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Why is the central tendon of diaphragm called a tendon?
Why is the central tendon of diaphragm called a tendon when it does not connect the diaphragm to any bone?

Is there a requirement that tendons attach to bones? Histologically, it's just dense connective tissue.

@kmm Ligaments are similar to tendons and fasciae as they are all made of connective tissue. The differences in them are in the connections that they make: ligaments connect one bone to another bone, tendons connect muscle to bone, and fasciae connect muscles to other muscles.        Wont this result in no difference in three,  if tendon wont connect muscle to bone or something(like lens of eye)?

Not all ligaments connect one bone to another bone. ex; ligaments of liver which connect liver to abdomen, and other organs.

The basic difference between ligament and tendon is that one restricts movements while other aides in movement.

A tendon usually connects a muscle to a bone, but not always.
According to InnerBody, the diaphragm muscle originates at the lumbar vertebra, lower ribs and sternum and inserts to the central tendon.

The central tendon — a flat aponeurosis made of dense collagen fibers
  — acts as the tough insertion point of the muscles.

So, the central tendon acts as the diaphragm's own insertion.
A similar example is aponeurosis of the external oblique muscle in the lower part of the abdominal wall (Brazosport.edu, Picture 10.11.a.).
A tendon is the connective tissue that is always a part of a muscle and it fixes the muscle during its contraction.
A ligament is the connective tissue that merely connects two bones or two internal organs and is not actively involved in their movements.


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How can calcium be a kept as a local signal in the cytoplasm?
We went through this in my class last week and it doesn't make sense to me at all.
It's small and it diffuses in and out so easily so wouldn't it diffuse out quickly and thus not be a local signal? Or where it's stored in the RER does that change things?

Diffuse out of where? Ions cannot pass through the membrane.

I may try to write up a full answer later, but for a quick answer: calcium does not diffuse out of a cell ever, it actually takes a lot of effort for cells to keep their calcium concentrations so low. Instead, cells have a lot of calcium buffering capacity, so when calcium comes in it only stays free temporarily. That's when it has the opportunity to have influence. As it lingers and diffuses away from where it influxes, it is constantly being picked up by chelators, so it doesn't have a chance to diffuse away from a local signal at any high concentration.

Ions can only pass through channels in lipid membranes, such as voltage gated calcium channels at presynaptic membranes. That might clear up a bit of the confusion. Chelators bind free calcium ions, preventing them from interacting with other signalling molecules.

@BryanKrause — Please follow the injunction you read when you click on the comment box: do not use comments for answers. It breaks the SE model.

As @BryanKrause says in his comment, net flux of calcium would not ever be from inside the cell to outside the cell. There is a large gradient the other direction. Per Berg, the cytosolic concentration of calcium in a resting cell is on the order of 100nM, while extracellular concentration is in the mM range.
Signalling occurs when channels open up and allow $Ca^{2+}$ to diffuse down that very steep electrochemical gradient (from extracellular or topologically similar sources, e.g., the endoplasmic reticulum).
At least part of your question seems to involve a concern that the signal would not be very long lived. Though your concern about it diffusing out of the cell isn't warranted, the question about the time dynamics of calcium signalling is interesting. Calcium signals are, in fact, often very brief (though in other cases they last much longer). This is actually a benefit, and is one reason these signals can have very localized, very brief effects. For localized membrane fusion events, e.g., exocytosis, the signal lasts on the order of microseconds. The control of the time and position of a calcium signal involves a large number of players, including sequestering proteins, various compartments and stores, and tight control of the balance between calcium on and calcium off signals. It is discussed in this nature review, and summarized in this simplified figure:

You might also be interested in looking at some videos of calcium signalling. There are a number on youtube. This is one example

Calcium ions hold a +2 charge, and thus are unable to diffuse through lipid membranes. It is stored in the ER, and released to act as a signaling molecule in the cytoplasm. Being unable to cross membranes it remains in the cytoplasm until it is actively transported back into the ER.

Overall, decent answer, please add some references though.

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Can frogs see clearly under and above water?
If humans attempt to see underwater, the image is blurred due to refractive differences in air and water that disrupt the normal refractive effect of the lens in the eye. A diving mask overcomes this issue. How then do frogs accommodate their lenses in both air and water? Are their images clear in water and blurry above, or vice versa?
As far as I know, their lenses are made up of epithelial cells and fiber quite similar to the human eye lens, or am I incorrect here?

Short answer
Frogs are nearsighted on land and farsighted under water.
Background
Frogs are reported to be nearsighted on land, but farsighted underwater (source: Chegg Study). Nearsightedness (myopia) is a condition in which near objects are perceived clearly, but objects farther away are blurry. Farsightedness (hyperopia) is the reverse. The human counterparts of these conditions are shown in Fig. 1. Humans focus images on the retina by changing the shape of the lens; to focus on near objects, light is more strongly refracted by making the lens more spherical in shape. For far-away objects the lens is flattened such that light is less refracted.

Fig. 1. Near- and farsightedness. source: Hyperphysics
In humans refractive errors are common and can usually be successfully treated with corrective lenses.
The cornea adds substantial refraction to the optical system of the eye, namely about 43 diopters. As a comparison, normal prescription glasses often have only a few diopters worth. In water the refractive index of the cornea is mitigated, as water and the cornea have about the same refractive index (source: lasikmd). Hence vision is blurred for humans under water, because images are focused far behind the retina, resulting in hyperopia.
Frogs have another way of correcting their retinal image. They focus on objects at different distances by using specialized (lentis) muscles to move the lens closer to or farther from the retina (Fig. 2), like the focusing mechanism of a camera (Douglas et al., 1985). However, the lentis muscles can adjust the focus only for approximately 10 diopters worth, with an accompanying shift in lens position of about 150 μm. Hence, because of the huge effect that water has on the corneal refraction (~40 diopters), a frog's lens cannot sufficiently correct the refractive state of the eye to achieve normal vision (emmetropia) both above and below water. Apparently it settled evolutionary spoken somewhere in the middle, namely myopic on land, and hyperopic under water.

Fig. 2. Cichlid eye. Accommodation results from the movement of the lens in the pupillary plane using the lentis muscles; the musculus retractor lentis, and the antagonistic ligamentum suspensorium. source: Vision in cichlids
Reference
- Douglas et al., J Comparative Physiol (1986); 158(1): 33–143

+1, Nice answer! Did you use a fish eye image (bottom, a cichlid) because of similarities with amphibians?

@Kara - Thanks! And yes indeed - the lentis muscles are not confined to frogs but are found in many amphibian eyes and fishes. You actually read my post didn't you ;-)

Oh of course, else why bother? It's funny, most students I've come across think the human/mammal zonules of Zinn are ancestral. For fun, you might be interested in looking at the Four-eyed Fish, Anableps anableps, solution to air-water vision.

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How to compute CNV from TCGA data
TCGA provide CNV data for each cases like this.
I want to know, how can I calculate CNVs from this data? What are standard  algorithms and methods used?

Hi. The link your provided cannot be accessed any more. Can you provide information about what or which files did you use to extract CNVs?

The files you're referencing are completely processed files in the SEG format. The basic files are calculated using both germline and somatic CNV, whereas files denoted nocnv are only somatic (the numbers will differ because they are calculated either together or not together, so don't mix and match).
Among many tools you can use IGV from Broad Instutute to view SEG files at somewhat of a high level, or you can use various R packages i.e. Bioconductor to do your own analysis. You will probably need to do this anyways to annotate the gene names to the data. You can find somewhat of a how-to here or here. IGV will know what genes it's looking at based on chromosome assembly, and you can open it rather easily using java web start. I'm far from an expert, however.
Beyond that, you do need to make some additional considerations based on your expertise. For example, in this article, the authors set cutoffs for INDELS by filtering out seg.mean values between -0.2 and 0.2 (ref). They also filter out any markers for which 'num.mark' < 10, where 'num.mark' is the number of actual affymetrix probes detected, to account for false positives.
And so what you're left with then is the chromosome, the segment the probe spans, and the log2 mean of the microarray intensities calculated. So for that region of the chromosome, loc.start to loc.end, a seg.mean of 2 would mean 4-fold change in copy numbers over the reference for that region.
I think the take home point is the leg work on the data has been done, and level 3 TCGA data like .seg files are ready-to-go sources of CNV data. You significant tasks will be annotating, visualizing and assigning biological/statistical significance to your data.

Thanks for nice explanation. Just to clarify, should I ignore the data if num_probes < 10 OR segment_mean between -0.2 and 0.2?

It depends on what you're intending to analyze. If you have a significant segment mean but barely any probes, it could just be noise or an actual SNP as opposed to a CNV. Then for segment means, they set cutoffs: If your mean is below your reference, it could be a deletion (negative expression), and you aren't analyzing deletions. They chose >0.2 because anything lower may be noise or no amplification (you could argue different numbers. The idea would be to filter for BOTH to obtain high-quality data.

