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How can you tell if a protein-coding gene is nuclear or mitochondrial?
New to genes, and have to read literature to find candidate genes for a particular study. I cannot for the life of my understand if all genes are placed into either the "nuclear" or "mitochondrial" category...are there more categories? Some are easy, like cytochrome subunit genes are always written as "mitochondrial" and then rhodopsin are written as nuclear...but other genes like ATPase etc. don't have those descriptions. When I search online further, it still does not clarify, so I am wondering now if there are just more categories to this?

Welcome to SE Biology. It will help people to answer your question if you note what resources you are using to confirm whether you are dealing with a genomic or mitochondrial gene. The databases vary in where they report this information.

I am still very early on in my research, so I am going through journal articles dealing with genes that differ in species found in one habitat vs. another. As of right now my only resource are journal articles. I am not sure what you mean by genomic or mitochondrial gene...i.e. the COI genes were obtained from genomic DNA, so I am not sure how to answer that.

I don't know what you mean by COI genes. I understood your question as a query about the location of genes; genome or mitochondrial genome. If you want to know the likely subcellular location of proteins, your question should ask about proteins and not genes.

http://biology.stackexchange.com/questions/40331/do-eukaryote-cells-contain-dna-that-isnt-part-of-a-chromosome-or-located-in-the
Would this be helpful?

Ahh okay, sorry this is me developing my vocabulary properly. I did mean the location of genes, nuclear or mitochondrial. I meant to use COI as an example where in the literature they always just outright call it mitochondrial. Then I come across something like ATP1 which is just called a membrane protein - so I didn't know if that meant just nuclear membrane or potentially mitochondrial membrane.

@MalharKhushu, I included a link in my answer. Thanks for the link.

I have limited my answer to refer to humans, but the advice generalises to other eukaryotic cells.
In human cells, almost all of the genes that code for proteins are located in the genome, which is located in the nucleus. The mitochondria have their own genetic material, however, the mitochondrial genes only encode for 14 proteins. The answer to this question also notes the existence of extrachromosomal circular DNA. There are also a number of proteins (1192) that are verified to exist but their genomic location is currently unconfirmed.
In your comments you mention ATP1 and note that it is called a membrane protein. The gene is located on chromosome 19 in the nucleus. The protein, that is encoded by the gene, can be found in a variety of places, including the nucleus and also the mitochondrion. The gene for Cytochrome c oxidase subunit 1 (CO1/COX1) is encoded in the mitochondrial genome and it localises to the inner membrane of the mitochondrion.
The links in this answer all point to Uniprot. This is what I use to get an idea of the basic functions of proteins. The database includes information genes but its primary purpose is to describe proteins and their functions. The information is roughly correct, it is not perfect. It includes a many species and links to a number of tools, including the gene ontology which attempts to characterise proteins using a controlled vocabulary.

@DNAngel, I'm glad to hear it. Biologists have created some great online resources. Remember that you have the option to accept answers that have provide a solution to your problem.


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Modulating the level of acetyl CoA

Describe what might happen if there were no mechanisms for modulating the level of acetyl CoA.

I am not sure what is meant by "modulating the level of acetyl CoA", or what mechanisms contribute to this. Presumably the citric acid cycle would be affected in some way because acetyl CoA enters it, but I'm not sure what exactly would happen.

What type of organism are we considering? Respiring or fermentating?

Probably respiring, but there is no additional detail in the question.

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Do xylem vessels in roots have lignin?
I learned that water enters xylem vessels in the roots after absorption by osmosis, but also that xylem cells are impregnated with lignin that doesn't allow water to pass through them to prevent water loss. Does that mean xylem cells in roots of plants aren't impregnated with it?

Xylem vessels contain perforations, too.

We have to consider the main function of lignin in xylem vessels, which is providing mechanical support for the plant. For the parts of plant above the ground, the stem where the xylem is located has to counteract the gravitational force pulling the plant down. Here's where lignin comes in to strengthen the xylem to support the plant. Remember that this is for many land plants.
Compare this to creepers, vines and aquatic plants. Lignin is absent or only present in small amounts as for creepers and vines, they have another external support, while for aquatic plants, it's weight is distributed on the surrounding water apart from the stem.
Now we can liken the case for aquatic plants to the xylem vessels in the roots of land plants. The roots of land plants are firmly anchored in the soil, and the plant's weight is distributed along the roots and soil, not just on the central root (for tapped roots). Hence there is not a need for lignin in roots of land plants.
And yes there are perforations in lignin as mentioned by @Always Confused, hence water can still enter the xylem vessel even when lignin is waterproof.

Do you have any reference that tells plant root xylem do not contain lignin?    Though right-now I can't find a source that tells separately about root-xylem wall composition; it doesn't seem they lack lignin. So far I knew, Lignin is a characteristic component of xylem vessels secondary wall. (also, Xylem and Lignin have same etymology, meaning 'wood').  Also, mature roots of shrubs and trees; go through 'secondary growth' (not to be confused with secondary cell wall), contain very much 'woody' secondary xylem. so I really doubt that root xylems could lack lignin.

You have "speculated" underground parts may need less-mechanical support since that is soil-embedded, and that could be a cause of no deposition of lignin in root xylem. Speculation is no-bad thing, but science looks for facts at first. A "guess" could not be accepted as answer until a verifiable source is given. thanks.

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What type of tree is this? (Coyote Hills)

I found this in Coyote Hills, Los Angeles, USA. Please provide the common name.

Do you have more close-up images of the twigs? could you find any see any flowers/ seeds etc (such as beneath the tree)? if possible photograph them.

some sort of  Taxodium?

Welcome to the Biology Stack Exchange. Please take the [tour] and carefully read through the [help] to learn more about the site, including what is on-topic and what is not, and how to ask a good question. Please ensure your post is formatted correctly as well.

For species identification questions, this page may help you about what things could help to answer.

Size: You can probably tell by the fence post; the tree is probably about 3 times normal human height

I guess it is Schinus molle (Peruvian pepper)

This does not provide an answer to the question. To critique or request clarification from an author, leave a comment below their post. - From Review

the person don't search a name of this tree? in facht i don't understand why it is not a answer of the question.

We like to see sources. A random species name doesn't say much.

which source could answer this question? i see no other possible like i did. and indeed it is not much, but better than not answer the question. we can discus this answer but i don't know the reason to don't give it a try.

Add a link to wikipedia is enough?


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What do bloodsucking animals actually feed on?
A number of animals, including mosquitos, leeches, ticks and so on, feed on blood. And yet, at least in mammals, most stored nutrients can be found in body fat as fat, muscles and liver as glycogen and digestive system as undigested nutrients, leaving very little in the blood itself. Normal blood sugar before a meal is 70-99 mg/dL, which at the high end means blood contains roughly 3.8 kilocalories per liter. This means that to gather a single kilocalorie from blood glucose, it would take 26 mL of blood, more than any leech could reasonably hold. Estimating the mass of a leech at 20g and scaling down human caloric needs linearly, 2500 kilocalories per 70 kg, yields a leech caloric requirement of 0.714 kilocalories per day. By this estimation, a leech would need to feed at least once per day to meet its energy needs, and yet data from the American Museum of Natural History states that a leech need only feed once every few months. The same math holds for other bloodsucking animals.
So what in blood do bloodsucking animals actually feed on?

What does the blood consist of, is the real question. And you seem rather focused on the calories. Yes calories are important for energy, however, our body needs fat, proteins, minerals etc to function. Also the caloric requirement, how did you scale that down? Simply by mass? What about other variables like organs, mobility, neural activity? A huge part of our caloric intake is used by our brain

There are advantages, too, for blood-sucking. Blood is liquid. So needs no cut, chew macerate etc process and small effort for digestion. It is easy to collect a little amount of blood from the host and then flyaway. but for tougher tissues it is not so swift. Might they leave more nutritious options for these advantages?

Lets find out how much calories are there in the blood. I am using this site for main reference, but will also add more references where needed. But before that, we should know that one donation of blood is about 1 pint (or 450 ml) blood1. But here, I calculate with volume 500 ml.

First calculate calories for plasma. Blood is denser than water by six percent2, so multiply that 500 ml donation times 1.06 to get to grams (because calorie content will be calculated from grams). Multiply that by 55/100 for men or 60/100 for women to get to grams of plasma. Now, multiply that by .07, because plasma is only 7% protein3, to get to grams of protein. Finally, multiply that result by four to get protein calories. Here, considering 55/100, I get 81.62 calories.
Now for sugar in plasma. Normal fasting blood sugar is around 0.09 grams per 100 ml of plasma (more familiarly expressed as 90 mg/dl4). Multiply the amount in grams time 2.75 for men or 3.00 for women, i.e., equal to how many hundreds of mls of plasma there are in 500 ml of blood, and then times four to get to calories. Result should be 1 calorie.
For plasma calories from fat, use 0.5 grams per 100 ml5 of plasma, times hundreds of mls of plasma, times nine - for calories from grams of fat - to get to calories.  Result is roughly 12 calories.
Next comes calories from red blood cells. RBCs are mostly water and protein, the protein almost entirely hemoglobin. Hemoglobin does not conform to the rule of four calories per gram because the heme portion of the molecule is not metabolized for energy. Use average hemoglobin values of 160 g/L for men or 140 g/L for women6, multiplied by 0.5 to get to the blood donation volume of 500 ml, multiplied by 0.96 to correct for using only the non-caloric heme portion of the hemoglobin molecules, then multiplied by four to get to calories. Hemoglobin is only 90% of the dry weight of RBCs7. Multiply one-tenth the amount of the hemoglobin weight in 500 ml times six (see below for why six) and add that to red blood cell calories. I get 353.28 here.
Finally, estimate calories for the other types of cells. Of the 500 ml blood donation, roughly one percent will be white blood cells and platelets8. Figure five grams, times one-third to get to dry weight, times six, to get to an estimated 10 calories. The "times six" is because some of the dry weight is protein or carbohydrates, which both have four calories per gram, and some is fat, which is 9 calories per gram.

