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How are cells of the cornea transparent?
We know that cells have mitochondria, chromosomes and other organelles so that's why they are opaque but can you say how the cells present in the eye cornea are transparent and allow light to pass through?

The pupil is a hole, there are no cells. What you probably mean are the cells of the cornea covering the pupil.

Yes i got the wrong term it is cornea

http://www.sciencedirect.com/science/article/pii/S1350946215000488

http://www.practicalfishkeeping.co.uk/features/articles/how-can-glass-catfish-be-transparent it's not totally clear how an entire fish can be transparent rather than white or pink, as the blood should flow in their muscles. check out the cool photo from the above page.

http://www.sciencedirect.com/science/article/pii/S0022519399909487

Most cells are transparent, which is why we can see cells using bright-field microscopy, where the light travels through the cells before you see it. That's how we can see inside onion cells and see structures like onion cell nucleii, moss cells, human epithelial cells and animal mast cells.
The human cornea is made up of five layers, each of which have different structures allowing them to be transparent: the outer and inner epithelial layers are very thin and naturally pretty transparent, and the middle layers have collagen fibres; based on that Wikipedia article, it sounds like there are several hypotheses for why these layers are transparent, but it doesn't look like there's a definitive answer yet.

Actually it is made up of myelin sheath

Collagen is transparent as well --- just look at gelatin. Also, there are no blood vessels in the cornea.


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Why is glycerol kinase absent from adipocytes but present in the liver?
Why don't adipocytes have the enzyme, glycerol kinase? Wouldn’t it be more efficient for them to utilise glycerol present to synthesize triglycerides than to get it from the liver? So what is the advantage of its absence?

I think it's worth mentioning, in explanatory note to question, that yes indeed lipocytes are being delivered triglycerides by liver - not by LDL though (reminder)  but by VHDL.

The short answer to this question is given in the Wikipedia article on glycerol kinase:

Adipocytes lack glycerol kinase so they cannot metabolize the glycerol produced during triacyl glycerol degradation. This glycerol is instead shuttled to the liver via the blood where it is: phosphorylated by glycerol kinase to glycerol phosphate and/or converted to dihydroxyacetone phosphate which can participate in [glycolysis or] gluconeogenesis.

[My de-emphasis of glycolysis]
To understand this requires one to consider the different functions of liver and adipose tissue and how they should respond to the fed and fasted state. Then one can appreciate that the differences in enzyme complement are one of the ways by which this is achieved. (The other is their differential responses to hormones.)
The role of the adipose tissue is to store fat (triglycerides) in the fed state and make it available for the other tissues in the body in the fasted state.
The role of the liver is to divert metabolism to the synthesis of fat in the fed state (at the appropriate stage) and to ensure that there is a supply of glucose in the fasted state for those tissues that depend on it (brain, erythrocytes) or a supply of ketone bodies for the brain.
The substrates for triglyceride synthesis are L-glycerol phosphate and fatty acids. There are two enzymes that can catalyse its production, glycerokinase (glycerol kinase) in the liver and glycerol 3-phosphate dehydrogenase in both liver and adipose tissue, as shown in my diagram below:

Fed State
The liver has surplus glucose so it can switch to fatty acid production from acetyl CoA (from pyruvate) and generate L-glycerol phosphate from the dihydroxyacetone phosphate intermediate of glycolysis, catalysed by glycerol 3-P dehydrogenase. This allows the synthesis of triglyceride, which is exported as lipoprotein.
When the triglyceride reaches the adipose tissue it is broken down to fatty acids and glycerol by the hormone-sensitive lipase. The glycerol cannot be used by the adipose tissue, but adipose tissue can synthesize L-glycerol phosphate itself in the same way as liver as there is glucose available for glycolysis in the adipose tissue. Hence the triglyceride can be resynthesized and stored.
Fasted State
The hormone of starvation, glucagon, initiates the breakdown of triglyceride in the adipose tissue. As already stated, the glycerol produced cannot be used to synthesize L-glycerol phosphate as the tissue lacks phosphoglycerate kinase. In starvation uptake of glucose is prevented hormonally, so that there is no glucose for glycolysis and hence no hydroxyacetone phosphate as a source of L-glycerol phosphate. Hence the fatty acids cannot be re-esterified and are released into the blood for other tissues, i.e. the response of the adipose tissue to starvation is that required.
The glycerol diffuses to the liver where it can be converted to L-glycerol phosphate because of the presence of glycerol kinase. What is the fate of this? It is not converted into triglyceride, it is converted to dihydroxyacetone phosphate by the reverse of the reaction shown. This is not glycolysed, but converted to glucose by gluconeogenesis, the enzymes for which are present in the liver. The glucose is released into the blood where it can be utilized by the brain, i.e. the response of the liver to starvation is that required.
References
This answer is based on lectures I delivered to undergraduates some years ago, which were drawn from various sources. The problem is that most biochemical texts tend to be organism-agnostic, and any discussion of mammalian tissues tends to be limited. Thus, I can’t find much useful to refer to in Berg et al. on line, except for support in section 16.3 for my assertion that glycerol returned to the liver in starvation is used for gluconeogenesis. I’ll update this later if I find anything more useful.

I think there is a typo in the first line of the paragraph above the diagram. It should be l-glycerol phosphate and fatty acids.

could you answer this please http://biology.stackexchange.com/questions/56029/effect-of-bile-salts-on-pancreatic-lipase-activity

@JM97 — Thanks for pointing out the typo. Fixed now.

@JM97 — Unfortunately I know next to nothing about bile salts. My background is chemical rather than medical, and my research interests were molecular biological. I was obliged to teach metabolism to biochemists, and I also had to mug up on certain medical subjects for lectures to professional students. However the bile never featured.

Refering to the wording of the question, "There are two enzymes that can catalyse its production, glycerokinase (glycerol kinase) in the liver and glycerol 3-phosphate dehydrogenase in both liver and adipose tissue,..." may be considered the gist of the answer? As the question (explanatory text) seems to assume that there is no synthesis of triglycerides in lipocytes at all. There is, though.  Thank you.

Brilliant answer, my voice. "Hence the fatty acids cannot be re-esterified and are released into the blood for other tissues, i.e. the response of the adipose tissue to starvation is that required." Implicit answer to a follow up question that would come from question erroneously assuming that there is no synthesis of triglycerides in lipocytes. Then, question should arise: why do lipocytes then only have that other enzyme.

Every learner surely will be surprised as there is some "prohibition" of using fatty acids for gluconeogenesis. Where do the fatty acids released by lipocytes go to? Surprise.  --- It would be interesting to hear from you - any occasion would do - on role of insuline. Lack of insuline in diabetes might be equivalent to "fasting". Implications for "metabolic syndrome"...

@PeterBernhard — I'll have a look at this when I have a moment. Having written it over four years ago, I will need time to rethink myself into the topic.

Refering to: where do the fatty acids go to? I believe you mentioned that - in starvation muscle need them. Then, in Berg I saw some diagram, where fatty acids apparently released by adipose tissue somehow diffuse freely to the liver (beginner should know: no Lipoprotein transporting fatty acids to liver, correct, in principle..). That was when I first got acquainted with subject. "Over", no answer expected, no need to be  moved to chat, just to let you know.

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Identifying three species of Datura
I have found a large, wild patch, some 200m long, of mainly Datura Stramonium, in our street. I have always been keenly interested and well read on the shamanic, and - very rare - medicinal uses of this species, but scattered amongst them, like family, are two other plants I don't know, but am convinced are also some kind of Datura. I would please like some help on identifying the other two based on the two photos I have of all three.

This is the well known - to me - Stramonium flower, the plant characterized by jagged leaves and the well known spiked seed pod of Jimson Weed seeds.

It looks like user29734's answer is correct, and the above is Morning Glory, but of course subject to confirmation. I now do recognize at least the purple flower as Morning Glory, but from some 30 odd years ago. And it now looks like what I confused with Datura Alba is really just another colour flower of the Morning Glory.
If anyone could please confirm my ID of the Stramonium, and confirm the identification of the second image as morning glory, and suggest what species.
These plants are all around my neighbourhood, with is the northern part of Randburg, South Africa. This city borders on the Northern side of Johannesburg. 1 It's a temperate climate, with very hot and rainy summers, and bitterly cold and dry winters. The soil is reddish and lacks much humus.
It is a semi-rural area, having been rapidly urbanised over the last ten or so years, when it was still just farms and small holdings. Farming is mainly vegetables or lucerne; and lots of maize further out from the city. We are a few km south of the Cradle of Humankind.
1 Strangely enough, there are two cities in the US with the same names, both in California, I believe. I know Johannesburg is.

In the second photo none is Datura

Please [edit] your question and where you saw these plants. Location is often very relevant when attempting to identify species.

Could the second photo be a Convulvulus/Calystegia?

@RHA, no, the flowers are far less flat and cone like, but wide, not like the narrow Stramonium trumpet shape. I only have dried ones with me now, but I will find a very good example tomorrow and photograph it well, isolated from the foliage, with separate pics of the latter.

@terdon I have added as much detail as I could guess you wanted. I'm no biologist, so only have a rough idea of which factors count, so a tried a shotgun approach.

@AlwaysConfused Yet they are densely interspersed with the Datura, with zero gaps and much overlapping of branches, and I have not seen them elsewhere.

@ProfK to me it seems the pink flower at second photo is from any species of Ipomoea (Convulvulaceae). The cordate leaves are seemingly of the same plant, or may be from some-other plant.

Yes, the second photo looks to me like a morning glory (Ipomoea).  Is it a vine?  The third appears identical to what I have growing as datura in my own garden.

@jamesqf Sorry for the OT, but how do you find growing Datura in you garden? I would imagine in requires quite frequent pruning. I wish to start doing the same.

@AlwaysConfused The leaves are definitely of the same plant, as I have picked flowers from the same stems as leaves.

@ProfK  why you removed the third image? Seemingly that was some sort of Datura.