Copy number variation (CNV) has traditionally been detected in the wet lab via FISH, fluorescent in-situ hybridization. By combining targeted DNA oligos to fluorescent reporter proteins, a region with high CNV will "glow more brightly" than a region that doesn't have as many repeats.
More recently, with next-generation sequencing, a common approach is to align sequencing reads to the reference genome. If a particular region in the sequenced sample has a large CNV, then there should be disproportionately many reads (2x, 3x, etc) reads mapping to the CNV locus in the reference genome compared to the rest of the genome.
For example, if our sequenced sample has a 3-CNV for region B:
$$A-B-B-B-C$$
then aligning our sequenced reads to the reference genome, which is:
$$A-B-C$$
will yield 1x coverage at region A, 3x coverage at region B, and 1x coverage at region C.
There are, of course, more sophisticated approaches. For a good review, refer to
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0059128

Thanks for the reply. In my link of TCGA, each CNV file contains a column num_probes, do you know what does this column means or what would be the interpretation of this column?

Yes - the data are most likely from high resolution SNP chip arrays (mostly affymetrix) , and these have probes for specific genomic coordinates. The intensities then get combined into distinct segments with similar copy number estimates to produce the segmented files you have. The number of probes on the array that lie in a given segment is the num_probes column.
What particularly are you planning to do in terms of downstream analyses?

Also consider , in addition to CMosychuk's suggestions, sticking things through ABSOLUTE (particularly if you also have a mutation MAF file, which you can grab from the MC3 project on SAGE Synapse). The advantage of this is the ability to estimate and account for purity and derive absolute copy number values. EXPANDS is another R package that can do absolute copy number estimation.

What is absolute copy number? How it would be helpful? Sorry, I am from computer background

Usually copy number data is relative, you get a ratio in terms of tumour vs normal; this does not tell you how many copies of a given gene are actually present in a tumour, and if so, in how many cells in a tumour.
Absolute copy number is the actual number of copies per cell. ABSOLUTE builds a probabilistic model and fits combinations of purity and ploidy to derive absolute copy number.


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What are the effects of the common cold in an immunodeficient person?
How would the virus causing the common cold (rhinovirus) affect the human body in the absence of a normal immune response? On the linked wiki page it is said that the runny nose and fever symptoms are in fact caused by the immune response, rather than the rhinovirus itself.
Suppose the immune system is severely impaired (immunodeficiency), how would infection with the rhinovirus affect the body? Would the host not develop any symptoms then?

I've substantially edited the question to expose the question core as best as I could. The wording was unclear imo. Your sub-question on where the common cold causes its effects I have removed to keep the question focused. Feel free to ask another, separate question on that though.

In one small study, rhinovirus in the immunocompromised led to significant mortality from lower respiratory infection:

Among high-risk patients with cancer, rhinovirus infections are often fatal. In a study of 22 immunocompromised blood and marrow transplant recipients who were hospitalized with rhinovirus infections, 7 (32%) developed fatal pneumonia. The remaining patients had infections confined to the upper respiratory tract. In 6 of the 7 fatal cases, rhinovirus had been isolated in bronchoalveolar lavage fluid or an endotracheal aspirate before death.

Note that this is in hospitalized patients; it says nothing of non-hospitalized patients.
This conclusion has been disputed.
In a slightly larger study among people with hematological cancers (presumed immunosuppressed because of same):

Respiratory viral pathogens are a common cause of morbidity in patients with hematologic malignancies. ...Both a rapid viral culture with direct fluorescence antibody (DFA) staining and a PCR-based assay (MultiCode-PLx Respiratory Virus Panel) were performed on patients with hematologic malignancies, who underwent collection of a nasopharyngeal swab or bronchoalveolar lavage from October 2006 to April 2007. Eighty-two samples from 70 patients were obtained; all patients had upper respiratory tract symptoms. Respiratory viruses were detected in 10 samples (12%) by conventional virological methods and in 31 samples (38%) by the MultiCode-PLx assay. ...40% of these patients had pneumonia in addition to the upper respiratory tract symptoms. [emphasis mine; note, there is no mention of mortality.]

So long story short, they have stuffy, runny noses, sore throat, cough, etc. Clearly the virus itself causes damage to the mucosa; that is integral to viral replication After entering a mucosal cell, the virus replicates, then the progeny virus is released by lysis of the cell. This damage itself causes inflammation (not the same as an immune reaction), pain, etc. The major difference seems to be a more severe and prolonged experience.
Respiratory Consequences of Rhinovirus Infection
Detection of respiratory viruses with a multiplex polymerase chain reaction assay (MultiCode-PLx Respiratory Virus Panel) in patients with hematologic malignancies

they have stuffy, runny noses, sore throat, cough, etc. that is response of immune system not of virus right?

@murmansk - please see answer. You asked about inmmunodeficient patients. Clearly the virus itself causes damage to the mucosa; that is integral to viral replication.

Thanks for this most interesting answer +1 The question really made me wonder.


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Difference between ‘tagging’ and ‘conjugating’ a fluorochrome to an antibody?
The Wikipedia entry on fluorescence repeatedly states that “a fluorochrome must be tagged or conjugated to the antibody”.
How is tagged or conjugated different? Is this a mistake or are these indeed different concepts?

Your link is a null link.  I'm pretty sure thought that tagging is merely an alternate way of saying the fluorophore is bound to something. Either directly to the macromolecule of interest or "conjugated" first to an antibody that has preference for said molecule of interest.

Conjugated and tagged mean the same thing here, although I would advise against using tagged here.
In the context of antibodies, tagging means the addition of a (short) peptide sequence to a protein. Either to do something useful (degradation tag, HHHHHH-tag) or just as an epitope for an antibody.


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Plant Nutrition
Alfie has two plants, A and B. He used some Vaseline to coat the top of the leaves on plant A and the underside of the leaves on plant B. He left the plants on the windowsill for a week and watered them regularly.
a) What do you expect happened to each plant?
Plant A: __________________________________
Plant B: __________________________________
b) Explain the result you have predicted for plant B

I think plant A would use a moderate amount of water and would use the least amount of water. I think plant B would use the least amounts because coating the lower surface causes the water loss similar to coating both surfaces (upper and lower).
What are your thoughts on this?

Is the plant a dicot or monocot?

I would try to think about the vaseline layer as a huge cuticle that our man "Alfie" just applied to the plants.
I think you have the right answer here. Just note that there is a typo in the first sentence of your thoughts. You missed a "B" in front of "plant". Took me a bit to understand.

Am I missing something? Plant B would have all stomata blocked.


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Ultra-violet radiation and Bacteria in Petri Dishes
My partner and I are planning on doing a science fair project on how long bacteria can be exposed to UV radiation. We were wondering what the noticable effects would be if we held a UV lamp to bacterial colonies in petri dishes. Would the bacterial colonies shrink?

Welcome to SE Biology. I have removed the word "question" from your title as all titles refer to questions. I also changed "rays" to "radiation". The former may be ok for a science fair, but it is not current scientific usage.

Think about what UV radiation does: It damages the DNA and thus the potential for the cells to replicate. If you blast them when replication is done and over, what do you expect to observe?

First of all, thank you both for editing my question and for the welcome.

I'd expect that the bacteria would no longer replicate.

A more interesting experiment would be to spread plate bacteria and irradiate them before they start actively growing. Then you can compare the effects of no radiation and different radiation on the amount of colonies formed.

I don't know if they would shrink. But, if it is possible for you to do an enumeration (perhaps by hemocytometry, if your school could provide the instruments) and serial dilution, you could test the percentage viability over time by standardizing an arbitrary cellular concentration (in cells/mL) to be spread plated.


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Are there genetic causes underlying the difference in circumference of the upper arm and foream?
Is there any genetic reason for the difference in size between the upper arm and lower arm (i.e., the forearm)?
In most women, it seems that the upper arm is larger in circumference than the forearm. However, in males it seems to vary - some men (like myself) have an upper arm with a diameter smaller than their forearm, while for example in body builders the opposite may be true, as they often have large biceps.