Add everything up. The total should be approximately 425 calories for women and 460 for men in 500 ml blood i.e. even 10 ml of a man's blood contains about 9.2 kcal (there's no definite answer about how much blood a leech drinks at a time). Now, as you say in your question that a leech requires about 0.714 kcal, it means that a leech can survive for almost 13 days by sucking just 10 ml of a man's blood (if they have to metabolize everything present in blood (except, of course, water)), which justifies your statement.

I see my error was assuming the only value in blood is in the glucose, and ignoring everything else

@theenvironmentalist yeah, but since the parasite has got only that much amount as its sole source of energy, it would definitely do everything to extract as much energy as possible ;)


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Why half of the protein is saturated when [L] =Kd
let's suppose the following reaction:

At equilibrium we can calculate the Kd (Dissociation constant) using the following formula:
Kd = [P][L] / [PL]  or kd / ka
We can then use the Hill equation to calculate the fraction of binding sites which are occupied:
occupied binding sites = [L] / [L] + Kd

When [L] euals Kd, half of the ligand binding sites are occupied (Lehninger principles of biochemistry)

Why is this true? This would mean that at equilibrium half of the binding sites are occupied?

As the other answer says, it is true for a simplified model. The model you describe has only one ligand binding site per protein, which makes it the most simple model there is.
It doesn't mean that this is the case at equilibrium as you asked. This is because Kd is not necessarily equal to [L] at equilibrium.  Hopefully this simple derivation will help:
As you said, we know the formula for the dissociation constant: Kd = [P][L]/[PL]
Suppose [L] = Kd. If we plug back into the equation above we get: [L] = [P][L]/[PL]
Doing some algebra we can derive: [P] = [PL]
Therefore, at equilibrium, when [L] = Kd, the
amount of free protein ([P]) and the amount of ligand-bound protein ([PL]) are equal. In other words, half of the protein is bound to ligand, which is exactly what you were asking about.
But now let's suppose that [L] =/= Kd. The reaction will still come to equilibrium, finding concentrations of [P] and [PL] that satisfy the equation Kd = [P][L]/[PL]. However, these values will not be equal. Either more or less than half of the protein will be bound to ligand.
Only in the specific case of [L] = Kd will half of the protein be bound to ligand when equilibrium is reached.

The Hill equation in that link uses the simplifying assumption that all ligands bind simultaneously and that the binding sites are identical. The reaction is then P + nL = PL,
and Kd = ( [P][L]^n )/[PL]
Then by rearranging you get the expression in the link.
The equation "fraction occupied binding sites = [L] / [L] + Kd" Is not the Hill equation. It is called the binding isotherm. You can see that if Kd = [L] then the fraction of occupied binding sites (let's call it theta) = 1/2. Thus half of the binding sites are occupied.

It is the Hill equation where the Hill coefficient is 1, which kind of defeats the purpose of using the Hill equation.


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Why is it thought that silicon based lifeforms never flourished on Earth?
Reading the recent ScienceAlert article "For the first time, living cells have formed carbon-silicon bonds", it is stated that despite the relative abundance of silicon in the surface of the Earth, there are no silicon based lifeforms.
Specifically, the article asserts:

Why silicon has never be incorporated into any kind of biochemistry on Earth has been a long-standing puzzle for scientists, because, in theory, it would have been just as easy for silicon-based lifeforms to have evolved on our planet as the carbon-based ones we know and love.

I have read the question and answers "Why are we carbon-based?", which looks at the importance of carbon, what I am seeking information of is why carbon and why not silicon in the first place. So, therefore my question:
Why is it thought that silicon based lifeforms never flourished on Earth?

You might be interested in this

Keep in mind that there might have been silicon based lifeforms on Earth, but we do not know as we did not find them. It is estimated that 99.99% of all species that ever lived on Earth are extinct.

Well, diatoms do use silicon dioxide to form their cell walls,   and some grasses incorporate it, so silicon is incorporated into biochemistry.

Good points, I have replaced 'developed' with 'flourished'

I dislike the use of "currently accepted" with regard to "theory" and something as speculative as the chemistry of life forms. If you are interested in theories, ask about them, but beware of trying to find comfort in things that other people "accept". I have edited your question to a form I think more suitable for a scientific forum.

At temperatures above -195C, "C" wins the day. "Si" based chemistry may be more versatile than carbon in some environments, for example in a frozen nitrogen atmosphere.
Silicon accounts for 43% of rocks, Carbon is less than 0.1 percent, except that carbon is similar to water for reactivity and dissolving stuff, and organic "C" compounds are a molecular sludge like flowing-dissolved-stone, room-temperature-lava: tar/margarine/oil/diesel/glucose/alcohols/acetone are sludgy, liquid, the molecules can rotate, flow, coalesce... Carbon molecules are fluid, sludgy, rotating, pivoting, kind of lego material, whereas silicone chemistry doesn't flow, it vaporises and precipitates out of any flowing state.
Carbon reacts with both the molecules of water, O and H, and almost everything else, to make millions and millions of compounds. Silicon can't bond H. It's like the difference in between lego technic and lego. Try making a robot from lego!
That gives life millions of times more chemistry building blocks compared to silicone, and permits life to interact with water. Silicon life can't really interact with water.

10/1 cosmic abundance of carbon vs silicon

A carbonaceous contrite meteorite can contain 70 extraterrestrial amino acids and other compounds including carboxylic acids, hydroxy carboxylic acids, sulphonic and phosphonic acids, aliphatic, aromatic and polar hydrocarbons, fullerenes, heterocycles, carbonyl compounds, alcohols, amines and amides.

If you put silicon in a flask with, metals, sulphur, nitrogen, water, etc, and do the same with graphite, and you mix and heat them all up, the carbon will tend to make a vast population of larger sludge molecules, tars, formadehyde, amino acids, and the silicon will tend to form rocky crystals, as found in geology.

SiO2 is sand, quartz, very unreactive, takes a lot of energy to make it, whereas CO2 is a relatively reactive solube compound.

Silane SiH4 is the equivalent of Methane CH4, but SiH4 oxidizes instantly in contact with water and oxygen and air and is totally unstable, not naturally occuring, and it's difficult to make it, it combusts and becomes elemental silicon and water.

A silicate rich meteorite will only contail a wide array of silicate minerals, which are simpler, mineralogical, unreactive substances compared to organic chemistry that can exist in a meteorite.

Carbon forms double electron bonds a lot easier than silicon because it is smaller and lighter with a small atomic radius.

Silicone carbide SiC is a very rare mineral which illistrates Silicon's fussiness in making bonds.

Silicon-hydrogen molecules react spontaneously with water and they exist more easily in suphuric acid, which kindof limits silicone to a square root of the combination possibilities available to carbon. The H reactions give it that extra connection ability, any time a carbonate molecule becomes unstable, it absorbs an H and it's stable. Silicone can't do that.

Silicon doesn’t want to let go of Oxygen, but it doesn’t want to attach to hydrogen. try burning or dissolving quartz and silicates, compared to carbonates and "C-H" compounds = organic compounds.

An AI life-form could make good use of silicon: it's unreactivity with water means that a silicon transistor brain can exist anywhere in frozen space, using metals and electricity for the animal's functions, and avoiding water. A robotic species of life would more probably be made of silicone, so if some alien life forms land on earth, they will probably be transistor and metal electric beings rather than carbon based ones.

Wikipedia page.

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Does chromosome cross occur over male and female or vice versa?
My understanding is homologous chromosome pair, which means male and female chromosome inside the DNA. So if that's homologous how does male do with female? Does it flip over and change direction, that could not happen as male chromosome 1 (say) is indistinguishable from female?
And what about the XY chromosome in male,say?
I know some are pseudoautosomal, but most are normal sex chromosome nucleotides.
So what about them?

What do you mean by "male chromosome 1 (say)" ?

What are you meaning here about "chromosome inside the DNA"? I think you need clearly understand clearly more-basics of genetics. What is your age (so that I can get an idea of which class/grade/standards you read in)?

Are you asking about "is there any crossing-over between any portion of chromosomes X and Y of male humans?"

The question is unclear to me but hopefully that will help a little bit.

My understanding is homologous chromosome pair, which means male and female chromosome

There is no male and female chromosome. Chromosomes have no sex. In humans, to the exception of chromosome Y all chromosome can be found in individuals of any sex.
There are paternally inherited chromosomes and maternally inherited chromosomes though. As you said the maternally inherited chromosome is indistinguishable from the paternally inherited chromosome when comparing their sequence (they may well differ in terms of epigenetic changes).

chromosome inside the DNA.

A chromosome is not inside the DNA. DNA is the name of the very long molecule from which a chromosome is (mainly) made of. DNA can be organized in different forms one of which is into chromosomes (another one would be a plasmid for example). While it would still sound funny, it is more correct to talk about DNA inside a chromosome than talking about chromosome inside DNA.

So if that's homologous how does male do with female?

This is very unclear...do what? Why would the paternally inherited chromosome (assuming this is what you mean by male chromosome) do anything with the maternally inherited chromosome rather than the other way around? While it is clear from the what follows that you would like to talk about recombination, I don't get where you're heading.

does it flip over and change direction, that could not happen as male chromosome 1(say) is indistinguishable from female?