@AlwaysConfused Because it turns out that is not a picture of the plant I was trying to identify, which is just a whitish type of ipomoea.

this(https://i.stack.imgur.com/92KbL.png)? quite strongly looks like Datura (as also wrote by @jamesqf). The shape of corolla and calyx looks same as Datura, including projections at margin of corolla. The stamens are same in length; and style is so long... it is quite unexpected in Ipomoea. Also it may look similar to Mirabilis jalapa, but it is not.

@ProfK: It does take a bit of space, but my garden is about an acre.  I do need to regularly prune the seed pods off before they're ripe (every few weeks during the summer/fall), or it will reseed quite enthusiastically.  They plants die back to the ground in winter here (USDA zone 6/7).  Very good nighttime fragrance.

The two left pictures look like garden morning glories, which are mostly hybrids of various species, some of which reseed quite well in my garden, and could have become naturalized.  The leaves on the right look something like Ipomoea leptophylla, but that's native to the US Great Plains area: https://plants.usda.gov/core/profile?symbol=IPLE and not common in commerce.  But there are a lot of Ipomoea species, and I'm no expert, just a gardener.

@AlwaysConfused It does, but the shape of the leaves in the image you linked to don't match the rounder leaves in my centre-bottom pic.

Yes the third plant (https://i.stack.imgur.com/92KbL.png) (seems to be  Datura) is completely different from the second one (https://i.stack.imgur.com/gkbpT.png) which is certainly NOT datura. And Datura indeed shows drastic variations in leaf size and teeth-depth in different populations of it.

There is no third plant. All three bottom photos are flowers, leaf, and end of stem foliage from the same plant, and the other plant being the top picture, Stramonium.

Okay, so as far as the blue and white flower goes I'm pretty sure it's a cultivar of ipomoea called Flying Saucer which is a hybrid of heavenly blue (I. tricolor) and Pearly gates (also I. tricolor) meaning it's a hybrid and no seed output.
As far as the white flowers go it is most likely Datura since it is part of a short shrub and the petals are spiked. However you should determine if it blooms at night because its possible it could be moonflower. It may also be brugsmansia or pearly gates.
As far as 'alchemical use' datura contains scopolamine which is potentially lethal if consumed in indiscriminate amounts.

I am only too aware of the potentially fatal  and extreme effects of scopolamine, both from extensive study and several very interesting personal experiences. The best treatment for an unexpected or unwanted scopolamine experience is physostigmine and acetylcysteine, for the anticholinergic poisoning, and benzodiazepines for the extremely elevated heart rate. Physostigmine occurs naturally in the Calabar bean.

The second flower is, I'm guessing by the valentine shaped leaf and violet tubular flowers, a morning glory vine (ipomoea violacea or ipomea tricolor). These plants both are closely related cultivars of ololioqui and tlitlitzen which had a history of shamanic use in southern Mexico.

Aaha,, yes, I think I now do recognize that from them growing in a friend's yard when I was very young. So all the psycho-active plants stick together then, like mafiosi.

@ProfK yes, oddly. The morning glory species contains lysergamide and and it's analogues. However, there is a plant which is native from Carola all the way down to Micronesia called Argyria nervosa which contains the same active principle as the mesoamerican plants.

I have edited my question, and included much better images of the ipomoea flowers, of two colours, a leaf, and some other foliage at the top of a 700 - 1000 mm high stem where the thin vines with leaves and flowers start.

That said, as I am studying this plant as an alchemist, where would I locate seeds on the ipomoea?

The seeds on ipomoea form after the flower dies. It sort of dissolves because of its structure and a bulb begins to grow at the ovule. You can observe this as sepal will begin to bulge. You will begin to see a greenish looking pod emerge but you want to extract the seeds from it only when the pod dries and becomes brown. This is assuming that the plant is not a hybrid. If it has grape shaped leaves and heart shaped leaves it won't produce seeds at all. Fascinating, I suggest you read psychology and alchemy by Jung and gionardo bruno and the hermetic tradition by Frances Yates. Excellent books.

Thanks for advice and the great suggestions, especially Jung, who is fairly  unique amongst modern psychologists to not discard and instead value the ancient and evolved bodies of knowledge in magick and alchemy. I am myself a Hermeticist and in particular a Thelemite.

The top plant looks like it could easily be D. stramonium. Daturas can be a bit tricky. You should either provide an estimate of the scale or measure the flower, then compare with this simple key of invasive Daturas (in Australia): https://www.samorini.it/doc1/alt_aut/ek/haegi.pdf. It helps to note capsule size and shape. (It is NOT a Brugmansia sp.; those are trees with pendant flowers.) Also, the second flower photo seems to me is clearly a morning glory, possibly as IDed by user29734, and the center leaf seems from the same plant(s) or closely related.

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How does the tRNA recognise the first methionine during translation?
The process of translation starts with the initiator tRNA identifying the codon coding for methionine (AUG). However, my textbook also says that there are various untranslated regions present on the mRNA. It was then that this question had occurred to me. How does the tRNA actually differentiate between the regions that are ought to be coded and that are not? One may say that translation always start with the methionine, but my question is different. For example, if the code is
5'...GUAUGCAUGAUC...3'
then when the tRNA arrives, it reads from which of them? Does it leave the first two nucleotides and read it as AUG CAU GAU and so on or does it leave out the first six nucleotides and read it as AUG AUC and so on?

I suggest you read further in your text book or consult a better textbook if necessary (look at NCBI Bookshelf on line) before posting here. Be advised that the answer is different in prokaryotes and eukaryotes.

There are different processes for recognising the initiator site in prokaryotes and eukaryotes.
In prokaryotes the process relies upon the Shine-Dalgarno sequence, this is a well conserved sequence throughout prokaryotes found upstream of the start codon. It interacts with the 16s ribosomal RNA to place the initiator codon in the A site of the ribosome.
In eukaryotes the process is somewhat more complex and relies upon a large protein complex which assembles on the 5' cap of mRNAs. This complex mediates an interaction between the mRNA and the ribosome, the ribosome then scans (using GTP for energy) 5' to 3' to detect the start codon.
One final process which is unusual but does occur is cap independent initiation mediated by internal ribosome entry sites (IRES). These are sequences which form structured loops which can mimic the interactions usually formed by the cap complex. These sequences appear in viral mRNAs allowing viruses to bipass anitviral mechanisms in cells.
You will need to do some reasonably extensive reading if you want to uderstand fully these processes and how they may be manipulated by cells to alter expression.

To explain this to a beginner, rather than encouraging him to do some more reading, I would leave out IRES and instead correct your description of eukaryotic initiation, which does not involve placing the AUG in the correct position but involves scanning from the cap to the first AUG in a suitable context.

@david I have adjusted as suggested I felt that introducing scanning left the obvious question, how does the ribosome know when it has reached the start codon? However upon your advice I have altered the answer. I have included IRES as these are important in viral infection and will point the reader to literature which could help understand the regulation of eukaryote initiation.

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Computational engineering of protein binding pocket
I have an X-ray structure of an enzyme with reported activity to a small molecule.
This activity is rather low since it is not the native substrate.
I can run molecular modeling simulations (e.g. using DOCK) to estimate the enzyme's binding behavior to different compounds. However, what I would like to be able to do is to mutate the binding pocket so that it better binds my small molecule of interest.
Exploring all possible amino acid substitutions is computationally too expensive, so I am wondering whether smarter ways of looking at this problem have been developed.
Can someone point me in the right direction? I've searched Google but can't really find a straight forward answer

Could you choose rational mutations that you think may facilitate binding and only study those? The results of one mutation may inform the next.

@canadianer There is probably a way. However, I would not want to have to reinvent the wheel if someone has done something like that before

You can try an evolutionary algorithm. If you can quickly evaluate the binding affinity you can initialize a set of copies of your protein but with random mutations. You can assign them a fitness score based on the affinity of the binding. The ones with highest affinity you replicate again with some probability of mutating each amino acid and you continue for as many generations as you need. If you find your parameters (mutation rate, population size, etc) correctly you can easily optimize the binding without knowing anything a priori about the different sites. There is a lot of literature on this, I suggest you do a quick Google scholar search on directed evolution or evolutionary algorithms to optimize binding affinity.
Paper on in silico evolution to optimize protein-protein binding

Thanks for the input. If I understand correctly they used in silico design and experimental optimization to get to the final result. They did not use an evolutionary algorithm. However, I think that this is generally a promising path to explore. I am just wondering whether so already developed such a tool.


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What is the advantage of having multiple pathways to activate complement?
We all know there are three pathways to activate complement: classical pathway, lectin pathway and alternative pathway. What is the advantage of having multiple pathways?

Although the initiating event of each of the three pathways of Complement (Clasical, lectin and alternative) activation is diferent, they converge in that all of them can cooperates with both the innate and the adaptative immune system to eliminated blood and tissues pathogens.
I think the major advantage is that when a individual has a deficient in a complement component  of ones these pathways the others can function to eliminate dangerous antigens or immunogens. However, if this complement component deficience is present in two pathways, patients can have the most severe clinical manifestation, suffering frequent severe bacterial infections.
Besides, these three pathway can function together to carry out a number of basic functions including:
Lysis of cells, bacteria, and viruses
Opsonization, wich promotes phagocytosis of particulate antigens
Binding to specific complement receptor on cel of the immune system, triggering activation of immune responses such as inflamation and secretion of immunoregulatory molecules that simply or alter specific immune responses
Immune clearance, which removes immune complexes from the circulation and deposites them in the spleen and liver

References please!

There can be many reasons for this, but generally redundancy in biological systems is very important in that it makes the system more robust. If one pathway fails, due to mutation or some environmental factors, the other(s) can compensate and the function of the pathway remains. In some cases it can also be used to tune the degree of activity or speed of activation.
Article on pathway redundancy


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Fatty acid oxidation in adrenal medulla?
Why adrenal medulla can not utilise fatty acids for generation of energy?
What could be the benefit for not having ability to use fatty acids?
Refrence 1
Refrence 2

Does it have something to do with feedback mechanism?

