text:
Water-bird that can take off vertically from the water?
If you look at ducks taking off, they take off at a pretty flat angle, building up speed before they finally get some altitude. This takes a lot of distance, it seems, for them to get high in the air.
But this lead to a question. Are there water birds that, sitting on the water, take off at a more vertical angle without the long run-up?
The best I can think of are flamingos, who cheat by having their feet on the ground, in the shallow waters. Some birds will dive into the water, grab a fish, then fly out at a high angle, but that's a bit different from sitting on the water then taking off.
Many birds are able to perform a vertical or near-vertical takeoff, on dry ground. Can any birds do this while sitting on the water?

I think this question is receiving inappropriate close votes. There is nothing opinion-based about this question.

Too bad you stipulate "sitting on the water"; that limits it to aquatic birds. A kingfisher can come up out of the water almost vertically.

@anongoodnurse Thanks for your downvote, it's becoming a tradition.

Oh, the pitfalls of commenting! It's not a tradition; that's a pretty arrogant assumption. I downvote you occassionally, and only when you give a bad answer, like the one you deleted yesterday (?) or the day before.

It was not even close of being a bad answer, the same way this one is not. The problem with that question, once again, is that the OP was not clear enough, and it was ambiguous. Anyway, I deleted it because of a comment OP left. And thanks for the "arrogant".

Excuses, excuses.

The answer to your question ("are there water birds that take off at a more vertical angle?") is probably this: no.
The explanation is quite simple: on land, the hindlimbs provide the main force for the vertical take-off while the wings (forelimbs), obviously necessary for continuing the movement generated by the hindlimbs, are not the primary take-off accelerator.
According to Earls (2000), that studied the take-off in some species:

The hindlimbs of S. vulgaris and C. coturnix produce the primary acceleration of take-off. The wings act either after the hindlimbs have finished producing force (S. vulgaris) or during the hindlimb action (C. coturnix), but in both species provide only 10–15 % of the total take-off velocity. (emphases mine)

Also, regarding extrapolating the conclusion to other species (idem):

Comparison with one other avian species in which take-off kinematics have been recorded (Columba livia) suggests that this could be a common pattern for living birds.

Now the problem becomes clear: sitting on the water, an aquatic bird cannot use its hindlimbs to provide the acceleration for the take-off. It has to use only its wings.
Then, we can suppose that using the wings for providing 100% of the acceleration in a vertical take-off is:

Energetically expensive, or
Physically impossible for the bird*.

*When I say physically impossible I'm not implying that this is "impossible according to the laws of physics"... I'm just saying that the bird doesn't have the necessary strength.

Source: Earls, Kathleen, KINEMATICS AND MECHANICS OF GROUND TAKE-OFF IN THE STARLING STURNIS VULGARIS AND THE QUAIL COTURNIX COTURNIX. The Journal of Experimental Biology 203, 725–739 (2000)

Basing an answer on "this could be a common pattern for living birds" is iffy.

I'm just quoting the paper.

What comment did I delete?

It's still there! And I said that because you downvoted my other answer, which was not a bad answer, and now this one in the following day... that's why I wrote "tradition".

Ah, wrong place. Strange to post that under the question. In any case, do you think all your answers are gems? They're not. And two downvotes in three days does not make a tradition. I actually upvote your good answers! But if you have a problem believing that, I suggest you take it to the mods.

Did you happen to realize that the OP asked about aquatic birds, and you based your answer on... a paper about starlings and quail?

@anongoodnurse Oh the vicarious embarrassment... of course I did! That's the whole point of my answer: I'm explaining the mechanics of how birds takeoff on land, showing that they can't do the same on water. Now I see that you didn't even understand my answer... I thought you were smarter than that. PS: no need to flag this comment, taking it to the mods or whatever, because I already deleted my account (it will be removed tomorrow).

How can you assume aquatic birds rely on legs so much for lift? That's my point. You could at least have found a paper on flight initiation of an aquatic species, not a starling, for goodness sake. And I am smarter than you think, by far. I hope you're not leaving because of my several downvotes. I certainly hope it's more than that.

I don't believe this is a bad answer. It is a bit assumptive, but highlights some useful facts to make a plausible hypothesis.

Yes. A duck can be observed taking off near-vertically from the water's surface in this video. Watch the first duck to take off (from about 0:08). Immediately after take-off, the duck has a very low horizontal speed, and works to gain speed by a combination of flapping and vertically beating its tail. The full process is as follows:
Beat 1: The duck gives a sudden start. Both wings are beaten once on the water's surface to take advantage of the extra resistance the water provides, compared to air. The duck presumably also pushes down on the water with its feet below the surface in order to gain extra lift, but this is not visible.
Beat 2: By the start of the second downbeat, the duck's body is clear of the water, but the feet are obscured by spray.
Beat 3: The whole duck is clear of the water, and is gaining some horizontal speed. This wingbeat is accompanied by a clear vertical flap of the tail.
Beats 4 onwards: The duck continues to accelerate horizontally, remaining clear of the water.
Because the duck comes near-vertically off the water's surface, and remains airborne thereafter, I'd define the take-off as vertical, and the subsequent flight as transitioning into a duck's normal near-horizontal flight. Similar take-offs by terns can be seen in this video (but starting from a dive under the water's surface, see from about 1:02).
More generally, many waterbirds can take-off vertically from the water's surface, without requiring a run-up. All that is generally necessary is to face into the wind, and spread their wings. If the sea-surface is basically stationary, but there is wind, then any difference in speed between the air and the water can be exploited to generate lift.
If there is no effective wind (i.e., the water and the air are moving at the same speed), then the birds have to generate the lift for take-off by expending energy. Some species can do this, but it gets harder with increasing body-mass and wing-loading. I have personally observed a juvenile frigatebird (a species that generally weighs around 1 kg, but with very low wing-loading) lifting off vertically from the water's surface on a windless day. Note that frigatebirds would not normally land on the water (their feathers are not waterproof), and trying out a water landing seems to have been a play behaviour on the part of the juvenile.

Love that you actually address water birds. I would upvote you, but your video doesn't support your statement about it. Maybe some literature or a different video? The question is, 'Can any birds achieve a vertical or near-vertical takeof while sitting on the water?' There are birs that can leave the water at a vertical/near vertical direction: kingfishers and penguins, for example. But they aren't starting by sitting on the water.

@anongoodnurse the OP has asked the question in two forms - the one you highlight, and the softer "Are there water birds that, sitting on the water, take off at a more vertical angle without the long run-up?". The video unambiguously answers the 'soft' version, and if the lift-off is defined as the act of getting into the air, given sustained flight after that (as in my definition), I believe it also answers the 'hard' version that you have highlighted.


text:
Why do some insects constantly move their abdomens?
Why do some insects, such as wasps, constantly move their abdomens?

Insect respiration is passive, with sclerotized tracheal tubes taking oxygen directly to the tissues, and moving carbon dioxide out. By pulsating the abdomen, the movement of gases through this system is accelerated. Wasps, as in your example, are relatively active metabolically, so it is not a surprise that they tend to use this strategy.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


text:
What is the striking speed of a Green Anaconda?
How fast does a green anaconda strike? The striking speeds of other snakes is readily accessible, but not that I can find for the anaconda.
If you have information for the size and weight of the anaconda, please include this with your answer. Any additional information about their striking is also welcome.

A herpetologist friend of mine recounted an experience of wading through a stream, and an anaconda reared up and struck him in the chest, and then pulled back. The strike ripped the man's T-shirt completely off. I can't answer your question, but remember that the strike was very fast, and was quite a shock to the man in the stream (although he was unhurt).

@KarlKjer Thank you for sharing! If I may ask, did the man comment that it felt like being punched?

Sorry, it was years ago. I vaguely remember that it did feel like being punched, but memories so old are likely unreliable.

Thanks Karl. I'm also investigating the strength of a snake strike, separately.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
Low migration rate in Papadopoulou et al. (2008)
In the paper "Speciation and DNA barcodes: testing the effects of dispersal on the formation of discrete sequence clusters" by Papadopoulou et al. (2008), is there an explanation as to why the authors simulated very low migration rates ($m$ between $10^{-8}-5\times 10^{-5}$)? The population size was 160,000, which produces $Nm$ between 0.0001-0.5. This is much less that a single migrant per generation.
Any insight would be most appreciated.

After a quick look-up, they don't seem to comment much on this choice of parameter unfortunately. Here are my quick thoughts.
They are dealing with quasi isolated species. They explored a range of values and I would like to assume that made sure that more extreme values won't yield to drastically different results.
These simulations can be pretty computationally intensive, it is possible that they considered $Nm$ to be the important statistic but they would assume that the results could scale up and down for different $N$ and $m$ values. In fact, they almost systematically refer to their migration rate as $Nm$.


text:
Are Zebras white with black stripes, or black with white stripes?
I'm not sure it makes sense, but are zebras black or white below the surface?

It is not like someone painted a zebra one color (say white) and then painted lines of the other color (say black) on top. But it does not mean we can't give some thoughts on the question.
What causes these patterns?
The colors are caused by pigments. Melanocytes either produce black pigments or do not and this cause the alternation of white and black stripes. The exact developmental pathway for producing these stripes is still very much unknown. All we know is that several environmental variables seem to affect this pattern. The most important correlate found so far is temperature, where higher temperature lead to darker and better defined stripes (Larison et al. 2015). This pattern can also be observed geographically (although there might have other important covariate driving this pattern, such as genetic typically)

So, are zebras black or white?
According to the Brevard Zoo, under their white or black fur, the skin is always black. This, I suppose, might lead others to rather claim zebras are black with white stripes.
From @iayork's answer, it appears that embryos are first black and then white tripes appear. This an extra reason to claim that zebras are black with white stripes. Note however, that I am not sure whether the skin of zebras are not first white, then turn black and then black fur and then white fur. Under such circumstance, one might want to argue that zebras are white with black stripes.
So if we take your question as phrased

[A]re zebras black or white below the surface?

If by "below the surface" you are referring to their skin, then they are black (according to the Brevard Zoo)!