The first answer explains that proximal limb segments do more "work" * using quotes to be careful w.r.t. technical definitions of work. Genetically, this is correct--it's the ancestral condition for tetrapods. It is also worthwhile to answer why it's beneficial for why proximal segments get bulky to do this work, instead of their distal counterparts -- i.e. why did natural selection favor this arrangement in the first place.
There is a biomechanical reason for distal limb segments to be less massive than proximal limb segments, especially in tetrapods: That moving masses farther away from the center of rotation, when force is applied between the center of rotation and the mass, takes a LOT more force.
Let's consider the arm from your example. We'll treat the forearm as a "load" which is supported by the upper arm and shoulder.
In this case, the whole arm is a Type 3 lever, with the force applied (by upper arm and shoulder) inbetween the load center of mass and the fulcrum (joint). Image from https://alexeinstein.wordpress.com/2014/09/03/lever-of-human-body/:

 In the picture, it's showing the hand (could be a weight in the hand, too) as the load, but for an empty hand the center of mass of the lower arm is probably slightly more proximal (but not more proximal than the muscle insertion).
In order to support the load that is the lower arm, the torques about the joint need to be balanced. So the torque produced by the muscles (by force AF in the diagram), needs to equal (or for bicep curls, exceed) the opposing torque produced by the mass of the load.
Torque is the product of the rotational force acting perpendicular to the lever and the distance along the lever to the fulcrum. (Reference is Wikipedia, but there's no argument about the definition of torque.)
Lets make up some numbers, and work through the example. Say that the weight of the lower arm (R in the diagram) is 10. And the distance from the center of mass to the elbow is also 10. Then, the biceps in this image needs to produce an opposing torque of at least 100. But the insertion of the biceps is very near the fulcrum, say at a distance of 1. So it needs to produce 100 times the weight of the load to create a balancing torque. For most joints in the body, the muscle insertion is nearer to the joint than the load--so the muscle will ALWAYS need to produce more than the load. So you can see how having a lighter forearm would be of benefit.
Now let's consider the whole arm, relative to the shoulder. I drew a picture for us. Suppose we only need 10 muscle mass to do day to day moving of things. Let's imagine a world where that 10 muscle mass is in the lower arm. If we have an upper arm of length 10, and a lower arm of length 10, and we hold our arm perpendicularly in front of us (so the center of mass of the 10 muscle mass is approximately at the middle of the lower arm(15 length from the shoulder), the weight of the arm is generating a torque of 150. This needs to be matched by the rotator cuff muscles, and it's a lot. The shoulder girdle insertion is quite close to the joint (let's say 2 length from the shoulder), so these muscles must produce 150 Torque / 2 length = 75 force perpendicular to the arm -- which means even more force overall, because the muscle is not acting perpendicular to the arm. That's a lot of force. (PS: red is showing lines of action of forces)
Now, suppose instead we put the 10 required muscle in the upper arm. (Another drawing for you.  We'll say the center of mass of the whole arm is now probably just before the elbow, at length 9 from the shoulder. The whole arm is producing a torque of 10 * 9 = 90 at the shoulder. The shoulder girdle muscles (with the same insertion distance of 2) must produce 90 Torque / 2 length = 45 force perpendicular -- much less. This holds in general--for a type 3 lever, the muscles will always have to do more work if the load is farther away from the joint.
Thus, placing muscle mass distally means the center of mass of the entire limb s farther from the body -- which means the body must produce a lot more force to support the mass than if the load is closer to the body. This is the same reason why it is easier to carry a heavy backpack in your arms than at the end of your arms. On an evolutionary time scale, it makes sense that the bulk of muscle mass has been placed closer to the center of mass.

How do I ping @AliceD ?

For a ping to work, AliceD must be involved in this thread. If you're unsure, just start typing @AliceD. If he's involved, the autofill will give you a choice to click on his name. Try it under my answer and see what happens. :) +1 btw. Very nice!

@Kara - I'm here and you've got my upvote. What a great answers here on this question.

Yes, there are genetic reasons for this. But your observation is either incorrect or abnormal.
The shoulder (and hip) muscles do the heavier work, thus have larger (and bulkier) muscles. The more distal the muscles, the more involved with finer motor skills (yes, even in the foot), so we're after finesse here, not strength. You can pick up 100 pounds primarily because of your upper arms. You can curls weights (not 100 pounds for most humans) because of your distal arm musculature. You can grip the weight because of your hand and lower arm muscles.
It's like this for most vertebrates. Have you ever seen a dog, cat, horse or other animal with skinny "thighs" and fat "lower legs"? A horse's thighs (between their back and their knee) are huge, their gaskins (between the knee and the ankle, also called the hock) are prominent, the rest barely visible.

Here is a Grizzly Bear:

Here is a frog:

This is the plan for almost all terrestrial vertebrates, including humans. Certain vertebrates may have different musculature depending on how they live.
If it is true that your forearms are larger than your upper arm, then it simply means you are using your forearms much more than your upper arms, something not common for man before the present age.
Horse: http://thinklikeahorse.org
Grizzly: The Grizzly Bear
Frog: antique drawing, French.

Nice answer, +1! something not common for man before the present age so it is common nowadays? Can you give more details about this?

how come all girls have bigger upper arm , is is t due to fat

@another'Homosapien' - No, it's not common at all. In fact, I have never seen this outside of infancy (infants have yet to work much, and their upper arms are sometimes significantly larger than their lower arms.)

@murmansk - No, it is not. The answer explains why this occurs.

Can you cite the sources where the images are from?

@another'Homosapien' - Oops. I meant the other way around!

@canadianer - done!

This answer is not entirely correct. Muscles get big from use, yes, but most big muscles are placed proximally to begin with, by virtue of physics.

@Kara - Why are the proximal muscles of the shoulder girdle larger than the proximal muscles of the forearm? Arguing from physics is a teleological argument in my opinion. They are that way because that placement - passed on from generation to generation from early ancestors - was the most effective. So, yes, it also makes sense from the standpoint of physics. But it's not because of physics. It's because of it's success in ancestors.

@Kara - Thinking about it, it's because of the laws of physics that it was the most successful plan. But... but. The muscle groups are larger. We are born with the gluteus maximus being the largest muscle in our body. Because it works is a less satisfying answer imo. But that's just one person's opinion.

@anongoodnurse -- yes, it is fundamentally physics. And it is also the plesiomorphic condition. I just wanted to point out WHY the physics works. Rarely are there examples of natural selection agreeing closely with physics. It was successful in ancestors in the context of physics.  However, success in ancestors would not also explain the effectiveness of lifting weights far away from the joint. My addition was more to address the "they are that way because of use" reasoning, I have no qualms with the "they are that way because of ancestry" reasoning.

@anongoodnurse I'm sorry if I've offended you. As a biomechanist, I'm inclined to explain ALL the physics. Even arthropods place bulky limb musculature close to the center of mass, and those limbs are independently evolved.

@Kara - not at all! I'm sorry I gave you that impression. I tend to be to the point, so combined with the inability to see body language and tone from the written word, I was interested in what you had to say. It's kind of a chicken-and-egg argument. I don't really know but what I have stated. I like your addition to the "discussion." The more good answers, the better!

Oh good! I was worried! I'm generally in your camp, as opposed to the adaptationist one, on this kind of question... I think this q. just reminded me of a time when I calculated the torques and forces on a pregnant woman's spine/hips. It was enlightening? ( Or en-ohgodwhy-ing. That.)

@Kara - Wow! What an interesting job you must have! (Seriously) Your answer reminds me of how when I was doing a neurological/musculoskeletal exam, I would tell men to put their fist to their shoulder and keep it there, while I tried to pull it down. And of course, because physics, I could pull it away. They would always look at me (a smallish woman) and say with a touch of embarrassment, "You must be stronger than you look..." Ha!


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Hybridization in Darwin's finches is rare or frequent?
I've talked to a couple of researchers today and read recent articles on the subject of hybridization of Darwin's finches. I'm confused about the consensus in the scientific community.
First, I was reading about hybridization in systems where adaptive radiation occurred. I came across this Honeycreepers paper: Knowlton, J. L., D. J. Flaspohler, N. C. R. Mcinerney, and R. C. Fleischer. 2014. First Record of Hybridization in the Hawaiian Honeycreepers: 'I‘iwi ( Vestiaria coccinea) × ’Apapane ( Himatione sanguinea). The Wilson Journal of Ornithology 126:562–568.
In this paper they are saying:

The Galápagos finches, for instance, hybridize frequently both within and across genera (Grant et al. 2004, Grant and Grant 2008).

But in the resources they cite, here is what I found:

Rare hybridization between the species, occurring partly as a result of misimprinting on song (Grant
  and Grant 1998)

From Grant, P. R., B. R. Grant, J. A. Markert, L. F. Keller, and K. Petren. 2004. Convergent evolution of Darwin's finches caused by introgressive hybridization and selection. Evolution 58:1588–1599.

Hybridization was rare at the level of individuals: only
  a few percent of all offspring are hybrids

From Bell, G. 2015. Every inch a finch: a commentary on Grant (1993) 'Hybridization of Darwin‘s finches on Isla Daphne Major, Galapagos’. Philosophical Transactions of the Royal Society B: Biological Sciences 370:20140287–20140287.

Hybridization was always rare.

From Grant, P. R. 1993. Hybridization of Darwin's Finches on Isla Daphne Major, Galapagos. Philosophical Transactions of the Royal Society B: Biological Sciences 340:127–139.