Interesting question. Do you have a reference showing that fatty acids cannot be used? The adrenal medulla is basically a specialized nervous tissue, and neurons are usually considered to be unable to oxidize fatty acids, but other cell types in the CNS do oxidize fatty acids, see for example https://www.hindawi.com/journals/bmri/2014/472459/

but the blood brain barrier is not present in adrenal medulla.

I was hoping for a reference to actual experimental data, rather than just somebody else claiming the same thing. I did find some textbooks that repeat this statement (without reference), so perhaps it's valid, but textbooks can also be inaccurate ... Also, the blood-brain barrier does allow fatty acid transport (contrary to statements in some textbooks :), see for example https://www.ncbi.nlm.nih.gov/pubmed/17901540  See also my related question http://biology.stackexchange.com/questions/34159/why-is-the-brain-dependent-on-glucose

Also, we should consider the possibility that there is no benefit. Some features of biology are not good for the organism, but evolution just hasn't come up with any better solution.


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How to drop a grid of points in DICOM images of a CT scan (imageJ? Horos?)
I have a series of DICOM images from a CT scan of a bucket of rocks. I want to systematically measure the size of the interstitial spaces. The reason I'm doing this is to compare it to a simulation I've made to check that my simulation is giving accurate data.
In order for the measurements to be comparable to data from my simulation, I want the method for measuring the gaps to be as follows: define a 3D grid of points within the rocks (say, every 5 mm). At each point that falls within a gap (not in the centre of a rock), measure the gap width from that point in the X, Y, and Z directions.
I've tried messing around with both Horos and ImageJ but I can't work out how to define points (ROIs?) in a systematic way, or to have them show up in all three directional slices of the scan (I'll need to measure two dimensions from one 2D image e.g. X,Y and then switch to the X,Z image to get the third measurement, but use the same defined point).
Ideally once I know how to drop points and understand how they work, I could program the software to automatically do these measurements. Can anyone point me in the right direction?
Thanks!


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Viruses and Transformation
Would the lysogenic cycle for the reproduction of viruses be considered a form of naturally occurring transformation since DNA from the virus is being incorporated into the DNA of the host cell?

The answer lies in the definition itself of transformation. See from here:

In molecular biology, transformation is the genetic alteration of a cell resulting from the direct uptake and incorporation of exogenous genetic material from its surroundings through the cell membrane(s). For transformation to take place, the recipient bacteria must be in a state of competence, which might occur in nature as a time-limited response to environmental conditions such as starvation and cell density, and may also be induced in a laboratory.

What is clear from this definition is that host cell needs to be competent for taking up extracellular DNA to call the process transformation. Also, the term direct uptake does not seem to fit here as, you know why, bacteria do not just go on collecting viral DNA from their surroundings.
Obviously, bacteria are not competent to take up viral DNA, nor the virus makes them so. The virus simply injects and joins its own DNA into baterial genome. Now, it would be some common sense to know that the host does not like it, so whether it is competent or not, is just a matter of debate (did anyone ask them?). In short, No, the process of lysogenic cycle would not be considered transformation as the bacteria are not made competent for this process.


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How does translational immunotherapy work?
I skimmed an article on a recent experiment which suggested that it was effective to inject induced colon cancer tumors with an attenuated salmonella variant. According to the article, this stimulated an immune response which suppressed metastasis of the cancer. How exactly does this work?

Tumors are commonly infiltrated with lymphocytes, including T cells, macs, DCs and B cells. The crux of the paper is that their attenuated virus secretes TLR ligands (Toll-like receptor) that resulted in an activation of tumor-suppressive M1 macrophages, a concomitant reduction in immune-suppressive M2 macrophage activity, and an influx of immune infiltrate to the tumor.
So M1 macs are activated typically by IFN-y and LPS stimulation, which is typically through TLR4. Their salmonella is attenuated and causes no disease, check one. It's gram-negative and thus has LPS, check two. It's engineered to secrete bacterial flagellin, a TLR5 agonist, check three.
M1 macs secrete IL12, important for polarizing T cells to TH1/TC1 phenotypes that are oncolytic, and IL10 which can elicit anti-tumor immunity though it's reputation is that of an immunosuppressant. M1 macs can also kill tumors of their own accord by producing nitric oxide which is cytotoxic to tumor cells. TLR4 agonsim on it's own accord also activates T cells in an NF-kB-dependent manner.
Whats also interesting is the inflammatory signal actuated by the macrophages actually tells other immune cells "hey come check this out," and potentially makes for a more robust anti-tumor response. The idea is that inflamed tissues secrete signalling or chemotactic molecules called chemokines which are picked up by chemokine receptors on leukocytes, telling them to enter the zone of infection (and thus the malignancy).
You'll also find, however, that despite immunological advances, modulating cells is a challenge due to the nature of each type of cancer's TME (tumor microenvironment). And so in your paper they tested it in a murine system in bladder cancer, but will it work in a human melanoma must be qualified, for example.


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What is coffee effect on muscles ? On sport performances?
Since coffee is a vaso-restrictor does it have any impact on sport performances ?
I mean does it go against natural way the body works (sending more blood to muscles due to the increasing needs) or does the body easily bypass this effect ?
Edit : I leanred that coffee has a great impact on sport performances but what realy interests me is to learn more about its vaso-restrictive effect , how doesn't it reduces performances ?

Did you do any research on the subject prior to posing the question here?  To my understanding, If information is easily accessible by a google-search, the moderators and other users here will ask you to do research in advance and possible rephrase the question to be more specific.

I learned that coffee increases performances but i don't find a lot to learn on it's vaso-restrictor effects which is what realy interests me

I would advise you to then clarify in your question that you have done prior research and now search for answers regarding a specific area. I am no expert on the subject you are asking about, so I apologize if my comments seem unnecessary. I am merely trying to improve your chances for finding a useful answer.

Ty for this comment , i'll edit the question ! :)


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is it possible for Cougars and Cheetahs to reproduce
I know that many big cat hybrids exist ie ligers, but I always thought it these hybrids were limited to members of the Panthera genus till I came across a cross between a leopard and a cougar. Now since cougars and cheetahs are more closely related to each other than to leopards could these two successfully reproduce?


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Why is carotene in carrots?
Internet says that the carotene is an important pigment for photosynthesis and UV-protection. That explains its accumulation in leaves. I suppose colored fruits are more appealing to animals, so that explains the fruits. But why roots? Why is carrot full of carotene? The only reason I can think of is human cultivation. Is there any specific reason carrots synthesize so much carotene? Are there other similar examples of so vividly colored roots?

Carrots are a vegetable selected by humans: "ancient" carrots were very different from "our" carrots. Their color was different, as well.
Probably, the artificial selection for edible carrots (with different taste and characteristics) led to the "collateral" activation of the methabolic pathways which can explain the biosynthesis of so much carotene, but this is just an hypothesis :)

We cannot really answer this; the only true answer is ‘because nature did so’. (Actually, it may also be ‘because humans bred carrots in that way’ but that answer would be just as unsourced).

They're uncommon in mainstream grocery stores (but starting to appear more and more), but one can find carrots of all sorts of colors out there.

I have asked on Biology.se and it appears to be on topic there. I will therefore migrate it. It does, however, come with the advice that adding some references would be a good idea if there are any, and including what your attempts at answering the questions are. There would otherwise be a chance that it might gat closed as low effort.

I mean... it's called "carot-ene". Carotene... carrot... it just makes sense.

Carrot (Daucus carota) is a biannual plant that accumulates massive
  amounts of carotenoid pigments in the storage root.

The root of the carrot was not orange before domestication.

Although the root of carrot plants was white before domestication,
  intensive breeding generated the currently known carotenoid-rich
  varieties, including the widely popular orange carrots that accumulate
  very high levels of the pro-vitamin A carotenoids b-carotene and, to a
  lower extent, a-carotene.

As stated in the comments people did this to give a better taste to the roots. This is simply economical more beneficial because otherwise only the leaves of the carrot could be used for consumption (and not the roots which are a major part of the carrot), wasting this root would result in a lot of waste (and thus a lot of money waste) and because of an increase in carotene (and other compounds which contribute to the flavour) this would save money and provide more tastefull and appealing roots.

It is likely that wild carrot plants had uncolored roots of a bitter
  taste and a woody core but were initially cultivated because of their
  aromatic leaves and seeds.

So the only reason (as far as I can find) is that this is ineed because of cultivation by stimulating a flux in the direction of the carotenoid biosynthesis
I think this picture will explain it all:

 (source)

I'm not sure how familiar you are with biology so I described this not in that much detail about the genes and expression of them etc. If you would like to know this I would highly recommend to read these articles:

Biosynthesis of carotenoids in carrot: an underground story comes to light. (which I mainly used to write this)
New insights into domestication of carrot from root transcriptome analyses

I'd swear an onion sneaked into that picture...

hahahah it's a parijse carrot @xDaizu


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How to consider ions charges while calculating ions steady-state equilibrium concentration
i recently tried to find answer for following problem:

"Assume that a membrane is permeable to Ca++ , K+ and Cl- but not to a
  large cation R+. The inside concentrations are [RCl] = 100mM and
  [CaCl2] = 200mM, and the outside concentration is [CaCl2] = 300mM. (a)
  Derive the Donnan equilibrium. (b) Find the steady-state equilibrium
  concentration for Ca++."

when i tried to write space charge neutrality equation, i encounter to a new question,
how should i consider that
a:for each Ca++ there is two Cl-

and
b:each Ca++ has 2 positive charge

in the past i only worked with the ions that had same charge or same number of molecule, for example considering we had only cl- and K+ and some large
cation R+ , this situation is simple but the above mentioned problem is totally different.


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Can proteins/peptides pass through the intestine?
I've heard somewhere said that :

Stomach cells do not absorb anything larger than single amino acids.

