text:
Is human vision sensitive to frequency or wavelength?
In a vacuum, there is a one-to-one correspondence between light frequency ($\nu$) and wavelength ($\lambda$), ie. $\lambda=c/\nu$. But in a refractive medium, $\lambda=v/\nu$, so while the frequency may remain constant, the wavelength may not.
I've seen that in biology, wavelength is mostly used. But, I recall reading that human vision is sensitive to frequency. So, is human vision sensitive to wavelength or frequency?

Huh. It's a question of what wavelengths of light will activate opsin proteins in the retina itself. If you changed the refractive index in the retina photons of the same energy(and therefore, frequency) should activate the same state transitions in proteins.

My guess is therefore frequency instead of wavelength, but if anyone has empirical data I would love to read the methods of that.

I found this answer relevant since he shows that if our eyes detected wavelength a red brick would look green seen from water.

@Aditya P no it wouldn't. It will still appear red because retinal fluid remains the same, so final wavelength reaching retina will still be same

It is not the wavelength or frequency that determines light absorption- it is the energy of the photon that matters. The energy of incident light should match the excitation energy of the chromophore. The medium itself can also affect light absorption by electronically interacting with the chromophore. Frequency is proportional to the energy (given by the relationship $E=h\nu$); while wavelength and velocity change in different media, frequency and energy remain constant.
The chromophore in the opsins (retinal) absorb energy to become active and you can say that they detect the frequency. However, sufficient number of opsins have to become active for the retinal cells to transmit the signal. So the overall light flux is also important. An interesting thing to note is that activation of the opsins hyperpolarizes the photoreceptor cell and reduces its tendency to fire.
Wavelength plays a role in diffraction and therefore diffraction is less in a medium with higher refractive index. Wavelength also determines scattering. So, while the opsins actually detect frequency, the wavelength can slightly affect the overall "vision" because of scattering/diffraction effects.

The energy of a single photon is proportional to its frequency. So if a single photon is detected, its frequency does determine the color.

The more important questions are: Does opsin detect single electron excitation by the photons, or integrate over a period of time and detect the total photon energy? An atom can absorb simultaneously two or multiple photons. I suppose, even if opsin can detect single electron excitation, it can not distinguish between single photon absorption and muti-photon simultaneous absorption. Is that correct? Both cases would imply the eye can not detect the true frequency of individual photons.

@Hans yes of course. Energy is proportional to frequency but I focussed on energy because the transactions (absorption/emission etc) are of the energy. Frequency is a sort of indicator. Regarding opsins: They detect energy of a photon (photon absorption causes a stereoisomeric change) but the retinal cells will respond only if a sufficient number of opsins are active.

Thanks for your answer. You say an opsin is able to detect a single photon. Is it able to absorb two or more photons simultaneously https://en.wikipedia.org/wiki/Two-photon_absorption#Two-photon_emission? Does a retinal cell fire only when the total number of active opsins presumably linked to it or the total energy of the absorbed photons exceeds a threshold? There is difference between the two. Either way, two different compositions of the incoming light can induce the same response from a retinal cell. Is that right? That would limit the resolving power of the retina regarding color.

@Hans as far as I know it is a single photon absorption. The firing of the retinal cells depends on total number of activated opsins but activation of opsins reduces the tendency to fire; there should be a threshold but I am not sure of how the threshold is established, at the moment. Usually different cells in the retina (rods and cones) express different opsins. Some residues in the opsin proteins can affect the absorption frequency of the chromophore (retinal). You can read more about cones/opsins on wikipedia or this linked post.

@Hans I am sorry for the misunderstanding: retinal cells fire less with increased number of activated opsins. I corrected the answer. However, I am not sure if (and how) this is thresholded.

Wavelength-frequency relation is $\lambda=\frac{c}{\nu}$ or $\nu\cdot \lambda=c$ in vacuum. In some refractive media you can substitute $c$ with speed of light at corresponding medium, essentially nothing changes. Speed determines the product of wavelength and frequency, not their ratio, as you suggested. Hence at different speeds frequency and wavelength will both decrease or increase, there is no reason to think that one of them stays constant and the other one changes.
If you still want to make a distinction and describe physical property of light with one of them, frequency $\nu$ would be more relevant as matter/light (photon/electron) interactions work as described by the formula $E=h\cdot \nu$

A short comment: c is always the speed of light, there is no need to "substitute" it, when you have another medium. The speed depends on the medium, so you have to know the specific constant.

Frequency is supposed to remain constant: http://physics.stackexchange.com/questions/59469/why-frequency-doesnt-change-during-refraction

As WYSIWYG wrote, energy is the answer, but to clarify the dependence of energy from momentum... sorry, the dependence of frequency from wavelength, have a look at the animation on this web page: http://www.acs.psu.edu/drussell/Demos/wave-x-t/wave-x-t.html, posted here in what I believe complies with fair use legislation:

It represents a sinusoidal wave, the basic component of any disturbance (as long as you can count on linearity, but that's another matter...).
Frequency tells you how fast the red dot goes up and down. This is what a receptor put in that specific position will sense: a disturbance (here it's the height of a string, in your case the amplitude of the electric field) changing $\nu$ times per second.
Wavelength, on the other hand, tells you how far the maxima and minima of the sinusoid are separated in the medium. In this case, two subsequent crests are separated by $\lambda$ meters. For a given disturbance frequency, this number depends on how fast the wave is allowed to travel in the medium. A slow wave will have a shorter wavelength (because it will travel a smaller distance in space during the time the red dot completes a cycle); conversely, a fast wave will have a longer wavelength.
Note: the speed can depend on the frequency of the disturbance - in that case the medium is said to be 'dispersive' and the relation between frequency and wavelength (or energy and momentum, or - if you are into quantum physics - between energy E and wavenumber k) is called a 'dispersion relation'.
In an isotropic homogeneous medium, the speed is the same in every point and in any direction and you can write
$$\lambda(\nu) = c(\nu) / \nu $$
The frequency is determined by the physical process in the source. It's very hard to change the frequency (i.e. the color, in the visible) of a light wave - you have to resort to nonlinear effects to do that. The wavelength is the result of the interaction with the medium, and changes all the time. But it's customary to express a sort of implied equivalence between frequency and wavelength based on the behavior the light wave would have in vacuum. Hence, when one says 550 nm photon, he is usually implying a photon with en energy corresponding to
$$E = h \ \nu = h \ c_0 /\lambda = 4.226 10^-19 \ J = 2.64 \ eV$$
Where $c_0$ is the speed of light in vacuo.
(Note: the latter value is computed from the one before diving by the charge of the electron).

In the context of human vision, wavelength and frequency are not mutually exclusive, but given by the first equation you pointed out in the question. That is, whenever the range of human vision is given they are not assuming that wavelength and frequency can change independently.

Say you change  the refractive index of the retina. Does the perceived color change?

Also, I think there's a typo in your first equation. I don't have enough points to edit or comment. $v \lambda = c$


text:
Can ovulation and menstruation occur simultaneously?
Is that possible that ovulation happens in the time of actual menstrual haemorrhage in human females - let say in a case that woman has 21 day cycle and her menstrual period is 7 days?
If yes, does it means that in this particular case the woman has lower chances to conceive?

Ovulation and menstruation don’t happen in normally cycling women at the same time. A basic outline of the hormonal cycle that triggers these events will make this clear.
Proliferative (a.k.a follicular*) phase
Beginning after menses (when the endometrium is thinned), the hypothalamus produces GnRH which stimulates the anterior pituitary to produce LH and FSH. These in turn stimulate ovarian follicles to develop. A dominant follicle produces estradiol which causes the endometrium to thicken (proliferate).
At a certain level of estrogen (actually estrogen/progesterone ratio), the feedback on the hypothalamus flips from a negative to a positive feedback loop. Thus, there is a GnRH followed by a LH surge. The latter triggers ovulation. Note that at this time the endometrium is stable due to relatively high estrogen levels.
Secretory (a.k.a. luteal*) phase
After ovulation, the high levels of LH trigger formation of a corpus luteum from the tissues left behind after ovulation. The corpus luteum makes progesterone. This hormone triggers a change in the endometrium from a proliferative to a secretory state. Progesterone also provides negative feedback to the hypothalamus and anterior pituitary, maintaining low levels of GnRH, LH, and FSH, so no new dominant follicles develop at this time.
If pregnancy does not occur, the corpus luteum will eventually (10-12 days) degenerate and stop producing progesterone. It is this abrupt drop in progesterone that triggers the sloughing of the endometrial lining. You can see these hormone shifts in an illustration like this:

The decline of the corpus luteum is correlated with a decline in serum levels of ovarian hormones including progesterone, estradiol, and inhibin A. Release from negative feedback provided by these hormones at the level of the hypothalamus and pituitary permits FSH to rise, and the cycle begins again.
You should now be able to see that:

Around the time of ovulation, the uterine lining is not fully developed and is stable due to the hormonal milieu. Menstruation does not occur.
Around the time of menstruation, FSH and LH are suppressed in a way that is not conducive to ovulation.

In theory, yes, of course there would be a lower chance of initiating a viable pregnancy (implantation rather than conception is the most obvious problem) were the endometrial lining to be unstable at the time of ovulation. The problem of luteal phase deficiency is along these lines. In this condition, the corpus luteum does not produce adequate progesterone during the luteal phase to develop the endometrial lining in such a way as to support a healthy pregnancy. However, ovulation and menstruation are still time-separated events for the reasons outlined above.
*Note that the first term is with respect to the endometrium; the second is with respect to the ovary.

Abbreviations:

GnRH - Gonadotropin Releasing Hormone; LH - Luteinizing Hormone; FSH - Follicule Stimulating Hormone

References

1. Anatomy & Physiology, Connexions Web site. Illustration is also from here.

2. Jerome Strauss, Robert Barbieri. Yen & Jaffe's Reproductive Endocrinology. September,  2013. Saunders.

Thanks for the answer, I don't understand why one can clearly say that actual hemorrhage is time separated from hormonal activity of the ovary and hypophysis - what feedback do provide endometrium itself to be independent in any way from the system? If it is not the "last" organ in the chain we should know how it itself influences changes in the chain...