Zebra embryos start off black and develop white stripes late in development. This is widely used to conclude that zebras are actually black with white stripes, and it's as good an argument as any for this essentially semantic question.


text:
What nutrition do flies find in feces?
How are flies able to extract nutrition in feces when the originating animal wasn't able to? What makes flies more capable?

I wonder how much (by percentage) of feces consists of bacteria. These would be added nutrients, wouldn't they? Also, feces are not entirely digested, so even if bacteria provided nothing extra, there would still be nutrition for the taking, with the right enzymes.

Someone's trash is another's treasure.

Bacteria comprise about 50% of the fecal mass. https://www.ncbi.nlm.nih.gov/pubmed/7359576


text:
Why does the olive tree produce a bitter tasting fruit?
What is the survival value for the olive tree to produce a bitter tasting fruit, even when it is ripened?
I realize some fruits and berries are species specific, i.e., meant for specific animals to eat and disperse the seed widely. Is this the case of the olive?

You guessed it correctly: seed dispersal by zoochory, specially when the animal eats the fruit to spread the seeds (endozoochory), is an intimate relationship between the plant and the animal: the fruit has to be attractive to that specific animal, not attractive to you or me.
And, as you also seem to know, the same fruit will taste differently for different species. We could explain that using the concep of qualia (see my answer here), but the case here is even simpler: different species may have different receptors and different sensory perceptions (not sensations, I actually mean perception) for the same fruit. The most famous case is that one involving birds and chilli peppers, which don't taste hot to them (birds lack capsaicin receptors).
All that being said, olive (Olea europeae) fruits attract birds, which are their main dispersal agent (REY et al., 1997; Spennemann and Allen, 2000).
According to Spennemann and Allen, 2000:

Worldwide, olives have proved to be a successful invader of disturbed lands, with birds as the principal seed vectors.

So, we can hypothesise that olives don't taste as bitter to birds... or, that birds do like a bitter taste. It really doesn't matter: what's important is that the fruit is eaten and the seed is dispersed.

A male blackcap (Sylvia) eating an olive. Source

Sources:

REY, P., GUTIERREZ, J., ALCANTARA, J. and VALERA, F. (1997). Fruit size in wild olives: implications for avian seed dispersal. Functional Ecology, 11(5), pp.611-618.
Spennemann, D. and Allen, L. (2000). The Avian Dispersal of Olives Olea europaea: Implications for Australia. Emu - Austral Ornithology, 100(4), pp.264-273.


text:
Identification of small creature
this is my first message here. Let me tell you why I came to this stackexchange:
A couple of years ago, I took an empty transparent jar (5 liters) and put in it some water (taken from a pond), some dirt and some randomly chosen acquarium-plant. And waited. It was (still is) an amazing experience! The jar went through a number of phases but is still alive, very green, surviving well without any maintainance for more than 2 years (maybe I have added 1-2 liters during this period of time, due to some very low evaporation).
Recently, a friend gave me as a gift a small 15liter acquarium and I decided to do another experiment of this kind. The larger acquarium (compared to the 5L jar) will also give me the possibility to observe better the environment and it's evolution.
Now 2-3 months have passed. The water is still quite yellow-ish, but from previous experience with the jar this has to be expected for the first year or so. [the jar became transparent/green from yellow all of a sudden after about 1 year of life]
However the jar is full of life, the plants are doing fine and there are a lot of little creatures.
QUESTION: could you help me identify one of these creatures? It is a very very small one and I'd like to know more about it.
In this video you can see a number of them going around a small piece of cotton that fall down in the acquarium yesterday.
LINK: https://www.dropbox.com/s/jrkoa5kswghiizm/Video%2011-01-2018%2012%2037%2055.mov?dl=0
thanks for any suggestion!

Those are probably Ostracoda, commonly known as "seed shrimp" a small freshwater crustacean.

The creatures in the video do indeed show the shape, size, coloration, and typical behavior of ostracods ("seed shrimp"), a type of freshwater crustacean (class Ostracoda) that is distributed worldwide (Martens et al. 2008). They lay eggs either on plants or directly in the water as plankton. Some researchers consider them to be potentially useful as bioindicators (e.g. Ruiz et al 2013), or even keystone species (Lawrence 2002). You can find many photos of ostracods on the Internet.
Lawrence, J. et al. 2002. Microb. Ecol. 44: 199
Ruiz, F. et al. 2013. Int. J. Environ. Sci. Technol. 10: 1115
Martens et al. 2008. Hydrobiologia 95:185


text:
Effect of heat-treatment of Vitamin C
When it is in the body, does it matter if vitamin C has peviously been heat-treated? Can the body still use it?
For instance, if vitamin C is added to 90 degree celsius water does it matter if you drink all of the water? Will you still gain the vitamin C?

Disclaimer: the denaturation is the process of protein unfolding from their native state. Since vitamin C is not a protein, it cannot denaturate. I think that the word you're looking for is simply "degradation".
Vitamin C can exist either in its reduced form L-ascorbic acid (L-AA) or in the oxidised form dehydroascorbic acid (DHAA). The active (antioxidant) form of vitamin C is the former; however, there are enzymes in our body that can convert DHAA back into L-AA.
In this article, the authors seek to evaluate the thermal stability of both L-AA and DHAA in broccoli. Their results are the following.

Thermal treatments (for 15 min) of crushed broccoli at 30 to 60 degrees C resulted in conversion of l-AA to DHAA whereas treatments at 70 to 90 degrees C retained vitamin C as l-AA.

So, cooking the vitamin C does not alter its structure and your body will still be able to use it. Another reason to eat broccoli, I guess.

Thank you for this information. This is exactly the response I was hoping to get.


text:
Why won't birds move an inch in total darkness?
One day, a bird flew inside my house. I locked the door. It landed on my TV and then I turned off the light. Then I touched the bird and it didn't even to try to fly or move.
Then I went to the kitchen and turn on the light,  and suddenly it flew into the kitchen.
Why won't birds move an inch in total darkness?

The bird could have walked on the TV but it didn't know where the edge was, and walking would have made it easier to see for a predator. If it had flown, there is no way it could have seen safely where it was landing. Walking and landing at flying speeds are different things. Turn the lights off on a bird, you give it an sensory sequence of events that it's ancestors hadn't experienced from 100 million years, other than flying in a cave perhaps.

@com.prehensible I made some changes to my question.

in a birds mind is a very weird place, very many weird scenarios exist. perhaps it's ability to panic is overridden if it's in the dark. also perhaps birds don't have any night time predators. he perhaps instantly switched to night mode and felt safe.

Most birds are diurnal and have vision adapted for daylight. Vision is among the most important senses for most birds, so much so their eyes have evolved to be quite large -- much larger than human eyes, proportionally to body size. In order to have excellent daytime vision, many birds also sacrifice some of the cells in the retina that allow for dim lighting conditions. (These photoreceptor cells are called rods and cones; cones are responsible for color perception while rods are more sensitive in dim lighting. Diurnal birds can have a lower percentage of rods than other animals adapted for nocturnal activity.)
Falconers have been exploiting this trait for millennia, by using a hood, diurnal birds of prey calm down in darkness.

Owls are a great example of a bird that can see in very dim lighting conditions, though they can't necessarily see in total darkness. They also rely on acute asymmetrical hearing in order to pinpoint prey in extremely dark conditions.
Your avian visitor likely can't see in dim conditions in which you can still see. To avoid injury, birds will hold still and wait for light.


text:
What is the exact frequency of Delta brain waves during Slow Wave NREM Sleep?
I saw a TED talk about researchers playing pulsating pink noise while a test subject is in Stage 3 Non-REM / Slow Wave / Deep sleep and observing an increase in Delta wave EEG activity. This seems to indicating that the burst frequency of the pink noise is matching the dominant frequency of the Delta waves. (Skip to 5:00 to hear a sample of the sound)
My question: While a spectral analysis shows a range of brain wave frequencies, and many sources define a range such as "0.5-4 Hz", I'd like to find a more precise dominant frequency of Delta waves.
The video inspired me to write my own small computer program to make my laptop play a similar pulsating pink noise pattern on the table next to my bed last night. I arbitrarily chose 1 Hz as the pulse frequency, and the following pattern:
30 min silent (to give me time to wind down and fall asleep)
  60 min sound
33 min silent
  54 min sound
40 min silent
  45 min sound
49 min silent
  37 min sound
57 min silent
  30 min sound
30 min silent

So roughly 5x 90-minute sleep cycles with an increasing ratio of silence to noise to mimic the ratio of REM to NREM as the night progresses. I've read that REM is characterized by un-synchronized brain waves and NREM is where you see large amplitude synchronized Delta waves which the sound experiment is trying to help stimulate. Tonight I will wear my FitBit bracelet with heart rate and sleep stage tracking to see if the readings match the sound schedule.
Bonus Questions:

How credible is the hypothesis that playing sounds can affect the quality of sleep?
Would a different sound than pulsating pink noise work better?
Does the phase matter?
Also, I couldn't help but notice that Deep NREM sleep seems to be the only time you see a single large amplitude frequency dominate on EEG and it's suspiciously close to the average Resting Heart Rate of 60 bpm...are Delta waves and heart rate related?

don't try to mess with your sleep.  all phases of sleep have important things going on in them.

Periklis Y. Ktonas and Atul P. Gosalia performed such an analysis. It was published in 1981 under the heading "Spectral Analysis vs. Period-Amplitude Analysis of Narrowband EEG Activity: A Comparison Based on the Sleep Delta-Frequency Band"
The bins were quite wide but their analysis showed peak power spectrum moved between 0.84 and 1.96 Hz at different times.
I think the paper would serve you well, as it highlights the difficulty in achieving what you have set out to achieve. The frequency is not constant, even over short timescales. It depends for the most part on a balance between the intrinsic, basal polarity of thalamocortical neurons, and the effect of synchronising, inhibitory input from the reticular nucleus. The latter is in turn subject to cortical feedback. There are huge numbers of neurons involved. The period between bursts, and the number of action potentials per burst, is quite variable.
Perhaps it might be possible to set up a device that alters the round in real time, based on the EEG measurement.
With regards to your 'bonus' questions:
(1) The video posted does show an effect on the thalamic rhythm, which is surprising, as it had been thought that in deep sleep, sound has no effect on the thalamocortical circuit, since it is gated at the thalamus. This shows the plausibility of the hypothesis. However, the video does not provide any evidence that this alteration in rhythm is beneficial. It is possible that it is not and this possibility should be eliminated.
(2) Clearly the sound has an effect on the rhythm, so it seems entirely plausible that there is an optimal sound to maximise the effect.
(3) It will be hard to organise the phase, given the continuous, rapid shifts in period, unless done in combination with EEG in real-time.
(4) I am not aware of any research attempting to correlate thalamic rhythms with heart beat, although it would be quite easy to do. However it is highly unlikely there is a correlation, since the thalamocortical period has a lot of variation moment to moment, whereas the heart rhythm does not. Also the thalamocortical rhythm is generaly somewhat faster.