Is that wrong?
How do biological toxins (peptides/proteins) from mushroom or bacteria like Botulinum come to our blood and affect our body after we eat them?
Update: In fact, i want to know if we drink milk, is there anyway IGF-1 protein from milk can pass through the intestine and affect our body. Because I see some arguments/debates about the IGF protein in milk can cause acne.

Related (duplicate?): http://biology.stackexchange.com/questions/36050/how-does-botulinum-toxin-enter-the-blood-stream-from-the-digestive-tract

Entire proteins can be transported across the epithelial cells of the digestive system.https://en.wikipedia.org/wiki/Transcytosis
This is common in neonatal infants aiding in immunity passed via proteins in mother's milk. It is much less common as you age. http://www.vivo.colostate.edu/hbooks/pathphys/digestion/smallgut/absorb_aacids.html
The process is termed "transcytosis" if you wish to search for whether this occurs for a particular substance. One such goup of proteins entering the body in this manner are prions. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5004172/

And viruses can pass through epithelial cells in this manner.


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Identification of brown film inside a plastic water bottle
What could this film be at the base of a plastic water bottle?

Also observed one around the neck.

May be water sediment or algae or cyanobacteria. Was they inside the bottle or outside the bottle?  Is it possible to you to see them in a microscope?

Is it possible to you to see them in a microscope?-No.They were inside.

I meant if a microscope is accessible to you (institute/ home). In the inner  wet portions algae may germinate. If unused, the bottle could be cut and the inner material could be scrapped, smeared and viewed under microscope.

I did understand what you said. No, it is not possible to view the film under microscope.

It could be algae or bacteria film, but also ironoxide.


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Lysis step during DNA purification
I am currently studying DNA extraction from various bio-originated samples. I am new to this field, and have learned how commercial DNA extraction kits work for bacteria.
I understand that the very first step is called 'lysis', and that this is supposed to break cells to pull out all the stuff inside them, including DNA.
I am studying cell-free DNA extraction procedure from human blood, and I don't understand why the lysis step is necessary in this context.
If lysis is to break cells, and cell-free DNA is already out of the cell and freely circulating, such a step seems unnecessary.
Is my understanding about lysis right? Then, why is the lysis step necessary during cfDNA isolation?

You want to isolate the cfDNA, and leave anything else in the plasma out of your analysis — essentially, the lysis step is part of the purification.
(See here)
(I'll elaborate with edits shortly)
Edit:
Actually, it looks like lysis is not a good idea in cfDNA isolation — lysing cells in your sample will result in contamination by genomic DNA, as discussed here. It would be better to stabilize/fix cells to prevent them from lysing, to avoid this risk.
In other words, your initial instincts were correct!

Thanks, you gave me a piece of confidence to solve this problem. Then is it okay to say that the lysis step for cfDNA is to clean or degrade other stuff in serum such as protein?

Let me know if this answers your question!

Yes absolutely it does! I never knew there could be WBC in serum... Then lysis step might cause a mess in my sample. Thank you very much :)

@Kidan My pleasure! Please do mark the answer as accepted if it helped you :)


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What is the Gaidukov Phenomenon in algae?
Apparently the Gaidukov Phenomenon occurs in algae so as to enable the algae to absorb the maximum light for photosynthesis. How does this happen?

This may be helpful. http://www.pnas.org/content/20/5/251.full.pdf

@Mesentery Thanks a lot!! Obviously this was of great help!!

You should provide a better background, and briefly explain the Gaidukov Phenomenon.


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Why is a magnesium ion essential for ATP activity in enzymic reactions?
The Wikipedia entry on Magnesium in Biology includes the following:

ATP (adenosine triphosphate), the main source of energy in cells, must be bound to a magnesium ion in order to be biologically active. What is called ATP is often actually Mg-ATP.

I don't understand why magnesium is essential for breaking the high energy bond in ATP?

One of the key reasons is that Mg covers the negative charge of the triphosphate and therby allowing Mg-ATP to bind to hydrophobic clefts in the active site

wouldn't the presence of mg hinder release of phosphate?

I will add that to my answer @JM97

As far as I know there are two main reasons for this:

promoting a nucleophilic attack

In general, Mg2+ interacts with substrates through inner sphere
  coordination, stabilising anions or reactive intermediates, also
  including binding to ATP and activating the molecule to nucleophilic
  attack (wiki)

 - assists in the leaving a pyrophosphate group and may also facilitate the cleavage of the bond between the α- and β-phosphates by its electron-withdrawing effect. (source)

wouldn't the presence of mg hinder release of phosphate?

As with all reactions this is dependent of the concentration of the molecules
involved as stated here:

The Gibbs free energy change (ΔG) due to ATP hydrolysis depends upon
  the concentrations of the various participants in the reaction. When
  the concentrations are farther from their equilibrium values, the
  absolute value of ΔG is greater. Under “standard” conditions (i.e.
  concentrations of 1M for all reactants except water which is taken at
  its characteristic concentration of 55M) the Gibbs free energy of ATP
  hydrolysis varies from -28 to -34 kJ/mol (i.e. ≈12 kBT, BNID 101989)
  depending on the concentration of the cation Mg2+. The dependence on
  Mg ions occurs because the positively-charged magnesium ions help to
  stabilize the ATP molecule. However, in the cell the conditions are
  never even close to the standard state values. (source)

The answer by Rick Beelo discusses the role of magnesium ions in relation to catalytic mechanism, but does not include a more general and long-accepted role of the ion. This is to hold the triphosphate ‘chain’ of ATP in a specific conformation and in this and other ways to enhance the binding to the enzyme, an essential initial step in the catalysis of any reaction involving ATP. Thus, in a section of the standard undergraduate text book, Berg et al. one finds the following:

How does the binding of the magnesium ion to the nucleotide affect catalysis? There are a number of related consequences, but all serve to enhance the specificity of the enzyme–substrate interactions by enhancing binding energy.
First, the magnesium ion neutralizes some of the negative charges present on the polyphosphate chain, reducing nonspecific ionic interactions between the enzyme and the polyphosphate group of the nucleotide.
Second, the interactions between the magnesium ion and the oxygen atoms in the phosphoryl group hold the nucleotide in well-defined conformations that can be specifically bound by the enzyme…
…Third, the magnesium ion provides additional points of interaction between the ATP-Mg2+ complex and the enzyme, thus increasing the binding energy.

This latter point can be seen in the 3D structures of ATP bound to enzymes, illustrated in Figure 9.50 of that edition, where the ATP interacts with an Asp residue through two water molecules bound to the magnesium ion:


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Would a clone of myself have exactly the same development (character, appearance) as me?
If I'd have a clone of myself (with my DNA) and I would record the development of that person, would I be able see exactly the same development as myself (same personality, appearance)? For example that at a certain time, that clone would look how I looked like when I was 8?

Appearance, personality etc. are also influenced by the environment (persons around your clone, geographic location, eating, sporting etc). So there are a lot of other factors which need to be the same. Further not only the sequence is important but also  epigenetics ( like methylation of DNA)

No, your clone would differ from you. Actually such clones exist in humans also. Monozygotic twins are clones. They certainly look alike but they definitely differ in some respects.
Understanding why this is true require one to understand the concept of heritability from the field of quantitative genetics. You should definitely have a look at the post Why is a heritability coefficient not an index of how "genetic" something is?. The main reason why you would differ is because our phenotype (personality, appearance, etc...) also depends on the environment we experience.

your come would be even more different becasue it would have a very different in utero environment, this can have a rather strong effect. You how to wonder how different monozygotic twins would be if they did not share the same womb.

@John I don't fully understand your comment due to the typos. Yes, of course, the correlation coefficient between twins depends on whether they share the same environment (again, see Why is a heritability coefficient not an index of how "genetic" something is?) which includes the uterine environment.

Sorry, that should say "Your clone" I was pointing out that the clone of an adult would have a drastically different in utero environment. This could lead to some surprising differences, in some organisms (not humans that we know of) it could even mean your clone is a diffrent sex. http://onlinelibrary.wiley.com/doi/10.1002/dvdy.23924/full

In eutherian mammals, sex is determined by sexual chromosomes though, not so much by the uterine environment. But it is true that the uterine environment can be very influential. It is also true that many species that do not have a uterus, parental care will affect sex determinism.

I did say not in humans, I should have moved that to the end so you knew I was referring to sex specifically. Now epigenetics may affect sex in humans by modulating the gametes but that will not have an effect on your clone.

Yes, not in humans and not in any species that have a uterus I would think as all uterian mammals have sexual chromosomes to determine sex. But I might be wrong. I have not read the paper.


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What is blue light?
What is the "blue light" often discussed in relation to human melatonin production, sleep/wake cycles, etc.?  A Google search seems to define it as light of a particular wavelength, suggesting that it literally means "light that's blue in color," but many articles seem to attribute blue light to the light emitted from computer/TV/etc. screens, which is not inherently blue in color.
What exactly is blue light?  For example, would adjusting the "blueness" of a colored light bulb, as if raising and lowering the "B" slider in an "RGB" color selector (raising "B" in the morning and lowering "B" in the evening), have at least a hypothetical positive impact on human circadian rhythms?

Blue light means wavelengths that appear to the human eye as blue when they are presented alone. This light is important for sleep/wake cycle regulation because this is the wavelength that cells that participate in this regulation respond to.
"White light" is light that covers the full visible spectrum; sunlight, for example, is fairly white. However, that light contains plenty of blue light as well as all the other colors - there is no actual wavelength for "white," it is a collection of all the other wavelengths.
Similarly, TVs and other screens emit red, green, and blue light. Because of our makeup of photoreceptors, this is sufficient to mimic any visible color. When referring to the blue light of televisions, people are referring to that blue component. If you disabled the blue channel somehow you would get a very strange picture but also activate less the cells that sense daylight based on blue light.
The reason screens are so problematic is that people stare directly at them and take in a lot of light. Other sources of bright, whitish light would have the same effect.


