especially if its wet and humid) and it is rich in detritus (eg:fallen leaves specially) also since they are cosmopolitan they can infest a rotting tree trunk (for loose parts since they can not bore into it like termites) which will provide a suitable shelter and food for them, also they are pretty tough since they can live for almost a year without food barely surviving on water. They are also agile/quick thus got large area at their dispense to explore for food. They aren't so voracious feeders hence can survive in bare minimum availability which is abundant on the floor itself. Personally i feel they should prefer locations like next to a cave entrance which is damp and dark and near the food.

But what do they eat?

They can infest the log if there is something for them to eat in there. If they can eat rotting wood then of course the log is made of food. But can they eat rotting wood?

They should eat loose parts rotting wood bark since they themselves can't bore into the hard wood which is water resistant, but once it is primarily infested with termites and degraded to a certain level they can infest deeper

Mostly they get sufficient amount from fallen leaves, they aren't as hungry as termites are for wood otherwise you would have seen libraries getting eaten in some really worse manner and it would have been so hard to get rid of them. Which concludes they are not voracious feeders

Where does it say in the references that they eat fallen leaves?

because there isn't anything else to eat on the lowest stratum of forest if we look by their preference of food, that they should be rich in cellulose and i don't see any other possibility here rather than leaves


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Can concentration of a protein be determined from a gel quantitatively (rough estimation)?
I've got a His-tagged protein in 6M urea, 500 mM imidazole buffer that needs to be quantified before dialysis to ensure there's enough protein worth dialysing. I ran out of my elution buffer which should be used for blanking. I made a fresh buffer with the same contents, it started giving me false results. I could interpret that problem is with the buffer (probably because of change in chemical batch) from the readings I got in BCA and Bradford assays. Hence, I ran a gel to get an idea of presence of protein. Are there ways to estimate protein concentration quantitatively from the gel?

I suppose you could get an estimate if you made a calibration curve with known concentrations of protein, then try to match the intensity of your unknown with the calibration curve. Probably wouldn't be very accurate. I recommend fixing your buffer and using the BCA assay.

Yup, I am doing that with a BSA standards. BCA assay gave me negative values for all the dilutions. I've tried fixing the buffer, it couldn't help me in any way. Thanks!

Yes, you can use SDS-PAGE as a semiquantitative estimate of protein concentration. You need to create a standard curve with a protein of known concentration to compare against. Quantification is done by densitometry. It's a quick and easy process, but keep in mind some limitations:

Band intensity depends not only on the amount of protein but also on the amino acid composition of the proteins and the dye used
The unknown protein and standard should be run on the same gel to remove variations in gels, electrophoresis, staining, destaining and imaging
Densitometry can be quite qualitative depending on how it's done

I'm not sure if you're looking for a protocol, but it's relatively straight forward. I usually load 2, 4, 6, 8 and 10 uL of 100 ng/uL BSA as a standard and 2, 4 and 6 uL of the protein of interest (based on past experience with my proteins and their purification). The gel is stained with Coomassie and the band intensity estimated with a program called ImageJ. A standard curve is created by plotting intensity as a function of mass, from which the concentration of the unknown can be found.

Wow! This is new to me. Thanks a lot!! Does a scanned image of gel work on ImageJ?

@piscean_1993 Yes, but you'll introduce artifacts into the image during printing and scanning. It's probably best to keep it digital if possible.


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Does adding antibiotic after 5-10 mins of innoculation affect the protein yield or growth?
I've asked a lab colleague the same question. She said, it would loosen the bacterial cells in the LB medium and plasmids would come out. Is that true? and why?

That is not true. If you had forgotten to add the antibiotic before inoculation then you can add it before the bacteria starts growing. Make sure you add it when the bacteria is still in lag phase. If you add it later then it won't be effective as some non-resistant (non-transformed) bacteria would have already expanded their population. Ampicillin and kanamycin are best effective when the bacteria are growing. Even though these antibiotics are considered bacteriocidal, you would end up having unnecessary biomass in your culture.
So 5min delay for E.coli is not an issue. (I think this happens to all of us: forgetting to add antibiotic).

But isn't it still true that the plasmids will get lost if there are no antibiotics as they normally contain the resistance gene?

@TheGreenOne They would eventually but not so fast.


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Can a plate with incompletely filled LB agar be used?
I am falling short of LB agar plates and I have a plate with less LB agar poured. I meant, the plate is not fully filled with the agar (it was the last plate I poured the medium into). Some part of plate is empty. Does this cause any contamination problems or moisture retention? Is it okay if I use this to streak a 5 cm line?

It won't be a problem other than that the surface would be uneven. Seal the plate with parafilm when not using to avoid moisture from accumulating inside. When you pour plates then swirl the plate gently so that the molten agar distributes evenly throughout the plate. The agar will be thin though, and you would have to streak gently so as not to cut the agar; you can add 0.5 % of normal agar-agar to make it a little dense.
Or else use  smaller plates (2 inch) if you have them in your lab.


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Neurophotonics vs. Optogenetics
What is the difference between the two? I see them frequently listed together in conference descriptions but can't seem to find anything that clearly explains the difference.

Neurophotonics refers to the use of light to study the brain, including measurement (i.e. microscopy, including the use of fluorescent molecules that allow measurement of ions or voltages in live tissue, but also including histological techniques) and manipulation (using light to activate, inactivate, modulate, etc neural activity).
Optogenetics refers to the use of genetically encoded (whether delivered via virus or in a transgenic animal) constructs that respond to light and are introduced into cells where they are not normally found, often neurons. Neurophotonics is a broad term that would include optogenetics.
In my personal opinion, optogenetics is a fairly specific term that is useful, though it certainly has some popular buzz around it. Neurophotonics is a new buzzword that encompasses a lot of techniques that have been around a long time, and while these techniques are constantly improved upon, the neurophotonics label isn't really necessary (but sounds fun).