Thank you for the excellent response (even if I'm a little disappointed to hear it). What do you make of the part of the TED talk where the presenter showed EEG readings that did in fact respond to sound?

OK, I have to admit that I haven't seen that effect before. There is a clear response to the sound in the wave. My statement that sound "has no effect on the thalamus" is incorrect, so I will edit it. But I think what you should look for is evidence that this artificial alteration of the rhythm is beneficial. You could be having the opposite effect to that intended. It would be interesting to compare the effect on rhythm shown with the effect of the sound of wind blowing through trees, or water babbling down a stream, so if you get that far, do share your results ;-)

Well, strictly, you should look for evidence that it isn't beneficial, of course ;-)

Heh yes well causality and health benefits are notoriously hard to prove - plus I don't have an EEG.  So far I've lowered the pink noise pulses to 0.8 Hz and tried it for a few nights. While it's impossible to say whether I've felt any different the next morning due to placebo, I do think I had/remembered more dreams which is surprising since SWS is supposed to be dreamless.  The other thing is that on nights where I have a hard time falling asleep the sound can be distracting, like disembodied breathing. On normal nights I'll wake up and notice it playing but fall back asleep without issue.

I thought you might be interested in this, a Nature news feature last week: https://www.nature.com/articles/d41586-018-02391-6


text:
What spider is this? BOLIVIA

I was in Cobija in northern Bolivia, and these spiders were hanging around a lamp post. There were over 100 of them.
The picture is not a good one, but I can describe them:

They were black with light blue stripes on their body, and the legs were black and yellow. They formed a big X with their legs.

Anyone know what spiders these are?

Read your text twice because others will read it 10-20 times, for words like spiser and picrure, it's a good forum to learn how to say things tactically without resorting to adding S on vocabularys.

Those are just Argiope, a common spider. The proper identification of the species may be impossible due to the poor quality of the image.

The size, shape and leg arrangement as it hangs upside-down in the web, marks this spider as an Argiope, as previously noted.  The big white band on the front of the abdomen suggests A. argentata, but the photo is blurry enough that some of those spiders might be A. trifasciata.  I'd be happy to put it down as Argiope species, in the hope that more, and closer photos of this neat and completely harmless (to humans) spider are forthcoming.

https://bugguide.net/node/view/2033

Again, thanks for your expertise in spiders, John, but please provide support and provide citations for images (preferably those from reputable sites that properly ID the species you include). Thanks!

What’s with them hanging out in numbers like that?

The normal reason for finding lots of relatively solitary spiders in an area is that there's lots of food there.  Anywhere near a light source is a good place for flying insects, depending on the surrounding area.  I've seen closely packed webs on a lighted bridge over a canal, for instance.  There needs to be some sort of support structure as well, for the spiders to anchor the webs to; the photo is fuzzy enough that whatever is there is hard to see, but I would assume a wire fence or some other wire structure serves as the base that the webs are attached to at the top.

The interesting thing to me about this photo, and thanks for the question, Melanie, is that we would expect to see this sort of congregation around a light source for night-hunting spiders, like the usual Araneid orbweavers.  Argiopes, in North America, at least, are mainly day-hunting spiders - which may be a factor in their practice of making those center stabilimenta in the webs.  You wouldn't expect a light source to be all that important to spiders that operate their snares in the daytime.  Perhaps something else is going on, or perhaps these spiders have learned that night is better.


text:
If animals die why dont plants?
I am not a Phd in biology so don't go hard on me.when I was walking to home after swimming class I saw a mouse dead and was intimidated by gods wonder but when I reached home I saw the Devil's ivy and my thoughts flung to the 450 year old tree in my city why didnt it die when the mouse did.

There are whole large groups of plants that die in a relatively short time.  Annuals, for instance, grow from seed to mature plant, produce seed, and die within the space of a year.  Desert ephemerals are even shorter-lived, compressing the whole sprouting to seed process into the few weeks after a rain.

rephrase that question to not talk about intimidation by gods, not Phd, walking, swimming, it's a mouse/tree longevity question only.

plants have a slow metabolic rate. to can go into stasis, they can freeze below -20, they can go without water. complex machinery breaks faster than simple stuff, i.e. a scythe versus a lawnmower.

Many plants don't have the lifespan of a mouse. Many animals don't have the lifespan of a tortoise. This isn't about Biology. It's about learning. Your question is based on misperceptions.

PhD in biology?

What do you mean by plants don't die? You don't have to have a PhD to comment on this! Haven't you seen dead grass or any dead plant in your life? Some trees have a long lifespan, like the banyan, but they do die. Even turtles have a long life, but that doesn't mean that they don't die.

Plants die of old age too. Trees tend to have a long lifespan but still.... they die of old age.
There are few species that seem to have negligible sensescence such as

giant tortoise
greenland shark
aspen tree root system
mussel

and some that even seem to never age (biologically immortalilty) such as

lobster
hydra
some bacteria
some yeast

but you most definitely cannot make such generality as "animals age, plants don't".


text:
How to pipe Bwa-mem output without saving SAM file
I'm trying to find circular ARN using the program CIRI2. CIRI2 takes as input SAM file from BWA-mem, but I would like to go straight to CIRI2 output without saving SAM file.
Is there a way to achieve this?

This is an English language list. Do you by any chance mean RNA rather than ARN? And although I may be wrong, I think you are more likely to get an answer on SE Bioinformatics than here.

I never used CIRI2 but I think you can do the same way as I used to pipe with samtools:
bwa mem genome.fa reads.fastq | samtools sort -O BAM -o output.bam -
So it would be something like:
bwa mem genome.fa reads.fastq | CIRI2 <your options>
I think you will need to precise that CIRI2 input is STDIN.
I hope it will help,


text:
Does minimizing hunger maximize weight gain?
Due to the "obesity epidemic," there is a lot of focus on the causes of weight gain. We typically talk about strategies to cause weight loss, but what about strategies to minimize/maximize hunger?
Is there a way that hunger can be cured by eating a certain distribution of calories as a function of time? For example, if I have 2000 calories of food and I can eat it at any time, how should I spread out eating it over a day to maximize/minimize weight gain?  What would be the physical differences for me if I ate a small snack every minute of the day versus eating all 2000 calories at once?
Likewise what about weight gain? Would it be easier to gain weight if someone waits until they are very hungry and overeats during that hunger window, or if they eat over a wider window?

No, there are hunger free "diets" that you will safely lose weight on. An analogy might be that minimizing spending does not get you out of poverty.

What I mean is, given you will eat the same amount of food in a day, how will eating it in different time-frames affect your weight loss/gain

The digestive system absorbs food 24/7, time of day of consumption has little effect on absorption,   the main difference is day and night. your body is super efficient at absorbing calories, they go straight into the blood, . The excess sugar also is stored as fat efficiently at all times that your blood is flowing, day/night cycles are the main variant, except that night time is only a pause, you can't circumvent digestion based on times consumed.

Part of the obesity problem is that people eat recreationally, rather than just when they're hungry.  Or from cultural expectations: do you (if mainstream American) really stop eating Thanksgiving dinner when you stop being hungry?

Regarding the question in your title: minimizing hunger could be synonymous with leptin responsiveness. For example, leptin deficient or leptin resistant mice are known to become extremely obese - this is because leptin, the 'satiety' hormone, not only signals for you to stop eating, it also elevates the body's energy expenditure and stimulates thermogenesis.
An interesting strategy I've heard, though I don't know how effective it is, is increasing leptin sensitivity through the composition of your diet.
Another interesting element is that hunger, which is mediated by hormones such as ghrelin, decrease energy expenditure by multiple metabolic methods. So being hungry isn't always conducive to losing weight.
I believe most of the answer to your questions relies in these concepts. If you're talking about food distribution throughout your day, schedule it so that you're not very hungry for prolonged periods. Same with food type, eat foods that satiate for longer periods of time, unlike foods such as white rice.
If you want to read up a bit more, I suggest looking into AMPK, and the role these hormones and food composition has on it. AMPK reading


text:
Are fluoroquinolone antibiotics (Cipro, Levaquin, etc) chemotherapy drugs?
I read a claim (I can't find the source) that fluoroquinolone antibiotics are actually chemotherapy drugs, or maybe to be more specific, are "chemotherapeutic." Is this claim true? Additionally, if true, does this claim apply to all antibiotics, or only fluoroquinolones?

Chemotherapy of what? Chemotherapy literally means using of chemicals to treat a disease/condition. All drugs are chemotherapeutics, technically.