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What is the structure of DNA polymerase III?
According to Snustard and Simmons the structure of DNA polymerase III is the following, where the clamp loader( γ -δ complex ) is present on one side:

But according to Lehninger the clamp loader is centrally located:

Which one is right? Besides where can I find a correct diagrammatic representation of DNA polymerase III?

I recently found this paper which supports the second mentioned structure of DNA pol III.

I don't know the answer myself, but if you have access to Nature Structural Biology I would start with this recent paper and work back from it if necessary. (I found it by searching the Protein Data Bank (PDB) for E.coli DNA pol III): http://www.nature.com/nsmb/journal/v24/n2/pdf/nsmb.3348.pdf .

It's a problem then.You might try looking at the visualizations available in the various PDB entries, but it would probably be much more work than is justified. Hope there's someone on the list that works in the field and can tell you or reproduce an appropriate figure.


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What is "contigs" in Picard's ReorderSAM?
I've used BWA to map my NGS reads against the hg38 genome, and I have a BAM file. I'm not doing genome assembly, and my reference genome file has the human chromosomes. Thus, I shouldn't have "contigs". But...

https://broadinstitute.github.io/picard/command-line-overview.html#ReorderSam

and quote:

ReorderSam reorders reads in a SAM/BAM file to match the contig ordering in a provided reference file, as determined by exact name matching of contigs

Q: What does contig ordering mean, for my whole-genome-sequencing experiment? In particular, what does matching the contig against a reference file mean?

I'm not familiar with picard and their reorderSam function, but as far as I know/understand from their documentation they mean this:
The ordering of the contigs while using a reference sequence.
Like this:

 Figure 5: Anatomy of
  whole-genome assembly. In whole-genome assembly, the BAC fragments
  (red line segments) and the reads from five individuals (black line
  segments) are combined to produce a contig and a consensus sequence
  (green line). The contigs are connected into scaffolds, shown in red,
  by pairing end sequences, which are also called mates. If there is a
  gap between consecutive contigs, it has a known size. Next, the
  scaffolds are mapped to the genome (gray line) using sequence tagged
  site (STS) information, represented by blue stars. © 2001 American
  Association for the Advancement of Science Venter, C. et al. The
  sequence of the human genome. Science 291, 1304–1351 (2001). All
  rights reserved. (source)

ReorderSAM (Picard)
So in Picard you have your INPUT (File), the reads in this file are then mapped on the REFERENCE (File). This can also be seen in their code:
// write the reads in contig order
109
            for (final SAMSequenceRecord contig : refDict.getSequences() ) {
110
                final SAMRecordIterator it = in.query(contig.getSequenceName(), 0, 0, false);
111
                writeReads(out, it, newOrder, contig.getSequenceName());
112
            }

(code source)

ReorderSam reorders reads in a SAM/BAM file to match the contig
  ordering in a provided reference file

Some more background
There are two main approches two obtain a genome sequence:

there are two "main" approches for this:  g. Second-generation
  sequencing technologies produce millions of short(a few hundred bp)
  strings of nucleotides (reads), which is ideal for resequencing when
  reads are mapped to a reference genome (reference-based assembly). De
  novo genome assembly based on second-generation sequencing is
  challenging due to difficulties with GC- or AT-rich and homonucleotide
  DNA stretches, which are under-represented in the sequencing output (source)

The characteristics of these are:
de novo

no bias towards a reference genome
no template to adapt to
the    assembly is normally more fragmented
it normally works better for large-scale/median scale differences (source)

reference mapping

less contigs
in most methods the reads that don't map are not used in the final sequence (this is also the case with reorderSAM: Reads mapped to contigs absent in the new reference are dropped
you look what is similar to your reference genome
SNPs and very small veriations are more easily positioned and compared among groups (source)

I would highly recommend to watch this short animation to differentiate between these two and understand what reference genome mapping is.


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Reason behind formation of positive supercoils during DNA replication/ transcription
When a twist is unwound without cutting the DNA strands or is removed by cutting the strand(s) and resealing, negative supercoils are introduced in the DNA.

From Cell and Molecular Biology -Karp
But strangely enough unwinding of DNA by helicase cause the DNA ahead of the primosome to form positive supercoils. Why is it so?

From: Molecular cell biology -Lodish
My speculations: Underwinding cause the adjacent DNA to overwind and as the DNA overwinds the associated stress developed cause the DNA to form positive supercoils (which would have happened naturally had new twists been introduced in the DNA (Time:1:54) ).
I think removal of twist creates negative supercoils initially but when the unwinding causes too much overwinding of adjacent DNA, the strain developed cause the already negatively supercoiled DNA to form positive supercoils.

It's hard to explain in text, so here's a video:
https://www.youtube.com/watch?v=J4YlcD59-yw
Imagine the shoelaces are two DNA strands in a double helix. They are topologically constrained at each end. As the pen (helicase) moves through the helix, it creates overwound DNA in front of it and underwound DNA behind it.

Does that answer your question?

I didn't follow the notification about this answer. I also found Genome Duplication, pg-12 mention it.


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Why do we die of old age?
Not sure where to ask this question and thought this would the best place.
I am not after any opinion or theological, philosophical answers.
I am after the science or biology research, experiments or facts.
I would like the answer to be focused on the following:
Why do we die? With the condition that there are no diseases or any outside factors contributing to death.
In a simpler way, what makes us die biologically, physiologically. Is there a trigger? Is it cellular?.... and so on
As per suggested comment, I have researched genetics such as cell regeneration dynamics, Organ's lives studies.
Yet I find very little on the brains involvement, nervous system, chemical or anything else on the multitude of systems we have including triggers or irreversible messages from any or these systems

Possible duplicate of What evolutionary explanations are there for death?

These answers are not what I am looking for! I need a scientific explanation on any level, like cellular or brain chemistry or how many heartbeats there is in a human... that sort of thing

here is a good answer about the scientific explanation: https://www.reddit.com/r/askscience/comments/3fmle0/what_really_causes_death_when_you_die_of_old_age/

This answer is too partial and diverges into diseases. Many people just die of old age without diseases and relatively well balanced, yet they still die.

What research have you done so far to answer your question?

Genetics: at one point, our cells regenerate less than what we lose: we get old! Is there a link? There's research on hearts: apparently, they have a certain amount of beats.... that sort of things. Yet I cannot find a complete explanation possibly linking all these factors, or is there another avenue I haven't found yet!

Possible duplicate of Why does evolution not make our life longer?

Again, these answers focus on specific issues of dying old, not the pure biology of what I am asking!

In the absence of disease (including starvation, electrolyte imbalance, etc.), there is no death. Old people die of diseases, even if those diseases went undiagnosed while alive.

A possible answer (plus probably a bunch of other factors) is the rate of cell death/damage exceeds that of cell repair as one ages. Search on google for 'The impact of aging on kidney repair' if you want to read more (EDIT: Here's the link https://www.ncbi.nlm.nih.gov/pubmed/18287400 )

We die of old age because the biological cost of making us live forever does not improve our chances of passing on our genes. In nature something else would kill us eventually so there was never a reason to evolve the ability to live indefinitely. There are multicellular organism  that are biologically immortal(all unicellular are), they live slow low activity lives. A lot of the evolution of more "advanced" life is trading regeneration or longevity for higher activity. Literally live fast die young, leave more offspring.


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Spectroscopy on plant leafs
I'm trying to do spectroscopy readings on plants where I shoot electromagnetic waves and look at their signature/profile.
I want to be able to do this at a distance, in the field and on live plants so that I can modify my rig later to automatically do this on multiple plants daily.
I have no background in spectroscopy, but I heard that waves directed  through leaves can then be received on the other end using something like waveguide spectroscopy. I do not know the frequency range I should be looking at and was wondering how can I identify the range of interest for my plants.
Let's say I want to approximate the chlorophyll content in leaves and see if the leaf is healthy or not and look at its change daily. Some references to learn about this would be very helpful. Thanks!


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Can a phenotype only have one allele?
A phenotype such as hair color
like blonde hair.
I am curious because mutations cause new alleles but does that mean that there always has to be a dominant or reccessive allele?

Related: https://biology.stackexchange.com/questions/111402/what-are-the-relative-frequencies-of-dominance-and-codominance-in-genes-underlyi

Can there be only one allele at a given locus?
An allele is a variant of a gene. If there is only one allele at a given gene, it means that there is no genetic variance at this specific locus (a locus is a position in the genome. It can typically correspond to a gene). It is not rare at all that the whole population is fixed for the same allele at a given locus.
Number of alleles
In courses, it is common to consider only the case of 2 alleles. In reality, there might be any number of strictly positive allele. At a given locus, you might have 1, 2, 3 or 11 alleles for examples. The reason why we typically teach about the 2 allele case is that 1 allele is not of much interest as there is not genetic variance at this specific locus and 3 or more alleles makes everything a little more complicated.
Dominance relationship
In courses, it is also common to consider diploid individuals, 2 alleles and the phenotypes of the three possible genotypes assuming $h_N = 1$ (see here to understand $h_N=1$). In reality, the relationship between two alleles may be vastly more complicated. There is a gradient from complete recessivity to complete dominance (passing through perfect additivity). It is also possible that the heterozygote is more extreme than any of the two homozygotes.
Dominance relationship - Number of alleles
As the number of alleles varies, any pair of alleles have a specific relationship of dominance. While empirical studies suggest that if allele A is dominant over B and B is dominant over C, then A is likely dominant over C, it is not impossible that C could be dominant over A. And again here, I am considering only cases of complete dominance but any scenario is possible.
Dominance relationship - Ploidy
The ploidy also varies from one species to the other (and also from one moment in the life cycle to the other for sexually reproducing organisms). If you have  a polyploid, then the number of possible genotypes is higher than 3 (even for a 2 allele case) and therefore the concepts of recessivity and dominance don't necessarily apply that easily.
Dominance relationship - Epistasis
Finally, there might have interaction between loci making that the relationship of dominance at one locus may depend upon the genetic background (that is the other variants present at other loci). Of course, it may as well depends upon the environment but let's not talk about that for the moment.