I took a look at the google search from the comment just deleted. It seems to agree with this conclusion. Quoting the two sources on the front page I see that directly address this, "women who have regular menstrual cycles typically will not ovulate during their period." and "It is impossible to ovulate while having a period." I tried to provide some background on why that is so.

I added a paragraph to try to better elucidate my summary of the feedback mechanism (which is extremely complex, beyond my top-of-the-head knowledge, and way too voluminous to include here in full detail). To my knowledge, it is most at the level of the ovary-->hypothalamus/pituitary rather than the uterus/endometrium. Women after a hysterectomy may still cycle regularly.

So, we have a case of a woman with short cycle: let say 21 days + long periods ie 7days. From this we know that her ovulation is 14 before the ovulation (it's well known "fact"), thus her ovulation can come on the day 7 the last of her periods when the endometrium did not ready to implantation. So, this particular women probably has lower chances to become successfully pregnant that women with longer cycle and shorter periods.

Perhaps. Remember, though, that ovulation and implantation are time-separated events. If conception occurs ~24h after ovulation and the embryo implants another ~3-4 days later, so there is some window for the progesterone from the corpus luteum to act on the endometrium. Also, a 21 day cycle in a normally cycling woman is unusual, and it would be even more unusual for it to be associated with a long menses since the rising sex hormones prior to ovulation will stabilize the endometrium.

Of course before periods... this type of typos we should ignore %))

If you don't believe her, read the Wikipedia article on it. But stop arguing with the answerer.

source: Stack Exchange

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Sequence based method for prediction of continuous B cell epitope
What is Sequence based method for prediction of continuous B cell epitope? What is the algorithm/procedure of this method? Can someone please explain this to me in simple language?

Why do you want to know, and do you have some background?

umm I am going through this for my research , but i have not studied biology for the last 8 years....

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Can the Donnan effect be reversed so phospholipids follow ions?
I know that there are flipases and flopases that facilitate this sort of thing, but I'm curious about other possible influences. Can the Donnan effect be reversed so that phospholipids follow ions? For example, calcium efflux from cells causes it to be more energetically favorable for phosphatidylserine (slightly more negative, and thus slightly more likely to follow a positive charge) to be ejected from inner to outer leaflet.

While moving lipids to match charge could work, I don't know about any examples. Lipids are large and flipping rates tend to be slow. My guess is that ions can react to lipid distribution faster than lipids can react to ion distribution.

Yea, i suppose, though membrane biophysics is still a mystery to me... Perhaps the flipases/flopases make it more energetically favorable for lipids to follow the ions and not just the reverse...

Flippases would increase flipping rate, but there are plenty of ion channels that would increase the rate at which ions can move back and forth across the membrane too.

I am refering to apoptosis, platelet activation, and any other scenario where phosphatidylserine moves from inner to outer layer... in these scenarios there is also a calcium influx...  I can't help but wonder if there is a connection...

I'm confused about what this question is actually asking. The title is unclear and the only actual question is can the donnan effect be reversed so phospholipids follow ions.

for example, why does phosphatidyl serine get exposed to the outer leaflet after calcium efflux from a platelet?

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text:
Epitope annotated protein
What is epitope annotted protein??  The book from which I got this term is : http://www.springer.com/biomed/immunology/book/978-1-4939-1114-1

Have a read through the wikipedia article. BTW, you could have gotten that by googling "epitope".

so basically epitope and epitope annotted protein means epitope??

Yes, they're the same thing.

First, when asking about a specific small term, it's best to check your spelling.  If you actually look at the sentience, you will note that you left out a very important hyphen:

Pellequer compared several propensity scale methods using a dataset of
  14 epitope-annotated proteins. [emphasis added]

The phrase means that the protein sequences (amino acid sequence) has the epitopes marked on them.  If you look at the cited paper, you will see the various tables and break downs of determined epitopes.  Pellequer's group did a lot of the early work when people were still working on techniques to "map" out the locations of epitopes (which are often not in linear segments of the protein sequence due to the protein structure).

authors: Дмитрий Першуков


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Somatic Mutations in meristem tissue in plants
In angiosperm, in which layer of the meristem does a new mitotic mutation occurring has chance to be found in a pollen grain or in an ovule?
I also welcome some insights about non-angiosperm plants.

You can see the wikipedia article on meristem.
The apical meristem differentiates into floral meristem that gives rise to flowers.
From this the cells specifically expressing APETALA3 (AP3), PISTILLATA (PI), AGAMOUS (AG) and SEPALLATA (SEP) would give rise to the stamen [ref].
CRC gene is essential for female development and plants lacking this will not produce pistils. So cells expressing this gene will give rise to female parts[ref].
Nonetheless mutation happening at any stage of the development of floral meristem can be transmitted to the pollens/ovules if the mutated cells stochastically give rise to that lineage.

Thanks. Do you know approximatively, how many cells are in the apical meristem?

Oh I don't have much idea. I didn't study much botany. I'll look up and let you know..


text:
Why can't neurons undergo cell division?
Many cells in the human body can divide and reproduce, making healing possible. Neurons, however, cannot reproduce, which makes diseases affecting the brain particularly crippling. Why can't neurons divide - that is, what makes them different from "normal" cells? Are there any ways to artificially stimulate neuron cell division?

Neurons do not divide due to the reasons mentioned in Cornelius's answer. However, some new neurons can be generated in adults (Ref: Neuroscience, 2nd edition).
Generation of new neurons in adults was first demonstrated in birds, where labeled DNA precursors could be found in differentiated neurons. Experiments in mammals and humans demonstrated later that new neurons are created in the central nervous system (CNS) in adults, although it seems to be restricted to some particular regions: granule cell layer of the olfactory bulb and dentate gyrus of the hippocampus. These new neurons seem to be local circuit neurons and interneurons (i.e. no long distance neurons).
How are the new neurons produced if neurons cannot divide? They come from neural stem cells (NSCs) that were preserved in the sub-ventricular zone during development. NSCs are presumed to play a part in brain plasticity in the adult brain. However, they have therapeutic potential. Check the brief information in wikipedia), or this perspective in Nature neuroscience that may contain further details.
References:

Neuroscience, 2nd edition. Purves D, Augustine GJ, Fitzpatrick D, et al., editors.
Sunderland (MA): Sinauer Associates; 2001.
Gene therapy: can neural stem cells deliver?  Müller FJ, Snyder EY,
Loring JF. Nat Rev Neurosci. 2006 Jan;7(1):75-84. Review. Erratum in:
Nat Rev Neurosci. 2006 Feb;7(2):167. PMID:
16371952 [PubMed -
indexed for MEDLINE]

There are also NSCs in the hippocampus which is the part of the brain responsible for memory. This and neuroplasticity of existing neurons makes new memories.

Morphological point of view
Neurons cannot divide because they lack centrioles.

Because centrioles function in cell division, the fact that neurons lack these organelles is consistent with the amitotic nature of the cell [1].

Functional point of view
New cells in the nervous system wouldn't do any good. The whole nervous system is based on interneuronal connections, so adding an extra neuron would mess up these connections and alter both the functionality and the "stored" information.

Each nerve cell has a specific place in our nervous system. Its job is all about taking a signal from one specific place to another one. Adding new nerve cells would mess up these very specific connections in a very complex system [2].

References:

SEER Training. NERVE TISSUE. Available from http://training.seer.cancer.gov/anatomy/nervous/tissue.html
UCSB Science Line. Available from http://scienceline.ucsb.edu/getkey.php?key=1710

Although I agree with your comment the notion that "New cells in the nervous system wouldn't do any good" is untrue. New neurons are generated on multiple sites in the adult brain. For example learning as well as recovery from injury may be accompanied by formation of new neurons from stem cells.

I'm not sure if I should write it here but I have a related question. How does the body recovery from stoke which is actually death of nervous tissue? @Cornelius

I agree with AliceD in saying the second point there is a bit confusing. The primary goal of cellular replication (and coincidentally what people mean when they ask about neurons not being able to do so) is to replace and heal the original cell. This is a bit like asking "why can't we regrow limbs like lizards can?" and answering with "there's no point in having a third arm, two is the most efficient system we evolved to have for the least amount of energy."

I would like to propose an "answer" from a personal belief (no sources) based on an evolutionary approach to this question.
If neurons were readily capable of division, that is, healing, they would require a different form, thus mandating a different function; ultimately, they would be less efficient at what it is they are supposed to do (transfer electricity)--thus, not advantageous for the organism (during the evolutionary period); thus, did not occur.
Think of this for a moment: in physical space, what would happen to the other neurons if one were to divide? It would push into them, possibly 'disconnecting' a pathway, or impairing it's ability to fire (possibly below the activation threshold)--a whole new host of diseases could emerge.
Perhaps plausible, there was at one point something similar to what I've described above (a mitosing nervous system). The question is, though, would it be more efficient than a non-dividing nervous system? Would it have fewer diseases?


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Can you get enough water by eating only fish?
Scenario: In a boat in the middle of the sea, no freshwater or food stores, no desalination equipment, no rain, but you can catch fish and eat it raw. Can you get enough water this way to survive, let's say for 14 days? (Enough clothes to protect against cold, shade available)
2, 000 g of raw Pacific cod contains 1,650 mL water, 350 g protein, 2,200 mg sodium (source: usda.gov)
By my calculation, you would need to excrete 2,800 mL of urine to excrete urea from protein metabolism (8 mL urine per 1 g protein; source: nap.edu), so after eating fish you would be in the negative water balance for more than 1,150 mL solely from urea.
My questions are strictly about fish as a water source, not about other water sources or survival time:

Does protein really expel so much urine that makes fish an inappropriate source of water?
Any other appropriate source of water from fish, apart from eyeballs? Can you somehow squeeze the water from fish?

small hole in your scenario - if you can cook fish, you should be able to boil seawater and condense the steam for desalinated water :)

I edited: No cooking, raw fish.

note protein levels in fish blood vary by quite a lot. so it depends on the fish in question.