Short answer: Yes, fluoroquinolones are chemotherapy drugs
In layman's terms, fluoroquinolone antibiotics kill human cells as they divide. Fluoroquinolones are a class of drug called "topoisomerase interrupters." Every drug in this class is directly labeled as a chemotherapy drug except fluoroquinolones.
This is not well known by the medical community and is in part why irreversible damage from fluoroquinolone antibiotics is not well understood.
Long answer: Fluoroquinolones are definitely chemotherapy drugs, and they're dangerous
A refresher on how fluoroquinolones work, in case you slept through molecular pharmacology :
If you want you can skip this first section and instead watch YouTube: Fluoroquinolones: Mechanisms of Action and Resistance
How topoisomerase works
Bacterial cells have double helix DNA, meaning two strands twisted around each other. When bacterial cells divide, the two DNA strands are separated (untwisted), and eventually each side is turned back into a full double helix, making two copies.
If you think of a tightly twisted rope (representing double helix DNA) and start to pull the two ends apart, the rope will twist tighter and tighter and eventually you can't untwist it further. Nature's fairly primitive solution is an enzyme called topoisomerase.

topo-: dealing with topology, as in the structure of the DNA
-isomerase: a class of enzymes (enzymes are usually bundles of proteins)

The job of topoisomerase is to cut the the double helix DNA strand, untwist it, and then glue it back together.
There are several types of topoisomerase, which we'll come back to.
How fluoroquinolones kill bacteria
Fluoroquinolones bind to the glueing action of topoisomerase. So, as part of normal cell division, topoisomerase cuts a DNA strand, untwists it, then tries to glue it back together. However, fluoroquinolones block the gluing action ("plug the glue bottle"), so the cell literally cuts up its own DNA. Insidious, isn't it?
Don't human cells have topoisomerase?
Yes, since humans have two sets of DNA, let's focus on one at a time.
How fluoroquinolones kill human mitochondria
Human mitochondria are bacteria, and they do contain double helix DNA and topoisomerase. So why don't fluoroquinolones kill mitochondria? Trick question: they do, and it's worse than that.
Human mitochondria keep around backup copies of their mtDNA (we often call mitochondrial DNA "mtDNA" to distinguish it) to use when there are replication errors in DNA synthesis. Fluoroquinolones "deplete" mtDNA, meaning irreversibly destroy backup copies. The organelle desperately tries to pull in backup copies as it cuts up its own mtDNA during replication, and may die, or may become permanently damaged.
Insidious, isn't it?
Many other studies have proven that fluoroquinolones kill human mitochondria as they divide. Interrupting topoisomerase isn't the only way they kill mitochondria, but it's an important one.
How fluoroquinolones kill human eukaryotic cells
Human "eukaryotic" cells (cells with a nucleus, such as tissue cells) also have topoisomerase. So why don't fluoroquinolones kill eukaryotic cells? Trick question, they do:

Compared to an [actual DNA poison], ciprofloxacin produced comparable dose-dependent SCE frequency increases

(an SCE, "sister chromatid exchange" is a marker for how genetically damaged a cell is)
and

topoisomerase type II and DNA gyrase are physiological targets for [ciprofloxacin]

Insidious, isn't it?
Like mitochondria, topo binding is a small part of the kaleidoscope of how fluoroquinolones cause permanent cellular damage, but it's an important one.
As you can imagine, fluoroquinolones killing a cell's main source of energy (mitochondria), while also causing the cell to irreversibly destroy its own DNA lead to human cells dying as they try to divide divide
Even clearer: Compared to other chemo drugs
There are several oral chemotherapy drugs on the market, one of which is Topotecan (notice the topo-?). Here's how they work:

Topoisomerase I inhibitors:  Ironotecan, topotecan
Topoisomerase II inhibitors:  Amsacrine, etoposide, etoposide phosphate, teniposide

And, as linked in the earlier study, fluoroquinolones are topoisomerase II inhibitors. (They probably bind to other forms of topo, but we don't know for sure).
Even clearer: Fluoroquinolones are used for chemotherapy
There are a few
"novel" studies using fluoroquinolones as chemotherapy drugs. In this study, ciprofloxacin is used to target leukemia cells.
Why are chemotherapy drugs used as antibiotics?
When (non-fluorinated) quinolone antibiotics were first invented in the 60s-70s, we didn't know about mitochondrial DNA, and certainly not how fluoroquinolones affect mitochondria.
Don't fluoroquinolones have a good safety profile?
No.
Fluoroquinolones were released in the 70s, but the FDA warning for permanent nerve damage wasn't added until 2013. Because the symptoms of permanent fluoroquinolone damage are so outrageous (permanent nerve damage, tendons spontaneously rupturing, organ failure, psychosis, and dozens more). Doctors simply didn't know (and still don't know) to look for the symptoms, so they aren't documented.
There have been other fluoroquinolones that had "good" safety profiles, passed all medical standards, and then were promptly removed from the market after they started killing patients outright. One such drug, temifloxacin, was removed because it caused so many cells to die that the kidneys became clogged, killing patients.
The fluoroquinolones on the market are all able to, and have, killed patients through multiple mechanisms, but it's more rare, and the permanent damage symptoms are not connected by doctors.
All fluoroquinolones have the same core method of action, and all have a fluorine moiety allowing them to penetrate anywhere in the human body ("hard to reach" infections), so even though the current ones haven't been removed from the market, it doesn't follow that they are safe.
Why continue to prescribe them?
I sincerely believe that if doctors understood how fluoroquinolones worked, they would stop prescribing them, and use them only in life or death situations. The FDA has already advised never to use fluoroquinolones for "uncomplicated" infections, but this advice is not known nor heeded.
If only doctors read studies from over 10 years ago:

In view of the present genotoxicity, ciprofloxacin should be administered with caution.

Holy moley... what an answer! I will take some time to digest it

I can't upvote answers (yet?) but thanks a lot! could you also answer about other antibiotics?

"The FDA has already advised never to use fluoroquinolones for "uncomplicated" infections, but this advice is not known nor heeded." How do you know? How many doctors have you asked about this?

23 so far by my count?

So, 23 doctors you've asked admitter that they used fluoroquinolones for "uncomplicated" infections? Or admitted they used fluoroquinolones? There's a difference.

Most antibiotics can affect mitochondria (macrolides, aminoglycosides, tetracyclines etc). This is a statement from wikipedia article on quinolones: The overall rate of adverse events in patients treated with fluoroquinolones is roughly similar to that seen in patients treated with other antibiotic classes.[23][24][25][26]

Plus, if some drug affects prokaryotic topoisomerase/gyrase then it doesn't mean that it will affect eukaryotic topoisomerases. Your answer is misleading (statements like "mitochondria is bacteria") and uses flawed logic. Your "short answer" is basically wrong if you are talking in context of cancer chemotherapy.

@WYSIWYG to clarify, I've talked to more than 23 doctors about FQs, those are just the ones that talk about treating uncomplicated infections with them. And there's more than that, some of them are in hospitals that have guidelines on what to prescribe, and all follow the same rules.

@WYSIWYG the study I linked to shows the dose dependent action on eukaryotic topoisomerase. Number needed to harm for FQs is misleading if you research the history of symptoms.

Yes they are chemotherapeutic drugs. They enter the cells and destroy the mitochondria of the cell and it can no longer produce energy. Problem is these antibiotics target all cells whether they are healthy or not so they are systemically poisoning your whole body. Hence the wide variety of problems reported by patients who have taken them. They are commonly given along with a steroid such as Prednisone. Unfortunately, those patients often suffer more acute damage.

Your reasoning is not entirely correct. Please cite reliable references. If you don't improve your answer, it will be deleted.


text:
Research databases
So I'm just a lay person who likes to read about human biology/medical research but I dislike reading what so and so thinks of certain studies from pop articles. I like reading them for myself and I was just wondering which peer reviewed databases are the most reliable and accessable in your guys opinions?  I think researchgate is pretty good but I find navigating around the sign up inconvenient since you have to be working with a relevant company to join.  I hope I worded this specific enough thank you all who answer much appreciated!

Too much informality and opinion in the question for the forum ( i didn';t downvote as you have 1, other humans delight in downvoting cos their innately apathetic) ... I check https://scholar.google.fr/ and i check  "abstract" with the keywords in google search.

So post with more formality and less opinion next time?

Yes it's good to practice writing same as the articles that you like to read rather than the pop articles than you dislike reading :) when someone downvotes you you get -20 and fast you are restricted from the website.

Your title is confusing. Databases are a resource for research but not research, and are not peer reviewed as such. You are not asking about databases but scientific research. This is likely to be voted as off topic because opinions are subjective (I wouldn't recommend you follow the advice of tsttst if you are a lay person.) Is Scientific American or New Scientist what you are after? The News and Views section of Nature and the corresponding section of Science are also good. But you get what you pay for, and journalism costs.

Pubmed is the major database for biomedical research articles. Especially if you know what you're looking for, it should be easy to find.
Google scholar will also compile things that are not peer-reviewed journal articles. Sometimes that's useful (e.g. PhD theses) but you will have to be a little careful.

. . . and if you create NCBI account, you can create alerts and get new papers about the topic of your interest delivered to your e-mail.

Google Scholar is good, since it searches all kinds of databases and gives you different options to view full articles.  If you use Mendeley and get Mendeley Desktop, you can import articles that you like and it will often suggest other articles you might like as well.  I know what you mean about the pop articles, they're often misleading ;)

I've known about Scholar for awhile and never checked it out till last night I only spent a couple  minutes on but it does seem pretty good. I've spent the last half hour on Mendeley on your recommend and I like it alot so far very organized and easy to use in my opinion thank you very much.


text:
Why is blood collected at crime scenes?
I have read that mature red blood cells (MRBs)do not have DNA.  So I am curious why crime scene technicians collect blood. Is it to collect and amplify segments of white blood cells?

A simple Google search of "DNA in blood" immediately provides an answer to the OP. VTC.

Blood was collected and analyzed long before DNA techniques.  E.g. blood typing could rule out suspects with a different blood typing, or the blood on a suspect's clothing could be from an animal...

I appreciate the comments.  Just to be clear, I wasn't being lazy when I made the question.  Of course I could use a search engine.  I've been exposed to this StackExchange for maybe two weeks, and I find the questions and the depth of knowledge that contributors bring with their answers to be amazing.  I plan to make a Toastmaster's speech on aspects of DNA later this month.  No one in the speech club knows anything about cell biology.  I'm sure they will be surprise to learn that MRBC's do not have DNA.  The input given to me was just what I hoped for!

three words; white blood cells.

There's still white blood cells with DNA.
Some forensic blood tests are:
Conventional serological analysis:

Analysis of the proteins, enzymes, and antigens present in the blood, for general doctor tests: (black/white/drunk/stoned/heroin addict/polio vaccinated/hiv pos...)

Restriction Fragment Length Polymorphism (RFLP) DNA :

Direct analysis of certain DNA sequences present in the white blood cells. This method also usually requires a "large" sample size to obtain significant results.