I don't get what kind of "flip" you are thinking about. You probably should have a look at the wikipedia article for cross-over.
In short, synapsis are formed during prophase I of meiosis and when segregation happen synapsis are resolved with a probability of $\frac{1}{2}$ of causing a recombination event. Synapsis occur as they allow matching pairs of homologous chromosomes together that will ensure their separation during anaphase 1. You should probably take some time to review the meaning of this paragraph.

And what about the XY chromosome in male,say?

Sorry, that's a bit unclear too.

I know some are pseudoautosomal, but most are normal sex chromosome nucleotides. So what about them?

Sounds like you misunderstand what a sex chromosome is and what pseudoautosomal mean.
In short, in humans, there is only one pair of sex chromosomes (XX or XY depending on the sex). The other 22 pairs of chromosomes are autosomes. There is no such thing as a pseudo-autosomal chromosome in humans but there is a pseudo-autosomal region on the Y-chromosome.
Most of the Y chromosome never recombine (while the X chromosome recombine in females only) as it is never present with another Y chromosome in the same cell. There is only a short sequence on top of the Y chromosome that recombines with the X chromosome, this region is called the pseudo-autosomal region. This region probably still exist to allow separation of X and Y chromosomes during anaphase I.

Please also note that you seem very focus on humans (without saying it and maybe without realizing it). The diversity of sex-determination is huge. You might want to have a look at Do males of all sexual species have Y chromosomes?

There is a difference between the processes of meioses and mitoses. Meiosis typically leads to 23 chromosomes in a new cell while mitoses typically leads to 46 chromosomes in a new cell. Because every normal human being must have 46 chromosomes, you need to get 23 from your father and 23 from your mother. Meiosis creates cells that are necessary for humans to procreate. Mitosis creates cells that help an individual grow.
Almost every cell in your body has its own 46 chromosomes. Red blood cells, for example, are cells that don't have chromosomes. When a cell has 23 chromosomes it is called a haploid cell, and when it has twice that much it's called a diploid cell.
Chromosomes are not specific to a gender. The sex chromosomes only confer gender depending on whether you get one copy of each of X and Y, or two copies of the X chromosome. So you could have a man passing 23 genes to his daughter and then the daughter passes some of those chromosomes ,after genetic recombination, to her son or daughter. It doesn't matter. The separation is more or less random.
During genetic recombination the homologous chromosomes cross-over by DNA strands being cut by biomolecule processes. The image of this process is called a Holliday junction. So they do flip over and change direction, but they are only strands (aka strings) of DNA.


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Plants with no chlorophyll
If chlorophyll or chloroplast is needed for the process of photosynthesis then how do non green plants with no chlorophyll get food

Welcome to Biolgy.Se. Most, if not all, plants without chlorophyll are parasitic plants.

Cuscuta, Rafflesia  etc? They are "green plants" in that sense they phylogenetically belong to the green plants. These parasitic plants hack  their food from their host.

You tagged this question [mushroom]. Mushrooms are not plants, they are fungi, and heterotrophs - they feed on decaying matter.

As @AlexDeLarge mentioned, all non-photosynthesizing plans are holoparasites because they lack the mechanisms for autotrophy. Although it is worth mentioning that it is not always chlorophyll that is doing the photosynthesis in all plants, and that even "non-green" plants can still photosynthesize (see note below).
There are generally two classifications of holoparasitic plants: those that require fungal mycorrhizal hosts called myco-heterotrophs and those that require other plants as hosts. Some examples of non-photosynthesizing myco-heterotrophic plants include those in the genus Monotropa. Examples of plant-specific holoparasitic plants include those in the genus Boschniakia.
In both cases, the parasite is partitioning nutrients directly from its host plant through a specialized root called the haustorium that penetrates the host's roots or hyphae, essentially bypassing the need for its own photosynthetic production. Technically, those parasites that attack other plants are still relying on photosynthesis (of the host), although indirectly.
This is a good review paper on some of these species:
Leake JR. 1994. The biology of myco-heterotrophic ('saprophytic') plants. New Phytologist 127(2): 171-216.

Note: For instance, when deciduous trees turn yellow and red in the fall, they are relying on the carotenoids, xanthophyll and carotene. So, while the plant is not utilizing chlorophyll to absorb light, the carotenoid compounds are incapable of transferring light energy directly to the photosynthesis pathway themselves, and thus still require chlorophyll as a pass-thorough.


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Digestion Enzymes in Carbohydrate Metabolism?
Digestion of carbohydrates is ending in small intestine with mainly disaccharidases. Isomaltose is broken down to 2 molecules of glucose by the enzyme called alpha dextrinase(oligo-1,6 glucosidase or isomaltase) which hydrloyze 1,6 linkage of isomaltose. In the case of glycogen metabolism there is debranching enzymes that are transferase and alpha 1,6 glucosidase. According to this informations can we say that alpha dextrinase (isomaltase) and alpha 1,6glucosidase are the same enzyme ?

The answer depends on what you mean by "same enzyme". Some people say "same enzyme" when they mean "same enzymatic activity" (as opposed to same protein). For example, the EC system often is said to classify enzymes, when it really classifies reactions. It's confusing :-/

1,6-glucosidases are a class of enzymes and not just one enzyme. It does not mean that all the members of this class are the same enzymes. They catalyse the same kind of reactions but their properties and substrate specificities differ. Check BRENDA for details.
BTW, dextrin-1,6-glucosidase is a synonym for amylo-alpha-1,6-glucosidase. Other 1,6-glucosidases are different enzymes with different EC numbers.


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Left Ventricle vs. Right Ventricle size in different Animals
Why are the right ventricles in chicken hearts significantly smaller than the left ventricles, whereas in cows the two ventricles are of roughly equal size.

The question is interesting +1. Can you please add a reference and/or a figure showing that they differ? If you happen to know whether these traits are shared among all birds and all mammals respectively, that'd be great to state it.

Of all the pictures I've found googling, the ventricle sizes of humans, chickens and cows appear to be: left ventricle bigger than right ventricle.. ? add a reference please.

I don't know where you got your information, but it's not correct. The bovine (cow) heart is very much like the human heart in that the right ventricle is significantly smaller than the left. It's important to note that the difference is in muscle mass, not volume of blood each ventricle holds. More muscle is needed to pump blood through the body than through the lungs.


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can animals override instinct?
I would say that one of features that separates human consciousness from animal is the ability override instinctive behavior. A human infant will jerk its hand away from a hot surface. An older child you can communicate with at the basic level may not although experimenting with this is no doubt unethical. An adult can consciously overcome this instinct.
Are there experiments testing this idea with animals? In animals that science claims are self-aware, it would be interesting to know if they can overcome the automatic reaction to negative instincts.
The first step would possibly be to see if one negative instinct can be overcome in the presence of another. Like will a really hungry chimp walk across a painfully hot surface to reach food? This seems likely but I am unaware of any such testing.
A more interesting example will would be cases of real animal altruism. Science is quick to tout what some call animal altruism as hardcoded and evolving genetically e.g. lions defending prides, mothers defending young. And I agree this can be hardcoded and genetic since I am not aware of lions NOT defending prides or mothers leaving young to predators.
However, these links show cases of what some may call true animal altruism. Dogs braving the danger of the highway to help other animals.
https://www.quora.com/Are-animals-capable-of-selflessness-Do-they-have-the-desire-to-help-others
Leopardess adopts baby baboon
https://www.youtube.com/watch?v=j9DOxH5RyWQ

The trouble is our motives don't have labels on them, "instinct", "altruism" etc. Different parts of the brain produce different responses to the same stimuli and it is then the job of the cerebral cortex to calculate which of the competing options to follow, some of these responses are "hard-wired" others not, but there is no single "instinct" which our conciousness, or that of other animals can, "overcome", just a range of competing options almost all of which are processed by the cerebral cortex in every creature that has one.

How do I move a question? Just repost?

@Isaacson You can hold your hand to a hot surface if you wanted. And the videos are indications of animals overcoming instincts. So its very likely consciousness can overcome hardwiring.

@AnoopAlex This is a common misconception that causes few problems in animal studies, but massive problems in human ethics. There is no evidence whatsoever that they are "overcoming instincts", there are just a range of potential responses to the various stimuli in the scenario and the animals are choosing one of them using either learned or novel patterns in the cortex. There is no way of distinguishing "hard-wiring" from "conciousness" in these types of actions, all of them go through the cerebral cortex to be decided on.

Ever housetrain a puppy?  Or consider that a horse's instincts are to flee from perceived dangers, including four-legged wolflike predators, yet with training you can ride your horse around all sorts of scary things, and take your dogs along :-)

@jamesqf: I realize animals can learn percieved dangers are not actual dangers but I was thinking more along the lines of when the threat is real. When a puppy or horse learns the people he sees wont harm him, he no longer fears. But the example I gave of burning hot surface to reach food presents a real threat. I realize there are ethical issues here so am also curious if there have been examples observed in nature.

you may want to look at the vast number of studies done on rats with electric shocks, you would be amazed what behavioral alterations are possible. https://link.springer.com/content/pdf/10.3758/BF03209595.pdf the branch or science you are looking for is called ethology.

What makes you think that altruism isn't instinctual? Certainly certain forms of it are, parents caring for their offspring for example. The examples you mention may be examples of an instinctual behavior applied to a non-typical subject.