If you have a man in a box scenario where you only look at numbers, the answer is, no, he won't last 14 days.[1]
The difficulty with this question for me is that the body doesn't always behave the way it's supposed to. The 3-3-3 rule (3 minutes without air, 3 days without water, three weeks without food) and the "100 hour rule" (4.166 days) aren't absolutes.[2] Some people die in hours, some 10 days. The variables are too great.
Guinness World Records puts the record for survival without water at 18 days[3] by an 18 year old male forgotten in a cell by the police. But he was in a cool basement, and licked the walls which had a small amount of moisture on them. Had he been sweating or 2 decades older, he probably wouldn't have lasted as long.
Water requirement under extreme circumstances varies. How much clothes is your male wearing? Does he have shade? Where in the ocean is he? How inactive can he be? Can he oil his skin with fish oil? But mostly, does he have a still suit (j/k)? These things all matter.
Eating protein without water isn't wise. Carbs are better, but your guy doesn't have them. The better thing for your guy, who can certainly live for 14 days without food, is to suck the water out of the fish, and what he can't suck out, wring out at the end. If he has access to the whole fish, the eyeballs and the spine also have water in them.* The body has all kinds of homeostatic mechanisms to preserve fluids, including continuous secretion of ADH (Anti-Diuretic Hormone), osmoreceptors and baroreceptors to regulate fluid volume and how much water is lost from the kidneys.[4] He'll suffer terribly; fluid will be sucked out of his joints and cells and his blood urea nitrogen will go up and his kidneys will be damaged, he'll hallucinate, he'll need hospitalization, but might he live? If he is young, healthy and hydrated going in, and other factors (a tarp for shade, etc.) mitigate his water loss, I think the answer is yes, he might.
*In 1953, a French physician and sea survival expert, Alain Bombard, set sail in a Zodiac inflatable dinghy with the only food and water officially sealed to discourage himself from using it. He started immediately with drinking small amounts of seawater, and would suck water from fish, and, if he had any fresh rain water, would eat raw fish. He sailed from Minorca to Barbados, eating supplied food and water only once. His rival survivalist, another physician, Hannes Lindemann, contested Bombard's claims, but did well at sea as well.
[1] The Biology of Human Survival : Life and Death in Extreme Environments
[2] Dehydration
[3] Andreas Mihavecz
[4] Fluid Physiology, Ch. 5, 6

Human eyeballs contain more than 98% of water, so I assume something like this would be in fish, so yes, this can be a water source. The water from "spine" would be cerebrospinal fluid (?), which content would be similar to plasma (lot of sodium), so not sure how effective in hydration.


text:
What determines the autumn leaf color?
It is autumn out there. Green, brown, red, yellow, and mixed-colored leaves drop from the trees to the ground. What determines the colors of the leaves?
Wikipedia tells me

Leaf senescence is the cause of autumn leaf color in deciduous trees.

Ok. What does the color code? If a leaf is red, why is it red and not yellow or brown or green or mixed-colored?

There is no color code for the leafs - the color results from biochemical reactions. Basically there are three colors: Green, yellow and red.

Green color is caused by the chlorophyll inside the chloroplasts,
when the leafs are active in photosynthesis.
Yellow color is caused by Carotenoids, which are present in the
leafs all the time, but are masked by the chlorophyll. The
carotenoids become visible when the amount of chlorophyll in the
leafs is reduced, which usually happens in the fall.
The red color is caused by Anthocyanins, which are usually not
present in the leafs. They are made during the late summer and can
also mix up with the carotenoids (color mix) to get intermediate
colors.
Brown color is caused by the cell wall of dry leafs which have no
other color.

For further reading these articles are interesting:

Unravelling the evolution of autumn colours: an interdisciplinary
approach.
The Science of Color in Autumn Leaves

There is also the hypothesis around, that the bright colors are a warning sign to insects, this is called the co-evolution theory of autumn colors. The color should warn the insects that the tree has a high level of defense and thus reduce its parasitory load. You can read more about this hypothesis here:

The coevolution theory of autumn colours.
The shared and separate roles of aposematic (warning) coloration and
the co-evolution hypothesis in defending autumn leaves.

What
There are two theories according to Jennifer Wells, Leaf Color Change:

Competition theory - states that nutrients are redistributed to important parts of the plant. Lack of nutrients in the leaves will decrease the chlorophyll synthesis thus the leaves change their color. The redistribution does not happen equally that's why some leaves are multicolored (see Ecology and the Environment at Cornell Blogs).
Mutual enhancement - states that specific hormones (senescence factors) work in conjunction and cause the color change.

All these happen under the influence of light - the absorbed dose of light is modulated by internal factors. The result is a reversed balance between carotenoids and chlorophyll (increase in carotenoids).
These carotenoids (fat-soluble) turn the leaf into orange and yellow depending on their concentration. There are also anthocyanins (water-soluble) which are responsible for red coloration.
Why

Chlorophyll and its derivatives, if not carefully processed by organized biochemical pathways in green cells, can be toxic when illuminated.

According to: Howard Sidney Thomas, Leaf senescence and autumn leaf coloration. Check also Figure 3 from this link (on the last page).


text:
Horned Mohawk looking insect. What is it?
Any ideas? I didn't know any other way to explain it.
I live in Indiana, USA if that helps.
Someone said it might be a "stink bug" but I'm not sure and not willing to find out!

Its definitely a True bug (Hemiptera), and based on its distinct pronotum and small head I'm guessing its a Wheel bug (Arilus cristatus). It is a common species that is also found in Indiana.
They are aggresive predators and are part of the family Reduviidae also known as Assassin bugs. Assassin bugs have a painful bite, and they inject a toxin when they stab their victim (so humans should watch out). This is not a part of the world I know well though, and there might be similar closely related species that I've missed.
Links:

Bug guide
Records in GBIF
Univerity of Florida: Entomology & Nematology

Some pictures:

I would have called it an assassin bug, but I guess you're more specific than that.

@user137 You are correct in the sense that it belongs to the family of Assassin bugs.

@ansarob Yes, they can have a nasty bite, and they inject a toxin when they stab a victim.

Right, this is definitely a wheel bug. Watch out for their bite!

This does indeed look like a wheel bug (Arilus cristatus) as @fileunderwater indicates in his now 4-year-old post.
I just wanted to add 2 bits of information:

Range: Most eastern US states, from New York to Florida, through parts of the midwest and central plains down through Texas, New Mexico and Arizona.

 Source: Bugguide.net

The University of Florida Entomology and Nematology further claims:

It has been reported from Rhode Island west to California, and south to Texas and Florida. Blatchley (1926) included Mexico and Guatemala in its range. Wygodzinsky (1949) recognized four species of Arilus in this New World genus, but only cristatus occurs in the United States

This source provides an additional map (informally created from collected resources) that shows inclusion of California, Vermont, and Mexico in the wheekl bug's range..

-

Wheel bugs are sexually dimorphic, so do not be surprised if you see a noticeable gradation in size between specimens:

 Source: Wikipedia

I don't believe there is documented geographical size differences, so ranges in size would be due to age or sex.

 Cited sources from quote (for convenience):

 Blatchley WS. 1926. Heteroptera or true bugs of eastern North America, with especial reference to the faunas of Indiana and Florida. Nature Publishing Company, Indianapolis, IN. 1116 pp.
 Wygodzinsky P. 1949. Elenco sistematico de los Reduviiformes Americanos. Univ. Nac. Tucuman, Inst. Med. Reg. (Pub. No. 473), Monograph No. 1: 1-102.

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text:
Is ebola non-contagious until symptoms appear? Why?
There's been a lot of talk lately about the man who recently came down with ebola in Dallas, Texas. While I live elsewhere, I keep hearing quotes from CDC and state officials that ebola is not contagious until a person shows symptoms. This is generally used in the context of "Don't worry too much; we have the situation under control." Is this true in all cases? Why?

First, confirmation from the World Health Organisation:

The incubation period, that is, the time interval from infection with the virus to onset of symptoms is 2 to 21 days. Humans are not infectious until they develop symptoms.

But

People remain infectious as long as their blood and body fluids, including semen and breast milk, contain the virus. Men who have recovered from the disease can still transmit the virus through their semen for up to 7 weeks after recovery from illness.

They also state that deceased people may still transmit the virus via body fluids.
As to why the patients become infectious only when symptoms show, there are several related ideas.  For example, from the CDC:

Ebola virus enters the patient through mucous membranes, breaks in the skin, or parenterally and infects many cell types, including monocytes, macrophages, dendritic cells, endothelial cells, fibroblasts, hepatocytes, adrenal cortical cells and epithelial cells. The incubation period may be related to the infection route (i.e., 6 days for injection versus 10 days for contact). Ebola virus migrates from the initial infection site to regional lymph nodes and subsequently to the liver, spleen and adrenal gland.

According to Dr. Ray Schilling:

Ebola virus disease has an incubation time of 8 to 10 days where the person may complain of some tiredness, but is not sick yet. This is the time when the Ebola virus multiplies. It  paralyzes the immune system and distributes itself through the organ system.

From there, the symptoms and effects of Ebola are fast, according to the article "Ebola Virus Pathogenesis: Implications for Vaccines and Therapies" (Sullivan et al. 2003):

Ebola virus replicates at an unusually high rate that overwhelms the protein synthesis apparatus of infected cells and host immune defenses

Every infectous disease works this way: if you had contact with x particles (virus, bacteria, etc...), then you have y% chance to get infected (depends on your immune system, luck, etc...), so it has a distribution. This is called virulence, and it can be measured with ID50 (infectious dose by 50% of subjects) and LD50 (lethal dose by 50% of subjects) values. According to animal studies the LD50 is very low by ebola, so it is highly virulent, but it highly depends on the mode of transmission. So this virulency is compensated by low transmissibility: people infected with ebola, but not showing symptoms release too small amount (or nothing) of the virus to infect others. By hemorrhagic fever you bleed out of every hole of your body, and that blood contains a lot of viruses, that's when it can infect others. So this is not a "Don't worry too much; we have the situation under control." case, it works this way currently. This can probably change due to mutations.