Polymerase Chain Reaction (PCR) DNA :

Analysis of certain DNA sequences that have been copied multiple times to a detectable level.


text:
Is there redundancy in the auditory system like there is in the visual system?
In the early visual system, there is a great deal of overlap between retinal ganglion cells, which results in redundancy of the signals that neurons carry to higher visual processing areas in the brain.
Is there a similar type of redundancy in the early auditory system?

There is certainly redundancy in the auditory system, well demonstrated by Gal Chechik et all
It is also clear that there is pronounced intersensory redundacy, involving auditory systems here
Another article discusses clear auditory redundancy in adults when participating in a task to discriminate between two sounds as quickly as possible
...the auditory system maintains and tolerates functionally independently represented redundant and contradictory predictions.
In terms of redundancy in development, it seems there have  been shown links in mice discussed by Dr Thomas Braun
Hope this helps!

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


text:
What is the mechanism behind cats' geolocating homing behavior?
Some cats, which are separated from their home, have the ability to travel back to their original home - even over long distances and land that they haven't encountered before. E.g., see the Time article on the mystery of the geolocating cat or the following blog entry.
Based on the material above there seem to have only been some suspected mechanisms a few years ago.

It is explained with path integration in behavioral neuroscience. Not only cats, but other mammals, birds and even insects use path integration to return to a starting point.
Here is a relevant excerpt from the book Beyond the Cognitive Map: From Place Cells to Episodic Memory (by A. David Redish):

Path integration is the ability to return directly to a starting
  point (sometimes called a home base or reference point) from
  any location in an environment, even in the dark or after a
  long circuitous route (Barlow, 1964; Gallistel, 1990; Maurer and
  Seguinot, 1995). Sometimes called dead reckoning, this ability
  has been shown in gerbils (Mittelstaedt and Mittelstaedt, 1980;
  Mittelstaedt and Glasauer, 1991), hamsters (Etienne, 1987, 1992;
  Chapuis and Scardigli, 1993), house mice (Alyan and Jander,
  1994), rats (Tolman, 1948; Alyan et al., 1997; Whishaw and
  Maaswinkel, 1997), birds (Mittelstaedt and Mittelstaedt, 1982;
  von Saint Paul, 1982), and even insects (Wehner and Srinivasan,
  1981) and arthropods (Mittelstaedt, 1983), as well as dogs, cats,
  and humans (Beritashvili, 1965).
Path integration in animals has been the subject of argument
  for more than a century, including a notable debate in 1873 between
  Alfred Wallace and Charles Darwin in which Wallace suggested
  that animals find their way back via sequences of smells
  and Darwin argued that animals must be using dead reckoning
  (see Wallace, 1873a, 1873b; Darwin, 1873a, 1873b; Nature, 1873;
  Forde, 1873; Murphy, 1873). The carefully controlled experiments
  of Mittelstaedt and Mittelstaedt (1980) and Etienne (1987) have
  demonstrated conclusively that this ability is a consequence of integrating
  internal cues from vestibular signals and motor efferent
  copy.

emphasis mine
Cats, dogs and rodents can use taxon navigation as well along with path integration. Here is a relevant excerpt from Neural compass or epiphenomenon?
Experimental and theoretical investigations into the
rodent head direction system (by Matthijs van der Meer):

“Internal allocentric” navigation. This type of navigation relies on a mapping of praxic commands to an allocentric spatial representation, allowing the animal to make a direct return to a home base after a complex outward path in the absence of cues, an ability referred to as path integration, discussed in detail in the next section. Returning by following an odour trail back, or navigating to a cue indicating the home base would be taxon navigation, but behavioural experiments have provided convincing evidence that rodents are able
  to do this without using external cues. As mentioned above, this ability requires some mechanism of continuously updating at least one’s directional heading (a “homing vector”) relative to the home base. This is an allocentric representation which does not need to be related to any external cues, unlike the next class of strategies; the reference point or direction can in principle be set to any location the animal desires.

emphasis mine
Further reading:

A connectionist model of path integration with and without a representation
of distance to the starting point (ROLAND MAURER, University of Geneva, Geneva, Switzerland) - Copyright 1998 Psychonomic Society, Inc.

Thank you for your great answer - and the introduction on a topic, I didn't know before! Happy that you getting the reward. For the sake of this Q&A site, I will accept the answer if the Beritashvili book indeed shows path integration in cat. As the above review appears to be the only place with a strong claim on path integration in cats, I'd like to assess, if there is direct support, or if there only is circumstantial support (which would still be sufficient to be listed in a focused review / book).

The book of Beritashvill (original source) does not speak about cats' geolocating behavior. - Nor does it establish a link between cats' geolocating behavior and path integration. - The source cited above, Beritashvill, talks about "image-based" behavior that can extend to non-visual cues. While Beritashvill makes some valid case for "image-based" behavior in cat regarding fear, the detailed experimentation on spatial orientation are with dogs. The only observation on cats is one experiment with a blindfolded cat, which can be conditioned to find food 2m away if carried in a box.


text:
Why are male gametes and female gametes not equally sized
Why is it that male gametes are smaller and produced in larger quantities than female gametes that are large and lesser in number. Why aren't the gametes equally sized, or their sizes the other way around. Is there an evolutionary advantage to this, or is it just how things evolved and would it not have mattered if the sizes and quantities were reversed?

Regarding the question "Why aren't the gametes sizes the other way around?", it's simply impossible by definition: in an oogamic system the female gamete is the bigger gamete. So, if the male gamete were bigger it would be automatically named female gamete. Regarding your first question ("Why aren't the gametes equally sized"), this excerpt from Wikipedia explains it succinctly: "The prevalence of oogamy in higher animals (sic) leads to the conclusion that this specialization of the gametes..."

"...results in their performing their respective tasks better and more efficiently than those tasks could be performed by generalist isogametes, particularly the ability to concentrate high-energy substances in a smaller number of ova."

Gerardo is correct that female designates the bigger gamete, so there's nothing important about the terms "male" and "female" here.  But I'd like to also respond to your initial question of how the difference in size would've evolved because I don't think it's trivial.
I can provide a rough summary of one explanation that was summarized in Dawkin's The Selfish Gene which was summarized from G. A. Parker's 1972 paper "The origin and evolution of gametic dimorphism and the male-female phenomenon."
It goes something like this:
The asymmetry could have evolved from originally equal sized gametes through the evolution of two divergent sexual strategies - a large investment strategy which opened the way for a small-investment exploitative strategy. The idea is that when gametes were all roughly the same size, some would have happened to be bigger than others. There may have been some advantage to this because the larger gamete could provide a larger initial food supply. However, this also could have created a condition for exploitation by individuals producing smaller than average gametes, especially if they could ensure their smaller gametes fused with the larger than average ones. This could be achieved by making the small ones more mobile and able to actively seek out the larger ones. Making smaller gametes would have allowed that individual to make more of them and potentially have more descendants, as they're not investing as much energy into any one gamete. The interplay of these two strategies would've continued in a runaway fashion, with the larger gametes evolving larger and larger to compensate for the ever-smaller contributions by the exploiters.  Eventually the larger gamete could become immobile since it's being sought out by the smaller gametes anyway. You can see where this is going, with the larger gamete becoming what we know of as eggs and the smaller as sperms.


text:
Small black slow-moving insect showing up in the home
In the past few weeks (winter) I've started to notice these insects crawling about various places of the home.

Slow-moving like a beetle.
Black all over.
Hard to see but they have two prongs sticking out of the front.
I own dogs and cats.
I live in Tel-Aviv, Israel.
I live on the second floor.

Very hard to capture in an image so I tried a video. Here's a Gif:

What is this species?

That's just a weevil: https://en.wikipedia.org/wiki/Weevil By the way, drop the like in "like a beetle": they are beetles.

@GerardoFurtado Thank you. I've actually never heard of them. Using your information as a starting point, I believe the ones we have are specifically the Rice Weevil.

@GerardoFurtado I wouldn't say just a weevil. This is very likely some type of grain/rice/maize weevil. If you've been seeing multiple of them, that likely means they are breeding in some container of grain (rice or corn perhaps) you have in your home and could be well on their way to an infestation if your grain source is large enough. I recommend you check all sources of dried foods in your home to see if you hear/see weevils in it or coming out of the container.

@theforestecologist I said "just" because a weevil is an easy species to identify, that's what I meant. Also, regarding your advice, you're talking to the OP, not me, right? It's not clear the way you wrote your comment...

@GerardoFurtado Got it. Yes, sorry, I  was talking to OP. I've had a weevil infestation, which is why I responded the way I did :p -- what a pain!!

@theforestecologist Yes, I know! I live in Australia, where I never saw them, but in South America (where I'm from) they are very very common, specially in beans. I'm vegan, so I normally don't do that, but a lot of people in South America simply don't care, they cook the beans/rice/whatever with the weevils. They say, joking, that "it has more proteins".

@Rotem FYI, for future reference,  I used https://ezgif.com/ to convert your video to a gif, which can be placed on a SE page directly.

Based on the hard-looking outer "shell" and elongated snout ("rostrum"), this is certainly a type of beetle called a  weevil.
Given the size of the weevil, the time of year and the location of your home (second floor in a large city), I would guess this is certainly some species of nuisance/pest weevil.
Candidates include:
Wheat weevil (Sitophilus granarius)

Range: Worldwide
Food: wheat, oats, rye, barley, rice and corn
Appearance: 3–5 mm long with elongated snouts; reddish-brown
Life History: 36-254 eggs in 5-20 weeks

Rice weevil (Sitophilus oryzae)

Range: worldwide
Food: wheat, rice, and corn
Appearance: 2-3 mm, long nose, brown/black in color with 4 orange/red spots
Life History: 300 - 400 eggs per month [source]
Note: can fly

Maize weevil (Sitophilus zeamais)

Range: cosmopolitan in warmer climes [source]
Food:  corn (maize), wheat, rice, sorghum, oats, barley, rye, buckwheat, peas, cottonseed, other types of stored, processed cereal products (e.g.,  pasta, cassava, other coarse milled grains), and even has been known to attack fruit while in storage (e.g., apples)
Appearance:  2.5 - 4 mm, brown with four reddish-brown spots on elytra, long/thin snout, and elbowed antennae

See this Wikipedia page for a comparison of the rice vs. maize weevils

Life history: 300 - 400 eggs per 36 days

If you've been seeing multiple of them, that likely means they are breeding in some container of grain (wheat, rice or corn perhaps) you have in your home and could be well on their way to an infestation if your grain source is large enough. I recommend you check all sources of dried foods in your home to see if you hear/see weevils in it or coming out of the container.
Given the relatively large number of eggs each female can lay and given the month long generation time, this is an infestation you'd like to stop quickly.
 Note: all info is from the linked/cited Wikipedia pages unless otherwise cited.