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Cytochrome Oxidase activity in neuronal cells
The abstract of this article says
"...the entire neuron is often not metabolically homogeneous; most of the oxidative activity is usually found in dendrites."
Why would the activity of cytochrome oxidase be localized in the dendrites of the cell? Is it because it has a greater surface area (more channels and such) compared to the rest of the cell?

How would oxidative activity mean only cytochrome c oxidase? It could mean more oxidation of glucose, which could be due to presence of more channels in dendrites than axon.

@Metroplex I do not know, the article is talking specifically about histo- and cytochemical methods for mapping activity of cytochrome oxidase. I do not have access to the full article (I'm working on finding it), but I thought asking "where's the full article" would be an inappropriate question.


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What is(are) the mechanism(s) that stop cells from fusing in vivo?
I just learned about the phenomenon of 'cell fusion' in which two diploid somatic cells can combine into some aneuploid cell in vitro and proceed to proliferate in culture. Apparently this can even happen interspecifically. My question is, what stops cells that grow naturally in the body from fusing all the time and creating abnormal cells?
Or, does this happen somewhat often and produce potentially cancerous cells, which are then destroyed by the body's normal regulatory mechanisms (I guess it could slip these as well and turn into a problem).
Could this be why we normally have many benign growths over the course of an animal's lifetime?
Any related reading would be super appreciated, thanks!

Maybe an easiest question is why and how do such a cell-fusion occurs?

@Untitpoi afaik it happens spontaneously among in vitro co-cultures, and that using some fusogen (like polyethylene glycol) 'speeds up' the process by disrupting the cell membrane. I'll investigate further, thanks!

@Untitpoi So I've looked into that a tiny bit more and you are totally asking the right question, thanks so much!

Interesting question, it would be strengthened by linking to a paper.

If as a result of the suggestion @Untitpoi made you have answered your question, it would be useful if you could include it in an answer here. This is quite permissible and good practice in such cases.

@David haha it does kinda sound like cheating, doesn't it? I'll compose an answer within 48h!


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What is the optimal sampling method for modeling of microalgae growth?
Recently, I am performing microalgae (Chlorella sp.) cultivation experiments for the mathematical modeling of microalgae growth with respect to time.
The main issue is that an analysis of lipid contents in microalgae requires a large volume of culture media per data point. Especially, in the early stage of the cultivation, the density of the microalgae is very low, so almost 20% of the total culture media needs to be consumed for obtaining just a single data point. Due to this limitation, sometimes, I measured only three times (the beginning, middle, and last).
More data points are obviously desired for the accurate modeling but it ends up with huge loss of the media. This may affect the quality of the overall experimental results. This seems like a sort of trade-off. The problem is that I cannot increase the size of the reactor volume at the moment.
Could anybody recommend how to come up with the optimal sampling number in this situation?
Any experience, ideas or recommended papers are welcome.
Thank you.

I would adjust the title of your question as it has more to do with lipid analysis rather than growth

For these kind of experiments, especially when you talk about modelling, it can be worth to set up a chemostat or at least a turbidostat. An example of such a study can be found in: Simultaneous growth and neutral lipid accumulation in microalgae by Klok et al. (Pubmed).
Alternatively you can use lipid dyes such as Bodipy but these are often very tricky to get to work and they might not penetrate in your Chlorella. Nile Red in any case is almost impossible to get working quantitatively despite it being used quite extensively, see details in this publication. Be very cautious when going down this route.


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Gel electrophoresis bands
Is there any way to calculate the number of bands formed due to sodium dodecyl sulphate-polyacrylamide gel electrophoresis for a particular compound of group of proteins? For example, how could I calculate the number of bad formed after electrophoresis of IgG (immunoglobulin G) under oxidizing or reducing conditions?

This sounds like a homework question, which are not allowed unless you show your attempt at the answer. Do you know what reducing conditions will do to a protein? Do you know the structure of immunoglobulins?

Okay, so I think I figured out what was required. Immunoglobulins have 2 light chains and 2 heavy chains. So 2 distinct bands would be formed (the heavier one at the back and the lighter one in the front) I suppose.


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Why do we have wrinkly fingers after swimming?
I found an explanation for my question here http://www.pitara.com/science-for-kids/5ws-and-h/why-do-we-have-wrinkly-fingers-after-swimming/, which suggests that water washes out sebum (special oil, which covers our skin) and water gets into outer layer of now unprotected skin by osmosis. This article also suggests that fingers are not really shriveled - they are water-logged. But is this right? I think I observed many times my wrinkly fingers after swimming, but I never felt that they are water-logged. Any thought on this matter would be highly appreciated.

One more paper to add: https://www.scientificamerican.com/article/why-do-our-fingers-and-toes-wrinkle-during-a-bath/

Great question, for which still no definite answer is known despite ~100 years of research.
A simple physical basis for the wrinkling however seems unlikely as glabrous skin without sweat glands does not wrinkle, and as wrinkling requires the activity of specific nerves.
Moreover plausible evolutionary ideas, which used to be popular, such an anticipated improved ability to grab, don't appear that clear in newer experiments.
For the information above, and an even more detailed answer, please see Haseleu, Omerbasic et al. 2014 http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0084949


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Ratio boys:girls born - how to explain?
My son studies genetics at school right now and they have been covering gender. It's well known that slightly more boys are born than girls. However, originally there's an equal number of sperm cells with X and Y chromosomes. From what I've read it sounds that fertilization is affected by different factors but it seems that on average it's about equally likely? At school, they told them that more fertilized female "embryos" die than male?? Could it be true? Question: Do you know how it happens that there is an equal number of X, Y-carrying sperm cells, but more boys are born?

This page has quite a nice overview of the topic: https://en.wikipedia.org/wiki/Human_sex_ratio#Factors_affecting_sex_ratio_in_humans but as far as I know, it's not well understood.