Hybridization occurs rarely (less than 2% of breeding pairs) but persistently across years, usually as a result of imprinting on the song of another species.

In Grant, B. R., and P. R. Grant. 2008. Fission and fusion of Darwin's finches populations. Philosophical Transactions of the Royal Society B: Biological Sciences 363:2821–2829.
Did I miss something, or is hybridization rare and not frequent? Maybe frequently is so vague that it includes, rare?

I actually just had to read a Grant & Grant paper, so hopefully, I can get this right. My understanding is that hybridization events have repeatedly seen to occur, but the events themselves usually do not repeat within a lineage, i.e. once a lineage becomes partially hybridized, it is unlikley to continue to breed with adjacent populations.
Due to the reproductive barriers that come from song patters of hybridized individuals (Grant & Grant, 2009), Repeated hybridations are unlikely to occur within a lineage, even when in the presence of a species with which hybridization can occur.
Grant, P.R. and B.R. Grant. 2009. The secondary contact phase of allopatric speciation in Darwin's finches. PNAS 106 20141-20148

Please cite the Grant & Grant paper. We strongly encourage the addition of sources here at Biology.

That's what I was thinking: "Galápagos finches have very low, but persistent, levels of hybridization events, compared to other system where speciation is near completion or completed or where there is high reproductive isolation" For the actual numbers and percentages of hybrids see: Grant, P. R. 1993. Hybridization of Darwin's Finches on Isla Daphne Major, Galápagos. Philosophical Transactions: Biological Sciences 340:127–139.


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What instances are there in which two species share the same binomial name?
Since binomials are required to be unique only within a kingdom, two species can share the same binomial name if they are in different kingdoms. I know of one instance of this, Orestias elegans: this name denotes a species of fish (kingdom Animalia) as well as a species of orchid (kingdom Plantae).
Are there other instances where one binomial name validly refers to two (or more!) species?

This is a fascinating and surprising tidbit of information that practically begs to be used as the point of a puzzle story.

But why on earth did anyone think it would be a good idea to allow such a thing?

There are four other instances of species-level hemihomonyms I can find:

Agathis montana can be either a critically endangered species of conifer or a parasitic insect.
Centropogon australis can be either a fish or a plant with a long red flower.
Asterina gibbosa can be either a sea star or a type of fungus
Baileya australis can be a moth or a yellow flowering plant

Deep in the Binomial Nomenclature wiki citations!

The "wiki citations!" link in the previous note was a (now broken) indirect reference to https://species.wikimedia.org/wiki/Category:Species-level_hemihomonyms ,

Looking for hemihomonyms here: http://www.irmng.org/homonyms.php

In addition to the five listed above, Wikipedia currently shows two others, for a total of seven:
Ficus variegata can be either a sea snail or a fig
Tritonia pallida can be either a nudibranch or an iris
See "Hemihomonyms" here.

Two others for posterity, since I haven't seen others bring it up. Rhaphidophora is a genus of flowering plants AND of cave crickets, and there are two species-level hemihomonyms. R. beccarii is an uncommon houseplant and its relative R. neglecta is much rarer, but both are still documented. There's hardly any record that the cave crickets with these names exist, but they both seem to be accepted species with type specimens and all. I looked hard for images of either one and came up empty handed.

Very nice first post, welcome to Biology. Please take our [tour] and refer to the [help] for guidance as and when, enjoy the site.


text:
What are the 2 general systems to understand the whole natural world?
In Graham Bell's book Selection, it's written:

To some it may be a cause of regret that the natural world cannot be understood in terms of a single set of rules and laws, but at least, so far as we know, the whole of the natural world can be understood in terms of just two general systems, and no more. This book is an account of one of these, in the context of biological systems. It is an account of the Second Science

The first system or process is Selection. What is the second?

I wonder if it might be genetic drift?

The categorization of the entire of knowledge regarding the natural world is sexy but the categories aren't necessarily natural (wiki > natural category). 99.999% of scientists (me included even if I am an evolutionary biologist) would disagree to consider the the process of selection would hold half of the knowledge we have about the natural world. It does not even hold half of our knowledge in evolutionary biology!

In any case, whether his saying makes sense (or even whether the question of what he says) is a matter of opinion and is therefore off-topic.

If you are interested the philosophical discussion of how to divide our knowledge about the natural world, you can give it a try on Philosophy.SE (once you figured what the second general system is) Or you could try to chat about it with Graham Bell directly over a coffee as you both work in the same University!

@Remi.b thanks for your comments. While you are there, you could ask what Dolph thinks about it? :D I still think that this is a legit question and that it could be interesting to discuss. I guess that saying it's a general question about biology or philosophical question is an opinion too. Maybe if the question is: what are the 2 general systems to understand the natural world in biology might be more biology related? What's your advice on how to edit that question so that it fits, in your opinion, into this forum?

@M.Beausoleil As a rule, questions that evoke discussion aren't good SE questions. The point is to produce questions that have an answer that can be accepted as the best answer out of fact and presentation, not out of rhetoric.

On reading the rest of that passage via google books I think you and others are simply interpreting it wrong. He isn't saying Selection is one of the two ways to understand the world he is saying that one approach is to reduce to basic principles, like physics and chemistry, and the other is that this isn't possible. He is saying his book is one example of an attempt to understand something that cannot be reduced to basic principles alone.


text:
Identify a small bug, possibly a plant bug?
We found this bug in a bedroom in southern California. It's small: the body is about 5mm and the length including legs and antenna could be up to about 10mm. It's mostly black, though the abdomen from the bottom appears to have gold highlights under light when I used a flashlight. In sunlight it appears somewhat brownish. It looks like it has wings which forms sort of an "X" pattern on its back. The legs are dark black or brown but may be somewhat translucent in sunlight to appear an orange-gold color.
What species is it? It looks to me a little like a plant bug (phylinae?) or roach or beetle but I'm not sure. And could this species bite?

I've seen this thing too. I don't know the species, but I do know it bites. Be careful!

This may be an assassin bug, Reduviidae. These may indeed bite.

This is a plant bug (family Miridae); going deeper isn't possible on the basis of a photograph, except for some common economic species (the key to genera in How To Know the True Bugs is almost 200 couplets long!).  Most species of the family are plant feeders (hence the common name); biting humans is unlikely.
Reasoning (from Comments):
The top right photo [from the OP's post] shows that the front wing has a cuneus (a section of the hardened part of the wing on the outer margin set off by a groove), which is characteristic of that family and the broad-sense "Anthocoridae" (which includes three smaller families); none of the photos show simple eyes (the eyes we see are compound), which eliminates "Anthocoridae" and the subfamily Isometopinae of Miridae; the remaining seven Nearctic subfamilies are still possible

Welcome to Biology.SE and thanks for your answer. It is difficult to assess whether your answer might be correct or not. I know it is very hard to ID insects to the species level and therefore I like your conservative approach, giving the family only. But could you please still provide evidence for your claim that this species belongs to Miridae, maybe by discussing some of its characteristics and compare them to the specimen on the original question? Thank you!

The top right photo here shows that the front wing has a cuneus (a section of the hardened part of the wing on the outer margin set off by a groove), which is characteristic of that family and the broad-sense "Anthocoridae" (which includes three smaller families); none of the photos show simple eyes (the eyes we see are compound), which eliminates "Anthocoridae" and the subfamily Isometopinae of Miridae; the remaining seven Nearctic subfamilies are still possible.


text:
Meaning of ‘NC number’ associated with a gene?‘
Genes in listings etc. often have a number of the type NC_000012.12 associated with them. How should this be interpreted?

I have edited your question so the title is more useful to others, in view of your original misunderstanding and the correct answer supplied by @JITZ.

This particular ID represent RefSeq accession number.
NC_ stands for a genomic molecule representing complete genomic molecule, usually reference assembly. Every sequence has a stable accession number, a version number, and an integer identifier (gi) assigned to it. RefSeq records can be distinguished from INSDC records by the inclusion of an underscore (“_”) at the third position of the accession number.

New sequences are no longer being assigned GI numbers (source) since they were redundant.  Use "accession.version" instead, e.g. "NC_000012.12".


text:
Help ID this South Indian fruit-bearing tree
So there's this fruit-bearing tree near my house in Kerala, South India. A senior neighbor of mine tells me that this fruit is edible. I tried it out, and it tastes alright. I want to ID this plant, know its botanical name, as well as whether it has any medical/commercial/culinary application.

The fruit is green when tender and red when ripe.