Instinct and learning drive almost all behavior in the animal kindgom. We are only considering animals with nervous systems in this discussion, but non-neural learning has been documented.
All animals have instinct. Instincts manifest themselves as desires that elicit "automatic" behaviors. A good demonstration of instinct is to skip a meal and then put yourself in the presence of your favorite snack. You don't have to think "I would like to eat now" before reaching for the bag, it happens "automatically". That is one of many instincts found in Homo Sapiens.
Instincts are encoded genetically and in terms of speciation, population size and generation times insects are more evolved than vertebrates. We would expect them to have instincts just as complex (if not more so) than mammals despite their far simpler brains.
Learning is found in many species, including in jellyfish, earthworms, snails, and many insects. The desire to learn in my opinion is largely instinctual as can be seen by the enthusiasm of a young child. If learning is instinctual, is learning to override instinct actually overriding instinct?
The very smartest animal species can occasionally exhibit "creativity" which goes beyond instinct and learning and can in fact fight against instinct. For example, Orcas beach hunt sea lions which requires overcoming their powerful instinct not to beach. The calves learn this from the mothers (often by doing "dry runs" with no prey within reach), but someone had to come up with this idea in the first place. Whoever that Orca was had to fight their own instinct without resorting to learned behavior.
Humans only have half the cortical neuron count of Orcas but are still above most Cetaceans and are the top non-Cetacean at over twice Chimpanzees and Elephants. Even at such a "lofty" spot in the animal kingdom, truly creative behavior is rare. But imitation is so good that these rare innovations spread around the world and became fixed in collective memory. Eventually, the accumulation of all these inventions led to modern technology (opposable thumbs also helped). There was only one Bitcoin but there are now >12,000 copycats.
Even though no animal species (human or otherwise) commonly breaks out of both instinctual and learnt behaviors, it happens in the smartest species occasionally and can have a big effect given enough time.


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What is the number of species known through paleontological evidence?
Essentially, this question could also be asked: how many species do all of the paleontological specimens in collections (or collections records) represent?
I recognize that species is a temporal concept when thinking about differentiation across time; but, natural history collection catalog specimens to species level, so there must be a reasonable basis to make this distinction.
Also, note that I'm not exactly interested in inferred species (i.e. if we have records of species A and species B, we might infer a last common ancestor, species C).

Very interesting question.
I remember reading about it in one of Stephen Jay Gould's great books (The Panda's Thumb? The Flamingo's Smile? Wonderful Life: The Burgess Shale and the Nature of History? Dinosaur in a Haystack? Probably in one of these).
He wrote exactly about this question, and the effort made by teams from many different countries to get to an "approximate" result. What really impressed me at the time (fifteen years ago) is that when Chinese scientists were invited to add material for a second analysis, the number of known fossil species doubled!
Please, if anyone find the exact source of this, I'll be glad to read it!
But maybe you can get an idea by looking at the number of fossil species for certain groups, and comparing with the number of estimated/known extant species. Keep in mind the rates of fossilization for each group, and also the fact that Nematoda and Acari might be the most overlooked groups in terms of species number (both seem to parasitize animals through most of the Animal Kingdom).

Short answer no one knows exactly, a single database of fossils does not exist. there are lots of specialized ones, for say pollen or dinosaurs, but not one complte one. each museum maintains their own. There are estimates based on type specimen publications but they tend to overemphasize some groups like vertebrates and under represent less... charismatic groups.  Accroding to this study http://www.pnas.org/content/99/6/3706.full
There are at least 280,000 named invertibrate species, (infered species are not given species names) hopefully that gets you started. This is a recognized problem and there is a lot of debate about how to fix it.


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Why is glycine considered a nonpolar amino acid but a polar molecule?
Glycine has a dipole moment, so why is it considered a nonpolar amino acid when discussing its occurrence in proteins?
Also, is the backbone of a protein nonpolar?

@AlwaysConfused please read the text that appears when you start to write a new comment - "Use comments to ask for more information or suggest improvements. Avoid answering questions in comments." You have been doing this a lot lately. Please stop.

@MattDMo On many cases users (including moderators) put brief/ simplified answer in comment. Such as this comment by you ( permalink  ) tells "Of course they do. If you take away a substance that is killing certain cells, of course the number of those cells will increase. I don't understand how that has anything to do with HIV infection and CD4 levels. –" ; which is an answer to a question.

As well, when it is not possible to write immediately an elaborate answer by an user, a small hint to the answer could greatly help the asker.

@AlwaysConfused That's fine for a short hint but your comments just get too long, spanning two or three comment boxes. If you have time for such a long comment then better give an answer.

@WYSIWYG Oh that second comment (note please that I used a bracket) was just a note to avoid a confusion since glycine donot have an '-R' or alkyl group in true sense. So far i could remember that H is not considered as an alkyl group; so often at structures in  in organic reactions sometimes wrote as -R or -H. It was just to mention; for glycine the side chain is also H.

@AlwaysConfused Please take heed of MattDMo's comment. StackExchange has a particular model for particular reasons. If you answer in a comment you break this model. The question is marked as unanswered and there is no way for anyone to up- or down-vote your comment/answer so that other readers can get a feel of whether the answer is likely to be correct. I feel very strongly about this and have made my views clear in an answer to http://meta.english.stackexchange.com/questions/2653/why-are-answers-being-posted-in-the-comments-on-the-question/8171#8171

@David and all other moderators Okay i'll try to follow to maintain structure. However, still, i had no intention to put answer as comment... and it was indeed a 'shor hint' but i unthoughtfully used >1 comments. As well since a valid answer came in; so I'm deleting that 2 comments under dispute. I'm sorry for if my comment any trouble with SE structure. Is it now okay?

@David Thank you for that meta post link. however my usage of comments were like this answer  to that same post.

I have altered your question by adding in my assumption that glycine is only considered non-polar in the context of proteins. This allows me to answer it more clearly.

I've started a discussion on this commenting-issue (short-hint as comment) in SE meta seeking clarification . However I'm respectful to SE structure so anyone dont mind

The first part of your question illustrates a common confusion of beginners between the physiochemical properties of free amino acids in solution, and the properties of that part of an amino acid that remains after it has participated in a condensation reaction to form part of a polypeptide. They are different. (It was for that reason that I modified the question to make it clear that the ‘consideration’ of glycine as nonpolar applies to it in its protein context.)
I have prepared a diagram to clarify.

As can be seen on line 1, all free amino acids at physiological pH are charged because of the pKa of the  α-amino and α-carboxyl groups (proline, as an imino acid is the exception). The chemical features common to all amino acids are shown in blue, for the second amino acid, and the unique feature — wherein amino acids differ — is shown in red.
To show amino acid 2 in the context of a polypeptide chain, I have condensed it with two other amino acids (1 and 3) to produce a tripeptide (line 3). (This is the situation most amino acids in a long polypeptide chain will be in, as there are only two that will be at the ends.)
You can see from the colouring that what is left of the amino acid in the protein — the amino acid residue — has lost the charges of the α-amino and α-carboxyl groups, which have become parts of peptide bonds. (A molecule of water is removed in a condensation.)
The properties that a particular amino acid endows to a protein are those of the ‘R-group’— R2 in the diagram. In the case of glycine, R is H, so that in the context of proteins we regard glycine as a non-polar amino acid (The C-H bond has a negligible dipole.)
Don’t confuse R with residue. It is a side-chain, designated using a common chemical abbreviation.

The second question was “is the backbone of the macromolecule nonpolar?”.
No. The backbone of a protein has partial charges on the oxygen and nitrogen atoms of the peptide bond, as shown below. This is because it has a partial double-bonded character. These partially charged atoms can (and frequently do) form hydgrogen bonds, either with another part of the backbone (secondary structure such as α-helix or β-sheet) or with polar side-chains.

I'm just converting @alwaysconfused's comment into answer (with a bit of more details).
Yes, glycine does have a dipole moment (15.7 D), but when it comes to biochemistry, then the dipole moment on the side chain is considered. Since the structure of glycine is:

H2N - CH2 - COOH   <--->   H3N+ - CH2 - COO-

So the side chain is:

-H-

which has, obviously, 0 dipole moment. Thus glycine, though polar, is considered non-polar in protein structures.

Source

Glycine has no side chains.
In a neutral solution; not forming a peptide bond, glycine has the following the following structure

H3N+ - CH2 - COO-

which is polar because of the -ve and +ve charge.
Once it forms a peptide bond with another aminoacids (aa), it becomes in the following form:

aa-----H2N - CH2 - CO ------aa

As you can see, it doesn't have any charges on it since the amino group and the carboxylic acid group formed bonds with another 2 amino acids.

I just upvoted your answer, but there is a mistake: every AA has a dude chain. The side chain of glycine, btw, is the simplest possible in chemistry: H.

@David: Pentavalent carbon corrected.


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What is the essential benefit of center-surround organization of retinal ganglion cells?
I am trying to understand the significance of the overlapping on-center off-surround and off-center on-surround organization of the retinal ganglion cells, also called center-surround organization. What is the advantage of such an organization from the point of view of vision?
To highlight the point of the question, wouldn't it be computationally and organizationally easier to simply have the retinal ganglion cells arranged in a non-overlapping fashion, and without the center-surround ability? Then there would be a straightforward correspondence between the incoming spots of light and the firing of adjacent neurons in the optic nerve.

EDIT:
I just realized this question is two-fold in nature.

Why the center surround organization?
Why is there an overlap?

I think the answer by Bryan deals well with the first question, but doesn't quite touch upon the reason for the high degree of overlap.
I admit the question is worded in an slightly ambiguous way.