The hypothesis that male embryos are more viable seems reasonable, but I've not seen any data to back that up. Also, it's purely speculative but you could imagine how particular proteins expressed with X or Y chromosomes could change how an embryo develops, which in turn could change how viable the embryo is.

The Y chromosome is smaller than the X. So sperm carrying the Y chromosome are very slightly lighter, and faster. I'm not an expert on this, but I wonder if it might be a possible reason.

@Jam That link says that sex ratio decreases as the father gets older. Maybe older men have a higher proportion of defective Y chromosomes? That could cause a greater number of male embryos to fail and bring the male to female ratio down.

This post seems to adress the question https://biology.stackexchange.com/questions/27582/why-do-we-have-more-male-infants-born?rq=1


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RNA extraction from soil
I have been trying to extract RNA from soil without success. I have used commercial kits (The Plant DNeasy kit) because I did not want to buy a complete new kit (Soil) to do 5 extractions. Is there any "in-house" protocol that successfully extracts RNA from the soil? Or, is there any tip that would allow me to extract good soil RNA using the Plant DNeasy kit?
Thanks


text:
in order to align genome multi-fasta files, do you ignore the chromosome sections?
I want to test my implementation of Needleman-Wunsch on two fasta files downloaded from https://hgdownload.soe.ucsc.edu/.
However, fasta files on this site are multi-fasta and therefore are split into sections each one belonging to a chromosome.
If I want to align the entire genomes in these files:

do I just ignore the chromosomal separation inside these files? thus do I stitch the chromosomes of each file into one big chunk?
or do I align combinations of these chromosomes?

If the fasta really are chromosomes, there will be one per chomosome. Check this in case the multi-fasta you have is an incomplete sequencing of an organism. There is a bioinformatics site on Stackexchange now at https://bioinformatics.stackexchange.com

Chromosomes do not form one continuous genome, so I would suggest creating a separate alignment for each chromosome.

If the fasta really are chromosomes, there will be one per chomosome. Check this in case the multi-fasta you have is an incomplete sequencing of an organism. If incomplete there will be many more fasta. There is a bioinformatics site on Stackexchange now at https://bioinformatics.stackexchange.com .You would get better answers there.


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Is NZT-48 real?
NZT is a fictional compound in a movie called limitless, basically it's a brain booster, it gives access to more simultaneous neuron activity.
are there any real cognitive enhancers out there?

As others have said, this compound is fictional. Leaving illegal compounds aside, I would vote for nootropics. And from them I find pramiracetam to be the best fit. I have found its action to be rather similar to the one described in the movie, although with no side effects. One of the most notable mechanisms of it is the highly selective potentiation of acetylcholine and improvement of brain blood flow. Papers on this chemical are easily accessible through Google, so I won't provide lnks.
However, no cognitive enhancers will do any good without proper motivation and conscious efforts. It is pointless to eat pills and hope that something will come and change who you are for the good. Cognitive enhancers need something baseline to enhance.
UPDATE
Looks like this question really belongs to CogSci SE, but I feel that I should complement this answer with some more information that is important to take into account.
Cognition/mind enhancement can be a double-edged sword for some people. Instead of giving pleasure directly, it actually enhances mind and calls for much more self-discipline and responsibility. For example, I practice meditation and some other mental disciplines for a long time already, and it came in handy to control and direct my mind. However, some people who tried pramiracetam reported that the intensity of their own mind was too much for them, they simply did not know what to do with it for they had no real task, motivation or big plan formed before administering the compound, and it could happen that they got themselves overwhelmed by many long-forgotten memories that rejuvinated in all their lucidity at the same time when the present day reality became much more integral and whole, without many pieces comfortably forgotten.
These memories could not necessarily be negative, but what about a super-fine image of the wallpapers pattern you were looking at when you were 3 years old, standing as bright as a day before your eyes when you try to sleep, eat or mate? And I am not even saying about the fact that recent events are perceived in much greater detail and integrity, senses sharpened greatly... Personally I was able to control my mind because I also practice it in daily life (without the enhancers), but this may not be easy for people who are not used to that.
Another issue such an enhanced mind could face is that people around remain as they are. The perceived difference can render them much less intelligent and almost dumb. A person with an "enhanced" cognition can find himself living in a world of dense people. This is in no way an offense, a similar condition can be observed when one with a body "enhanced" by a stimulant can run 3 miles and still feel not even slightly tired, while an average untrained person will extinguish in under a mile. It is true that there are lots of smart people in this world, but one has to be ready for a sudden shift of perception that could occur. I remember reading reports of piracetam users who say that while they became more effective in integrating knowledge, people around did not, and situations occured when "obvious" things were not immediately understood by the surrounding people which caused irritation and conflicts. One has to be careful as this may lead to social disadaptation.
This again calls for discipline, ability to love and appreciate other people, and actually rises many unusual ethical questions. As with any gain, one must always remember that love and understanding are essential.
Another example of a two-fold effect is piracetam - an older, less potent but nevertheless useful nootropic. While it has an effect which may with high probability result in enhanced cognition, it also rises agression due to stimulating the secretion of the thyroid gland. So again, this calls for enhanced discipline. (do not mix the terms "piracetam" and "pramiracetam" in this text, they mean different compounds).
In any way, it is always important to apply conscious approach to your own behavior and thinking, be it with or without enhancers. But with enhancers, the responsibility is times greater.
One more point to notice. While nootropics do not exhaust body in any way (they are not stimulants), it is very important to provide oneself with sufficient nutrition and sleep, and avoid drug usage such as nicotine, alcohol and other psychoactive drugs. Failing on any of that may significantly reduce the useful effect and in case with illicit drugs cause unpredictable consequences. Dietary supplements such as omega-3, lecitine, vitamins can also provide some support.
Disclaimer: aside from compiling information available online, what I am saying is also supported by personal experiences of 2 courses each 6 months long, taken with a pause of 1.5 years between them, 600mg pramiracetam 2 times a day. I don't smoke or drink alcohol. Both times the experience was life-altering.