This looks like Muntingia calabura, the Jamaica Cherry.

pic source

pic source
It is indigenous to tropical America and often planted in Asia.
It is edible and used in jam, cake and fruit drinks. The bark is sometimes used as rope. Source: "Tropische vruchten, Nowak&Schulz 1999"

Googled it and confirmed. This is what I was lookin' for. Thanks again!


text:
Why male gametes doesn't go through antipodal cells in chalazogamy
Male gametes in double fertilisation enter the embryo sac through synergid cells even in chalazogamy i.e. when polen tube enters the ovule through chalazal end. Regarding the fact that compatibility reaction has already taken place (i.e. they are the right gametes) after pollination then why male gametes doesn't enter through antipodal cells? Is it just because of filiform apparatus that affiliates the entry of male gametes through only synergid cells or is there something else as a reason?


text:
Will meat rot in alcohol below freezing?
I understand that freezing slows decay but I'm wondering what will happen if meat is kept in below freezing temperatures while submerged in a liquid that has a lower freezing rate, like alchohol?

The meat will still freeze

A chemist's perspective:
Ethanol and water are miscible, meaning they are perfectly soluble in one another in all proportions. So given enough time, the alcohol will likely seep into the tissues and cells of the meat, and some water will seep out into the surrounding alcohol bath. The liquids might not equilibrate very well on a reasonable time scale, that is, the bath surrounding the meat could remain mostly alcohol with some water, and the tissues of the meat could contain more water than alcohol. This is because the biological barriers of the meat interfere with the diffusion of the fluids to reach a mixture of equilibrium proportions. However, in theory, cell membranes are permeable to ethanol, so given enough time soaking we might build up a useful concentration of ethanol within the meat.
Note that it doesn't matter so much what happens outside the meat - being bathed in a substance that remains a liquid below 0 °C won't necessarily stop the meat itself (well, the aqueous solutions within it) from freezing. That is why the considerations of solubility and permeability are crucial. As I said, for ethanol we have perfect solubility with water (miscibility), and possibly sufficient ability to diffuse throughout the organic catacombs of our meat. So, assuming ethanol can sufficiently perfuse the tissues and enter the cells, what would happen?
Water has a higher freezing point (not "freezing rate") than ethanol (0 °C > -114 °C). When you mix some ethanol into water, the freezing point of the solution will be lower than the freezing point of the pure water. The freezing point of pure water is depressed by the addition of ethanol. Here is some data on the freezing point of water solutions with different amounts of added ethanol:

(Note that the freezing point at 100% ethanol seems to be -111 °C according to this data; this should technically be freezing point of pure ethanol itself, so we would expect it to be the -114 °C figure I quoted earlier. But that small discrepancy between this experimental data and the traditionally accepted number will not affect our analysis.)
So, as you lower the temperature, the water-ethanol solution in the meat will begin to freeze. It will freeze at some temperature lower than normal because of the ethanol present. Note that the normal freezing point of water in meat is already going to be lower than 0 °C due to all of solutes inherent in such a biological system (ions, sugars, metabolites, maybe a few stray amino acids, etc). As it freezes, the water will freeze first and leave the ethanol behind.
So, inside the meat, you will see the meat freeze at slightly lower than normal, with some liquid remaining in the tissues which would be the ethanol. Outside the meat, in the bath of ethanol which has drawn some water out of the meat, you will see that water forming ice on top of the liquid, which will become purer and purer ethanol as the water freezes out of it. The process I just described is fractional freezing, and you may be interested to know it is how "ice beers" (Keystone Ice, Natty Ice, etc) are made more alcoholic.
Now, if the proportions of ethanol and water are just right, something interesting happens. Instead of the water freezing first and precipitating out of the ethanol, a special eutectic solution is formed that freezes all at once. (Perhaps you've heard of fractional distillation and azeotropes, the the boiling point analogue to fractional freezing and eutectic mixtures). On the graph above, the eutectic mixture is achieved at the very minimum value, around -118 °C. Note that freezing point of the eutectic mixture is lower than the freezing point of pure ethanol alone. Unfortunately, for the specific case of water and ethanol, reaching that special point of bonus freezing point depression requires the solution to be almost completely ethanol (about 93%). That would be the holy grail of lowering the freezing point of your meat, but it's likely not feasible to replace that much water with ethanol throughout the meat.
So, in conclusion: It's what happens inside the meat that counts. If you bathe meat in ethanol, a useful amount of ethanol may permeate the meat. The freezing point of the meat (rather, the aqueous solution within it) will be lowered the more ethanol perfuses it. In theory, you could even drop that freezing point below that of ethanol itself, but it would require replacing nearly all of the water with ethanol.


text:
Plasmid harbouring subunit S of type I R/M system
We have an assembly of a genome of a Lactobacillus species. The genome also contains a 7.5kb plasmid.
Aside from the "usual plasmid genes" the plasmid contains:
 - toxin/antitoxin system
 - Subunit S of type I R/M system (No R or M subunit)
Now, to me this seems like an interesting case. It looks like the plasmid is "exploiting" the R/M system of the host (Bacterium seems to have type I R/M system indeed).
This could have the effect that the plasmid is increasing the fitness of the host (and itself) by making the R/M system more flexible in terms of target sequences by the R/M system (Phages, etc.).
My questions are now:

Does anyone know an example of such a case. Did not find any.
Do you think it works the way I suspect.
Could this be interesting for Biotech applications since phages in diary food environment are a problem.
How would you test if this plasmid has this effect?


text:
RNA isolation problem
I have isolated RNA from cell culture (T25 flask, mouse cells) with trizol. I've measured the sample on Nanodrop, and this is what I've got:
A260 (10mm): 16.408
A260/A280: 1.98
656.3 ng/ul
How is this possible? What could go wrong here?
Thank you!

What is your problem? The A260/280 ratio? The yield? I don't understand (actually see) the question.

The absorbance A260: 16.408

The absorbance is directly proportional to the amount of nucleic acids (and proteins). Can you show the absorbance curve of your measurement?

no :( this is all i've got

Without any further data, we cannot give you any advice. But the A260 is not wrong, it shows that you have some RNA here. It is most likely still contaminated with Phenol though, this is what the high A260/280 ratio says.

Do you think RNeasy mini kit would help? Thank you very much for your help :)

I can't give you any advice as long as you are not sharing your protocol etc. Trizol in my experience gives fine RNA.

The 260/280 is almost 2, isn't that technically pure RNA? If the A260 readout alone is bothering you, read this article under Quantification of DNA

i used this protocol (RNA isolation procedure for cells) http://www.abcam.com/protocols/rna-isolation-protocol-cells-in-culture except I added 200uL chloroform, 500uL isopropanol and on the end I added 15uL DEPC treated water (because the last time there was small amount of cells).


text:
Why is pollen used as a dietary supplement?
Sporopollenin is the hardest biological substance and can't be degraded by any know enzyme (my school textbook). Then why is pollen used as a dietary supplement if it can't be digested?
Also, pollen depends on nutrients from the plant itself either before or after pollination (before if pollen leaves anther at 3 celled stage and after if it leaves anther at 2 celled stage). Then how would it be rich in nutrients?

But at some sites called as "germ pores" , sporopollenin is absent, so the enzymes may enter it via this, and the digested products may exit via this.

Do you have any citations that suggest that pollen supplements are indeed rich in nutrients or have any beneficial value? All of the evidence I am aware of is that pollen is used as a dietary supplement because people are willing to buy it at a price greater than the cost of producing it. There doesn't have to be any benefit to something sold as a dietary supplement.

Bee pollen contains high concentrations of reducing sugars, essential amino acids and unsaturated/saturated fatty acids. It contains minerals such as Zn, Cu, Fe, and high K/Na ratio and significant quantities of several vitamins. Note that the composition of it varies greatly depending on their botanical type and the techniques used by industries. It is basically the collection of pollen grains from flowers made by worker honey bees with nectar and salivary substances.[Source 1](Page 1)  [Source 2]

[Source 1](Page 4)
The claimed benefits of bee pollen are based on biological and therapeutic activities. The main components are phenolic acid derivatives and polyphenolic compounds. They are known to possess properties such as anti-oxidant, anti-aging, anti-carcinogen, anti-inflammatory, anti-atherosclerosis, cardio-protective and improved endothelial functions. However, it is unknown that treatments with such products are effective or not and how to minimise the health risks.[Source 1](Page 5) [Source 4]  [Source 5]  [Source 6]
Different studies were conducted in mice on the nutritional effects of bee pollen. It improved food digestion and also improved reproduction rates. Chickens fed with bee pollen had a better development of the small intestine. This suggested that bee pollen helped in early development of the digestive system. Bee pollen is also taken as a supplementation by athletes for improvement of performance. Controlled experiments indicated that no positive benefits were obtained. However, the number of training missed due to respiratory tract infection was lower in the bee pollen treated group.[Source 1](Page 5)

Pollen digestion:
Doubts have been raised, whether the tough shell of pollen can be breached and digested by humans. It was discovered in animal experiments that pollen did not retain its content after leaving thedigestive tract. This gave rise to the hypothesis that the nutritional content of pollen was released by the digestive juices in animals (Schmidt & Schmidt, 1984; Roulston & Cane, 2000). In humans it was once shown that pollen was absorbed in the digestive tract (Jorde & Linskens, 1974) or that it was partly digested, (Franchi et al., 1997) whereas there were differences in the degree of digestion of poppy and hazelnut pollen, with an average degree of digestibility of 15% for carbohydrates and 53% for proteins.
In this case it has been hypothesized that pollen was insufficiently digested and that cracking would improve the digestibility and bioavailability (Rimpler, 2003). Different companies offer cracked bee pollen, claiming that this product is better digested. On the other hand, there are many studies in humans with whole bee pollen showing that a part of the bee pollen content is digested and is bioavailable. However maceration of pollen for several hours in water or other liquids is recommended in order to improve digestibility, this method is used also for other heavy digestible grain products.[Source 1](Page 3 & 4)

Flower pollen:
Non-bee pollen are called flower pollen. Extensive health relevant research has been conducted on pollen prepartions from non-bee pollen. It is marketed under names such as Cernitron, Cernitol, etc. It is known to decrease prostrate hyperteophy in rats, but there was no relevant changes in blood levels of LH, FSH, testosterone or dihydro-testosterone.