@NeelSandell Please, let me know if it answered your question or not.

This is actually a really good question.

Can a phenotype only have one allele?

Yes. Some diseases arise only from one known allele. Some common phenotypes can be predominantly controlled by a single allele, but are affected by more than one. On an individual level, it is common to see one allele creating the phenotype, such as rare diseases cause by de novo mutations or familial rare disease. On a population level, it is harder but not impossible to find a phenotype that has only one allele for everyone because genes typically contain many alleles.

Mutations cause new alleles but does that mean that there always has to be a dominant or recessive allele?

No, there doesn't. In fact, we've lied to you in school a little bit to make things less complicated. It is easy to teach dominance and recessive alleles and do punnet squares, but the reality is that dominant alleles have little effect on complex traits like height or how much education someone receives. You've stumbled upon the same intuition that led Fisher to develop the currently prevailing additive model in 1918.
All complex traits, i.e., most things that aren't a rare or Mendelian disease, do not have important dominant/recessive alleles. Instead, each allele contributes a little bit regardless of if other alleles are present or not. So not only does there not have to be a dominant or recessive allele, but it is the norm for there not to be.
Dominant alleles arise naturally due to loss of function mutations. They are very important in the discussion of monogenic genetic diseases, and frequently contribute to the phenotypes of rare disease, even though they are rarer than additive alleles.

"dominant alleles are quite rare" I would take issue with this. Simple example: loss of function mutations necessarily leave a dominant allele (LOF is recessive). Granted, they are certainly numerically rarer overall, especially as you say for complex traits or neutral variation. But you will encounter them quite often in doing genetics on things people care about! Related: https://biology.stackexchange.com/questions/111402/what-are-the-relative-frequencies-of-dominance-and-codominance-in-genes-underlyi

Good point; I will edit it with that in mind

This may depend on how precisely you wish to define an allele. Cystic fibrosis is a disease effected by mutations in a chloride ion transport channel. Because this is an extensively studied illness, now over 500 different mutated versions of the gene are known. Each of these genotypes gives rise to the disease although there is much variation in the severity of the disease pending the exact mutation.
https://www.ncbi.nlm.nih.gov/pubmed/8949420


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How can soft tissue exist in dinosaur fossils?
In this article the author explains that they found soft tissues inside of 68-million-year-old dinosaur fossils. How can that be possible? It was believed that soft tissues cannot last more than a million years and that DNA degrades even sooner.

Our findings challenged everything scientists thought they knew about
  the breakdown of cells and molecules. Test-tube studies of organic
  molecules indicated that proteins should not persist more than a
  million years or so; DNA had an even shorter life span.

What is the evidence that the fossils were real?

Uh, that link is to "An annotated list of links to further reading about dinosaur soft tissues" What is left to answer?

In a nutshell the organic matter got encased in such a way that oxygen was limited at first and ultimately the casing materiel sealed the organic matter left completely off from oxygen.

This question seems more sutable for Biology.SE than here.

@MaxW, you are smarter than scientists because they would never think of that.

@Ilya Melamed, ok let's migrate

keratin and collagen are an incredibly tough molecules so if it is isolated from the environment (oxygen and bacteria) it could easily survive for that long. Not all proteins are equal some are very robust other very fragile. We have long known protein and carbohydrates can survive for incredible lengths of time under the right circumstances, amber is famous for it. Rapid deposition of minerals can produce a similar if less powerful result.
In this case the keratin was encapsulated by water deposited minerals that sealed it away from the outside environment. There are other examples as well, natural mummification can lead to some preservation in the form of biofilms and impressions. But the most dramatic are amber encased specimens. Amber is a quick forming and creates a perfect air seal.
here is a dinosaur tail preserved in amber.

"The bone slice was from a dinosaur that a team from the Museum of the Rockies in Bozeman, Mont., had recently uncovered—a Tyrannosaurus rex that died some 67 million years ago—and everyone knew organic material was far too delicate to persist for such a vast stretch of time. " it doesn't seem the sample was preserved in keratin.

I think I found the answer http://www.livescience.com/41537-t-rex-soft-tissue.html

not preserved in keritin, MADE of keratin, I assumed you were referring to the discovery of beta keratin in dinosaurshttps://news.ncsu.edu/2016/11/moyer-claw/. In the case of the study you are referring to the material in question is collagen which is also very tough. It is the rapid mineralization of rhe fossil that seals the bone.

in the link I provided they talk about iron which creates formaldehyde and that can preserve tissue. It's just little funny to me how easily they can find the answer and the whole community takes it as solved.

I was part of that community, if you think figuring out how it happened was easy you are mistaken, there were dozens of paper back and forth. Several argued that that particular piece was not even original but a bacterial byproduct, it is still not confirmed to be original, That is why I assumed you were talking about the beta-keratin finds they are unmistakably original material. And remember you are looking at the editorial about the science not the original research.

lol, you are a joker. It should take something like to build a hydron collider to test and prove these theories and you say it took some dozens papers going back and forth?

You don't understand what testing means, testing does not mean reproduce in a laboratory. Ask another question about it so someone can answer or try reading up on it, http://www.brynmawr.edu/geology/documents/scientificmethodCleland.pdf


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How does the body count time in the short term?
So I've done some research and found out about the different circadian cycles that use chemical clocks to help us keep time in the long term (hours, days, etc.). This doesn't seem to explain how we can so accurately count seconds. Musicians can count time extremely precisely in even shorter intervals than seconds. Is it a chemical clock responsible? If you could explain the whole process to me it would be great. Thanks.

I've nominated this question for reopening because it is clearly about counting time in the short term, whereas the duplicate marked is merely about circadian rhythms. This question explicitly differentiates itself from circadian time and is talking about time on the order of seconds.

"One mississippi, two mississippi..."

There is a significant difference between (consciously) counting time, and simply being aware of it. Musicians are aware of time, but we don't count time when performing. Once a musician begins performing, the music is "alive", and the musician must keep playing in order for it to stay living. Because of this, their assessment of timing is relative, so to speak, and (fairly) easy to maintain without thinking. I would also say that the impeccable accuracy in a musicians ability to adhere to timing simply comes from their extensive practice of the (given) composition; I speak from experience.

@Charles But what biologically enables musicians to do so? By practicing, they must be essentially just fine tuning whatever biological function that helps us keep time. As an analogy when riding a bike, at first we must consciously make an effort to balance. Eventually we fine tune our vestibular system to the point where we can subconsciously do it. I am look for that "vestibular system" for hearing. At least I think this is the way it works. Am I right?

Detection of rhythm is a separate function from general musicality, but both can be affected by the same brain damage, or they can be independently affected:

A range of rhythmic deficits has been described, including the inability to reproduce rhythmic patterns or to discriminate between them, and the inability to perform music rhythmically, or to keep time to music, including dancing in time. These deficits may occur in combination with other musical deficits, such as impaired vocal and instrumental skills ... rhythmic and metric organisation can be differentially impaired in brain damaged patients, supporting the relative independence of functions of the rhythmic system. In terms of cerebral lateralisation, Peretz and Morais [43] suggested that metric organisation may be ascribed to the right hemisphere, whilst smaller rhythmic groupings are encoded by the left hemisphere. ... Neuropsychological studies of groups of patients, however, have generally shown more variable lateralisation effects, particularly in recent research [25,36,46]

--Modelling rhythmic function in a musician post-stroke
So it seems that the detailed neuroanatomy and function of rhythm isn't completely understood, but it is a fairly specific function.  One suggestion is that it's  linked to language ("We conclude, then, that this effect is linked to language dominance and not handedness." -- Rhythm and dominance), but I don't know how widely this is accepted.  Possibly Common neural mechanisms for explicit timing in the sub-second range. offers more insight, but I don't have access to the full article and the abstract isn't very helpful.


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Ethics in Paleontology
Ethics in Paleontology
Fossils help researchers understand the evolution of many lineages of plants and animals. But, who actually owns fossils? What if an important fossil (say a transitional fossil like Tiktaalik or Basilosaurus) were found by an amateur fossil hunter and sold to a private collector? Should there be regulation of fossil hunting to prevent loss of scientific information? Should all "important" fossils be turned over to museums?

I'm voting to close this question as off-topic because it is not about biology.

It depends entirely on where the fossils were dug up. In the US fossils on private land belong to whomever owns the mineral rights to the land, that landowner can do with the fossils as they will. On public land the fossils belong to the government and to get a permit to dig them a paleontologist must have a place to store them, this is part of the permitting process (digging on public land without a permit is a felony). Most of the time this place is something called a repository, a public institution that has facilities to store and care for fossils, usually a museum or university and has contingencies so that the fossils will not be lost if the facility were to fail or close. Now this is for vertebrate fossils becasue of the nature of invertebrate fossils (chalk for instance is made entirely of fossils) the laws can be a bit more lax.
Private collectors can only collect on private land, which usually involves making an agreement with the landowner. Keeping collection records is always a good idea if for no other reason than to show where a fossil was found.
I have worked with both types of collectors private and public, good private fossil hunters will differentiate rare fossils and common ones and will donate rare ones to museums while selling common ones. Bad one will sell everything, which often does lead to fossils disappearing or in some cases being outright destroyed by those who disapprove of evolution and the fossil evidence for it. For this reason most journals will not accept publication made using private collections, becasue it makes repeatability impossible.
Now this is all in the US, other countries have different laws some more strict some less so.


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Plant identification: San Francisco, USA

I am taking a biology lab class and I need to identify all these plants which are from the San Francisco area.
My question is how can I find the right keyword to find their names on internet? Or can you recommend any book that I can find in library?

some pictures with more details would be great. the plants are all quit jung - which make it difficult. also some additional inforamtion about the context: it look a little bit like a peatland?  is it a kind of garden? or what is the type of landuse in your side?