You are assuming that light comes in perfectly in spots, and that the purpose of vision is to replicate a "bitmap" of the incoming light. This would actually be very inefficient computationally.
In reality, vision relies on detecting salient features. Imagine a simple scene, maybe like this one:

Most of the white space of the wall is pretty uninteresting: you have no need to really process that information besides knowing it's one solid area. What is interesting in the image, if you are trying to understand the space your are occupying, is to see the edge between the floor and the wall. In fact, that's what really tells you this is a wall and a floor: if you only had the upper 1/4 of the image, you would just have a white box: you wouldn't know if this is a floor, a wall, a ceiling, the paint on someones car. The edge between the floor and wall gives you the needed context.
Lets think about how center-surround organization would respond to this image. In the whole blank white space, white light is hitting both the center and the surround: these cancel and there is little response. However, imagine what happens for an on-center off-surround cell right at the edge with the floor. That cell is getting white at its on-center, but only on about half of it's off-surround: the other half of the off-surround instead gets the darker wood floor. This cell would therefore respond to the imbalance in the average surround vs average center!
You can then combine many of this circular receptive fields to detect straight edges, like this:

From https://grey.colorado.edu/CompCogNeuro/index.php/CCNBook/Perception
Note: the LGN (thalamus) receptive fields are very similar to the retinal ganglion cell receptive fields. In V1, primary visual cortex, these receptive fields are added together to make "simple cells" which respond to edges.
I think this picture comes closest to answering your question about how overlapping receptive fields can be useful.
This image from the Wikipedia page on receptive fields shows what you get when you put a scene through a center-surround filter: note how all the edges are emphasized!
Other benefits: this type of detector works well over a range of light levels, for example different steps of gray will appear the same, even though the pixel intensity varies a lot. This way, you get similar responses to edges in both a dark and light room. These detectors also help to sharpen images. Note that computer vision uses some of these same strategies as well!
What if you wanted to detect spots of dark instead of spots of light? We often think of eyes as being "light detectors" but they are just as appropriately described as "dark detectors." Imagine you are a rodent looking up at the sky, for example: an important, salient stimulus for you might be a dark spot where a hawk is blocking light from the sky. Therefore, having an off-center, on-surround type of cell is just as useful as the opposite (and indeed, the retina contains both types of retinal ganglion cells).

It is interesting that you mentioned computational inefficiency in your second sentence. Do you think the lack of center-surround org. is the reason why deep neural nets take so many training samples before they work well?

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


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Why are there no Nissl bodies in the axon?
What could be the significance of not having Nissl bodies (endoplasmic reticulum) in the axon hillock (a part of the cyton) and axon? Does it have something to do with the processing of action potentials?
What prevents Nissl bodies from entering the axon hillock even though they can enter dendrites (which are much narrower)?

Can you add more details? Otherwise it looks-like homework question.

Looks much better. Nominated for reopening.

Molecularly, Nissl bodies are the densely clustered ribosomes on the ER. The basophilia is due to the RNA in the ribosomes. The question you have raised is a very significant one. For perspective, I quote a book Fundamental Neuroscience, 2002 (2002 is pretty old for neuroscience!)

The hillock is a region where materials either are committed to the axon (cytoskeletal elements, synaptic vesicle precursors, mitochondria, etc.) or are excluded from the axon (RER and free polysomes, dendritic microtubule-associated proteins). The molecular basis for this sorting is not understood. Cytoplasm in the axon hillock does not appear to contain a physical "sizing" barrier (like a filter) because large organelles such as mitochondria readily enter the axon, whereas only a small number of essentially excluded structures such as polysomes are occasionally seen only in the initial segment of the axon and not in the axon proper.

But a recent paper GG Farias et al. 2015, proposed the presence of a special area in the axon hillock known as the Pre Axonal Exclusion Zone (PAEZ) that tries to explain this polarized sorting by differential binding of microtubule motors.

Although the paper mainly talks of the sorting of axonal and somatodendritic vesicles as seen in the picture, they also seem to apply for the RER which actually are the basis for Nissl's granules.

This structure excludes not only somatodendritic vesicles but also larger organelles, such as the Golgi complex and the rough ER, in effect constituting the cytoplasmic boundary for the somatodendritic and axonal domains..... The exclusion of the rough ER and Golgi complex, in addition to somatodendritic vesicles, at the PAEZ suggests that a common restriction mechanism may operate for all of these organelles.

Well, as you might have understood by now, it's not a matter of the size of the axon/ dendrite since same sized vesicles are being diverted in either direction and as previously mentioned, even mitochondria enter the axon.

Logically I would say that since there is more entry and exit of substances at axon hillock , a large organelle like rer would hinder the transportation by its presence at there, also er too needs to be in proximity with the nucleus for its activity , therefor it cannot enter axon and far away into dendrites.


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How large is the immune repetoire and at what age does it finalize?
There seems to be a large disconnect between the Wikipedia's article on the immune effector repetoire and Janeway's Immunobiology 9th Edition, a standard textbook widely used to teach immunology to pre-meds. In the Wikipedia it puts the size of the repetoire at 100,000 unique receptors, but in Janeways it says the repetoire has typically 10^8 or between 100 million and 1 billion receptors. Also, in Janeways it implies that the repetoire is largely finalized at some point, although it gives no specific age, but in the Wikpedia article it claims that new T cells are constantly developed by the body throughout a person's lifetime.
How many unique T-cell receptors typically circulate in the body at one time and at what age is the immune repetoire largely decided (if any)?


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Dorsal root fibres
How can dorsal root fibres be unmylinated though are responsible for conduction of pain and temperature? How is their conduction so fast without even being myelinated? Is presence of only one axon( indicating that a single axon travels from skin to dorsal root ganglion) enough for such fast conduction?


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Will sperm cells exhibit chemotaxis towards sucrose?
I was wondering if sperm cells will exhibit chemotaxis towards sucrose? One of my friends told me that sperm cells die in presence of salts. So I guess sperms will move away from salt. Can someone give me any reference related to this area.

UPDATE (Answer for why sucrose?):
So I should have made things more clear. I was thinking to do an experiment by taking some sperm cells and its effects on sugar and salt and then to see it under a foldscope microscope. Since I am not a biologist, I wanted some guidance. The common available substances which came to my mind was sugar and salt.

If you google "sperm chemotaxis sucrose" you learn some things of interest. Notably, wikipedia's article on sperm chemotaxis indicates that the important chemoattractants for sperm (the things that attract sperm via chemotaxis) are various signaling molecules given off the by the egg.
It is not clear why you would necessarily think that sucrose would attract sperm or that salt would repel them. In the first case (sucrose), it is not obvious why sperm would expect to see sucrose. If I remember correctly, sucrose is actually pretty rare in animal physiology except as an energy source in plants that animals eat; and sucrose is largely broken down into monosaccharides before it even leaves the small intestine, so it's not like it's circulating in the body. For instance, a lab protocol for studying animal sperm chemotaxis suggests adding sucrose as a densifying agent that doesn't interfere with chemotaxis, suggesting that sperm are pretty independent of sucrose. In the second case (salt), it is not obvious that sperm would necessarily avoid the things that kill them. Those things may be correlated with doing their job! Most sperm cells are expected to die in the human reproductive strategy.
In plain terms: there are huge numbers of sperm which are competing really hard with each other to find and fertilize an egg, not to find sucrose or to avoid salt. The chemotaxis that sperm exhibit will tend to help them accomplish this goal. So it seems (according to wikipedia) that they follow the signals that say 'egg', not the ones that say 'sugar'.
Update:
Sorry, only just saw update on Q. Thanks for the clarification- sounds like fun! I've been curious about the foldscopes.
If what you want is to do an experiment, then I think you've actually got a great start with knowing first that salt interferes with their motility. That is a control experiment, e.g. the very first thing you should do, to make sure that the world works the way other people say it should. (First rule of experimental science: never trust anyone!). Look up a protocol which suggests a sperm-inhibitory concentration of salt (ideally kosher salt, not table salt which has a bunch of other stuff like iodine in it). Put sperm in that concentration of salt and then also in a medium where they should show chemotaxis (the protocol I linked to could be helpful here). See if you can reproduce the salt inhibition, ideally in a medium that is otherwise identical to the medium that allows chemotaxis.
Next, try other stuff. Unfortunately, chemoattractants are probably proteins/small molecules you can't buy at the supermarket. But you could try to get creative. I can't ethically recommend that you try to find a human source, because that gets weird pretty quick, though it is the obvious suggestion (I assume you are talking about human sperm). Potentially there is an animal source for such things which isn't too expensive.
However, you could say to hell with chemoattractants and chemotaxis, and try to just understand sperm motility. You could try other osmotic shocks, with simple cheap chemicals like glycine. It looks like there is some literature that calcium ions affect sperm motility. Or you could play with pH, using vinegar or lye, or temperature. I bet that all of those affect sperm motility (probably for the worse). Or you could try the effects of various weird hippie herbs from the health food store. It sounds like you are just looking for an easy, fun experiment, and if that's your goal then I suggest you try a bunch of things and see what happens. That way you're more likely to find something interesting.
If what you want is a more elaborate experiment, then I think it is worth your time to sit down and try to read up on how sperm work, and then design an experiment that really clearly tests a hypothesis. I am not an expert here, but the Yoshida article I link to looks like it has a good literature review.
Hope that helps.

Please see the update for why sucrose?


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Is phosphofrucrokinase1 PFK1 found in the liver?
I am trying to understand glycolysis control. One thing I am stuck on is whether there is PFK1 in the liver, or only PFK2.
Edit: As far as I am aware, there is no pfk2 in muscle cells, only pfk1. This is entirely under allosteric control of ATP/AMP ratio to control the rate of glycolysis compared with gluconeogenesis. In the liver there is pfk2 which ensures that there is hormonal control of the rate of glycolysis. However is there also pfk1 so that there is a rate of glycolysis sufficient for liver cells to survive, irrespective of the hormone signals?