Totally, without motivation, all that is excess energy without a proper outlet. still interesting though, that we're nearing a future where we could have more access to our thoughts, more control over our lives.

@AlyShmahell I thought that I should build up on your position and express some more concerns directly related to the issue and possibilities

I'm glad you did. it's both such an interesting subject and a sensitive one. it requires as much care and planning as pushing forward into research and application. now it's my turn to build up on your information, I'll be researching what you provided in the update. and next question it's going on CogSci ;)

Yes there are a few out there, though the mechanism is quite different to the film. Things that increase the activity of dopamine and norepinephrine particularly in the prefrontal cortex where a lot of your higher functions like decision making seem to be. Things that do this can include amphetamines (ritalin and other adhd medications) along with things like modafinil.

That's very interesting, but isn't dopamine responsible for reward-driven-motivation? is that to say even intelligence is increased by increasing the promise of reward?


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Is it possible for a person to eat so many carrots that one turns orange?
I once read that Jerry Rubin (a famous 1960s activist) ate so many carrots that he turned orange. (This was in the East Bay Express, around twenty years ago.) I assumed it could be true, though he would have to eat hundreds or thousands of carrots; while a close family member thinks it's ridiculous. Is it medically/biologically plausible?
(I hope this question is appropriate to ask here--I'm new to this forum.)

@TanMath: As I said, this claim was from an article in the East Bay Express, around 20 years ago. The article was about history/politics/ "where are they now" about Jerry Rubin, or the Yippies (a hippie group that included Rubin and the more famous Abbie Hoffman).

Beta-carotene, the pigment that gives carrots their orange colour, can accumulate in the skin if taken in excess amounts. This condition is called carotenosis. Since beta-carotene is a lipohilic (fat loving: dissolves in lipids), its absorption is facilitated by dietary fats [1].
There is one report that says that excessive consumption of beta-carotene containing fruits and vegetables can lead to carotenosis [2].
Also have a look at this Scientific American blog.

Prince, Martin R., and Joan K. Frisoli. "Beta-carotene accumulation in serum and skin." The American journal of clinical nutrition 57.2 (1993): 175-181.
Wageesha, Nekadage Don Amal, et al. "Studies on hypercarotenemia due to excessive ingestion of carrot, pumpkin and papaw." International journal of food sciences and nutrition 62.1 (2011): 20-25.

Thanks. But how many carrots would an adult need to eat?

@user24353 That I am not sure of. It may vary between person to person and would also depend on the kind of diet one is having.


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Hypanthial disc
Can anyone illustrate what the hypanthial disc is?  It is descriped throughout the key to Rosa in the Flora of North America.  I think that I understand that the hypanthium is the hip which is formed from fused flower parts.  But, which part is the disc.


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Resolution of gel electrophoresis
My professor mentioned the resolution of the gel in gel electrophoresis. He stated that agarose has large pores and thus low resolution whereas polyacrylamide has the opposite.
I don't understand what resolution has to do with this. Can someone explain?

Resolution size of the gel simply means the distinction that can be made between molecules very close in size.
If you were looking to distinguish between a 100bp fragment and a 200bp fragment, then agarose will give you that level of differentiation.
But if you were looking to distinguish between a 190bp fragment and a 200bp fragment then you would likely want to us polyacrylamide. The PA gel has a higher resolution because you can distinguish between smaller differences on molecule length.
Think of it in terms of a simplified idea of a microscope, at 100X, you can probably distinguish between cells, maybe make out a well stained nucleus. where as at 1000X you can start to discern other organelles. You are seeing a finer degree of detail at the higher magnification. There are many factors that go into the resolving power of a microscope and the example based on magnification is simplistic and doesn't really address optical resolution, but it is an illustrative example of resolution in a gel. You can think of agarose as the 100X and PA as the 1000x, if that helps.


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What changes would allow cutting mRNA-based vaccine safety testing to 18 Months
I see a lot of skepticism among my fellow citizens following an interview that Bill Gates gave the BBC on the topic of Corona vaccines. The Gates foundation is funding several study ventures on Corona vaccines, conventional vaccines as well as experimental mRNA vaccines. In the interview he said:

"We'll need to fund the ten most promising constructs because we don't know in advance which on will prove to be safe and effective [...] so we gonna have to take something that usually takes five or six years and get it done in 18 months (6:09)
  [...]
  There is an approach called RNA Vaccine [...]
  that looks quite promising but we can't count on that, so we'll back 4 or 5 of that and 4 or 5 using a conventional approach, which unfortunately, the schedule on that would probably not so quick. (6:45)

There are people on the internet that criticize that Gates would want to trade security for speed in getting the vaccine out and cite this comparison (18 months instead of five years) to make a point how unsafe that would be. I interpret the interview insofar that Gates believes that the new technology itself would provide for some speed gains (longer time needed with conventional approaches). Similarly, this review (Section "Good manufacturing practice production") mentions that mRNA vaccines are easier to produce than their conventional counterparts, for example because life viruses and toxic inactivation chemicals are not involved in the process and thus do not need to be removed reliably.
However, I lack the knowledge to judge how big the speed gains due to the mRNA platform could be. Also, the same review as above mentions in the section "Safety" that there are more problems in clinical trials than there were in preclinical ones, so there still seems to be considerable need for basic research left. Similarly, I do not know how long the phase of vaccine clinical trials normally is and how much it could be reduced by logistics without loss of information. Finally I don't know what studies could be left out for an emergency approval of the vaccine to cut the approval time if the benefit would outweigh the risk.
I would be grateful if you could help me on the questions in bold.


text:
How is it that ionic diffusion is independent of other ions?
This question arises from the explanation of what the resting potential of a cell membrane is. In the Goldman formula, there is no interaction between different ion types.
If diffusion is caused by random movement of ions and collisions, then how is it that the K+ ions do not seem affected by the very high concentration of Na+ ions outside of the membrane? Shouldn't there be an effect due to the fact that outside, the ion concentration overall is higher than inside? How come they are all independent?