Symptoms usually begin with a sudden influenza-like stage
  characterized by feeling tired, fever, pain in the muscles and joints,
  headache, and sore throat.1[12][13] The fever is usually greater
  than 38.3 °C (100.9 °F).[14]
This is often followed by: vomiting, diarrhea and abdominal pain.[13]
  Shortness of breath and chest pain may occur next along with swelling,
  headaches and confusion.[13] In about half of cases the skin may
  develop a maculopapular rash (a flat red area covered with small
  bumps).[14]
In some cases, internal and external bleeding may occur.1 This
  typically begins five to seven days after first symptoms.[15] All
  people show some decreased blood clotting.[14] Bleeding from mucous
  membranes or from sites of needle punctures is reported in 40–50% of
  cases.[16] This may result in the vomiting of blood, coughing up of
  blood, or blood in stool.[17] Bleeding into the skin may create
  petechiae, purpura, ecchymoses, or hematomas (especially around needle
  injection sites).[18] There may also be bleeding into the whites of
  the eyes. Heavy bleeding is uncommon and if it occurs is usually
  within the gastrointestinal tract.[14][19]
Recovery may begin between 7 and 14 days after the start of
  symptoms.[13] Death, if it occurs, is typically 6 to 16 days from the
  start of symptoms and is often due to low blood pressure from fluid
  loss.2 In general, the development of bleeding often indicates a
  worse outcome and this blood loss can result in death.[12] People are
  often in a coma near the end of life.[13] Those who survive often have
  ongoing muscle and joint pain, liver inflammation, and decreased
  hearing among other difficulties.[13]
The time between exposure to the virus and the development of symptoms
  of the disease is usually 2 to 21 days.1[10] Estimates based on
  mathematical models predict that around 5% of cases may take greater
  than 21 days to develop.[11]

wikipedia - Ebola virus disease

The LD50 of mouse-adapted EBO-Z virus inoculated into the peritoneal
  cavity was ~1 virion. Mice were resistant to large doses of the same
  virus inoculated subcutaneously, intradermally, or intramuscularly.
  Mice injected peripherally with mouse-adapted or intraperitoneally
  with non-adapted EBO-Z virus resisted subsequent challenge with
  mouse-adapted virus.

1998 - A Mouse Model for Evaluation of Prophylaxis and Therapy of Ebola Hemorrhagic Fever

Although outbreaks of Ebola virus have largely been confined to
  endemic regions, their high fatality rate, ability to transmit
  person-to-person, and low lethal infectious dose make Ebola virus a
  dangerous threat to public health and pose a great risk for
  researchers working with these viruses as well as health care
  personnel treating patients during outbreaks. Furthermore, their
  potential to be developed into aerosolized biological weapons also
  causes grave concern for their use as a bioterrorism agent ( Bray,
  2003).

2008 - Protection against lethal challenge by Ebola virus-like particles produced in insect cells

Some interesting story about the topic (others were not so lucky):

In 2004, a virologist at USAMRIID was working in a BSL-4 laboratory
  with mice that had been infected 2 days before with a mouse-adapted
  variant of the Zaire species of Ebola virus (ZEBOV) (2). The virulence
  and infectious dose of this variant of ZEBOV are unknown in humans;
  wild-type virus has a case-fatality rate of up to 90% (3).
The person had been following standard procedure, holding the mice
  while injecting them intraperitoneally with an immune globulin
  preparation. While the person was injecting the fifth mouse with a
  hypodermic syringe that had been used on previous mice, the animal
  kicked the syringe, causing the needle to pierce the person’s
  left-hand gloves, resulting in a small laceration. The virologist
  immediately squeezed the site to force the extravasation of blood.
  After decontamination of the blue suit in the chemical shower, the
  injured site was irrigated with 1 liter of sterile water and then
  scrubbed with povidone-iodine for 10 minutes.
In terms of exposure risk, the needle was presumed to be contaminated
  with virus-laden blood, although it was suspected that low levels of
  virus were present on the needle. The animals had not yet manifested
  signs of infection, and much contamination may have been removed
  mechanically when the needle pierced the gloves. The local
  decontamination of the site also reduced potential for infection.
USAMRIID medical, scientific, and executive staff concluded that the
  person with potential exposure warranted quarantine in the MCS.
  Contact plus airborne precautions (gown, gloves, N95 mask, eye
  protection) were used, with a plan to upgrade to BSL-4 precautions for
  signs or symptoms of illness. These extra precautions were instituted
  while the patient was asymptomatic for several reasons: 1) the timing
  of initial clinical manifestations with regard to potential for
  shedding virus were not known for this specific isolate in human
  infection; 2) there was interest in ensuring all infection control
  procedures were being followed appropriately in advance of clinical
  illness; and 3) there was interest in reducing any potential
  confounders, such as a caregiver transmitting a febrile respiratory
  infection to the patient, which might lead to unnecessary procedures
  or additional isolation. The person was monitored for routine vital
  signs; daily laboratory studies (coagulation studies, blood counts,
  chemistries, viral isolation, D-dimer) and regular physician
  assessments were performed.
Over the next several days, discussions were held with several
  internationally recognized filovirus experts regarding potential
  treatments or postexposure prophylaxis options. Local and state public
  health officials were also notified. The consensus opinion was that
  there was no safe, readily available source of immune plasma and
  little evidence existed to support its use. Emergency investigational
  new drug (IND) protocols were established for treatment with
  recombinant nematode protein (rNAPc2) and antisense oligomers, with
  the intention to consider implementation only if the patient
  demonstrated evidence of infection.
Ultimately, none of the 5 mice had confirmed viremia at the time of
  the incident. The patient did not become ill or seroconvert and was
  discharged after 21 days.

2008 - Managing Potential Laboratory Exposure to Ebola Virus by Using a Patient Biocontainment Care Unit


text:
How TCGA CNV values are calculated?
When I download CNV SNP array data for ovarian cancer from TCGA data portal, I see some very small numbers like -5, -6 in the "Segment_Mean" column of the segmentation data files. I am very new to genetics, and I don't understand how that much deletion can occur in the gene. We have 2 copies of each gene in our normal cells, and my intuition tells that the minimum loss for a gene in a cell can be -2 (both copies of that gene are lost). So, could someone please explain shortly how this -5, -6 copy number losses are computed?


text:
How to identify genes?
You and me are different at DNA level. My eye color gene is different from yours. So, my DNA is different from yours. How can a scientist identify a certain gene in a chromosome (and its function) if chromosomes are different? How can we talk about "the" human DNA when nobody share the same (except twins)? Please, this is a practical question about how scientists identify genes, not a philosophic one (a question that bother me every time I read about discoveries in genetic)

Humans share about 99.9% of their DNA, see this link (http://biology.stackexchange.com/questions/21699/what-percentage-of-dna-do-people-share/21706#21706), so the phenotypes you referred to are caused by allelic variations i.e. small changes in the genome but the genes are still identifiable as being A or B or a homologue of the two.

First of all: We are not very different on the genetic level - the identity is somewhere around 99.6 to 99.9%. See here for details. If this wouldn't be like this, things like blood transfusions or organ transplants wouldn't work.
To identify genes there are different routes. "In the old days" (meaning before the possibility of massive high throughput sequencing or DNA microarrays), genes were usually discovered when they were connected to a disease which had a noticable phenotype. Researchers then tried to find out which protein or pathway was affected and from there went backwards to identify the genetic region. This way of discovery was relatively slow. An example for this kind of identification is the identification of the Mitf gene which is important for the development of pigmentation.
If you sequence DNA (doesn't matter here if these are complete genomes or only parts of it) you can identify genes based on homology with already known genes. You can also predict the presence of genes in a certain sequence based on regulatory sequences in the region before the gene (the promoter). These sequences are known and also highly conserved, so this gives a good estimate. Predicted genes usually need to be verified experimentally.
What is done today are the so called "genome wide association studies". Here you take a big cohort of people which all share one phenotype (for example blue eye color). Then you take a second group of people which do not show this phenotype and analyse their genomes (usually by sequencing or SNP genotyping). Then you compare the two groups to find the differences. Ideally you can then more or less directly identify a causative mutation which is responsible for the phenotypic difference between the two study groups. This usually needs also to be verified further.

GWAS is what I was looking for.


text:
Can Galactose be synthesized with photosynthesis?
I know that galactose can be found in sugar beets and some gums so I thought plants could synthesize galactose but in my book the answer to the question "Which of these can be synthesized with photosynthesis in plants" was only fructose and glucose. Is that correct?

i suspect that this is only true if you expect the galactose to be made directly by carbon fixation from photosynthesis.  galactose and other sugars are often made by enzymes that convert from one type of sugar to another...

Yes, that makes sense, but the question was asking direct synthesis by photosynthesis, so I think the question (or rather the answer to the question) is incorrect. Thanks for your answer

you ask, you learn...


text:
programmatic fast search of 100-1000 short reads to a public server and obtain list of nearby genes
What are the options for programmatic fast searching of 100-1000 short reads to a public server and obtain list of nearby genes where the reads map?
Input: ~100-1000 short reads
Output: GFF list of genes it maps to or nearby genes
Genome UCSC is restrictive to the number of searches and AFAICS it won't allow programmatic use.
Any ideas? I've asked this question to another forum without much luck:
https://www.biostars.org/p/114124/

i think if you have your script slow down and submit the searches over a longer amount of time this can work with blat/blast

This can be done offline and wont require too much of computational resource.
What you will need:

A fast short read aligner such as STAR or even bowtie (STAR is faster)
Genome sequence (you will have to build index for the genome for your aligner)
A GTF annotations file (get it from GENCODE or any other standard genome repository for your organism of interest)

Before you align remove redundant reads. Keep their counts if necessary.
Align the reads using any of these aligners and obtain the alignment co-ordinates. The default output is SAM format for STAR and a tabular format for bowtie (bowtie also gives SAM).