In patients with prostatic adenoma the improvement was in nycturie, important decreases in the residue post-urinate and in long term treatment, also decrease in the diameter antero-posterior of prostate. The urinary debit did not suffer any changes. The effect on the other symptoms usual in the hyperthrophie benign of prostate was not of statistical significance (Bruneton, 1999).[Source 1](Page 7)

For industrial benefit:

Improved bioavailability is important in the pharmaceutical industry in that it reduces costs and increases the effectiveness of drugs. Previous studies have shown that this enhancement is possible using exines from pollens and plant spores. In one example the ingestion of ethyl ester derivative of EPA (eicosapentaenoic acid) encapsulated in sporopollenin microcapsules from L. clavatum spores improved the bioavailability of EPA in the bloodstream. In these trials, six volunteers ingested 4.6 g of fish oil containing 20% of the EPA ester, both alone, and encapsulated, as a 50% fat content powder, respectively. The bioavailability of the active was defined by area under curve (AUC (area under curve) 0–24 h). The mean AUC 0–24 of EPA from ethyl ester with exine was remarkably 10-fold higher than the corresponding for ethyl ester without exine encapsulation.
In other unpublished studies involving human volunteers, ingesting a lipophilic active, the enhancement of bioavailability has been very similar. The mechanism by which such enhanced bioavailability is achieved is intriguing and some preliminary experiments have been undertaken to explore possible explanations. Recent in vitro studies (unpublished studies) revealed that the exine shells exhibited gut mucosal adhesion properties. In addition, in vivo experiments on mouse microtone sections of intestinal walls of mice fed with exines showed the exines to lie between the gut villi. The unique morphology of exine shell surfaces probably evolved to help pollen particles to become attached to insects and thereby aid the process of pollination. It is possible therefore that this same morphology could help the exine’s adherence to and close association with the gut wall leading to an increase in the period of contact between the encapsulated drug and the biological surface, thereby enhancing its absorption and bioavailability.[Source 3]

Hazardous components of pollen:

Trace amounts of hepatotoxic pyrrolizidine alkaloids were found in pollen of Echium vulgare, E. plantagineum, Senecio jacobaea, S. ovatus, and Eupatorium cannabinum (Boppre et al., 2008).  In Middle and Northern Europe these pollens are not among the main pollen grains gathered by bees, however in Southern Europe the two Echium plants are more  diffused and are gathered by bees in larger amounts (Campos et al., 1994; Serra Bonvehi, 1997). [Source 1] (Page 5)

Therefore, it should undergo tests to approve it's purity as allergies can be caused.
References:
1 : Future of bee pollen(Research gate)
2 : Pollen composition and standardisation of analytical methods(Research gate)
3 : Hollow pollen shells to enhance drug delivery(NCBI)
4 : Bee pollen: chemical composition and therapeutic application(NCBI)
5 : Biological activities of commercial bee pollens: antimicrobial, antimutagenic, antioxidant and anti-inflammatory(NCBI)
6 : Biological and therapeutic properties of bee pollen: a review(NCBI)

I am skeptical about the broad claims about health effects to say the least. I will have a look on the journal article in question tomorrow, but this is a ten year old review which seems to have not been cited. This is usually not a very good sign.

@Chris The page says that it has 21 citations and 90 references.

It is also in a journal that only existed for two years. It's pretty hard for a journal to generate any positive reputation in that little time. Also one of the authors appears to be affiliated with a company in Switzerland that I wasn't able to find any information about, but there is no conflict of interest disclosure in the paper, which is quite troubling.

As I said, I will look at it tomorrow when I have journal access. This is not possible from home. But it smells a bit funny to me.

@BryanKrause Still, such an article can be cited. But it is even not listed in the Pubmed.

@Chris It simply isn't in a journal indexed by pubmed. Google scholar shows that it has been cited 45 times (though some could be duplicates or not real citations), but I don't necessarily take that as a measure of quality.  Paging through the citing articles many of them are in fairly red-flag journals, as well.


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What is the course of inter auricular line?
BACKGROUND: The interauricular line is the line connecting two auricles.

I wish to know the exact route through which this line passes. I want to be sure whether it passes through the parietal prominences, or in front of them.

Could anyone create a tag for cephalometry?

@JM97 Please do not create new tags for every single possibility. This tag is relatively pointless at the moment and will most likely be orphaned.

Do you mean the interaural line? If so it is ventral, rather than in front, of most of the parietal bones. This seems like a really odd question - you are using fairly outdated/underused terminology, and the answer is pretty clear if you know what landmarks you are talking about it and just have a look at a skull.

No I didn't mean interaural line. The terminology is used in my textbook but it doesn't say anymore about its course, so I wondered what could it be.

Please state the source of your background in the question. That way people trying to answer your question can [possibly] look up your information.

I found very little use of the term interauricular line in a web search (only about 800 results in Google), and those that gave some sort of definition suggest that it is indeed the same thing as the interaural line. The auricles in this case are a sort of outdated term for the external ears. The interaural line isn't a real thing, it is just a reference point that refers to an imaginary line between the openings of the ear canal. The interauricular line is the same thing but is poorly named, because it is still referring to a line between ear canals, not really the auricles themselves.

Up front - I have never heard of this term and I could not find information on the interauricular line. The only thing I was able to dig up was the term auricular line, which is (Fig. 1):

[The] [l]ine pass[ing] perpendicular to the anthropological baseline,
  through the cent[er] of the external auditory meatus.

Fig. 1. Auricular line. source: Radiology Key
The anthropological line being (Fig. 2):

[The] [l]ine join[ing] the infraorbital margin to the superior border
  of the external auditory meatus.

Fig. 2. Anthropological line. source: Radiology Key


text:
Worm inside a millepede
I found a dead millipede lying on the ground in Wayand, Kerala (India). I put it in a bottle and brought it home. After around 5 hours a worm came out of it. It is about about 1.5 cm long and segmented.
Any idea if its a larva of some sort?

Edit:
It's been about five days since I posted the picture of the larva , and it seems to have pupated last night. The pupa is approximately 0.5 cms in length. All that's left is to see what happens next.

Do you have a picture of the millipede?

Give it nutrients and see if it grows into anything!

Yes, it is a larva, and it could be any of a number of insects that parasitize millipedes, like the Phoridae.

It looks like a dipteran larva.

Can i get a more specific answer? And also, how would you suggest I raise it?

Yes that seems to be a larvae but at the same time I know that it is a millipede but the larvae it self reminds me of a carpet beetle.

Anything happen yet?

Yes, it was a dipteran larva. A housefly emerged from it yesterday, 9 days after  the larva pupated.

There is something wrong with this question. You are saying a housefly emerged from the larve. Housefly larvae are not 0.5 cm big.

@ObiwanKeNoobie they also don't parasitise millipedes, which I think is more of an issue here.

Do you have the adult that emerged? If you post a photo of it it might be identifiable.

Definitely some sort of fly (order Diptera). Specifically, you found the legless larva, or maggot, of a fly that then developed into a pupa.

 Source: Univ of Florida IFAS
The above picture represents the life-cycle stages of the common house fly (Musca domestica).

M. domestica is one of the most common and widespread flies in the world:

This common fly originated on the steppes of central Asia, but now occurs on all inhabited continents, in all climates from tropical to temperate, and in a variety of environments ranging from rural to urban. Source

According to Wikipedia, M domestic larvae take 2-5 days to metamorphose into a pupa.