Most importantly, the whole Goldman-Hodgkin-Katz model is, well, a model. It is a way we would like to find and explain phenomena, given pen and paper.
Often, scientists build models in order to explain data in hand, but even then, they will have to add something from their imagination. For example, early astronomers saw planets moving differently from stars, and came up with the idea that, you know, planets do not circle the earth, but maybe around some points in space, which in turn circle the earth. That didn't work well, so they created the heliocentric model, where planets and the Earth circled the sun. That was still perfectible, and Newton suggested the planets do not move on circles, but on ellipses. Each generation of astronomers had almost the same data in hand, but chose to make some assumptions in their models.
The same goes with the lack of interaction between potassium and sodium ions: it is a theoretical assumption. As models go, the GHK model is quite good, because it fits experimental findings better than any other model. Its assumptions have a great chance of being true, of reflecting the physical world. I guess you really asked what are the physical facts that underlie the assumption of ion independence. The fact is, you are looking for explanations for a fact that may be or may not be - so any response you will receive is, to a degree, speculation.
My thought is that the number of water molecules (55 molar) that may collide with an ion is far greater than the number of cations (up to a few hundred nanomolar, about 100 million rarer). Perhaps the number of ion-ion collisions is negligible. There is one bottleneck, in the actual channels, but there different species do not meet, because each has its own channels.
Another, more factual, is that the model is imperfect, and independence is more of a wish than a complete truth. Quoting from http://books.google.com/books?id=SmJoSwnwSh0C&lpg=PA353&ots=3fvI19Sk5Q&dq=ghk%20ion%20independence%20fails&pg=PA353#v=onepage&q&f=false : "The rich literature on how ion channels fail to obey the independence principle is reviewed in Chapter 14 of Hille (1991), and some specific models will be studied in the following chapter."

Thanks for this quick reply, which helps to a certain extent. But now that I thought about it for a while... If one assumes that the interactions between cations are negligible, and that therefore K+ diffuses "as if Na+ wasn't there", wouldn't that also mean that inside the cell K+ would hardly diffuse, because... well they don't interact with each other, thus hardly ever collide and thus don't diffuse?

In solution, potassium ions collide with each other as rarely as with sodium ions. The issue is net movement. When looking at a semiporous membrane that allows 1/10 of the ions hitting it, there will be no net movement, if 10 Na ions bumble on one side, and 10 Na ions on the other; nor if you have 100 on one side and 100 on the other. But there is predictable movement, if one side holds 10 times more Na compared to the other side, regardless of absolute numbers, and regardless of the number of K ions hanging around.

Hi Nick, and thanks again for taking the time to help me! I think I finally understand what you mean. Are you saying, that the diffusion is only caused by how many potassium ions hit the channel on either side? That would make sense to me... I had a quick Wikipedia search and found that there are inward and outward potassium channels, so that potassium that hits the membrane from the outside can flow into the cell too. The fact that there are inward and outward channels also helps with all this. Thanks again!

The number of ions moving one way is dependent on the number of ions of that kind. If one in a thousand hits the hole, like the balls in lottery, it matters how many balls one is juggling. More green balls will pass if more greenballs are bouncing. But we have two movements. Most ionic channels allow equal passage both ways.

(continued) The GHK model implies no direction selectivity. GHK does not distinguish permeability for moving K in from permeability for moving K out. (In reality, this assumption is not 100% correct. Rectifying channels make a distinction between directions. So here's another reason why GHK is a simplified model.)

(continued) The net movements is a balance of two movements. The fact that we have the electric+osmotic imbalance makes ion X undergo net leakage towards, say, the cytosol, in physiological conditions. But in the lab, where one can play with concentrations and voltages, most ions will allow net reverse flow.

Thanks Nick! it's all a lot clearer now, very interesting topic I find, much more interesting than they show you in a classroom!

Maybe I'm missing something here (and it's not my area of expertise) but...
the GHK formula includes the parameter Vm which is the transmembrane potential. This parameter is determined by the intracellular and extracellular concentrations of all ions. A high external concentration of Na+ will therefore influence the net movement of K+.
One of the assumptions of the GHK equation is that the ions do not directly interact.

Hi Alan, in the GHK formula, the movement of K+ is independent of the other ion concentrations, you can see this by setting the permeability of all other ions to 0. According to the GHK model, if the ion cannot pass, it will not have an effect on the membrane voltage. But have a look at Nick's answer!


text:
Do skull bones have pain nerves (nociceptors)?
I recently attended an awake brain surgery  for deep brain stimulation and it seemed to me that only the skin surrounding the drilled hole got local anaesthesia. I know that the brain itself does not have nociceptors, but what about the skull? And how does this compare to other bones in the body? Would you feel a hole being drilled in your skull? Would you feel your leg being chopped off if the surrounding tissue was numbed?

Thanks for your answer Alexandria,
As you didn't seem entirely confident about the innervation in the skull bone, I ended up asking the neurosurgeon, and she indeed only anaesthetises the skin surrounding the drill hole and the subcutaneous tissue as the bone does not have nociceptive innervation in that area.
So you are right for the leg: if chopped off, you would still feel the pain from the nerves in the bone. In the case of deep brain stimulation however, the skull does not have nociceptive innervation in the area where the holes are drilled.
This leaves the question of why there are some exceptions to bone innervation, but that's a problem for another day.

Yes, bones can be innervated. I say "can be" because although I'm not certain that ALL are, I know that most are. "Innervation" is your key word to learning more about the presence or absence of nerves reaching to any body part. Googling "are bones innervated" yields plentiful results, but the short answer is yes.
If you were to chop your leg off with surrounding tissue numbed, you would still feel it for this same reason.