Column-3 of SAM shows the name of the reference sequence
where alignment happened (chromosome)
Column-4 is sequence start
Column-10 is read sequence. Add the length of this to column 4 value to get stop site.

The columns are tab separated
Now define a window that you define as proximal/nearby (lets say 500nt).
Now all you have to do is find genes that lie $\pm500nt$ from your start/stop sites. In your reference GTF parse for the lines that have the feature "gene".
I am giving an example using awk. You can use any programming language you are comfortable with. Check the GTF format also.
Assuming that you made a file (reads.txt) from your SAM output in this format:
Chromosome <tab> Orientation (+/-) <tab> Start <tab> Stop

I am giving an example awk script:
example.awk
#!/bin/gawk

BEGIN{FS=OFS="\t"}

NR==FNR{
    a[$1 FS $2][$3 FS $4] # store the co-ordinate information from your reads file
    next
}

$3=="gene" && ($4 FS $7) in a{ # quick parse for reference chromosome and orientation

    i=$4 FS $7
    for(j in a[i]){
        split(j,jj,FS)
        if(jj[1]>=$4 && jj[2]<=$5)
            print $0";contained"

        else if($4<=jj[2]+500 || $5>=jj[1]-500)
            print $0";partial overlap/proximal"
        }
}

call it like this:
awk -f example.awk reads.txt annotations.gtf

NOTE: In the above script I have not considered antisense proximity. If you want to allow that then don't parse for orientation. Also gawk version < 4.0 doesn't allow multidimensional arrays. So install gawk>=4.0
The output is by default a GTF because you are printing selected lines of the reference GTF.

If I am going to run this locally, which of the aligners will let me run the system as a client/server? I wouldn't want the aligner to take 5 minutes to load the reference in memory and 5 seconds to align my 1000 reads...

It wont take so much time to load the reference index. STAR uses a binary index and bowtie uses a compressed burrows-wheeler index. Both are quick to load. And if you see bowtie paper they say that one of the reasons bowtie is fast is because it loads the index fast. However, making index from fasta will take some time

These aligners were designed for reads in the order of ~50-200nt. However I don't think they would not work (or work subobtimally) with longer reads. In such a case you can split the longer reads.

I am doing alignment of ~1000 different reads of 50-250nt each, not "1000bp reads"

I am reading SSAHA documentation and it seems to be able to do client/server.

You can implement client/server kind of thing in this also. You just need to make a proper interface. I have used these tools and they work fine. If you want to save time on back to back multiple jobs then you can keep the index loaded in the RAM (for that you need to edit the source-code a bit)


text:
are the spontaneous generation and evolution the same idea but in a different time scale?
I was in my biology class, learning the history of spontaneous generation and how this idea was discarded. I told my teacher that is the same as evolution but in a different timeline. I Argue that evolution does not explain how life formed, but complemented by abiogenesis. Ultimately it is almost the same thing. Therefore it could not rule out spontaneous generation.
I got an F.
My appreciation is so wrong?

Do you mean to say 'spontaneous generation and abiogenesis are the same idea'?

Yes, ultimately it is almost the same thing.

You are right in the sense the evolutionary biology doesn't try to explain the origin of life as it is not within its scope. Other fields of biology investigate the question of origin of life (abiogenesis).
Now, there is a very important difference between spontaneous generation and evolution. Life originated at some point and the through repetitive speciation events, created the whole diversity of species existing on earth. You could say that what really happens is that there was one spontaneous creation of life (although there is more a continuum from non-living to living things than a sudden switch from non-living to living) out of non-living things.
The main fallacy of spontaneous generation is that under the spontaneous-generation-conceptualization of life, every species are made de novo and independently which is definitely not the case as in reality species speciate (split in two) causing the existence of to two new species. There are tons of fallacies hidden behind the spontaneous generation conception of life, one of which relates to the concept of species and another one is the origin of within population variation.
So, in short spontaneous generation is definitely something different from a single abiogenesis and evolution and the hypothesis of spontaneous generation has been ruled out a long time ago already.
So I am not so much aware of the grading philosophy in your school but your argumentation was wrong and probably the F was worth. Next time, you will probably want to discuss your opinions with your teacher before the test to make sure you agree.

Evolution is about descent with modification.  Spontaneous generation doesn't have that.  It's about modern organisms emerging from raw molecules.  If flies spontaneously appeared from rotting cow meat, why would they have DNA that made them look like they were evolutionarily related to other insects?


text:
What happens when you mix type A with type B blood (and v.v)
What happens when you mix different blood types that are not compatible?
For example, if a patient has type A blood and receives type B blood, or v.v.?

The blood type of people is determined by proteins which are anchored into the surface of the red blood cells. Cells can either express the A, B, A and B or no marker, resulting in the blood groups A, B, AB and 0. People which have a certain blood type (for example A) have antibodies against the other blood type (in this case B).
This will lead to the attachment of antibodies against the subtype which you don't have (so B for people with A and vice versa) on the transfused blood cells and their lysis. Depending on the amount of blood transfused, this can also lead to a very serious immune reaction. This works like in the figure below (from here):

To avoid this reaction a sample of the blood, which is about to be transfused is mixed with blood from the patient before the transfusion takes place. This looks like this:
For more information look here:

Acute hemolytic transfusion reaction
Transfusion reaction - hemolytic
Genes and Blood Type
Adverse reactions to transfusion

Whoever sownvoted the answer, what is the problem with it? I can improve it, if I know the criticism.

I didn't down vote, but I'd say it needs a few more words about the 'very serious immune reaction' you've mentioned.

What determines blood types is the type of antigens found on the surface of the blood. A blood cells have A antigens on their surface, B has B antigens, AB has both, and O has no antigens. What is an antigen?
According to Wikipedia:

an antigen (Ag), or antibody generator, is any substance which provokes an adaptive immune response. An antigen is a molecule that also induces an immune response in the body.

Now, not only is the blood important here but also the plasma. The plasma contains antibodies. Antibodies are (according to wikipedia)

a large Y-shape protein produced by plasma cells that is used by the immune system to identify and neutralize foreign objects such as bacteria and viruses. The antibody recognizes a unique part of the foreign target, called an antigen.

Members of the A group have B antibodies in their plasma, members of the B group have A antibodies in their plasma, AB has neither, and O has both.
Now taking this all into account and to answer your question, if B blood is given to a patient of type A, the antigens on the surface of the A blood cells would react as if the incoming B blood cells are foreign, harmful substances. To from the book "Blood Groups and Red Cell Antigens"1,

If incompatible blood is given in a transfusion, the donor cells are treated as if they were foreign invaders, and the patient's immune system attacks them accordingly.
  Not only is the blood transfusion rendered useless, but a potentially massive activation of the immune system and clotting system can cause shock, kidney failure, circulatory collapse, and death.”

The same would result if A blood is given to a B blood type patient, the B blood cells would initiate an immune response to the A blood cells.
To further expand on your question, this is why O is the universal donor. There are no antigens on its surface that will illicit an immune response from other blood groups. It also has both A and B antibodies in its plasma. Similarly, AB is the universal recipient. It has both antigens on its surface meaning that neither A nor B antigens will illicit an immune response from other blood groups.

This answer is too much simplified. You should at least take the Rhesus factor into account when discussing transfusion compatibilities. You can find why here.


text:
Stardust or the elements in our bodies
How do we know we are made of stardust? As our cells divide, are our atoms repurposed from existing materials or spontaneously generated? Do we consume materials after we are born that contain elements that were in stars? This I would understand. Or, as our cells are initially dividing after conception, but before birth, are we already repurposing existing materials to grow?

The saying that you are referring to is from Carl Sagan, when he stated that:

"We are a way for the universe to know itself. Some part of our being knows this is where we came from. We long to return. And we can, because the cosmos is also within us. We're made of star stuff,"

Quote source
In answer to your question, yes, we are 'repurposing' the elements that make us up, as are all living and non-living matter.
Chris Impey, professor of astronomy at the University of Arizona is quoted in the article Are We Really All Made of Stars? (Melina, 2010) as stating:

the fact that the carbon, nitrogen and oxygen atoms in our bodies, as well as atoms of all other heavy elements, were created in previous generations of stars over 4.5 billion years ago. Because humans and every other animal as well as most of the matter on Earth contain these elements, we are literally made of star stuff

The elements that make up the cells etc in humans and any life forms, as with the materials that make up the Earth itself were ultimately formed by nucleosynthesis processes (mostly fusion and neutron capture) in stars, explained in the webpage Origin of the Chemical Elements as being:

the early Universe consisted almost entirely of the element hydrogen, with a small amount of helium present too. Hydrogen, therefore, is thought to be the starting material from which all other elements have been built. This is consistent with the very high abundance of hydrogen in the solar abundance profile. The process may be thought of as a series of fusion reactions which weld together simple atomic nuclei to build increasing complex atomic nuclei.

Unless you are inside a star or a fusion reactor- Matter is neither created nor destroyed. However, fission of unstable isotopes is fairly common on earth's surface.
You may accumulate one of such isotopes but usually the ones that are generally absorbed in our bodies such as C-14 have very long decay times (more than your lifetime). So for all practical purposes you are created from the atoms of existing matter and these keep getting recycled from the environment.
Now the composition of different stars is different and statement like "Do we consume materials after we are born that contain elements that were in stars", is too farfetched. Many millions of years have passed since earth came out of a star and lot of nuclear reactions have happened in this time. So the composition is of course different.