Those are grow under the shade of the pine cone tree which is near by my college. I have no idea how to use the word to find them on google. Yes I can post clearly picture if you would like to help me pick some word to find them. Thanks

I'm going to refrain from giving you the answers because the point of the assignment is to  learn how to do it yourself.
You should likely start  by using a dichotomous key (likely provided by  your instructor).
You could also try  searching the Jepson California eflora or CNPS Identifying Native Plants for online keys.
Check out  the California Native Plant Exchange website if you don't know the name of the plant but know the general area where you saw it.
If you don't know what general type of plant  you have,   you should try keying  the plants to family  first  to get better search terms.  Try here.
If you don't know plant terminology  used  in  these keys,  try  "Plant Identification Terminology: An Illustrated Glossary" (Harris & Harris, 2001)

I am from another country who just move in here and  I already try all those words that you show me but still did not get how those plants look like some kind of group. That's why I try to ask more specific word.

@SiriwanLaoketkit This is not a guide to keywords for google, it was a guide to identification  key websites and books which help you identify plants, usually by a step by step questionnaire. https://en.wikipedia.org/wiki/Identification_key


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Why do we fear the night?
I always feel more afraid in the dark than in light conditions. Is this a common phenomenon in all the people? Does it have biological underpinnings?

This is more a psychology question than a physiology question and is probably better asked at http://cogsci.stackexchange.com/

Possibly related: http://biology.stackexchange.com/questions/55700/why-are-fearful-stimuli-more-powerful-at-night?rq=1

This question was closed as a duplicate as mentioned above, since the OP deemed the other question as a sufficient answer for this one.

Our ancestors were hunted by predators active at night. This is our inheritance, it is not something pathological.


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Why is it desirable to couple chemical production to growth?
I have the following question in systems biology:
a) Draw a graph showing the relationship of growth (Vbio) and Vefni for the system here. (Let the horizontal axis represent Vbio and the vertical axis represent Vefni)
My first thought was that it would simply be straight line from (0.5,0.5) to (1,0). But now I'm thinking that I have to take V4 into account as well.
b) Determine one or more reactions that are such that if they are taken
out the production of M4 is coupled to growth (growth-coupling). Draw a
graph showing the relationship Vbio and Vefni for the mutant.
Here I thought it would be V1 and V4. I'm not sure though because I haven't found a good explanation for what growth-coupling is exactly.
c)  Why is it desirable to couple chemical production to growth? i.e. what advantages do those systems have over the ones where no such coupling is present?
Here I have no idea.

What are the various terms supposed to mean? $V_{efni}$ etc.? I used the internet to translate and it looks like efni and aukaafur∂ mean respectively "stuff" and "byproduct" in Icelandic, but I'm not sure that fully explains the question. I guess $V_{bio}$ means biomass? The answer looks good but it's hard to puzzle out without this info.

Why is it desirable to couple chemical production to growth?

When designing new metabolic pathways for chemical production, one has to keep in mind that the purpose of it is to get scaled up (i.e. to reach industrial size).
From the industrial point of view, the faster/simpler a process is, the better. Growth coupled chemical production means that only one step is necessary in order to produce the desired product (before downstream processes). Otherwise, one would have to produce the biomass first (growth step) and then to proceed to the chemical production step. One step is cheaper and faster than two, not mentioning the intermediary steps that could be necessary (cells washing, centrifugation, filtration ...).
The main drawback of growth coupled chemical production is that the final yield ($mol_{final~product}/mol_{substrate}$) is hindered by biomass production. This can be a real issue if the substrate is expensive.


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Example of well understood/modeled biological mechanism
I am working on modeling psychiatric disorders, where multivariate time series data - which I think is necessary to do any interesting modeling - is only broadly available recently, due to the availability of surveys via mobile devices.
To get into the dynamic systems modeling literature, I would like to look into a biological mechanism, which is well-modeled, by which I mean that the error/misfit is negligible for many applications. Basically, I am looking for a (historical) example, where I can follow the steps that were taken to get from the observed (maybe experimental) data to a good model, with the hope that I can learn some lessons for my own work. Ideally, it would be an example with about 5 < p < 20 variables.
Any hints and suggestions are greatly appreciated and my apologies if this is a too trivial question.

Assuming you are talking about analytical modelling and not about statistical modelling, you can learn about modelling in general by learning the basics of math. This book from Otto and Day talks about analytical modelling in the fields of evolution and ecology.

while @Remi.b has a good point, I would counter from own experience that getting hands dirty with data is the best learning method for me. there are thousands of examples of biologically interesting mechanisms with data and models, but it would be very helpful to know more about what you want to do. Does it need to be time series data? Or psychiatric data? There is for instance really great data and models on molecular networks running plant circadian clocks from Andrew Millar's group (http://onlinelibrary.wiley.com/doi/10.15252/msb.20145766/abstract).

I would point out that, assuming (as the other commenter noted) you are interested in analytic rather than statistical modelling (which seems a little unlikely to me given your area), most mathematical models are derived from first principles (often from physics) or other assumptions.
This suggests (to me) that looking at models of totally unrelated systems is not so useful; the whole idea of such models is to formalize your domain knowledge!
But I'll give some examples anyway.
For example, consider
 biophysical models of neurons or continuum mechanical models of cardiac tissue, both of which have rich histories of mathematical models developed over decades of work, based on both theoretical and empirical considerations (albeit largely from physics).
Perhaps slightly more related (or at least empirically driven) are the advances in systems biology, which tend to derive from some underlying laws of chemical kinetics, but utilize enormous amounts of (multivariate, temporal) data in fitting (often non-linear stochastic) systems of differential equations. Methods for computational protein structure prediction tend to use a mix of ad hoc rules (for computational time-cost reasons) and physics-based considerations in their models.
Evolutionary biology and population dynamics also have wonderful models (see the book from the commenter above).
My guess, given that your question does not have much detail, is that you would prefer statistical, i.e. probabilistic graphical or stochastic process, models instead.
Let's suppose you have a bunch of variables over time (e.g. the actions or status of a person) but you want to estimate an unobservable quantity (e.g. say, the degree to which they are insane [not my field, sorry]).
One simple probabilistic model is the hidden Markov model.
It has many examples of applications in sequence biology.
It also lets you figure out, in a way, which variables are important, and let's you tune certain parameters (e.g. it's order, which here describes how much the person's state at time $t$ affects their state at time $t+\Delta t$).
In terms of predictive modelling power, though, the state of the art is in deep learning models for time series.
Anyway, I'd consider what your goal is more carefully. If you indeed have a strong idea of an analytic model (motivated by some theory you know), then by all means formalize it. However, if you want the data itself to suggest a model for you, then use a statistical approach.
Note: apologies if this answer was too trivial, I was not sure what you did and did not know.


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Does size correlate with sensory abilities?
On average, do smaller animals have senses inferior to those of bigger animals?  I ask because it seems like a somewhat logical assumption: smaller eyes would in theory collect less light, and smaller ears would in theory collect less sound.
Or is size just irrelevant?

this is a broad question that probably depends greatly on the types of senses that you're referring to. what research have you done trying to fine an answer to this question?

Size is not likely to have anything to do with sensory acuity. A simple example can be seen in the fact that rodents have much more sensitive sense of smell than humans, and some birds have much sharper visual senses than humans. It has much more to do with the number of olfactory/light sensors, sensory pathways to the brain and how that information is processed by the brain (i.e how much priority is assigned). Sensory organ size per se is less relevant (think of elephant ears).

can you add some references or links to back up your answer? posts without any evidence of reference material don't get very far on BiologySE - even if this maybe common knowledge to you, you still need to try and provide some references that others might be able to read more to better understand the answer

Guess thats true. Unfortunately my answer comes from years of working in scientific research animal facility, with small animals. References for something more on the 'common knowledge' spectrum would be very labor intensive and difficult to find. I will remove my answer shortly as i cannot provide a citation. Just want to give the poster a chance to view this answer and maybe help them get where they need to get.


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Caterpillar identification: Peru

Could you please help me identify this caterpillar (Amazon rainforest, Peru)?
Is it a species of Megalopygidae???

Did you take this picture? If so, could you provide more information about where it was found (e.g., on the ground, on a tree, etc.).

Yes - On the trunc of a living tree - During the day - Tamshiyacu Tahuayo Regional Conservation Area.

It resembles a Puss mouth or flannel moth caterpillar. The adult moth is beautiful and the bristles of the caterpillar are very irritating.. It does indeed belong to the Megalopygidae

It is an pink flannelmoth because there is no other insect which ressembles it

Usually pinkflannelmoths have orange coloured centers

The proposition that something is something because it looks like it is completely falacious. I could say that a person is an ape because they look alike. Perhaps it is an undiscovered species?

But with just one photo from the top view you can't expect the answer right

I do agree with your there

Please provide supporting facts.. simply saying, "I couldn't find anything better" isn't the best logic to use.


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Hardy Weinberg equilibrium

Hardy Weinberg would predict that the frequency of normal females, to carrier females,
  to affected females for colorblindness is equal to p$^2$ + 2pq + q$^2$=1. You
  were told that q=freq of the recessive allele. If p+q =1 (frequency of the dominant allele +
  frequency of the recessive allele=1 or 100%) and q=.08, what is the frequency of the
  normal allele in the population? What is the frequency of carrier females in the
  population (ie heterozygous females)?

I get that the frequency of the normal allele is p = 1 - .08 so 0.92. However the frequency of carrier females is giving me an unrealistic number. Using p$^2$ + 2pq + q$^2$ =1, the value for pq comes out to be a negative value. Is it safe to just multiply p and q since that is what we're essentially solving for using the full HW equation? This would make the value (.08*.92) = 0.0736. Would that be the way to approach the problem even though it asks for females only?

Welcome to Biology.SE. Homework questions are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy.