What research have you done on your own to try and answer this question? A simple Google search using the title of your question will quickly answer it. Homework questions and questions that show little or no prior research effort are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy.

I have read quite a lot about this, but Google was not answering my specific question. I will edit my question with the research I have done so far and the specific point of my confusion.

If you read the Wikipedia article on PFK1 that came up at the very top of the Google search I mentioned previously, the very first paragraph in the body of the article answers your question.

PFK2 (PFKFB2) doesn't appear to be present in the liver. The two sources I have used agree that PFK1 (PFKL) is present in the liver. They diverge regarding the levels of expression of PFKL.
This is the expression of the three 6-phosphofructo-1-kinase and one 6-phosphofructo-1-kinase genes according to the Human proteome map (mass spectrometry).

I can't see a huge dynamic range across the proteins in the liver, although the liver specfic gene (PFKL) is the 'winner' there.
The Human protein atlas (immunohistochemistry) is also a useful source for information and it provides a very different answer. Using immunohistochemistry it shows robust signal for PFKL but not for PFKFB2 in the liver.


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Are Y spermatocytes faster but less resilient than X spermatocytes?
I have heard somewhere (but did not find any suitable reference) that spermatocytes carrying a Y chromosome are usually faster but less resistant than those carrying an X chromosome.
Is this true? If so, which are the actual reasons?
There is a remote but theoretically plausible explanation indeed for the difference in speed, as the Y chromosome is much smaller and lighter and thus would make the Y spermatocytes less heavy than the X spermatocytes. Possibly, the larger number of genes on the X chromosome (missing in Y spermatocytes) could imply that they can still have some incremental translational activity.

Spermatocytes only carry one sex chromosome - either $X$ or $Y$. They are haploid, not diploid. Are you asking why $Y$ spermatocytes "swim" faster than $X$ ones? Please add a citation to your claim that one is faster than the other.

@MattDMo Sorry for the typo, indeed I meant X vs Y spermatocytes. I have corrected the typo. I did not find any suitable reference for this, so it might just be and urban legend.

If you can show it is a suitable claim, then the question would be nicely suited for Skeptics.SE. (I am not saying it is off-topic here).

@Remi.b I am expanding it now. There is theoretical basis indeed (see edited entry).

@fileunderwater fantastic answer to  Why do we have more male infant born? addresses your question.

As a side note, the "lighter" argument is not particularly convincing for swimming, since sperm swimming isn't limited by mass, but by viscous resistance (see "Life at low Reynolds numbers").

I searched and found a letter which clearly mentions about misinformation that sperm with Y chromosome swims faster than X carrying sperms.I think this link may help https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1440662/
The letter says "The widely held idea that spermatozoa bearing the Y chromosome (Y sperm) swim faster than those bearing the X chromosome (X sperm) seems to have originated from Shettles's work in 1960, using phase-contrast microscopy.He claimed to have observed, “two distinct populations” of spermatozoa. After attempting to count the chromosomes, he concluded that the smaller heads contain the Y and the larger the X chromosome. There were no intermediate types.
The following year he reiterated these findings, adding that smaller headed spermatozoa can migrate more rapidly and fertilize the egg more often in the distal part of the tube.
Reading Shettles's reports in Nature and other peer-reviewed journals, many researchers thereafter believed that Y sperm swims faster than X sperm. The finding particularly influenced research on sperm separation.
Although several attempts have been made to correct this impression, it was not until the development of computer-assisted sperm analysis (CASA) that reliable observations could be made. So far, researchers have found no morphological differences between human X sperm and Y sperm.4 Neither mature sperm nor their precursors possess significant morphological differences between X and Y genotypes, and Y bull sperm does not swim faster than X sperm."
You can see the reference and read more
1. Shettles LB. Nuclear morphology of human spermatozoa. Nature 1960;186: 648-9. [PubMed]
2. Shettles LB. After office hours: conception and birth sex ratios: a review. Obstet Gynec 1961;18: 122-30.
3. Moruzzi JF, Wyrobek AJ, Mayall BH, Gledhill BL. Quantification and classification of human sperm morphology by computer-assisted image analysis. Fertil Steril 1988; 50: 142-52. [PubMed]
4. Hossain AM, Barik S, Kulkarni PM. Lack of significant morphological differences between human X and Y spermatozoa and their precursor cells (spermatids) exposed to different prehybridization treatments. J Androl 2001; 22: 119-23. [PubMed]
5. Penfold LM, Holt C, Holt WV, Welch DG, Cran DG, Johnson LA. Comparative motility of X and Y chromosome-bearing bovine sperm separated on the basis of DNA content by flow sorting. Mol Reprod Dev 1998;50: 323-7. [PubMed]
Hope this help!


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CNS memory structure
I'm new in biology. could you please let me know if the following 2 assumptions are correct
A nerve cell in the CNS along with its loop back neurons (Collaterals) is a memory unit. It will trigger per given spikes pattern (example – from the PNS). The said pattern should be “close enough” to enable the memory unit to resonate.
A memory unit is a cyclic sub-graph with its “root neuron”. An inhibitory neuron eliminates multi resonance of the memory unit.

These things could be correct in a very specific implementation of biologically-inspired neurons for an artificial neural network, and might be reasonable assumptions to taking a graph-theory approach to understanding biological neural networks, but they don't capture the known subtleties in our actual biological understanding of how brain networks work.

For example, "memories" as abstract concepts are held in populations, not single cells, though single cells can have "some memory" - pattern completion can be performed by networks, as well. Neurons may resonate in some contexts but resonance is not necessary for recall or encoding of memories. Inhibition has many roles: it can prevent unwanted resonance (for example, seizures), help discriminate similar stimuli, control gain, suppress expected outcomes to highly unexpected events, etc.

Thanks Bryan. Let me ask you, given arbitrary episode how does the brain determine its start & end ? or when does brain conclude "I do not know" / "i do not remember" / "I do not recognize" ?

We don't know :) There are many studies that use psychophysical tasks to begin to answer some of these questions. Some have shown that estimates of confidence can be derived from activity in the prefrontal cortex - answers like "I don't know" require a bit of metacognition so it is somewhat difficult to study. It's actually quite a big deal to be able to recognize when you know and don't know, and one could imagine a fully functional animal/robot without those abilities.

i assume that the answer to this question may address my question  (though it's chicken  - egg  issue)

The concepts you raise in your question are not founded in neurobiology. We do not know what the biological correlates of a "unit of memory" are in the central nervous system.
Although oscillations are widespread in the brain, the relationship between oscillations and memory storage and recall is a subject of active research. The way you state this process in your question is not justified by any experimental evidence that I am aware of.
Memories do not have a "root neuron" — as I wrote above, we do not know how memories relate to neurons. Inhibitory neurons simply provide inhibitory input currents to their post-synaptic targets. Any relationship with "resonance" or oscillations relies on explicit assumptions about emergent network properties, and these are currently unfounded.


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The relationship between the shape of the bacterial DNA and the blocking of replication machinery
I was reading a course about tolemers when I arrived to this phrase :

[...] The ends of a linear DNA molecule cannot be replicated by the cellular replication machinery (which may be one reason why bacterial DNA molecules are circular).

I want to know what is the relationship between the circular shape of the bacterial DNA and the blocking of replication machinery ?

What research have you done to answer this yourself? Please read the Wikipedia articles on telomeres and telomerase to understand what happens with linear chromosomes. You should also read about DNA replication in both prokaryotes and eukaryotes. Homework questions are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy.

It’s not a homework question, it’s a question out of curiosity, I’m trying to understand an idea proposed by Liz Parrish to reverse aging by adding some portions of telomers to the human DNA, so I want to know, how the shape of the bacterial DNA makes the bacteria immortal (if I can say so).

Prior research is still required, regardless of whether the question is an academic assignment or not. Additionally, please [edit] your question to add and expand upon what you just put in your comment, as it makes the scope of your question completely different than what you originally asked. Remember, you need to include as much information as possible in order to get the answer you're looking for. Include what research you have done, what you understand so far, and where exactly you're stuck.

This has been covered elsewhere (I highly recommend this page ) but it basically has to do with the priming of the strands and the fact that all polymerases work from the 5' prime to the the 3'. I made a quick schematic to illustrate (the explanation is below):

The priming is done with RNA during DNA replication in the cell, unlike PCR where you use DNA oligo's to prime. This RNA-DNA is called the Ozakazi fragments. After replication RNAse H will remove these primers leaving only DNA's and gaps. In the middle of the sequence the gaps can be filled in by the normal repair machinery but at the ends there is no 3' terminus to fill in the gaps. That is where the telomerase comes in and fill these gaps with a fixed sequence (also based on an RNA template but that is going into details).
If you have a circular chromosome there is always a 3' to complete the gap.


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Bending your little finger without bending ring finger
It is possible to bend each finger without bending any other, except one for most people. It is more difficult for the ring finger, but when I try to bend my little finger independently my ring finger bends as well. I don't know if this is because of the muscle or  bone configuration, but I'm interested in the answer.

Is it possible to bend the little finger independently, and if so why is it so hard to do so?

I can bend all fingers individually and keep all other fingers straight at the same time. So... practice more. :-)

@AnoE lucky! I certainly can't

Yeah, I don't deny that - I just gave you an exception to the rule you assumed in your first sentence, "It is possible to bend each finger without bending any other, except one.". ;) To help you feel better, it requires quite some effort to do this kind of bending - the other fingers do want to come along unless I tell them in pretty clear terms that they shouldn't.