It might be helpful to think about where elements in general come from. Here is a plot of relative elemental abundance.
Note that the Y axis is logarithmic, so H and He are much much much more common than anything else. You'll notice that Li, Be, and B are rare, and C, N, and O are fairly common, and are the main components in biological chemistry. Fe is relatively abundant, and after Fe elemental abundance falls off. The explanation for the abundances comes from the processes involved in nucleosynthesis.
Big bang nucleosynthesis was the generation of hydrogen and helium within the first 3 minutes of the universe as the quark-gluon plasma cooled and formed the protons and neutrons. As the universe expanded and cooled, it lost the energy needed to keep making atoms within 20 minutes, so only very small amounts of Li, Be, and B could be made.
Stellar nucleosynthesis is the creation of "heavy" elements by nuclear fusion in stars. This is how we get C through Fe. As the stars age and use up their fuel, they generate elements up to Fe because energy can be released from fusion of atoms up to iron, past iron fusion takes more energy than can be released.
Elements heavier than Fe must be created through supernova explosions. This is the only natural way to get enough energy to jam the nuclei together. This only works well for elements up to uranium, where nuclei become unstable and decay at relatively fast rates. These unstable elements are produced in nuclear reactors and particle accelerators. Note that supernova explosions don't just make heavier elements, they are also responsible for blasting the elements made in stars into space where they can form new stars and planets. This is where the matter that makes us comes from, hence the stardust.
Another method for generating light atoms is cosmic spallation, where a cosmic ray hits an atom and blows some protons and neutrons out of the nucleus. This material becomes light atoms, such as Li, Be, and B.
Here is a periodic table that shows where each element comes from.

What was what source of this periodic table? As far as I am aware, at least in our solar system Uranium is the last naturally formed element. Edwin McMillan and Glenn Seaborg were credited with the synthesis of Neptunium and Plutonium respectively.

@AMR I believe I found it on wikipedia, probably in one of the links I posted in the answer. Pink elements are produced by supernova, it may be that Np and Pu were detected in small amounts from other supernova, making them "natural", but I'm not a physicist.


text:
Mechanisms of Flagella
I know that dynein arms and microtubules are involved in the contraction of certain parts of the flagella to produce a wave motion, but I don't understand they are related to the 9+2 structure of the basal body.
How do flagella work in prokaryotes and eukaryotes?

Flagella in prokaryotets is very different from that of eukaryotes.
The main structural protein in a prokaryotic flagellum is flagellin. The flagellar motion is caused by a molecular motor similar to Mitochondrial ATP-synthase; molecular motion generated by the chemiosmotic energy.
Eukaryotic flagella or cilia are made of microtubules with dynein attached on to them and cause the movement by the energy generated by ATP hydrolysis.
See the wikipedia article. It is clear enough.


text:
What is the scientific opinion on plus lens therapy?
Plus lens therapy is the theory that most myopia is environmentally triggered and that conventional corrective minus lenses increase nearsightedness over time. Thus the hypothesis that applying plus lenses for nearsightedness will invert the environmental pressures and halt or reverse existing myopia.
What is the scientific majority and minority opinion on plus lens therapy?

Are there any sources on this theory that are non-commercial?

@Chris I've found a variety of sources of differing levels of empirical induction on plus-lens but as yet no clear conclusions from scientists; as least in the limited places I've looked (I'm not a biologist). Since the therapy only requires $10 plus lens, commercial incentives are limited.

Personal anecdotal evidence: After a year of +1 diopter lens, my permanent eyesight has improved somewhat (was only mild myopia to begin with) in a 8 - 12 hour x 7 day a week computer environment; where I've worn lenses about half the time. As plus lens are only a partial replication of natural long distance, I suspect you could run the risk of strabismus if you undercorrect too much at short distances relative to your level of myopia. Hasn't happened to me, but then I no longer get a decent blur point at +1 and will probably need to increase to +1.5 to progress closer to 20:20 or higher.

Plus lens therapy can indeed reverse myopia, but it does take time. Your eyes did not develop myopia in a few days.
The eye represents its environment. Fitting chicks, monkeys etc. with minus lenses always INCREASED the amount of myopia, while plus lenses always reduced myopia and resulted in hyperopia (lens compensation).
Putting monkeys in a confined environment showed a myopic shift. Monkeys in an open
environment showed a refractive state about +1.00 diopters.
IMPORTANT: As I have said: Unfortunately, it does take time! Do not expect results after 1 week of plus lens therapy. That is why so many people give up and think that myopia is irreversible. You also do not build muscles after 1 week.
Kind regards.
EDIT:
Optical defocus and effects in HUMANS: http://www.ncbi.nlm.nih.gov/pubmed/20592235
Defocus on chicks: http://www.iovs.org/content/44/7/2818.full
Monkeys in a confined environment: http://www.iovs.org/content/2/6/571.short

Welcome to Bio SE. It is recommended to provide some references- specially for some of the statements in your answer. For example, could you cite the research done in monkeys? Or any other research supporting that plus lens reverse myopia?

The human eye is dynamic and always represents its visual environment. Thus, why was myopia so rare in early mankind, but now so present?
It can not be only caused by genetics. The worst thing you could do is wearing your full minus lens prescription while doing near work. When you think of how your myopia initially started (a lot of near work) and then you wear your minus (unfortunately, often over-prescribed), you are in your "initial" state again. And the cycle repeats itself - over and over again.
By reversing myopia, you must also consider prevention. When you do a lot of near work (long-term), wear plus lens to protect your eyes. It makes your eyes as if they are looking in the distance and thus relaxing your eyes effectively.
Try the following: Measure your Snellen score, then do near work for 3 hours or so and then check your Snellen again. You will see your sight will get worse (in this case temporarily). If you continue, your eyes will adapt and become myopic.
Unfortunately, plus lens therapy is not mainstream. Often people say "it does not help" or "it causes cataracts" and so forth. But therapy needs to be applied over a long-timeframe. Consider it as a "long-term diet".

Can you support your assertions with any decent studies?

Welcome to biology stack exchange. We usually ask for answers to provide some citation to support their conclusions, and I can't find the references you say you added in your first sentence. I would also suggest you change the style of the answer, the capitol letters and bold text makes the answer appear confrontational and the overall tone of the answer appears very opinion based.


text:
Possibility of Human cloning
Technology has evolved so much as to clone animals. But, what about human cloning?
Is it really possible to create humans in lab? Or is it that technology has not advanced to that level..?
Why cant it be attempted..?

This is mainly not a technical, but a severe ethical problem.

As Chris said, it is possible to clone a human but there are ethical issues.

generally people are pretty scared of what science can do because they don't understand the risks and benefits properly - look at a lot of GM food and the sacremongering that goes on. I doubt we'll be able to convince many that cloning should be tried with humans any time in the next 50 years!

@AbhishekK I tend to differ. Not everything which is technically possible should be done from an ethical point of view. And ethics are clearly not hindering the scientific development.

I think even with a dedicated human cloning project one would be several years away from success, after all cloning tetra wasn't easy.  I agree with Chris that ethical concerns are not hindering research, but rather help focus it when used correctly.  I can think plenty of recombinant viruses that should not be made for ethical reasons as a less controversial example.

Cloning of animals typically involves:

Taking nucleus from healthy adult cell of animal to clone
Taking a healthy egg and replace the egg's nucleus with nucleus from source animal.
Implanting egg in female, stimulating the pregnancy process.

This same process should work on humans BUT:

"Is it really possible to create humans in lab?" No. Animal cloning doesn't work this way, so human cloning wouldn't either. Animals aren't "created" in lab. The one artificial step is the modifying the nucleus of the egg cell before the pregnancy process initiates. The rest of the egg->embryo->infant pregnancy process is traditional nature and there is no working lab process available to replace natural pregnancies.
Cloning animals is very high risk, it involves lots of trial and error, and involves lots of mistakes, botched pregnancies, abortions, and birth defects. The core concept of replacing the nucleus in an egg cell makes sense, but the practical reality of that procedure involves cell damage and pregnancy risks. With non-human animals, no one cares. With humans, purposefully causing lots of botched pregnancies, miscarriages, and birth defects will make most people squeamish.
Donor Eggs: If the process worked perfectly, a single donor egg would suffice. Since the process doesn't work perfectly, many donor eggs are required. Getting those donor eggs is a very invasive process that I would not want my wife, sisters, or daughters to subject themselves to. With lab animals, who cares, scientists can be as invasive as they want, and harvest all the eggs that they need. Humans have rights which really impedes this type of risky work.

Today, cloning humans is possible, but at prohibitively high cost and risk. It is inevitably going to happen, but the costs and risks will impede its popularity. Process improvements that deliver more safety and reliability will allow human cloning to become more popular.
UPDATE: "Why cant it be attempted..?" It definitely is being attempted. Panayiotis Zavos is one doctor who has been very public about his attempts to clone humans:
"In April 2009, he claimed to have cloned 14 human embryos and transferred 11 of those to wombs."
AFAIK, none of these efforts led to a live birth. I'm sure other doctors have attempted and even more are considering it and waiting until it's a little more practical and realistic.


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Questions about insects eating flour and living in the cracks of a wooden cutting boards
I have a large wooden cutting board which is used in my kitchen mainly for preparing egg pasta. The wood type is Populus (poplar or aspen or cottonwood).
The main ingredients used with the cutting board are: flour (mainly soft wheat flour), hens' eggs, white sugar, butter, and baking powder.
After the food preparation, the cutting board is cleaned by scraping away the ingredients remains.
The board has some cracks and some small unknown insects are living inside the cracks.
The board has also a lot of holes due to woodboring beetles but I think the woodworms operated long time ago and they no longer live in the cutting board.
The unknown insect has an approximate length of 1 mm (along the direction of their movements) and a width of 0.3 mm. The unknown insects do not have wings, they just walk. I am not able to see how many pairs of legs they have.
The color of the insect is pale brown.
The cutting board was free from these unknown insects some months ago but then they appeared.
My questions:

What insects are they?
Are these insects poisonous to humans?
How can I get rid of them?

Update
The unknown insects could be Acarus siro, I will try to get a picture of the insects.
Update 2
Here is a picture. The bottom part of the image is a one Euro coin, the top part of the image is a caliper (each bright area is one mm tick).

Some more pictures:

Can you show an image of the beetles?

@Chris There are no woodboring beetles in the cutting board, there are just their holes. Unfortunately I do not have a suitable camera equipment to take a picture of the unknown insects I am asking about, they are too small (1mm x 0.3mm).

Buy a new cutting board. :P (plastic ones would solve all your problems). We can't ID a bug without a picture, either.