I had an infestation once -- bag of dried corn. Vacuuming wouldn't pull the buggers out of my carpets, so I was forced to pull them out one by one using a headlamp and tweezers

Thank you. Source was eventually tracked to a bag of dry pasta.


text:
Use lab agar for cooking
Our lab manager suspect that something wrong with our lab Bacto agar (Difco). So she decide to throw it to the garbage. I think that it's just a waste to throw that thing.
Can someone think of reason why don't use that agar for molecular cooking in my kitchen?
(My lab manager think that i am totally crazy without give any reason)

I'm voting to close this question as off-topic because it has nothing to do with either biology or biological techniques. There may be some other SE site (Health, Domestic Science?) where it is appropriate, but that's for the poster to find out.

If there are reasons to not use it for lab stuff, maybe there are reasons for not using it for cooking either.

Technically agar has first been used (and still is) in the kitchen and then adopted to the lab.
In the 19th century, gelatin was used in the microbial laboratory. The problem is that gelatin is much less thermostable than agar and at higher cultivation temperatures plates will melt and get liquid again.
In 1882 the german microbiologistt Walther Hesse (at that time an assistant in Robert Kochs laboratory) followed the suggestion of his wife Fannie Hesse to use Agar instead of gelatin. See the two references for some interesting details.
I personally would never use anything which comes from the lab in my kitchen since you never know if there are any contaminants in there. This is also probably the reason, why your lab manager doesn't want you to have it.
References:

Walther   and   Angelina  Hesse-Early Contributors  to  Bacteriology
History of the agar plate

What kind of contamination should I suspect? We use specific spoon to take out the agar from the box that used only for this.

The agar doesn't care where it is prepared, however, I am 100% with Chris on this one, I wouldn't use any coming from the lab for fear of contamination. I don't know what kind of organisms you work with and what you may find in your environment but generally it is not a good idea to mix things that were used in the lab with things that you use in your kitchen.

I don't think that I need to worry from the bacteria that I have in my lab more then the normal bacteria that I (probably the same) have in my kitchen. I am more worried if they use something in the production of the Agar that is toxic to people.

@Moshe I think more about lab chemicals which are present where agar gels are prepared like Ethidiumbromide. Or people using dirty spoons/spatulas before going into the agar. The agar itself is prepared from algae and my guess (although I don't know for sure) is that the lab agar is pretty clean.

@Chris TNX. like I said before we dedicate special spoon for each reagent in the lab. so i don't think that i need to worry from that (BTW the box is open but i pretty sure that they used it only once or twice). PS - ethidium bromide have very bad reputation compare to the risk that it made https://bitesizebio.com/95/ethidium-bromide-a-reality-check/

If we are worried about stuff from the lab being so contamined that it could be unhealthy, shouldn't be worried about that same stuff contamining other experiments? I would expect some experiments to be even more sensitive to contaminants than our dishes are.

@Pere In general you are right. But: This is a general precaution to avoid harm. We have a number of substances in the lab that can be nasty.


text:
Is there a double helix RNA?
I wonder what is its function and if it can be the genetic material for a living organism. If not, why?

Yes, double-stranded, helical RNA exists. It can occur naturally, a famous example would be Rotavirus, as well as synthetically in the lab.
Please note, however, that viruses strictly speaking do not qualify as a living organism.
References:
RNA double helix structure identified using synchrotron - McGill University
Double-stranded RNA viruses - Wikipedia
Rotavirus - Wikipedia

dsRNA can also occur in mitochondria, since they have circular genomes, both strands of which get transcribed. This can cause problems if the mitochondrial dsRNAs accumulate and leak out into the cytoplasm, since dsRNA is highly immunogenic: https://www.nature.com/articles/s41586-018-0363-0

Single-stranded RNA (like DNA) can also fold back on itself, creating base-paired helical regions, as in tRNA. It is thought plausible that originally RNA served as both the genetic material and as the structural material before DNA and proteins came about.

As the OP asked for double-helices and did not mention dsRNA, I would like to point out a tool developed by my close colleagues, that predicts secondary structures of RNAs from sequence.
http://rna.tbi.univie.ac.at/cgi-bin/RNAWebSuite/RNAfold.cgi
Here, base-paired regions are assumed to be in helical conformation.
You will see that most RNA sequences have some theoretical potential for auto-base-pairing with small, albeit temporary, helices.
Further, you asked about function of helical RNAs, which I more generally interpret as "structured" RNAs: Important terms or examples that you can further research are: 1."Rybozymes", which are RNAs with enzymatic functions; "Aptamers", which are RNAs found or created by SELEX that can bind biomolecules and even inorganic compounds with high specificity; 3. RNAs that have important functions in "RNA-protein complexes" as found in the ribosome, splicosome, telomerases, nucleases, RNPs and more..


text:
Intermediate of Krebs cycle that can form Chlorophyll?
This was a question in a test in my school today.
Q) Which intermediate of Krebs cycle further can form chlorophyll?
A) Oxaloacetic acid
B) Citric acid
C) Succinyl CoA
D) Fumarate
Given answer was (C).
How can Succinyl CoA form chlorophyll? All I could find was related to porphyrine ring. Can anyone explain it or recommend a good source?

I think you will find my answer indicates what your teacher wanted. I would explain politely that the question was wrong as regards the porphyrin ring of chlorophyl for the reason explained by March Ho, and illustrated in my answer.

The standard treatment of this topic is covered in Section 24.4.3 of Berg et al., available freely online:
Succinyl CoA is a precursor for porphyrin in mammalian cells by condensing with glycine to form δ-aminolevulinate as shown in this diagram from that book:

This reaction is catalyzed by mitochondrial δ-aminolevulinate synthase.
To quote from that reference:

Two molecules of δ-aminolevulinate condense to form porphobilinogen, the next intermediate. Four molecules of porphobilinogen then condense head to tail to form a linear tetrapyrrole in a reaction catalyzed by porphobilinogen deaminase. The enzyme-bound linear tetrapyrrole then cyclizes to form uroporphyrinogen III, which has an asymmetric arrangement of side chains. This reaction requires a cosynthase. In the presence of synthase alone, uroporphyrinogen I, the nonphysiologic symmetric isomer, is produced.

This is illustrated in Fig. 24.35 of that section, which also shows that uroporphyrinogen I gives rise to protoporphyrin IX, the precursor of haem:

As regards the synthesis of plant chlorophyl (which also contains a porphyrin ring), the review quoted by March Ho contains the following statement:

The porphyrin ring with its conjugated double bonds is assembled in the chloroplast from eight molecules of 5-aminolevulinic acid…

(5-aminolevulinic acid is the chemically preferred name for δ-aminolevulinic acid.)
However the review goes on to explain that although 5-aminolevulinic acid synthesized in plant mitochondria uses the same pathway as mammals, that produced in the chloroplast and used for the synthesis of haem that gives rise to chlorophyl uses a different pathway, termed the C5 pathway, in which — as March Ho stated — glutamate is the precursor:

I suspect that the person who set the question is an animal or biochemist who thought he would try a variant of the standard question “which intermediate is a precursor of haem”, and ventured into waters where he was out of his depth.

Thanks for the explanation of what the question was intending to ask. Given that, it makes a lot more sense that the question referred to a specific molecule, since it was the molecule stated in the textbook.

This is a poorly set question. If any one member of the Krebs Cycle is used as the raw materials in a biosynthetic pathway, it will follow that all of the other members are also part of the same biosynthetic pathway, since they are part of the same cycle.
The full biosynthetic pathway of chlorophyll is a very complex process, and there are dozens if not hundreds of different steps and enzymes involved. This is one paper that attempts to cover the issue.
In short, the porphyrin ring region of chlorophyll is generated from glutamate, and the phytyl tail region of chlorophyll is generated via the phytol synthesis pathway, via the geranyl phosphate pathway

I think it is a poorly set question, but not for the reasons you state. It is fairly clear what is meant. I do feel a complete answer needs to point out the animal/microbial pathway for synthesis of δ-aminolevulinate, which, is what is causing the confusion. I feel a little bad about using your info on the C5 pathway of synthesis in chloroplasts in my answer, but I have acknowledged you and,  again, I feel it needs spelling out.


text:
Extra-mitochondrial conversion of Acyl Carnitine to Acyl CoA
Normally fatty acids in the form of acyl CoA are converted to acyl carnitine in a reaction catalysed by carnitine palmitoyltransferase I (CPT1), which is also known as carnitine acyltransferase I. This allows them to be transported across the inner mitochondrial membrane by a translocase when the acyl CoA is regenerated in a reaction that is chemically identical but catalysed by a different enzyme, carnitine palmitoyltransferase II (CPT2).
As a result of observations I have made (detailed below) I wish to known whether acyl carnitine that has not entered into the mitochondria — either present in the cytosol or blood/plasma — can be converted back into acyl CoA without entering mitochondria?
Essentially, does a reaction like that catalysed by CPT2 occur outside of the inner-mitochondrial matrix?
Elaboration
I'm studying plasma metabolites. During fasting there is an increase in plasma acylcarnitines due to increased fat utilization/beta oxidation. If the fast is broken, acylcarnitines are typically supposed to drop. Oddly, some people experience an increase in plasma acylcarnitines 0-30 minutes following eating - but then they drop after the 30 minutes. I'm confused as 30 minutes after food ingestion, elevated circulating insulin levels are still present and should be still working to inhibit the majority of fatty acid oxidation - yet the odd increase and then drop in acylcarnitines after 30 minutes of food intake still exists.
So it leaves me with the question, is there another pathway in which acylcarnitines are converted back to acyl CoA outside of the mitochondria? In short, how does the cell recall fatty acids that are destined for the mitochondria?