Although the OP mentions that a housefly emerged from the pupa, I'll caution the OP that many flies look like house flies to the untrained eye. Houseflies typically deposit their eggs in fecal matter or dead flesh, so finding a maggot deposited into the body of a living millipede seems unlikely behavior from the common house fly. (Edit: Though I see now that the OP said the millipede was dead, so this is not an unlikely candidate).
IF the larva was deposited when the millipede was still alive, then other genera would be more likely.
One example would be a Sarcophagid (or flesh fly; family Sarcophagidae), which some species being known to be internal parasites.
As for proper ID, according to Wikipedia:

Generally, only males of this family can reliably be identified to species, and then only by examination of dissected genitalia. The literature is incomplete or scattered for all regions

Here are some images for a fairly widespread species, Sarcophaga crassipalpis (which is very unlikely to be your species, but demonstrates general appearance of this family):

 Source: Univ of Florida IFAS
Your specimen might still belong to another group of flies, the tachinids (family Tachninidae), which very often parasitize other arthropods.
It'd be very difficult to differentiate most of these taxa without up-close examinations of specimens.


text:
Link between cell area and efflux pump?
I conducted an experiment involving a fluorescent F-actin stain called sir-actin which is removed by an efflux pump. After increased time and removal of the medium containing sir-actin, the cell actively removed the sir-actin using the efflux pump but an increase in cell area was reported when the images were processed in matlab. I was wondering if anyone can propose a possible cause for the increase in cell area with the removal of sir-actin by the efflux pumps. The f-actin of the cytoskeleton was also found to have a reduced length with increased time. Thanks in advance. I also used MSCs and the cells were alive until fixed at each time point and then imaged.

When you added medium with sir-actin, were you also refreshing growth factors that caused the cells to grow?  Did you compare cells that effluxed your sir-actin with control cells that also received new media for the size you are concerned about?

@akaDrHouse Yes, growth factors were refreshed and it was compared to a control where the cells were fixed and then stained. All cells were passaged 8 times (P8).

It wasn't clear from your answer if the control cells also were given fresh media and allowed to incubate for the same amount of time as the sir-acting treated cells. I'm assuming yes.

@akaDrHouse the control cells were left to incubate for 5h and then fixed then stained and imaged. The test samples were incubated for 5h with sir actin and after the 5h period the sir actin containing medium was replaced with sir-actin free medium and incubated for additional hours (T0, T1, T3, T6) before being fixed and imaged.

So those controls don't actually mimic the treatment conditions. You may want to have controls that receive the media change again (same as the treated) for the different time points.  However, since you have a T0 time point where the treated cells actually do mimic the controls, does that set of cells still display the difference in cell area compared to controls?


text:
Actual determination of the DNA sequence in the shotgun approach?
I'm studying bioinformatics and I'm confused by shotgun sequencing. In Sanger sequencing we break up the DNA and use ddNTPs in order to determine the exact position of each neucleotide. How exactly does shotgun sequencing help us determine the sequence structure?
If we break up the sequence randomly and then stitch it back together by looking at the overlapping parts, how does that tell us what order the nucleotides are in? How exactly are the nucleotides read so that shotgun sequencing helps us?

The wiki page seems to provide a simplified schematic (the first table and accompanying text). What is not clear to you exactly?

@AliceD Basically, I'm under the impression that sanger sequencing isn't used in cases for very long DNA strands. Shotgun sequencing works better here but I'm not sure how shotgun sequencing accomplishes the same thing that sanger sequencing does? Sanger sequencing tells me the position of the nucleotides and therefore the structure of the DNA strand. How does shotgun sequencing do this?

Fair enough I guess. I'll leave this one up to our molecular biologists to assess. I held my last pipette back in 2001 O.o  Auch, I'm getting old

Does this answer your question?

@AliceD Not exactly. I appreciate you taking the time to search for things though. The only thing that makes sense to me is that the shotgun sequencing involves breaking up the dna strands that are too long, performing sanger sequencing on them, and then looking at overlap. But it doesn't seem to say that on the Wiki, and it says a LOT of other stuff that I don't relaly understand what it's for.

Would it answer your question if I said that shotgun sequencing isn't actually a sequencing technique, per se, but a method of assembling a large number of short sequence reads generated by Sanger sequencing? In other words, to sequence long DNA molecules, you would break it down into short fragments that Sanger sequencing can handle and then reassemble the reads based on overlapping nucleotide sequence.

I have modified the emphasis of the title seemed to be on assembly which did not reflect the question. The poster appears to know about computer assembly of sequenced fragments, what he appears unclear about is how the identity and order of the bases in the fragments are determined before this reassembly. (Or perhaps he thought it was part of the reassembly process, but in any case it is this determination that he is unclear about.)

@David Great, thanks a lot. There was a lot of things that I was confused about not having a background in biology but this has helped tremendously. The title does better reflect what I was after.

The question appears to confuse the method of identifying and determining the order of bases in a fragment of DNA — Sanger* sequencing, Maxam–Gilbert or more modern ‘next generation’ methods — with the strategy for selecting fragments to analyse and reassemble into the larger contiguous sequence from which they were derived, of which shotgun sequencing is one.
Shotgun sequencing is a strategy in which the selection of fragments to sequence is random, the method of sequencing is a matter of choice (it was often the Sanger method when it was first developed), and the assembly is done by computer programs that identify matching stretches. (It fails — or is not completely successful — if by chance the fragments do not cover the whole DNA with suitable overlaps or there are certain types of repeated regions.)
Shotgun sequencing should be contrasted with what might be called ordered sequencing strategies in which one generally starts with a restriction map of the whole DNA and initially selects specific fragments to clone and sequence (by whatever method seems best). On the basis of the sequence of the fragment one can choose to sequence further from a position within the already sequenced fragment, and this procedure repeated. Here there is no apparent assembly step as this is inherent in the choice of fragments to sequence. (This is much slower than shotgun sequencing, and cannot be automated so that it is much more expensive. However, it is more precise.)
Coda
Part of the confusion may arise from the fact that modern automated methods of sequencing genomes are designed to work on a mixture of many uncloned fragments of DNA, so inherently involve the shotgun sequencing strategy. They tend to employ technologies other than the classic Sanger method. If a ‘manual’ clone-based ordered sequencing strategy is required to ‘finish’ missing or ambiguous regions of a genome, this would most employ the Sanger method of determining the sequence. Hence, the contemporary writer might employ what is, in fact, a misleading contrast.
*Fred Sanger was an eminent Nobel laureate, so his surname is capitalized.

I hope this is clear. I can add a diagram if necessary.

This is clear! Thank you for explaining. Would it still be possible for you to provide a diagram as they usually drastically improve my understanding.

In Sanger sequencing we break up the DNA and use ddNTPs in order to
  determine the exact position of each neucleotide.

No.  Sanger sequencing doesn't do this.  The results of one Sanger sequencing reaction is a string of nucleotides, about 700-1200 bp long.  There is nothing in that which inherently gives that string a position.
"Shotgun" just means that you aren't take advantage of any kind of known mapping information to target your sequencing reactions; you sequence everything randomly, and let a computer sort out what overlaps with what.


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Why the "cfr." in 'Cirrhipathes cfr. anguina' and not "cf."?
Recently I stumbled upon the species name Cirrhipathes anguina. In the literature it is often mentioned as Cirrhipathes cfr. anguina. What does cfr. mean? Does it carry the same meaning as cf.?
Edit: If the same, why is cfr. used in this case and not just .cf?

Thank you for the answers. Given that you answered at the same time and equally well I added another question :)

I've seen both cf. and cfr. used in literature. According to Wiktionary, cf. is an abbreviation of the Latin confer whereas cfr. is an abbreviation of the Italian confrontare, both of which mean compare. It's probably just a stylistic choice by the authors, perhaps depending on their country of origin. I doubt you'll get a better answer than the ones given.

It's the same as cf. Both abbreviate confer-- meaning the specimen has most of the defining features of the species indicated, and the ID would likely be confirmed with comparison to reference material.
Ref: Sigovini, M. et al. 2016. Open nomenclature in the biodiversity era. Methods Ecol Evol. 7: 1217-1225. http://onlinelibrary.wiley.com/doi/10.1111/2041-210X.12594/abstract

Whoaa that was a simultaneous post :-) +1

The Wikipedia page explains cf. as:

In biological naming conventions, cf. is commonly placed between the genus name name and the species name to describe a specimen that is difficult to identify because of practical difficulties, such as the specimen being poorly preserved. For example, "Barbus cf. holotaenia" implies that the specimen is believed to be Barbus holotaenia but the actual identification cannot be certain.

And from Habitas it becomes apparent that cf. is indeed synonymous to cfr., both being abbreviations for confer:

cf., cfr., confer. : Latin, compare (with)
character, taxonomic : any attribute of a member of a taxon by which
  it differs or may differ from a member of a different taxonomy.