Btw, although the question is quite clear, the phrasing is a bit inaccurate and misleading. Is it the question as written for your homework?

Yes, that is the exact wording of the problem!

check your math, the value for pq comes out to be a negative value is incorrect

Thank you, got the value to be .0736. Would this be correct as to being the frequency of carrier females?

Carrier females= 2pq= 2 x .08 x 0.92
Because carriers say with genotype  Aa (A=dominant, a=recessive)  can arise due to two types of inheritances;one when A is from father and a is from mother and the other when it is just opposite.


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Insect identification - Is this a bedbug?
This bug was found on a couch in Cape Girardeau, Missouri. The couch, and the two beds in the room show no signs of other bugs. Is this a bed bug that I should worry about or something harmless? It was slightly larger than a common tick.

Having had bedbugs before, this definitely looks like one. You need to dig deep into all the cracks and crevices of the furniture; if the furniture is not sealed (e.g. material on the underside is only stapled on at intervals of 6-8 inches -- if you can slide a butter knife under the material, a bedbug can go there) they could very well be inside the furniture.

Also look for droppings. They'll look like little brown or black spots about the size of a grain of sand, in/around where the bedbugs nest. In a small infestation (one or two errant bugs) you might not see any, but if you have more than a few, you might be able to spot the droppings. See https://www.bed-bugs.com/images/bedbugs.com-blood-smears-on-mattress.jpg for a minor example, or Google image search for "bed bug droppings".

Unfortunately, you're the first I've seen on here actually to have a bed bug.
See  this picture  from University of Kentucky for comparison:

Here is one moving (more footage & info here):

Below is a picture from Bed-Bugs-Handbook.com demonstrating the relative size and appearance of 6 different life (molt) stages:

From Left to Right: Nymphs to adults both before (top row) and after (bottom row) feeding and becoming engorged with blood.

General Info:
Bed bugs are parasitic insects of the cimicid family that feed exclusively on blood. Cimex lectularius (or the common bed bug) is the most well known species as it is the one that feeds primarilly on human hosts and infests human dwellings. These insects often dwell in beds, couches or other upholstered furniture, and they are also known to live in cracks and crevices in walls, behind wallpaper and wood paneling, or under carpeting (Krueger 2000).
They usually feed nocturnally, and in the absence of allergic rashes from their bites, their presence can go unnoticed. The first signs of a bed bug infestation are often the bed bugs themselves or small dark stains bed bugs can leave behind.

See this EPA page for more information about locating bed bugs in a potential infestation.

Description
From University of Florida:

The adult bed bug is a broadly flattened, ovoid insect with greatly reduced wings (Schuh and Slater 1995). The leathery, reduced fore wings (hemelytra) are broader than they are long, with a somewhat rectangular appearance. The sides of the pronotum are covered with short, stiff hairs (Furman and Catts 1970). Before feeding, bed bugs are usually brown in color and range from 6 to 9.5 mm in length. After feeding, the body is swollen and red in color (USDA 1976).

Nymphs and larvae are smaller than adults, with late-stage nymphs being about 4.5mm long. (see here for size ranges). However, only adult females can lay eggs (see here and here for sexing tips). Their small (~1/10") white eggs are laid in clusters in mattresses, furniture, or in cracks in the wall, baseboard, or floorboards. (See here for more egg info).
Do you have a problem?
From Wikipedia:

Certain signs and symptoms suggest the presence of bed bugs; finding the adult insects confirms the diagnosis.

However, other than being a nuisance (e.g., having a "gross" factor + some skin conditions such as rashes), bed bugs have not been known to transmit dangerous human diseases (e.g., see Dolling 1991 and Kolb et al. 2009)
What to do:
Below, are a number of reputable and useful resources for handling and ridding yourself of bed bug infestations:

Bed Bugs: Get Them Out and Keep Them Out (U.S. EPA)

How to Treat Bed Bug Bites and Find the Pest (U.S. pest control company Terminix)

Bed Bugs: How to Get Rid of Bedbugs (pest-control company Orkin)

Finally, a quick search for "bed bug" on this site as well as visiting this reddit page can provide info for a myriad of species that are often mistaken to be bed bugs (e.g., carpet beetle larvae, psocids, fleas, ticks, etc.). Again, unfortunately, you're the (un)lucky winner and do in fact have a definitive specimen.

Citations:

Dolling W.R. 1991. The Hemiptera. Oxford University Press, New York, New York.

Kolb, Adam, Glen R. Needham, Kimberly M. Neyman, & Whitney A. High. (2009). "Bedbugs". Dermatologic Therapy. 22 (4): 347–52. doi:10.1111/j.1529-8019.2009.01246.x. PMID 19580578.

Krueger L. 2000. Don't get bitten by the resurgence of bed bugs. Pest Control 68: 58-64.

Wow. This is a very good answer, also for latter bad bug identification searches. Thank you for putting this together!

Note that in extremely rare cases, this might be a variety that lives with swallows (martin bug, oeciacus hirundines) , so when you find them in a room with a window, where on the outside of the house there are swallow nests, you might want to check if they come from there.

Thank you for the assistance. This was identified at a VRBO rental and now many, many of the babies have been found crawling on just about everything. So on to another site to find an answer for how to avoid bringing them home.

@NickCriswell I had a lot of success using thermal treatment. I put in a drying cabinet at 60 C my luggage and (washed) clothes, and in the freezer what didn't take the heat.

It never ceases to surprise me how unfamiliar people are with what a bedbug is.


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Which two organelles absorb acid?

I stain an unknown acid with purple dye. Later, you find the cell in two organelles. What are they?

I am guessing that one of them is lysosomes, because they break down unwanted elements. What would the second one be? Mitochondria?

Take a look at this.

@SanjuktaGhosh So my answer of lysosomes and mitochondria is correct?

I think the acid / base terminology is confusing in histology. In my understanding, this is not about pH, it's about charge. "Acidic" stains are deprotonated, and therefore negatively charged molecules, and so they are attracted to positively charged structures. Most proteins are positively charged, so protein-rich structures tend to be stained, while nucleic acids (which are negatively charged) are not.

It is about pH in the sense that acidic dyes will be deprotonated and negatively charged at neutral pH. If the pH is lowered below the pKa of the dye, it will become neutral.

The principle of staining works in such a way that acidic dyes stain the complementary basic components of the cell hence acidic dye rather than staining lysosome which is acidic will stain the relatively basic components of the cell.

What are complementary basic components? Specifically the complementary aspect.

So it stains the nucleus and ribosomes?

Hi. I am not sure of basicity of some cell organelles. Hence I have provided how staining works because I saw wrong answers; it definitely does not statin nucleus because nucleic acids are acidic in nature.


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What is the diet preference of American cockroaches?
I found a research article1 on the diet preference of German cockroaches. It reveals that those cockroaches prefer to eat bananas most. I wonder if it is the same for American cockroaches. And also, can American cockroaches survive on wood and water alone?
 1. El-Sharabasy, H.M., Mahmoud, M.F., El-Bahrawy, A.F., El-Badry, Y.S. and El-Kady, G.A., 2014. Food preference of the German cockroach, Blattella germanica (L.)(Dictyoptera: Blattellidae). Cercetări Agronomice în Moldova, 2(158), pp.81-88.

Bananas? In Germany? Bananas!

American cockroaches (Periplaneta americana) are omnivorous and opportunistic feeders, and as a result, they eat a large variety of foods. They will eat almost anything.
Favorite foods: They are particularly fond of fermenting foods$^{4,6}$ and also prefer sweets$^2$.
Common foods they eat: plant materials, dead animals, sugar, oil, cheese, beer, tea, soap, leather, bakery products, paper, starch in book bindings, manuscripts, glue, hair, flakes of dried skin, soiled clothing, glossy paper with starch sizing and generally most human or pet moist food or other organic matter $^{1,3,5}$. They have also been observed feeding on dead or wounded cockroaches of their own or other species as well as their own cast-off skins and egg-capsules$^6$.
 According to EOL:

 Some of [their food] items, such as cellulose, can not be digested by normal means. However, like cows and other grazing animals, cockroaches have a symbiotic relationship with a bacteria that allows them to digest such substances.

As a result, they could almost certainly survive on just wood and water.

Citations:
 {1}  Bell, William J. and K.G. Adiyodi. (1981). American Cockroach. Springer. pp. 1, 4. ISBN 978-0-412-16140-7.
 {2} Barbara, K. A. 2014. American cockroach. University of Florida Institute of Food and Agricultural Sciences. Retrieved 11 February 2017. http://entnemdept.ufl.edu/creatures/urban/roaches/American_cockroach.htm .
 {3} Jacobs, Steve. "American Cockroaches". The Pennsylvania State University. Retrieved 11 February 2017. http://ento.psu.edu/extension/factsheets/american-cockroaches .
 {4} Jones, Susan C. 2008. Agricultural and Natural Resources Fact Sheet: American Cockroach (HYG-2096-08). Ohio State University. http://ohioline.osu.edu/hyg-fact/2000/pdf/2096.pdf.
 {5} Milne, L. & M. Milne. 1980. National Audubon Society Field Guide to Insects and Spiders. Knopf, New York, NY. p 393. ISBN: 0-394-50763-0.
{6} Periplaneta americana: Palmetto bug. Encylopedia of Life. Retrieved 11 February 2017. http://eol.org/pages/1076920/hierarchy_entries/51102706/details .


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Can Mother-to-Child Transmission Occur in Relation to Mycotoxins or Mycoestrogens?
There are 17 officially noted cases in which leukemia or melanoma cancer cells crossed the placenta from mother to child. Other crossings include metals (or metalloid elements), such as mercury or arsenic (just as an example). There are also crossings of bacteria, viruses, and general foodborne illnesses.
With all this in mind, my question is: "Can a mother who is hosting a mold, transfer that to her unborn child?"
(Please don't supply an answer about how the child is at risk during the birthing process or caesarean section. Other than that, even opinions are welcome. Thanks in advance.)