It sounds like a flour beetle, try the red (or rust red) flour beetle, though they are more than 1mm in length. You can probably kill them by putting your cutting board in the oven at 250° for an hour or two.

@anongoodnurse Does the flour beetle have wings?

@anongoodnurse I treat them with Ethanol 95% so, at least, they will get drunk :-)

No, the flour beetles are flightless. If you look at google's images (there are three main kinds of flour beetles; red is the lightest), you should be able to tell, especially from the head shape, which it is, if any.

@anongoodnurse Red flour beetles are not flightless. Beetles have their flight wings hidden under a protective shell that is made from specialized wings. Also, flour beetles are a potential source of allergens, so if you're making these noodles for other people, I'd get a new cutting board. If you're the only one eating the noodles and aren't allergic to the beetles, it's up to you.

@user137 - you're correct. It's the confused flour beetle, which it closely resembles, that can't fly. Thanks for catching that.

That picture does not look like a flour beetle. Almost looks like a termite. Don't know if the size is consistent with termites.

The pictures aren't very good, but just for the sake of it I'm going to put Springtail (Collembola, primitive hexapod) out there as well. It fits well size-wise (<6 mm, often less than 1 mm) and they have quite diverse morphologies. However, they are connected to moist environments, and it seems unlikely that a cuttingboard would be the main point of infestation. They might hide in cuttingboard cracks thought. It's not the Acarus siro from your update 2 (eight legged mite)

I agree with @user137 that termite is a possibility (antennae look a bit off though). It is definitely not a flour beetle.

Neither flour beetles nor termites get that small.

This is a species of psocid (of the family Psocoptera, AKA booklice).

Species are best differentiated by their abdominal structure and antennae. Without a better (more magnified) image and info about the OP's location, identification to species is not possible. Though its small size will definitely narrow the options.
If I had to guess based on the limited detail (and my limited knowledge), I'd say it's a species in the genus Liposcelis or related genera.  See Oklahoma State's ENTOPLP ID key for examples and info. I've included 2 random images of Liposcelis species for reference: the (TOP) is Liposcelis brunnea and (BOTTOM) is Liposcelis corrodens.
You can find info about prevention and removal from Oklahoma state, King's College London or the Orkin man.
UPDATE: Though I, myself, cannot identify this psocid to species, according to this KCL article, Liposcelis bostrychophila is the most likely candidate. [See here for ID notes].

From the KCL article:

Liposcelis bostrychophila is the principal psocid pest species in the UK and in Europe. This single species, which is mainly an inhabitant of households, is responsible for virtually all of the psocid related complaints in the UK (Turner & Ali 1996)...Recent estimates are that 30% of households contain this species.
Several other small (about 1mm long), flattened, wingless liposcelid species (eg. Liposcelis corrodens, L. pearmani and L. brunnea) can become quite common in industrial sites, particularly in the summer months but are uncommon in domestic premises.

The insects are in the northern part of Italy.

@AlessandroJacopson: Thanks for the location update. Though after reexamining your low-resolution photos closer I don't believe they contain the detail necessary  to identify this psocid to species. I think this might be the best ID you will receive. If you're satisfied, please accept the answer. Thanks.

I agree with the ID (and have upvoted) but, just for the record, this could be improved by responding to "How can I get rid of them?" within the body of the answer (you use an external link for this) and also by addressing "Are these insects poisonous to humans?".


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What is the mechanism responsible for the periodicity of hiccups?
Hiccups (singultus) are caused by involuntary spasm of the intercostal muscles and diaphragm, producing a sudden inspiration with associated glottic closure. It seems the neurobiology of the reflex has been relatively well worked out (nicely summarized in this review):

Afferent limb: the vagus, phrenic, and cervical sympathetic chain
Central mediators: the hypothalamus, medullary reticular formation, and brainstem respiratory centers
Efferent limb:  primarily mediated by the phrenic nerve but also including the intercostals, and secondarily the recurrent laryngeal nerve to cause glottic closure

To my knowledge, hiccups are always cyclical, with a period of between 1 and 30 seconds. According to the afore cited article, this interval is relatively constant it a given individual. The cycling stops after some time; efferent vagal tone can suppress it, or it stops spontaneously. My question is:

What is the mechanism responsible for this periodicity?

Something must be triggering that afferent limb every 1 - 30s, but I can’t think of a normal physiologic process that triggers the firing of one or more nerves with such periodicity and then stops abruptly.

Check out Van Der Pol (chaotic) oscillator. It can be used to model heart rhythms. If a stimulus is applied to the oscillator, it will return to the curved envelope discussed in the article.
However, if "pushed just right", the oscillator's current state will be pushed towards the very center of the loop, and it will stop oscillating. This is the mechanism by which a sudden blow to the chest can stop the heart.
Reading up on hiccups, their "almost regular" interval sounds similar to a chaotic oscillator. The abrupt stop may represent pushing the oscillator towards the middle of the limit cycle, from which it cannot recover, effectively stopping hiccups


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protein-binding sRNAs
I am actually a computational biologist, pardon me if my question description is a bit off-note, my curiosity is driving me on
A bit of background and context:
In bacteria, a regulatory protein termed CsrA binds certain structures in the UTR regions of genes and prevents their translation. These structures are short hairpin-like and all have AGGA nucleotides in the exposed part. There are sRNAs that isolate the protein from its targets, a common feature of these sRNAs is that they have several repetitive hairpins that more or less display AGGA nucleotides in the exposed part. So basically, the sRNAs mimic the structures on the targets of the proteins and that makes them potent competitors for protein binding against the genes actually targeted by the protein. By relying on this mimickry the sRNAs bind CsrA, isolate it from its targets and remove its suppression on gene translation.
My question: Are there any other examples that illustrate similar mechanisms of analogy/mimickry of sRNAs to bind protein?
What I tried
I've skimmed through a lot of literature to identify other similar systems in bacteria where sRNAs have conserved repetitive structures but to no avail. I hope someone with deeper experience directs me to such examples in any living organism, preferably bacteria but I am open to suggestion.
I found CRISPRs but these are  DNA based, I have come across few other cis-acting sRNAs which target mRNAs and aren't protein-binding. So could it be the case that sRNA mimickers aren't very pervasive in bacteria after all ?!

The sRNA mediated regulation in bacteria operates via diverse mechanisms. This case of sRNA competing with a mRNA for a protein is a passive kind of regulation. This might be good for finetuning but may not be very efficient. It is much better to actively regulate a mRNA by direct binding. Also, it will work only if the concerned protein is in limiting concentrations.
I haven't come across any examples of what you are interested in. There may be one similar situation in case of a eukaryotic system. miRNAs can be titrated away by long RNAs that bear multiple binding sites for that miRNA, thus making the miRNAs unavailable for binding to the target mRNA. These long RNAs are called ceRNA (competing endogenous RNA) or miRNA-sponges (this term is mostly used if the RNA is exogenous). However this is not really a protein-RNA interaction even though RISC complex contains proteins.


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Why does K+ have more concentration inside of the cell compared to outside of the cell? Why is Na+ and Cl- the opposite?
Can someone tell me the fundamental reason why K+ has low concentration outside of the cell and more inside of the cell?

Is this a homework question?

By "why" are you looking for the purpose (physiological/evolutionary) or are you looking for the mechanism (membrane transporters/ion channels)?

Just why. Why is it not Sodium that is dominant on the outside of the cell?

@ProjectBacklog it is sodium that is dominant on the outside of the cell.

I maintain that there is no "just why?" here. It's either "for what purpose?" or "how is this accomplished?" To try to cover both seems too broad to me.

Why nature has done it this way around is difficult to explain. What is certain, however, is that the membrane potential which results from the imbalance of these ions across the membrane is used for a variety of purposes, such as transport of other ions and molecules, action potential generation in neurons among many other things.
How it is accomplished is mainly through the Na+,K+-Atpase pump and secondarily through Cl- channels that exchange Na+ for Cl- to lift the amount of Cl- outside the cell.

The question is kind of broad and once narrowed down I am happy to include citations if and where needed.

Your question isn't all that precise but I think looking at individual ionic equilibrium potentials begins to give us some understanding.
Looking at the equilibrium potentials(EK for potassium and ENA for sodium) for these two ions and their channels you have that EK = -90mV and ENA = +60mV in a typical neuron. This means that at these voltages you will have no NET flow of that ion across the membrane. Inside a cell you will have a certain amount of negatively charged ions called anions which will not diffuse, or move across the membrane regardless of the concentration gradient. To compensate for this (because the inside and outside of the cells like to have equal charges when there are not action potentials) you need a certain amount of a positively charged ion on the inside. NOW, there is no NET flow of EK at a negative voltage, this is around the same voltage of the entire membrane resting potential (this varies). If you look at the numbers and consider the voltage at which an action potential occurs, then you cannot have sodium be the cation inside the membrane since ENA = +60 since an action potential propagates when the membrane is driven towards a positive voltage.

A few remarks here (1) "..you will have no NET flow of that ion across the membrane" - There is a leak current yes, but when the channels are closed you can assume there is no flow. (2) "called anions which are impermeable" - ions are never (im)permeable, the membrane is (not). (3) "they cannot and will not move across the membrane regardless of the concentration gradient" - you just claimed there is a net flow of both ions? (4) By calculating the Nernst potential, you already use the pre-existing concentration gradients, so of course you cannot swap the ions to meet the Nernst equation.

@ChrisStronks When I say there is no net flow of ions I mean this for sodium and potassium. At resting membrane potential the exchange of these ions across the membrane is essentially equal, sodium and potassium are cations. The anion I'm talking about which will not move across the membrane unless you break the membrane and remove them are proteins and other molecules essential to the cell. Also, equilibrium potential for a specific ion is different from the resting membrane potential. The resting membrane potential will however tend towards the potassium equilibrium potential.