Yup, it was indeed! Great minds and all that. :)


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What's the proper way to determine whether dose response curves +/- another variable (besides dose) are statistically different?
I have an experiment wherein I measured uptake of a certain molecule into cells when delivered using Carrier A vs Carrier B. In other words, for example, I delivered 1, 2, 3, 4, 8, and 10 nmoles of DrugX to 6 wells of cells per dosage, HOWEVER in 3 wells DrugX was delivered using Carrier A and in the other 3 wells DrugX was delivered using Carrier B. I would like to statistically determine whether the dose-response curve I get when I used Carrier A for delivery is any different than the dose-response curve I get when I used Carrier B for delivery.
My initial thought was to run a paired T-test, but then I realized I would have to report results at each point and I would like to report on the curve as a whole. My next thought was to use a two-factor ANOVA, however from what it looks like, when it determines whether or not there is variance due to the change in carrier it looks at the average and variance of all the responses. Another thought I had would be to calculate area under the curve, but I'm not sure how. I finally settled on running a nonlinear regression on the Carrier A data, then on the Carrier B data, then as the dataset as a whole and compared the resulting fit curves. I got a nice p-value, however the $R^2$ values are lower than I'd like (about 0.9) because the curves didn't model especially well.
What would you do? What is the industry standard?

For the ANOVA you would want to focus on the interaction terms, those would tell you if there is a difference in the effect of drug depending on carrier for each level of the drug. Same thing for a regression, you should be comparing models that allow for interactions with carrier, not just a main effect of carrier (it's possible you did this, I can't really tell from your brief description). If the drug effect follows some expected pattern, a generalized linear model might be better than a nonlinear regression. I can't speak to industry standards, however.

Might be worth asking this on stats.stackexchange, too? I have seen paired t-tests with results at each point reported in the literature, but I dislike this quite a bit. I suspect the answer depends on what aspect of the dose-response curve you care about: is it the saturation value? The 50% peak response?

What is the expected shape of the dose-response curve in this case? Or if there is no expected shape, what do the curves look like?
If there's a transformation of the data that makes it look linear, I would also suggest fitting a generalized linear model (i.e., with a non-linear link function) and looking for a significant main and/or interaction effect of Carrier B, as Bryan Krause suggested. If there isn't such a transformation, there are likelihood-ratio tests you can do using non-parametric regression, but you might not have enough data (see e.g. EDGE from the Storey lab).

Good call on not using multiple t-tests. The reason being, assuming a 95% confidence interval, each time you run the test you are "allowing" a 5% possibility of making a Type I error - this means that you incorrectly reject the null hypothesis in favour of the alternative hypothesis. If you run one t-test, there's a five percent chance of making an error. If you run two t-tests, there's a ten percent chance of making an error.
Between a regression model, or ANOVA, it does not matter. As the mathematics behind each are pretty much equivalent.
What you really want to look for, is the slopes of both models. If the two models have a statistically significant difference between their slopes, then this is indicating an interaction effect.
Two examples of (some, but not all) possible interaction effects:

Carrier A & B have a similar effect on dose-response at 2mmol. But as the dosage approaches 10mmol, Carrier B causes a dose-response that is nearly double that of Carrier A.
Above 5mmol, Carrier B creates a greater dose-response. Below 5mmol Carrier A creates a greater dose response. At 5mmol the dose-response is nearly equivalent.

I agree, t-tests are not appropriate. I don't think an ANOVA is great here either because you are not concerned with an average. With dose response curves, you typically are more concerned with an effective dose or a lethal dose derived from a model fit to the data.
There are well-developed standards for this type of analysis as it is common in pharmaceutical development, ecology, and enzyme kinetics. The most commonly used and acceptable models used to analyze dose response data are 3 or 4 parameter logistic models that end up looking s-shaped. You can find a brief overview of this here.
If you are familiar with R, there is an entire statistical package developed to compare dose response curves called drc. This is a general description of the package and its use. This paper describes more concisely the use of the package and the theory involved.


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Longest lived land mammal when subtracting sleeping time?
Recently, it has been found that wild elephants only sleep two hours per night. Wild elephants also live quite long, the median life span is 56 years. Now, 56 years lived with 2 hours sleep per day amounts to about 51 years spent being awake, while a human being who dies at the age of 80 who sleeps 8 hours a day will have spent about 53 years being awake (here we ignore the larger sleep requirement during infancy, taking that into account may put the elephants ahead of us).
So, we see that taking sleeping time into account greatly affects the comparison between waking lifespans of animals. The question is then what land mammal has the longest lifespan when subtracting sleeping time i.e only counting the waking hours. Some sea mammals like whales are known to live for a very long time, but that may be due to very peculiar features of such mammals who have adapted to living in the oceans.

You cannot calculate it so mechanically. If you read just the Wikipedia article https://en.wikipedia.org/wiki/Sleep_in_non-human_animals#Sleep_duration, you'll find that the type of the sleep differs a lot between animals, so you cannot get comparable data just by "subtracting sleeping time". When you sleep and when an elephant sleeps, it's not the same experience :)


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polarity of DNA
If currency exists in a solenoid, we can know the polarity.

However, there is no currency in DNA.how to define its polarity then?

@tomd Sorry for my poor comprehension. A DNA molecule has two chains. If at the same end of the chains both have 3'-hydroxyl and at the other end both have 5'-phosphate, then the DNA have the same polarity. If at the same end of the chains, one has 3 and the other has 5, then  the DNA has the opposite polarity, right?

DNA is never structured so that both 5' ends are at the same side, the strands are always antipolar to each other. The structure doesn't work in the opposite direction. Think about a 2-way road: you can define a direction ("polarity) for each side of the road. Proteins that interact with DNA in a directional way are just like the cars on the road: they could feasibly go in either direction with respect to the whole molecule.

@BryanKrause I hate the word always ;)

@canadianer Ugh, you're right, I hate it too and chastise others - you caught me. I even used italics to emphasize my mistake. Ok so...in most forms of DNA, like the common helix people are most familiar with, the ways you are usually going to learn about it in a basic molecular biology class, the strands are antipolar :)

@BryanKrause Haha, yes the italics were particularly damning. Didn't want to be overly pedantic, but the counter examples are interesting. Of course, you're right in almost every instance.

@canadianer No worries for the pedantry, totally warranted in this case and I thank you for it.

@tomd Please note that the polarity of DNA does NOT refer to chemical polarity (or electrical polarity), but rather structural polarity. Polarity in chemistry refers to a net dipole moment of charge density due to uneven sharing of electrons. While DNA happens be a polar molecule in this sense (it is water-soluble), that has nothing to do with the polarity of DNA's structure (that is, the ability to distinguish be the 5' end and 3' end).

Biologists occasionally play a bit fast and loose with chemistry terminology. I think this is one of those examples. Here is the definition of Chemical Polarity via wikipedia: "a separation of electric charge leading to a molecule or its chemical groups having an electric dipole or multipole moment." If you object to the source, please note that the American Chemical Society tasks professional chemists with verifying wikipedia articles on chemistry topics. (https://en.m.wikipedia.org/wiki/Chemical_polarity?wprov=sfla1)

When people discuss the 'charge' of DNA being negative they are referring to the charge within the molecule.

The Phosphates (big red red and blue in the space filling diagram) have a negative charge and make the DNA both water soluble and negatively charged.
One can also talk about the 'directionality' of DNA which simply means that all DNA is 'read' and synthesized in the 5' to 3' direction (referring to the sugar backbone carbon). That's simply how all enzymes make DNA and RNA molecules and how we define the direction of the DNA code.
As far as I know there is no current running through the DNA itself and no pole in that sense.

"When people discuss the 'charge' of DNA being negative they are referring to the dipole moment within the molecule." The way this is worded seems misleading. Does DNA even have a net dipole moment? Or if you meant the individual dipole moments of each nucleotide, perhaps "moment" should be pluralized. It is also misleading because a net charge (such as DNA's negative) is not required for a dipole moment to exist. Furthermore, a molecule may possibly have multiple charges within it, and not have a net dipole moment (if the charges are arranged symmetrically). I think it would be far better

to discuss the negative charge here without trying to associate it with dipole moments, because the two are not correlated here.

@electronpusher A DNA molecule is single-stranded, and has a negative net-charge because of the phosphates and I'm not aware of a symmetric positive charge. I agree a net-charge isn't necessary for a dipole moment, but wouldn't a net charge existing mean that a dipole moment must exist?

The symmetry would be from a like charge, for instance molecule with a negative on the right side and a negative on the right side could have no net dipole moment (assuming the atomic arrangement is symmetrical as well). Whether a single strand of DNA has a net dipole moment would depend on its configuration. If it adopted a spiral configuration, like it does as half of the helix, then the negative charges on the phosphates would all average out spatially. That is, if you looked straight down the helical acid, you wouldn't see any point on the circular cross section that has more

charge than the rest of the points (assuming a sufficiently large number of nucleotides). By the way, here is an example of a net-charged molecule with no net dipole moment: (https://en.m.wikipedia.org/wiki/Cyclopentadienyl_anion?wprov=sfla1).