@Anoe edited to 'most people'. You're obviously an exception :P

Cheers for making me feel exceptional!

We just ran around our school campus surveying people about this out of interest and found that 20/47 (42.6%) can move independently. So in the minority, yes, rare, no! @AnoE

@Sirens wow, I had no idea so many could! I guess that may depend on for instance if it was like a musical school, and they’ve played piano, or perhaps at a certain age it gets easier. Very interesting though!

Oh, also, we did ask people who could bend if they played piano and only two who could bend said they could. One who played for six years but couldn’t was also very embarrassed

This does not have to be the case always, For example if you are a pianist you need all your finger to work independently.
OK, So coming to the main question.
In simple words, They are all interconnected. See the image [Source: Google Images]

They share flexor tendons (The flexor tendons allow you to bend your fingers) , If you try to move one, other is objected to come along.
Yes it is possible, As I mentioned before if you are a pianist, you don't have much choice. It is possible by little bit training.

I can move and bend them individually but if I try to take any one (of above 2) finger up to palm I fail. Does pianists can move that individual fingers up to palm?  or they too face some degree of  this connection?

@AlwaysConfused, it is like other areas where you can be more or less flexible (like doing the splits or whatever). I can bring all fingertips to the palm individually, but I also stretch my hands/lower arms etc. in all kinds of ways due to several kinds of sports where that is necessary.

The image that you have posted is the extensor group of muscles...change the image to the one showing the flexor group

Do you have a references that pianists can actually make their pinky and ring finger move 100% independently? I play piano and moving my pinky does influence my ring finger, but it is not at all an issue since they are independent enough. Playing the piano is essentially the same as typing on a computer keyboard, which all of us apparently can do fine, even with our pinky fingers.

To follow up on @biogirl's comment, an image like https://upload.wikimedia.org/wikipedia/commons/thumb/d/d1/Wrist_and_hand_deeper_palmar_dissection-en.svg/1000px-Wrist_and_hand_deeper_palmar_dissection-en.svg.png would also be clearer and easier to see!

To shed some light on why this is happening in the first place, it may be helpful to understand the innervation of the muscles on these fingers.
There are two nerves that innervate the little finger, both branches of the superficial ulnar nerve. One of them is exclusive to the little finger, but the other (the common palmar digital nerve) actually branches again and innervates both sides of the gap between your little finger and ring finger. This explains why contracting your little finger muscles causes some (but not complete) contraction of your ring finger.
These connections can be modified and trained with practice, like many other movements we can improve with practice.

Iannotti, Joseph P, and Parker, Richard. Netter Green Book Collection : The Netter Collection of Medical Illustrations: Musculoskeletal System, Volume 6, Part I - Upper Limb, Volume Vol. 6 : Musculoskeletal System, Volume 6, Part I - Upper Limb (2). Saint Louis, US: Saunders, 2012. ProQuest ebrary. Web. 29 November 2016.


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I am not understanding how water passes through root hair cells
Why do people say that water moves into the cell because the water concentration of the cell sap is low ? the cell sap is surrounded by a membrane so if any water moves into the cell it must be because the concentration of water in the cytoplasm is lower than the surroundings. I am thinking that water from the cytoplasm moves into the cell sap solution and as a result , the concentration of water in the cytoplasm decreases so water moves in from the surroundings.

Maybe people use a bad shortcut of what https://en.wikipedia.org/wiki/Osmosis is?

Is ytour question: "What is osmosis?"

though the situation is similar is same as osmosis in jars; Upvoted and watchlisted. Because one popular explanation for why "osmosis is sort of diffusion" tells; the "concentration of water" in an aq. solution of something; is lesser than concentration of "water" in pure water! because pure water is 100% water, but an aq. soln of something is not 100% water. So on presence of membrane; pure water (high conc of water) diffuse into soln (low water). But I couldn't accept it anymore when I came to know that, adding little salt to water make it contract (contd)...

...(contd)... link so the concentration of water (moles per liter) actually increased still water would go to the salt side from pure-water side. It became clear only when it was explained to me with concept of free-energy changes in mixing.


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The effect of 3D structure and solubility of the binding site of enzyme on its affinity Km and maximum activity Vmax?
Could some one provide me with some resources or papers where I can read more about the following:
1- How can the 3D structure of an enzyme affect its Km and Vmax? (some papers, books or articles will be very neat).
2- How can the solubility of the amino acids of the binding site of an enzyme affect its Km and Vmax? (again some paper, books or articles will be very helpful).
Or maybe some description about that with some references? I spent some time in searching but unfortunately with no attractive results.
I just resay that I am inneed for some resources or papers about the two points in addition to some word explanation.
Thanks in advance!

Probably the big reason you were unsuccessful in your previous searches is that nobody quite knows exactly how enzymes' 3D structures lead to particular kinetic parameters.
It's wrapped up in the concept of "how the heck do enzymes work, anyway?" -- surprisingly, it's a question we don't really have a good answer to. The leading concept currently - influenced in large part by catalytic antibodies - is the transition state stabilization theory. That is, enzymes work by preferentially stabilizing the transition state, reducing the activation energy of the reaction. (A good overview of the theory can be found in Structure and Mechanism in Protein Science by Alan Fersht, one of the must-reads for anyone interested in enzymes.)
But that's probably not all of how enzymes work, or at the very least "bind the transition state well" is a rather coarse overview of the process. There's thoughts that the precise arrangement of active site sidechains are involved in a quantum mechanical interaction with the transition state. This is the "theozyme" concept put forth by Kendall Houk and colleagues.
The role of enzyme flexibility in catalysis is a highly disputed topic currently. The dynamics of proteins are an important concept for the understanding of the full reaction pathway, but there are some people who think that an important contribution of the protein is funneling vibrational energy into the appropriate bond motions for catalyssi. Nobel prize winner Arieh Warshel is (vocally) against it, though, favoring an electrostatic view of catalysis. (That is, enzymes work by stabilizing the charge distributions found in the catalytic pathways.)
So the long and the short of it is that we really don't understand how enzymes work, so we're rather far from being able to predict how the 3D structure changes the catalytic parameters. There are a number of efforts (particular from David Baker's lab) trying to use computational modeling of 3D enzyme structures to design enzymes, but the results have been rather modest. While such enzymes have been designed, their activities have been modest, and nowhere near the activity of native enzymes.
Doing the reverse - trying to predict the catalytic activity from 3D structures - is difficult, given the lack of knowledge. That's not to say people haven't tried. For example, there's been some efforts to use machine learning to predict catalytic constants from different mutants in a series. The problem with machine learning-type approaches is that the results tend to be only applicable for the particular system they've been trained on, and there's only limited interpretability of the results.


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How to pipette accurate volumes from BSA solution without air bubbles?
I'm new to immunohistochemistry and there's one step I'm having problems with. Generally I can pipet volumes pretty accurately and avoid air bubbles, but:
1) The BSA solution that I made (with PBS and BSA crystals - then vortexing) had a lot of air bubbles that wouldn't settle over time
2) I couldn't avoid air bubbles in my pipet even though I placed the tip under the layer of bubbles
How should I improve my technique? (Also, will having slightly different concentrations of the blocking and primary antibody serums greatly affect the result?)
Thanks,
L

Never vortex the BSA solution. The best way to prepare a BSA solution is to put the BSA powder on the buffer solution (or water) instead of the other way round. Tap or rock the tube to dissolve the BSA. If there are some tiny clumps then pipette very gently (use 1ml tips; cut the tips if needed) but tapping/rocking should usually do the job.
From CSHL protocols:

For a 10% (100 mg/mL) stock solution of BSA, dissolve 1 g powdered
  Fraction V or molecular biology grade BSA in 10 mL of distilled H2O;
  to avoid clumping, dissolve by layering the powder on the surface of
  the liquid. Gently rock the capped tube until the BSA has dissolved
  completely. Do not stir. Store in aliquots at −20°C.


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Plant growth in blue light
For the past two weeks, I have been in a group of 3 studying how different lights affect plant growth. So we growth two chickpeas plants and put one in white light and the other in blue light.
These are the results:
Days    Blue light    White light
           (cm)          (cm)
__________________________________
 1          6.6           8.2
 2          8.5           9.9
 3         11.0          11.6
 6         15.8          16.0
 7         17.2          17.6
 8         18.0          18.2
 9         19.6          18.7

The blue-light plant didn't really branch out a lot whereas the white-light plant branched out a lot.
My question is:
What caused the white light plant to not grow as fast like blue;
Why did the white light plant branch out?
What I read about the second question:
Experiments with blue light resulted in plants that are wider than usual. This can be explained by reference to the fact that more flowering buds (more branches) could form by reason of diminished apical dominance at the growth point.
http://www.canna.com.au/influence_of_colours
I don't understand why the blue lights plant did not branch out a lot like the white light ones?

Hi and welcome to Bio.SE. There are a lot of factors that need to be considered here; temperature, time exposed to light, moisture, earth/fertiliser used, size of potting etc. In order to somewhat account for the variation that will be introduced even if all those factors are controlled, you will need to repeat the experiment and see if any trends emerge. For example, could we be sure of the conclusion (blue lit plants grow more than white lit plants) if we re-ran the experiment and it showed exactly the opposite was true?