This is a rather precise question in a specialized biochemical area, but seems rather strange to me. Is there a reason for asking? If you can explain a little further it is more likely that someone will be able to help you. At the moment all I can do is summarize what I can glean from standard biochemistry texts.

@David I updated the question to reflect your comment. I understand this is a harder question, not a lot research out there on it, but I was hoping to throw this out there to see if anyone has heard anything or can point me in a direction to research further.  Regarding the strangeness of the questions, it is basically introductory metabolism (beta-oxidation) with a twist.

Your clarification was helpful, and after a first go at an answer I have modified your question to provide the background biochemistry for anyone not familiar with it.

The introduction to Ann N Y Acad Sci. (2004) 1033:17–29 lists the various carnitine acyltransferases and mentions CPT-1a, CPT-1b, CPT-1c (tissue specific) but states there is only a single CPT-2 in humans. It does not appear that there is any other variant, so extra-mitochondrial conversion of acyl carnitine to acyl CoA would require a post-translational variant of CPT-2, or CPT-1 working in the reverse direction.
The discussion of carnitine metabolism in Berg et al., Section 22, implies the reaction is near equilibrium. Hence, if the concentrations of substrate and product were appropriate it would be thermodynamically possible for CPT-1 to operate in the reverse direction.
Thermodynamically possible does not necessarily mean enzymically possible. I am not familiar with kinetic studies on CPT-1 and CPT-2, but imagine that CPT-1 has a higher affinity for acyl CoA and carnitine than for the product acyl carnitine, and that the reverse situation holds for CPT-2. I imagine that the ability of CPT-1 (or one particular isoform) to catalyse the reverse reaction in physiological circumstances would depend on its Km for acyl carnitine and the concentration of the latter. It might be worth seeing what kinetic analysis has been done.
The ‘appropriate’ situation for (2) might be if something were preventing utilization of acyl carnitine in the mitochondria of ‘target’ cells.
If you work in this area you will know better than me that there are various clinical conditions and sub-clinical conditions (e.g. obesity) that result in abnormal utilization of acyl carnitine. Could the abnormal instances you observe be for such individuals?

I don't claim that this is a complete answer, but it tries to address the question in terms of possibilities. It has been modified since I originally wrote it.

Awesome, thanks for editing the question, and providing a more than substantial answer. Personally, I was thinking that there could be affinity exchanges, perhaps a short-chain acyl-coa might be a preferred substrate of CPT1, and thus might remove carnitines (somehow) from long-chain fatty acids in favor of switching the carnitine group onto a short-chain acyl-coa. That is just a completely unresearched guess though. I do work in the field of metabolomics, but surprisingly this is an unanswered question. But anyway, thanks again for the informative response.

@Aaron43 — Glad you found my remarks of use. I appreciate the difficulty of interpreting metabolomics data. One problem is that classical biochemical metabolic research went out of fashion because it seemed more or less finished and there were newer and more exciting fields that deserved research funds. However now that the old guys are gone there's a serious shortage of people who understand metabolism to interpret all the new omics stuff. I looked down on it too, but was obliged to teach it in the later stages of my career. Discovered that there are lots of interesting questions left.

lol, the complexity and the almost infinite number of metabolic interpretations that can come from something as simple as plasma metabolite concentrations, really makes the field seem like chaos. Even my own work I have to step back sometimes and just say wtf. Ha, but thanks again for the info.


text:
Why is a cellular structure necessary to satisfy the definition of alive?

I was looking at this image and reading through the Wikipedia page for viruses and it says that to satisfy the definition of "being alive" the organism must have a cellular structure, but it seems to me that if an organism has all these other factors without a cellular structure, it is still seemingly alive, no?
So why exactly does an organism need a cellular structure to be alive? What is the rationale for that criteria?

A quote I remember from the Campbell's Biology textbook said something like "if you take all the individual components of a chloroplast and put them all together in a tube, you won't have a functional chloroplast"... That's why the structure of a cell and its organsiation matter, even if it doesn't explain why the structure is absolutely necessary for a cell to work. Similarly, the textbook would say that having all the pieces of a bike in a box won't lead you anywhere, but a little bit more structure could make a bike and lead you somewhere. I hope these examples can help.


text:
Decision-making in tree limb growth?
Sorry if this is a naive question, but it occurred to me as I was walking across campus today; How does a tree decide which limb is allocated the most resources, and thus grows the largest?
My first thought is the first branch to deviate from the base receives the most energy investment, and so on, but I don't have the time (or will) to actually test that. Does it have more to do with efficacy of the limb for photosynthesis? Or is it largely due to chance/unknown variables?
Thanks in advance, I feel this is something I learned back in botany and just forgot completely.

There is Milton’s Law of resource availability and allocation.
It states that branches act as if they were different individuals, and they grow relative to the availability of their own resources.
The cells that grow are called meristems, there are different kinds of meristems, cambium ones that grow the trink, apical meristems that grow at the top,
Apical dominance is phenomenon where one meristem prevents or inhibits the growth of other meristems. As a result, the plant will have one clearly defined main trunk. For example, in trees, the tip of the main trunk bears the dominant meristem. Therefore, the tip of the trunk grows rapidly and is not shadowed by branches.
If the dominant meristem is cut off, one or more branch tips will assume dominance. The branch will start growing faster and the new growth will be vertical.
Over the years, the branch may begin to look more and more like an extension of the main trunk. Often several branches will exhibit this behaviour after the removal of apical meristem, leading to a bushy growth.
The mechanism of apical dominance is based on the plant hormone auxin. It is produced in the apical meristem and transported towards the roots in the cambium.
If apical dominance is complete, it prevents any branches from forming as long as the apical meristem is active. If the dominance is incomplete, side branches will develop.


text:
cloning and blue white screening in pet21a
I am using pet21a as a carrier vector for my gene, with R.E BamHI and XhoI,in reverse primer I haven't added any extra nucleotide sequence so that it should code for the histag towards C-terminal. Am I doing so correctly?
Another question: after transformation to DH5alpha, I am getting only white colony(X gal stock was 20mg/ml about 200ul and IPTG 100mM stock about 40ulon surface of plate)... why I am not getting blue colonies?

pET21A doesn't encode the lacZ α-peptide necessary for blue-white screening by complementation. Since DH5α has the lacZΔM15 background, only the lacZ ω-peptide is produced and thus β-galactosidase is inactive.


text:
Why do plants produce and store both amylose and amylopectin?
Since both forms of starch has its primary purpose of storing glucose and hence releasing energy, why are there 2 variations of this sugar? Is it possible for an organism to contain/depend only on 1 but not the other?


text:
What is the difference between gene expression and protein synthesis?
I have no idea what I'm supposed to do. Can someone please help me? What is the difference between gene expression and protein synthesis?

The difference between gene expression and protein synthesis is that of the whole to one of its parts. Note: not all genes code for proteins, but every gene codes for something.

This is a really poor question. "I have no idea on what I'm supposed to do" What are you talking about? How should we know what you are supposed to do when you don't explain the context of your question? What level course are you following, what books are you using, how did this question arise? Please take the Tour explaining how this list works and read how to ask questions properly.

According to the homonymous article of Wikipedia

Gene expression is the process by which information from a gene is used in the synthesis of a functional gene product.
These products are often proteins, but in non-protein coding genes such as transfer RNA (tRNA) or small nuclear RNA (snRNA) genes, the product is a functional RNA.

As shown by this picture, gene expression consist of genetic transcription, that results in a mRNA, maturation of the mRNA (splicing, incorporation of a poly(A) tail, capping, ...) and finally protein synthesis by means of translation of the mature mRNA.
Again, the homonymous Wikipedia article tells us what is protein synthesis:

Protein synthesis is the process whereby biological cells generate new proteins [...]. Translation, the assembly of amino acids by ribosomes, is an essential part of the biosynthetic pathway, along with generation of messenger RNA (mRNA), aminoacylation of transfer RNA (tRNA), co-translational transport, and post-translational modification.

The following picture describes the process of mRNA translation by ribosomes that results in a polypeptide.

Once folded in its proper 3D structure, the polypeptide becomes a functional protein.
In order to work properly, some proteins need post-translational modifications, which is (citing Wikipedia again) the covalent modification of proteins following protein biosynthesis and goes beyond the scope of this answer.


text:
Is the xylem like a tissue paper?
I am a 5th grader learning about the plant transport mechanics and I learnt that the xylem is made up of dead cells.So if water travels up the xylem and water travels only 1 way, is it like how water travel up a tissue paper?