If anyone wants a reference, specifically, chapter 6 in "From Neuron to Brain" fifth edition by Nicholls and others. However to get a overall picture of what I'm talking about I suggest going over chapters 4 through 6 in that book.

agreed, but your answer still does not address the question I think, as the question deals with any type of cell, while you focus on action potentials.

yes, because action potentials don't just occur in neuronal cells. My answer may not be the "fundamental reason" but it does provide a reason for the difference in distribution of potassium and sodium in a variety of cells termed excitable cells(those which produce action potentials). Aside from this all cells, not just excitable cells have the static - electric properties of resting membrane potential, ionic potentials and concentration gradients. Differences in distribution here can be blamed on pumps and leak channels.


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To get Standard ECG from PhysioNet?
I am trying to get standard ECG by using PhysioNet's ATM with parameters

but I get

It should be something like

How can you get complete standard 12-lead ECG out of Physionet database?

Programmatically attempt here http://biology.stackexchange.com/q/52955/86

PTB Diagnostic ECG database here.
Review here.

I don't think that all leads are available.
I looked at the Signals combobox for different databases. This combobox seems to be the list of all available leads.
For example, take a look at iafdb (Intracardiac Atrial Fibrillation Database). It will plot you an ECG containing leads II, V1 and aVF and some other leads.
Another example is the EEG database eegmmidb (EEG Motor Movement/Image Dataset) which contains many leads.
Look also at the mimic2wdb/39 (MIMIC II waveform database, version 3 part 9) which contains 4 ECG leads and some other parameters like breath rate.

I do not understand how this work has managed to use Physionet's data and got such a 12-lead solution: http://web.utk.edu/~xzhao9/research/Physionet2011/ECGQuality.html Do you?

Is any of these databases AAMI standarded? There is no 12 lead AAMI databases available online. I verified the St. Petersburg database and it is not AAMI - big entanglement of energy. They have problems with some analog components and other things - too many unknown variables.

How can you get programmatically data with rdsamp? I extended the thread here http://biology.stackexchange.com/q/52955/86

As another answer suggested, it's a matter of choosing a database that has all of the leads. The St Petersburg INCART 12-lead Arrhythmia Database (incartdb) contains all 12 signals. Here is the directory. The tracings are available by selecting it from the drop-down menu on the page you linked.

Is this AAMI standard data?

@Masi I don't know. There are several email contacts listed on the page I linked. You may want to write to them to obtain more info about the data.

I contacted them. I will write here when I get the answer. In ambulatory ECGs, there is the situation that MIT-BIH is the only available AAMI standard data when also requirement that two datasets of one patient (particularly patient #201).

@Masi does it need to be ambulatory?  Was the UT example from a database?  I didn't think they had one.  Anyway looking at St Petersburg it appears to be AAMI

@AtlLED It does not need to be ambulatory. What is UT? Do you have reasons why ST Petersburg is AAMI?

@AtlLED St Petersburg database is not AAMI. I verified this through a long process made by me and my friends. They have problems in many components of their system. So there is no AAMI standarded 12-lead databases online.


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Can anyone remind me of the name for the inter-scapular space on the back?
It's one of those names which are often said not to exist, like philtrum.

ELU deals with:— Word choice and usage; Grammar; Etymology (History of words’ development); Dialect differences; Pronunciation (phonetics and phonology, dialectology); Spelling and punctuation. Biology.SE actually have a [human-anatomy] tag.

"Inter-scapular space" is defined as the space between the scapulae.  It was most likely created by doctors who had no name for the space.  Yet another expansion of the English language by those who have need of a word or phrase to describe something that has no word or phrase already.  I found no other definition.

They do have a word, I just can't remember it; that's why I defined it as inter-scapular space.

@Michael - actually, in surface anatomy, it's called the interscapular area (as you can see here.


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Creating Sperm via cell culture adaptation
I am wondering if it is theoretically possible to create "artificial sperm" via cell culture adaptation. That is at very high level, can you replace the genes of one sperm cell with those of another sperm cell and still have a functioning cell?
An area of application would be male infertility due to "weak sperm". Here you would take a "strong swimmers" from a donor, replace the genes with those from infertile male, and used the cultured adaption in fertilization.

Are you asking about getting a cell culture to produce sperm cells through cleverness, or about the sperm cloning? From a technical point of view, if you can cut and paste the genome from a sperm to a different cell, it doesn't make a huge amount of sense to put that genome into a different sperm for fertilization. It's a bit like giving your friend some cupcakes by mailing him a brick, then breaking into his house and making the brick/cupcake substitution while he's asleep. Put the genome straight into the egg, why mess around with the extra step?


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How likely is it that through dog breeding, tail-wagging has been disassociated with happiness?
I am not a biologist, so sorry to anybody for misinformation in this post.
If I understand correctly, dogs evolved the ability to show emotions through various sounds and tail-wagging in order to better communicate with their symbiotic partners, humans. Is it possible that recently, dog breeding has disassociated this with the communication of emotions due to the fact that humans like dogs which are more naturally happy? Considering that they have been tamed, and therefore their actions wouldn't be a good indicator, it seems plausible to me.
Please correct me on misinformation.

Welcome to Biology.Beta. Just to make sure I understand your question: You ask whether it is plausible (or whether it really happened) that dogs do not feel anymore happiness but still waggle their tail because they are selected to make humans think they are happy but not to be happy per se?

I am asking about plausibility, unless there is some accessible source of knowledge to answer definitively. Other than that, yes- that is what I am asking.

Well...yes that sounds plausible to me! I guess one answer should incorporate some elements of the additive genetic covariance between traits and how such covariance evolve in order to address whether it is likely or not to have first evolved both traits together because they were correlated and then correlation fell down (eventually because being always happy is not a good thing) so that traits could evove independently.

Evolution of the G-matrix is still poorly understood today. Hopefully we won't have to discuss too much about the M-matrix. If I feel courageous I may try to give an answer along these lines later.

Dogs are very cunning. Wouldn't surprise me one bit if they evolved tail-wagging without being happy, just to get another biscuit.

P = zero, or so close to zero as to not be worth contemplating or discussing


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How to calculate relatedness in haplodiploid organisms (mainly full sisters and full brothers)?
I have tried to calculate the relatedness for haplodiploid organisms, but cannot understand the calculations behind full sister and full brother.

(taken from Wikipedia: haplodiploidy
I have managed to solve the other cases. Since female will have ZZ:

female will share 1/2 of her genes with daughter
female will share 1/2 of her genes with son
female will share 1/2 of her genes with mother
female will share 1/2 of her genes with father

Since male will have only Z:

male will share 1 (100%) of his genes with his daughter
male won't share anything with his son (unfertilized eggs leads to male in haplodiploidy system)
male will share 1(100%) of his genes with his mother
male won't share anything with his father (unfertilized eggs leads to male in haplodiploidy system)

Even though I figured out how others work, I wasn't able to calculate r for fullsister fullbrother? How can it be 3/4,1/4,1/2,1/2?

Is this a homework question? If so, you should sow us the work you've done so far, including the ones you already figured out.

The table is taken from Wikipedia: Haplodiploidy, right? If so, you should include a reference.

This is a relative thing in haplodiploidy system.

r = Mother's side + father's side(in this case)
D--Daughter
S--Son
F-Father
M-Mother

Note:

You can get the below things from the question image itself.(All that you need to do is to read male and female appropriately as son,father,mother,daughter based on the context.So simple!)

1.rMD=1/2
2.rMS=1/2
3.rDM=1/2
4.rDF=1/2
5.rFD=1
6.rFS=0
7.rSM=1
8.rSF=0
case 1:
rDD=(rDM*rMD) + (rDF*rFD)
rDD=(1/2*1/2)+(1/2*1)
rDD=3/4

case 2:
rDS=(rDM*rMS) + (rSF*rFD)
rDS=(1/2*1/2)+0*1
rDS=1/4

case 3:
rSD=(rSM*rMD) + (rDF*rFS)
rSD=(1*1/2)+(1/2*0)
rSD=1/2

case 4:
rSS=(rSM*rMS) + (rSF*rFS)
rSS=(1*1/2)+(0*0)
rSS=1/2

It is useful to think in terms of the proportion of genetic material that an individual gets from each parent and the amount of this genetic material that will be shared with another individual (on average), and then sum this together i.e. as:
$ relatedness = prop_{mother} * shared_{mother} + prop_{father} * shared_{father} $
A female will share 50% of the genetic material from the mother's side and 100% if the material from the father's side with her full sisters: $0.5*0.5 + 0.5*1 = 0.75$
A female will share 50% of the genetic material from the mother's side and 0% if the material from the father's side with her brother: $0.5*0.5 + 0.5*0 = 0.25$
A male will share 50% of the genetic material from the mother's side with his sister (and doesn't get any from the father's side).
A male will share 50% of the genetic material from the mother's side with his brother (and doesn't get any from the father's side).
Remember also that this only holds if the female has only mated once.

A female will share 50% of the genetic material from the mother's side and 100% if the material from the father's side with her full sisters--then it should be 0.50.5+11 right? and A female will share 50% of the genetic material from the mother's side and 0% if the material from the father's side with her brother: 0.5∗0.5+0*0 right?

A female still gets 50% of her genetic material from each parent, so it should be 0.5 in both calculations. The first case you suggest would lead to a relatedness of 1.25, which is clearly impossible.

Yes but are we using 0.5 because 1.25 is impossible?

No, because 50% (0.5) of the genetic material in a female comes from each parent.

okay relatedness=propmother∗sharedmother+propfather∗sharedfather Does this generalised statement apply in all cases other than haplodiploidy to calculate relatedness?

@ecolover In the general case it should hold, but I haven't considered it from all angles. Overall, you should be careful when thinking about/calculating relatedness in species with peculiar chromosomal makeups. The sex determining system is also important part, and there are in fact deviations from the general pattern for certain ancestral pairs (due to the inheritance of X & Y chromosomes). For instance, Paternal grandmothers are more closely related to their granddaughters than grandsons (see paper).

@fileunderwater I'm sorry for not informing you earlier but I've quoted your answer in a different post without your consent. After being pointed out by a senior user of that site, I realised I should have done this before. If you don't approve of this I'll flag it for closure.

@Tytoalba Forgot to answer this. No worries. That is ok.