With all the research I did this is my understand of why the plant that was exposed to blue light grew taller than the plant that was exposed to white light.
The results of this experiment proves the hypothesis that the plant that was exposed to the blue light will grow taller than the  plant that was exposed to white light. Chlorophyll is a green photosynthetic pigment that is found in most plants. The chlorophylls are found around pigments in the photosystem, chlorophyll helps the plant to get the right wavelength of light. There are two types of chlorophyll a and b. Chlorophyll a absorbs red and violet wavelength best, but it absorbs very little blue light. Chlorophyll b absorbs a lot of blue light. Understanding chlorophyll  b will explain why the blue plant grew taller than the white plant. It grew taller because in both of the photosystems there were more chlorophyll b then a, therefore there was a lot of pigments that absorbed the blue light and the plant was able to use the energy to produce more ATP which in the end resulted in more growth.  There were many factors that we could not control  temperature, time exposed to light, moisture, earth/fertilizer used, size of potting. In order to get an accurate result of different light affecting the growth of plants some of these factors must be implemented.
Sources:
http://scienceline.ucsb.edu/getkey.php?key=3155
Can someone Confirm if this is right?


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Why does getting soap in your eyes cause redness and irritation?
I am wondering why do eyes become red after getting soap in them. What is the cause behind it?

This is because of the soaps chemical nature. They are alkaline agents and human eyes have a very low tolerance for alkalinity. Human eyes are roughly neutral with a pH of around 7, and soaps are around 7.5 to 9.
The eye can't handle the alkaline object as it is potentially harmful to the eye so it will start watering to get rid of the alien substance. Blood vessels then enlarge, coming closer to the surface of the eye, making them appear red.
Most soaps are tested before released to make sure if they come into contact with eyes they are non-toxic. Baby soaps have a lower pH as well to make sure that the baby doesn't come to harm.
Either way, its probably best not to put it in your eyes.
See here for more information.

Seriously, the page you link looks (in general) as realiable as yahoo answers.

@TomášZato looks can be deceiving

This does not answer the question. Yes, soap/shampoo has different pH values from the standard eye environment, but that is not a really surprising answer. Why do different pH values cause redness? If we could make a "soap" that contains almost the same ingredients as actual soap but has its pH fixed to 7 still cause red eyes? Will any other substance that is wildly different from water but has ph=7 also cause red eyes? What is the function of the redness (if it has any except to tell us that we rather not put that stuff into our eyes). Etc.

@AnoE I don't think its a function, more a reaction

Yeah... take my longer comment up there as an incentive to enlarge the answer to the (rather interesting) question. But if it is just a nonfunctional, arbitrary reaction, it would be at least nice to see details about the actual way it comes to pass (i.e., why does the eye get red, why does it not just start watering profusely to dilute the substance down to usual pH values).

@AnoE if I understand right, the red is simply blood vessels having grown larger and come closer to the surface, which is why we can see the red colour.

Anecdotally, "tear free" shampoo still hurts my eyes.

Basically, the eye would react to anything that is not similar (w.r.t osmolarity and pH) to the solution that covers it. Eye will react to neutral substances too. Tap water (without chlorine or other such chemicals) would also hurt in the beginning.

So how do red eyes help to get rid of that pH change?

When soap gets into the eye, Our immune system reacts to the foreign substance, it releases a chemical known as histamine as a part of the inflammatory response.
Now as result of this, blood vessels in the eyes become enlarged, dilated or swollen.
It leads to redness in eyes.

Source

XXX has chemicals is not a way to start an answer on scientific page.

Why so much downvotes, Any reason.

What is the mistake in the answer. Is it scientifically incorrect ?

This is a scientific page. You're free to chose whatever formulation you like for an answer, but you should also include references.

@Tensor_Product, the downvotes are likely because you do not answer the question. You are more or less reformulating the question with a few more words.

Do you have a source that histamine is released in response to irritants, rather than allergens?


text:
Essential fatty acids function
Why are essential fatty acids so essential? I know that if taken less then it would cause diseases, but what metabolic role do they play? Are their importance is just because of their structural role?

''Please add details to narrow the answer set or to isolate an issue that can be answered in a few paragraphs.''

Essential fatty acids consist of two main EFAs - Omega 3 (Linoleic acid) and Omega 6 (Linolenic acid).
These two play vital roles in the following:

Growth and development
Brain functioning
Skin health
Hair growth
Metabolism
Reproductive system health
Cell membrane integrity.

The fact that are bodies can't make them makes them very important in our diet. They are most important in our cell membranes.
Omega 3 is an amazing anti-flammatory. It does this by blocking the inflammation pathways in the cell.
We need more Omega 3 than 6 - about a ratio of 2:1.
This is a pretty good page if you want more information.

thanks, but how do they achieve those functions?

@JM97 editing...


text:
Why do cell membranes let small non-polar molecules through but won't let small polar molecules through?
If the hydrophobic hydrocarbon chain of the phospholipid prevents the movement of polar molecules through the membrane. Why does the hydrophilic phosphate head of the phospholipid not prevent the movement of non-polar molecules?

You might be interested in this.

See if this helps: http://biology.stackexchange.com/questions/52371/why-lipophilic-molecules-can-pass-phospholipid-bilayer-in-spite-of-2-hydrophili/52384#52384

Possible duplicate of Why lipophilic molecules can pass phospholipid bilayer, in spite of 2 hydrophilic layers?

Polar molecules needs electrochemical gradient and protein carrier. ...whereas non polar molecules needs kinetic energy and these molecule continuously bouncing to come out from the cell membrane through the channel provide by lipoprotein structure of cell membrane and concentration gradient also effective for movement of molecules all types of molecules.

The plasma membrane consists of hydrophobic and hydrophillic characteristics. Towards the outsides, they are hydrophillic, so they can create bonds with water. The insides are hydrophobic, allowing no water inside and keeping them tight together due to the polar forces.
An non-polar particle (if small), can pass through this because it does not interfere with the hydrophobic/hydrophillic (polar) nature of the plasma membrane. However, polar particles would not have the opportunity to move in, because the insides (hydrophobic) are literally afraid of water, or charges, don't allow polar substances to pass through.
So only hydrophobic (nonpolar), gases, and small particles (nonpolar) can pass through. There are exceptions of $H_2O$ passing through the membrane in small amounts because their electric charge is very minor.

First, we should understand what causes molecules to be hydrophilic or hydrophobic.
A molecule is hydrophilic if it contains atoms with different electronegativities, that is atoms that pull electrons with different strengths. The factors determining the strength of the pull are the size of the atom (including the pre-existing electron shells) and the number of protons. Make the atom too big and electrons are too far from the nucleus, make it too small and there is not enough protons to pull the electrons. An atom that has a balance between these two factors is oxygen which has the second highest electronegativity in the periodic table. Oxygen was thought to be the maker of acids, which is literally in the name. Now we know this is not the case because all you need is to be more electronegative than hydrogen so that it becomes essentially a proton that goes into solution. Anyway, the electronegative atoms in a polar molecule form hydrogen bonds with oxygen and hydrogen in water molecules because they have opposite partial charges. This includes water forming hydrogen bonds with other water molecules that gives rise to cohesion, surface tension as well as hydrophobic interactions which we shall explain in the next paragraph.
What happens with hydrophobic interactions (not bonds) is that water molecules want to pair with each other so they push the so-called hydrophobic molecules out of the way and clump them together. They are not hydrophobic in the literal sense, they essentially don't pair with water because they are not polar enough. Examples are hydrocarbons, where hydrogen and carbon have very close electronegativities.

The cell membrane is formed of phospholipids, these are molecules with polar hydrophilic phosphate heads and non-polar hydrophobic fatty acid tails. These molecules align so that the phosphate heads face water and the fatty acid tails hide inside the membrane.
Polar molecules can't pass the membrane because they are being pulled by water outside and not being pulled by the membrane which has the hydrophobic fatty acids inside. Channels essentially form hydrophilic passages for these polar molecules so they can pass according to their concentration gradients.
Non-polar molecules are essentially hated by both bodies of water, extracellular and intacellular fluids. The question then becomes: why don't they stay inside the membrane with the hydrophobic fatty acids? Well, we need to think about this in terms of forces. You essentially have two forces:

Surface tension of the water that lines both sides of the membrane and keeps the hydrophobic molecules inside.
Pressure force (or normal force) that arises as the hydrophobic molecules accumulate and push on the surfaces of the membrane.

It has to happen that eventually the hydrophobic pressure overcomes the surface tension unless you put infinite amounts of salt in the water which increases the surface tension, or you freeze the water. It then becomes clear that the molecules are more likely to have a net movement towards the body of water that initially had less of them. This is known as simple diffusion.

Outside membrane there in water and inside membrane there is lipid.
Hydrophilic molecules are more stable in water as compared to lipid so they prefer to stay in water and not go inside lipid.
Hydrophobic molecules are more stable in lipid as compared to water so they prefer to leave water and move freely into lipid.
You are saying that hydrophilic part of membrane will obstruct the movement of hydrophobic molecules but do not forget that they are already in water, which is polar, so it doesn't matter to them.
Analogy :- 'If you are on roof of your house you can very easily jump to roof of adjacent house' similarly hydrophobic molecules which are already unstable in water can move towards hydrophilic part of membrane because they are equally unstable there.


text:
Where can I find an image of the gut/anatomy of the mealworm?
Specifically, I'm a student working on an experiment involving the dissection of the mealworm (Tenebrio molitor) but for the life of me, I can't seem to find an image anywhere on the internet. Speaking to Carolina.com also got me no results. We're looking to dissect the mealworm and extract its gut/GI tract. However, at the moment it seems like we're going in blind. Is there anyone out there who can provide some insight?

The best I could find which showed the inside of a mealworm not just the outside was this:

Taken from here. Hope this helps with your dissection.

There is a paper called: biodegradation and Mineralization of Polystyrene by Plastic-Eating Mealworms: Part 2. Role of Gut Microorganisms. I. Here you can find a picture of the midgut lumen.