Can you put in some references please

Sure thing: http://www.mananatomy.com/basic-anatomy/nerve-supply-bones and http://www.ncbi.nlm.nih.gov/m/pubmed/12123694/as well as http://www.ncbi.nlm.nih.gov/m/pubmed/19425099/

Sharp acute pain in response to acute physical breach comes mainly from the superficial periosteal innervation, and not much from internal bone innervation.
I am an orthopedic surgery internee. It's in our routine to drill ~3-5mm dia rods (steinmann pins) through bones of lower limb including femur, tibia and calcaneum. We too only inject anesthetic deeply into the skin, but that probably covers the perisoteal innervation too. At the end, when we doo the drilling, despite the great width of these aforementioned bones in comparision with the skull, patient seems calm while we transit through bone, and is only uneasy when the two skin ends are breached.


text:
How is a synapse held in place?
Here is a question I've never asked myself until now: All textbooks show synapses with a decently large synaptic cleft between the axon terminal and the dendrite. How is this connection held in place mechanically? How is the axon terminal attached to the dendrite?


text:
Allele-specific bisulfite sequencing
When evaluating methylation status at various CpG sites after sequencing, how much consideration should one give to random single base pair insertions and deletions. Suppose there is a CA dinucleotide; can we assume that the CA is native to the sequence or results from a G deletion especially when the latter is suspect once comparing to other sequences. Is there really a set standard sequence to compare it?

Welcome to BiologySE! Thanks for your question...can you give a little more detail about your question, specifically the rationale behind it so other individuals can follow along and better understand what you're asking? You may want to check out the help center as well, for some great tips on how to ask a great question... http://biology.stackexchange.com/help

Are you talking about when a single read in your deep-sequencing experiment has differences in base composition compared to other reads mapping to the same locus?  Are you suspecting a duplication event where the original copy is CpGpA and the copy you are referring to is CpA?

I agree with Vance, we need a little more detail to better answer your question. From what I can tell, you are asking whether a single nucleotide polymorphism (SNP) that results in the addition of a cytosine base to your sequence is of concern when examining the methylation signature of that sequence.
I would first determine whether the polymorphism is common in the population using NCBI. The more common the polymorphism, the less likely it is to have a serious effect. However, that is not to say that it doesn't have any effect.
I would then examine how much the methylation of that one site varies compared to samples without the additional cytosine base.
Finally I would determine the importance of the location of the SNP. Is it located in a CpG island? Or is it located on the shores, shelves or 'open sea'? (see work by Sandoval et al.)
Without knowing all the above it is hard to make a call on how important/unimportant the SNP is in your methylation analysis.


text:
Scaling down amount of DNA for transfection: what factor to consider?
I am interested in transfecting HEK293 cells with a BAC. One paper suggests using 24 ug of DNA to transfect a 55-cm^2/10 ml culture plate. I am using an assay optimimzed for a 96 well plate so I am interested in scaling down the amount of DNA.
If I consider by volume: I will be going from 10 mL to 100 uL, scaling down by a 1/100, suggesting 0.24 ug of DNA.
If I consider by cell number: I will be going from 10^7 cells to 10^4 cells, scaling down by 1/1000, suggesting 0.024 ug of DNA.
If I consider by cell concentration: I will be going from 10^6 cells/mL to 10^5 cells/mL, scaling down by 1/10, suggesting 2.4 ug of DNA.
What factor should I scale down by? I want to say that it's volume but I don't really know why.
Thank you for any help or suggestions!

Are you using lipofectamine? They provide tables to sort of help streamline the process: 3000 reagent, 2000 reagent.

Hi - No, I'm not using Lipofectamine but I did see the table online. I'm wondering why they decided to use volume instead of cell # or conc which seems much more intuitive to me.

Well if you think about a plate-based transfection, only a certain number of cells will viably fit into a well, and you want them in a replicative state. So you try to get them 90% confluent, which is easier visualized in a 6-24 well format, but for 96-well other groups have worked out the best cell/well in their protocols already. Consensus is at around 50,000 cells per well. So the cells numbers are actually standardized for the plate format. The only question that remains is how much volume of reagents will work with said cell counts!

Wait, I don't think that answers the question. If the cell # is standardized, then amt of DNA transfected should be scaled down according to cell # not volume

If you know how many cells will give you confluence in a 96-well format, you just scale down on the size of the well. So 1:100 or 0.2 ug DNA.


text:
Query individuals with both WGS and RNA-Seq data
Using the SRAdb R package, I am looking to query individuals who possess both WGS and RNA-Seq data on the SRA. So far I believe I have been able to query specific samples with both WGS and RNA-Seq experiments, however a specific sample, provided by the sample_accession, is not exactly what I'm looking for.
For example: I'm interested in finding human data in which one human was used to derive WGS data, and several tissues from that same human were used to derive RNA-Seq data.
Is there any easy way to accomplish this using SQL and/or R?
So far, this is my approach to identify samples that have both WGS and RNA-Seq data, using the local database, SRAmetadb.sqlite:
con <- dbConnect(SQLite(),'SRAmetadb.sqlite')
query <- dbGetQuery(con,
                    paste(
                          "SELECT
                            sample.sample_accession,
                            sample.scientific_name,
                            experiment.experiment_accession,
                            experiment.library_strategy
                          FROM sample
                          JOIN experiment ON
                            sample.sample_accession = experiment.sample_accession
                          WHERE experiment.library_strategy in ('WGS','RNA-Seq')
                          GROUP by sample.sample_accession
                          HAVING COUNT(DISTINCT experiment.library_strategy) = 2"
                        )
                    )

With this approach, I can see query contains 181 human samples that have at least one WGS experiment and one RNA-Seq experiment. That's great, but I feel I must be missing out on data that came from different samples but the same individuals.

Why do you feel so?

A liver sample and a brain sample from the same individual would have different sample_accession values, correct?

And it's remarkable to me that there are only 4 Mus musculus samples that meet this criteria, using the method above


text:
Can you measure ECG from a single location?
I want to make a DIY bracelet to measure my ECG. All I need is the interbeat interval.
Can I design a bracelet on one arm only, with two electrodes slightly spaced from one another, and figure out the beat from the conduction timing differences down the arm?

I am afraid you cannot build the classic ECG using only 1 hand.
Probably, you can measure HR - heart rate accordingly to pressure detection and similar sensors and from that you can simulate ECG by picture. Simulate I mean you cannot build any reliably ECG curve on the monitor, but can show some waves after every heart beat.

I definitely want to stick with electrical activity for now-- it's proved more reliable than pressure or photoplesmograph sensors at the wrist. I'm curious whether you think it's possible to only extract the heart beat from 2 electrodes on a single wrist. We don't need the classic ECG waveform, only the heartbeat  .

With a single electrode, it is impossible to get an EKG as it has to have biopotential from two points (it is impossible to gett voltage from a battery using only one terminal).
Regarding EKG from single arm, yes it is possible to get clean EKG from shoulder.


text:
Difference of coverage between amplicons
I have 2 fastq files and I generated BAM file (indexed and sorted) of some reads. I aligned them to a reference genome (hg19).
I am working with different primers.
FORWARD
1. TTGCCAGTTAACGTCTTCCTTCTCTCTCTG
2. CCCTTGTCTCTGTGTTCTTGTCCCCCCCA
3. TGATCTGTCCCTCACAGCAGGGTCTTCTCT
4. CACACTGACGTGCCTCTCCCTCCCTCCA

REVERSE
1. GAGAAAAGGTGGGCCTGAGGTTCAGAGCCA
2. CCCCACCAGACCATGAGAGGCCCTGCGGCC
3. TGACCTAAAGCCACCTCCTTA
4. CCGTATCTCCCTTCCCTGATTA

Therefore I have different amplicons. How can I plot the coverage of these different amplicons. And what could explain big difference between them?
Thank you very much for your help.

I answered before about things which will effect coverage in NGS http://biology.stackexchange.com/a/57169/990

BEDTools, among other software suites, will give you a coverage histogram.  Biggest source of bias in PCR efficiency is just that some primers work better than others, there is sequence bias in the PCR amplification stage of the library prep too.  GC content contributes to this.

Well, to plot the coverage I would use something like Python Matplotlib. Take a look at this example:
import matplotlib.pyplot as plt
import matplotlib

amplicons =  ('TTGCCAGTTAACGTCTTCCTTCTCTCTCTG',
      'CCCTTGTCTCTGTGTTCTTGTCCCCCCCA',
      'TGATCTGTCCCTCACAGCAGGGTCTTCTCT',
      'CACACTGACGTGCCTCTCCCTCCCTCCA')
countAmpl = (1635, 4734, 2156, 3085)

fig = plt.figure(figsize=(10,8.5))

subplt = fig.add_subplot(111)
subplt.set_ylabel('Count')
subplt.set_xlabel('Amplicons')
subplt.plot(amplicons, countAmpl,  linestyle='-', marker='o', color='blue')
for tl in subplt.get_yticklabels():
    tl.set_color('blue')

plt.savefig("amplicons.eps")

Check other types of charts in Matplotlib if you think you need something else.
You can also try to open and visualize the BAM in IGV from the Broad Institute.
Regarding the difference in coverage, I would say that some are from a repetitive region. Or the amplification depth of a region is greater than for the others. Or maybe the aligner found similar regions and decided that the amplicon aligns well in all those regions.

These amplicons are all of coding exons, so repetitiveness is not likely to be a problem.  Unless the read is quite short, it won't align to the wrong place.


text:
What are unmapped reads?
I am mapping some reads to a reference genome (hg19). I used bamtools to have the percentage of mapped vs unmapped reads.
Total reads:       1150004
Mapped reads:      1052983  (91.5634%)
Forward strand:    624067   (54.2665%)
Reverse strand:    525937   (45.7335%)
Failed QC:         0    (0%)
Duplicates:        0    (0%)
Paired-end reads:  1150004  (100%)
'Proper-pairs':    1046208  (90.9743%)
Both pairs mapped: 1049400  (91.2519%)
Read 1:            575002
Read 2:            575002
Singletons:        3583 (0.311564%)
Average insert size (absolute value): 534.479
Median insert size (absolute value): 215

My question:
What represent exactly these unmapped reads? What information do they tell us? How can we analyze them?
Thanks

In transcriptome (RNA-Seq) libraries, unmapped reads are reads that fail to map to known exons. More often than not, they represent genomic DNA. RSeQC has tools to help identify genomic (also sometimes called intergenic) sequences.
For the most part, the percentage of unmapped reads just provides you with QC information, like how much gDNA you purified along with your mRNA. It's unlikely to be very useful beyond that, but it really comes down to what you're looking for in those sequences.
If you're doing DNA-Seq, then unmapped reads generally represent reads that failed to map unambiguously to known sequences. This will depend on a threshold (usually provided by the user) for alignment stringency.


text:
What tool to use to map reads (samtools, sequencher,...)?
I am a beginner in Bioinformatics. I have 4 files:
2 fastq files (aln1.fastq and aln2.fastq)
2 bam files (aln.bam and aln.bam.bai)
I know that:

the raw file is aligned to hg19 human genome.
The sequenced file is pair-ended from Miseq sequencing platform.
This file is the result of an amplicon sequencing design.

I also have sequence information about the primers (4 forward and 4 reverse) and 2 adaptors.
And I have to answer these two questions:

What is the constitution of each read, for example (adaptor + primer + amplified
region) ?
Which gene region did those reads mapped to ?

My question is what kind of tool do I have to use to respond to these questions? samtools? sequencher? FastQC? Can anybody help me just to start because I am totally lost.
Thanks

The aln.bam file is likely a binary and compressed version of a file in SAM format, indicating where reads have aligned. I guess it has been generated by some alignment program using the two fastq files.
For a start, you might use a program to visualize where the reads have mapped.
For instance, you may use IGV and load your aln.bam file to see where in hg19 they aligned. IGV will also use the aln.bam.bai file to help it find the aligned reads in the aln.bam file.
As far as I know, sequencher is used to clean and assemble Sanger sequencing data, but my experience with that program is almost 10 years old.
Samtools is a command-line program that can help you extract information from the aln.bam file. You may use it to count how many alignments are present in a given genomic region, for instance, using option -c of samtools view. See the manual for more details: http://www.htslib.org/doc/samtools.html

thanks. I opened my bamfile with IGV but how can I know which chromosome to choose and which region to zoom in?

If you don't see the reads at large scale, then I'm afraid you cannot know, just using IGV, where to zoom to see them. You need to identify regions of interest with other means. For instance, samtols view -c aln.bam chr1 should give you the number of alignments in chromosome 1 (provided it is named chr1). samtools view -H aln.bam should give you, among other information, the list of chromosomes that you can query (preceded with "SN:").

Samtools is not an aligner; it is used to analyse alignments. FastQC is for analysing the read qualities and average composition. You can get to know the adaptor sequence by running FastQC.
The next step is adaptor trimming. There are many tools that do that. Trimmomatic is currently popular. You can find the adaptor composition of each read by subtracting the read length post trimming from the read length pre-trimming (this would be same for all reads).
Then you have to align your trimmed reads to a reference, using an aligner. Again, there are many aligners available; Bowtie, STAR and now a new one called HISAT. STAR and HISAT are faster than Bowtie.
Since you already have the alignments (aln.bam) to hg19, you do not need to perform alignment. You want to know, to which genes do these reads map to. This information is not available unless you have the genome annotations. The annotations are available in the form of GTF/GFF files. You can obtain the association between genomic locations and the reads using the BEDOPS toolkit as mentioned in this Biostars post.
I don't have much experience with this tool. What I would do is convert the BAM to SAM (using samtools) or to BED (using bedtools:bamtobed) and parse the columns of the SAM/BED file describing the read locations with the GTF file. See this link for the details on the SAM format. You can use any scripting language like awk or perl to parse.
Samtools does have an option to filter the reads according to regions specified in the BED format but it will not automatically annotate them.
samtools view -hL regions.bed aln.bam > aln_filtered.sam


text:
An experiment to test if a bacterial resistance gene is on the plasmid or chromosome?
So I have an E.coli strain phenotypicall resistant to the antibiotics ampicillin and rifampicin. How do I test if the AmpR gene is carried on a plasmid and not on the chromosome?
In summary, I thought perhaps you could isolate the plasmid, put it in an ampicillin sensitive bacteria, then see whether or not the bacteria die.
I also thought you could use PCR on the plasmid with primers complementary to sequences adjacent to the AmpR gene. I'd use a positive control with the gene of interest and a negative no template control.
Do these sound about right & are there any other methods or controls I should consider?

I remember another method. Isolate the plasmid and use restriction enzymes specific to ampR (Pvu I & Pst I). If the plasmid is cut, then the resistance gene should be on it.

You could try to isolate a plasmid, transfer it into non-resistant bacteria and see, which resistances they develop through the transformation.

Based on the situation you have described, isolating the plasmid from the ampicilin-resistant strain of E. coli and allowing it to be taken up by a separate, non-resistance strain of E. coli would be the most efficient, and cost effective method of determining whether or not the AmpR gene is located on the plasmid or the bacterial chromosome itself.
In order to do this, you would need to first grow a culture of the ampicilin resistant strain, from which you could induce lysis of cells in order to obtain a solution containing free plasmids.
Several different plasmid isolation or mini-prep procedures exist that are typically quite effective, if done correctly.
Additionally, many specific "plasmid-isolation" and "plasmid-purification" kits exist that would offer the materials and instructions needed to undergo this process: Isolating your Addgene Plasmid DNA from Bacteria
After properly isolating the plasmid from your ampicilin-resistant strain, you would then need to insert that plasmid into a non-resistant E. coli strain. Bacterial transformation via electroporation is a commonly used technique that causes increased permeability of bacterial cell membranes, enabling the plasmid to enter or be taken up by the cells.
Once these cells have been allowed to "recover" they can then be grown in liquid or solid culture containing ampicilin. Growth would indicate the AmpR gene is present in the bacterial strain, and that the plasmid is responsible for carrying this resistance. Likewise, no growth would suggest that the gene must have be present on the bacterial chromosome instead.


text:
Construct a restriction map of a linear fragment of DNA using the following data?
I've attempted to do the single digests, and the double digests, but cannot complete the map.... I've attached what I've done so far

DNA Sizes of Fragments (bp)
uncut DNA 900
DNA cut with EcoRI 500, 350, 50
DNA cut with HindIII 600, 300
DNA cut with BamHI 400, 300, 200
DNA cut with EcoRI + HindIII 350, 300, 200, 50
DNA cut with EcoRI + BamHI 300, 250, 200, 100, 50
DNA cut with HindIII + BamHI 300, 200, 100

Why are you listing only one of the possible fragment orderings for each cut result?  (e.g. only 500, 350, 50 and not the other five arrangements, like 350, 50, 500 and 50, 350, 500)

^This. You need to list all arrangements possible. It is equally possible for the enzymes to cut in any order (theoretically). Unless specified in which order they are used.


text:
Phenotype-Genotype for multi-hybrid crosses
It's generally easy to figure out genotype and phenotype frequencies using a Punnett square for monohybrid and Dihybrid crosses. But what about situations involving 5 or 6 traits? Is there a simpler way to get about this?
As a sample problem:
If we have two organisms crossed, one with genotype AaBBcCddEe and the other with genotype aaBBccDdEe (lowercase is recessive and upper case is dominant), how many individuals would have the genotype AaBBCcDdEE?