I'm in year 5 too; and (with a bit of help of my dad) I have some bits of answers (my challenge of the day).
A paper tissue is principally made of cellulose. And cellulose is a polar molecule. And so is water. So, the paper will easily absorb water.
See these short clips [1] for water polarity and here for cellulose [2].
In plants, xylem vessels are also made of cellulose and that helps the small molecules of water to stick to the vessels walls.
Think of it as a lot of tiny drinking straws made of wood.
There are at least two reasons why water manages to 'climb up' from the roots to the leaves through the xylem.
During the day, when the sunlight is available, water will be consumed by the leaves during photosynthesis [3]. For each molecule of glucose, 6 molecules of water are needed.
So the water already present from the xylem in the leaves needs to be replenished by water (sap) from the twigs, which is replenished by the water from the xylem in the branches,... And so on, till the water is pulled from the roots.[4]
Remember little molecules of water cling to each other because they are polar.  This is why they tend to pull each other up, as they are consumed in the leaves [1'].
And this is why it is important that both the water molecule and the cellulose molecule are polar.  If H2O would be like CO2, there would be no vascular plants as we know them.
But there is no sun, so no photosynthesis, during the night.
Then the stomata, which are holes used by vascular plants to "breath" (
transpiration), are usually closed.
There is also another reason why water moves up the xylem. Here it is.
Roots not only 'pump' water, their role is also to capture nutrients.
These nutrients are like salts, not table salt, more like ions (potassium, phosphorus, zinc, mangnese, etc) which are needed by the plant cells.
So the water is a bit more 'salty' inside the roots.  Water outside the roots tends to try to diffuse into the roots in order to compensate the relative saltiness [5].
This in turn pushes the water from the root below the ground towards the branches.[4]
What is remarkable is that the whole cycle of water is passive, the plant does not spend energy to move the water 'upwards' to the leaves.
Here are a few sources which I can recommend and from which I learned most of these things. Crash course biology.
They talk fast but it's quite funny.
[1] water polarity: 'Water - Liquid Awesome: Crash Course Biology #2'
https://youtu.be/HVT3Y3_gHGg?list=PL3EED4C1D684D3ADF&t=171
[1'] To picture molecules of water pulling one another up the xylem... well:
https://youtu.be/IlmgFYmbAUg?t=154 (Monkey chain in Madagascar 3)
[2] cellulose: ' Plant Cells: Crash Course Biology #6'
https://youtu.be/9UvlqAVCoqY?list=PL3EED4C1D684D3ADF&t=255
[3] Photosynthesis ' Photosynthesis: Crash Course Biology #8'
https://youtu.be/sQK3Yr4Sc_k?list=PL3EED4C1D684D3ADF&t=75
[4] For a simple presentation of xylem, I use Simple English in
https://simple.wikipedia.org/wiki/Xylem_vessel
and 'Vascular Plants = Winning! - Crash Course Biology #37'
https://youtu.be/h9oDTMXM7M8?t=373
[5] Osmosis (water compensating solutes) "In Da Club - Membranes & Transport: Crash Course Biology #5"
https://youtu.be/dPKvHrD1eS4?list=PL3EED4C1D684D3ADF&t=148
Ian (and dad <= all errors and approximations are his :) ).

Ah, and yes, this is me in the avatar. When I was one.

Thanks for your highly informative answer. But at night, if the temperature is still higher than 0° so won't some water evaporate through the stomata?

@Joshua, under normal circumstances, stomata are closed during the night.
https://youtu.be/IlmgFYmbAUg?t=154 but you are also right to add that photosynthesis is not the main reason why leaves consume water. Water evaporation is also the way plants regulate their temperature in warmer conditions.

Yes, the analogy is quite correct with respect to the mechanisms involved. In xylem as well as in tissue paper there are there are tiny pores throught out them through which water rises up. This mechanism is called cappilary action of water which you shall study in high school physics course. In fact tissue paper is made up of the same substance that xylem is made up of, i.e Cellulose.When you dip tissue paper in a bucket it spreads in all directions but imagine looping it to form a pencil like shape. Now thats like a real xylem.
Hope it helps.....


text:
Import of H+ ions into the thylakoid space during photosynthesis in plants
Why are H+ ions pumped into the thylakoid space as the electrons pass through the cytochrome complex from PS2 to PS1 during photosynthesis?

This is covered in most texts of biochemistry. Have you tried to find the answer yourself as explained in the Help Centre? Try, for example, Section 19.3 of Berg et al. online.


text:
Text or source (preferably free) for learning developmental biology
I might have to take a graduate level course in developmental biology, of which I have never taken a course in before. The course website lists no recommended texts. Therefore, I assume we will be doing a more independent study, and I would want to have a book or source to better facilitate that study.
Any recommendation, free or not free, is welcome.

Gilbert's Developmental Biology is an excellent text. It is in the 11th edition, though the 6th edition is available free on NCBI bookshelf.

I ended up buying the 9th edition since I felt the 6th was too old, and I could not figure out how to access a .pdf form of the 6th. Thanks :D

@RoSiv Many free text books on NCBI are only accessible by searching. You can get into whole chapters/sections if you just search for the title. Of course, the actual book is much more user friendly; I hope you enjoy it.

For a very quick and free introduction, you can have a look at Khan Academy > Developmental Biology.
Of course, before studying developmental biology, you will need basis in molecular biology and molecular genetics.

Yea I kind of found myself thrown into the whole grad school life. Just hoping to knuckle through.


text:
What portion of America needs the Flu vaccine for herd immunity effects to become substantial?
I've been looking at the effectiveness of Flu vaccines, which are in my subjective opinion abysmal, and the concept of herd immunity.  I see many articles which argue that we all need flu shots to help support the weaker individuals via herd immunity.  However, I see very few documents actually indicating how effective this process is.
Most of what I have found on the topic is interested in the Herd Immunity Threshold (HIT), which appears to be the point where vaccinations drive the Rq of the disease (reproductive rate in the presence of the vaccinations) below 1 such that the disease spreads to fewer and fewer people with each generation, like removing the heat from a fire such that it cannot sustain itself.
There are two particular aspects of this which I believe are required to answer the question which I cannot seem to find a good answer for, which have been preventing me from answering my question:

What is R₀, the basic reproductive rate, for influenza?  I have seen estimates ranging from 1.2 to 3.  As best as I can tell, even a poor vaccine would be very effective if it was 1.2 but it seems like it would do very little against the higher R₀ values.
How substantial of a knee in the curve is there regarding the number of immunized individuals vs. the herd immunity effects?  If there is no substantial knee in the curve, that should indicate that there are valid herd immunity arguments for influenza even if the vaccines are substantially ineffective.  If the knee in the curve is sharp, then herd immunity arguments would only be valid if we could reach that threshold.

It appears some of these questions may have been answered in "The vaccination coverage required to establish herd immunity against influenza viruses" by PedroPlans-Rubió in 2012, but I do not have any access to Preventive Medicine, the journal it was published in.

The flu vaccine is a poor choice for this kind of analysis because of the tremendous number of variables involved: what was the dose inhaled/how intact is the 'victim's' immune system/how close is the match between the vaccine and the circulating (ever mutating) virus, etc. The world's epidemiologists struggle with this anew every year. The question is better for a virus like varicella.

@anongoodnurse True, it might be easier to analyze another virus, but influenza is the one I am interested in.  It is actually the variability and uncertainty surrounding influenza that draws my attention to it.  I see a great deal of certainty expressed regarding the influenza vaccine, but I'm having trouble finding numbers that back those certainties up.  For example, the anti-vaxers love to tout the ineffectiveness of the vaccine (perhaps 10% this year!), but I find it hard to find out what effectiveness is actually needed.  Maybe 10% is actually enough if we all do it!

I can't answer; the effectiveness changes every year. I can say, though, that as a young doctor, I recommended the vaccine but didn't get it. Four years in, I contracted influenza. I never missed a flu shot again, and never got the flu again (even though I treated such patients every year.) Decades passed. I contracted influenza again this year - only the second time in my life - in a year that the vaccine is a notoriously poor match. Maybe because I received the high-dose vaccine, my course was very mild. Others who have been immunized (chiefly infants) have died. How can you get hard facts?

Cort, you might want to look at the Cochrane Report. Keep in mind, though, that they don't only include influenza A&B (what the vaccine covers.)

Quoting Jhung et al. 2011 talking about H1N1 2009 epidemics

Although estimates of R0 from past pandemics vary, the R0 of previous pandemic influenza viruses generally range from 1.5 to 1.8 for the 1957 H2N2 and 1968 H3N2 pandemic viruses, and 1.8–2.4 for 1918 H1N1 influenza A strain, with a high estimate of 5.4 by Andreasen et al [see also White et al]. During the current pandemic, White et al used CDC case-based data from 1368 confirmed and probable cases with a date of report on or before 8 May 2009 and estimated the reproductive number of pH1N1 virus to be between 2.2 and 2.3. Estimates decreased to 1.7–1.8 after adjustment for increased case ascertainment during the initial pandemic period. In a sensitivity analysis making use of previous estimates of the mean serial interval, White et al estimated that the reproductive number was between 1.5 and 3.1. Fraser et al used data from the initial outbreak in Mexico to estimate R0 in the range of 1.2–1.6. Yang et al used reported case clusters in the United States to estimate R0 to be 1.3–1.7. Most estimates of R0 for pH1N1 virus, therefore, have indicated that the virus was at the low end of transmissibility, compared with the strains that caused the 1918 pandemic, and was comparable to or slightly less transmissible than the strains that caused the 1957 and 1968 pandemics.


text:
Are peanut proteins similar to chicken meat proteins?
I'm studying amino acids content in vegetable food. I was looking at peanut protein and noticed its similarity with chicken meat, as you can see in the table below (quantities are measured in grams). Third column is first column minus second column. Green amino acids are the essential ones.
The biggest difference (-1.11) happens for Lysine, but Lysine quantity (0.901) is still bigger than the lowest one, which is Tryptophan (0.2445). So in this case, is Tryptophan the limiting factor in protein synthesis? (Tryptophan amount is < than any other amount).

The table below lists the optimal profile of the essential amino acids (first column). Second column is obtained by dividing the values in table 1, first column, by 25.3055 and multiplying by 1000.
Notice that Lysine is the only one amino acid less than the reference (36<51).

So the questions are:
1) Have peanut proteins a limiting factor (if yes what is and why?) or can be considered a complete protein?
2) If the answer to 1) is "yes it has a limiting factor" what vegetable foods rich in lysine can be eaten with peanut in order to obtain all the amino acids? And how to calculate the ratio of peanut and the complementary foods to eat in order to get the proper profile of the essential amino acids?

Source for first table (first and second columns) https://ndb.nal.usda.gov
Source for second table (first column) http://nutritiondata.self.com/help/analysis-help

I'm not sure if biology is the correct site to post this question, so if you know a better one let me know, thanks.

I posted an answer to a similar question here: https://health.stackexchange.com/questions/9124/is-all-protein-the-same/9130#9130

You're not using protein as it is to maintain your body. It's first
  broken down to the individual amino acids, which your body can then
  use to build new stuff.
If you're lacking one of the essential amino acids, you can only build
  as much new protein until that runs out, and all the other amino acids
  are just excess. A protein that contains all the necessary amino acids
  is called a complete protein, and you could calculate the differences
  in the so-called quality of the protein.
A perfect protein (i.e. from egg/milk/soy) will contain amino acids in
  exactly the ratio you need, some protein contains so little of a
  certain amino acid that you'd need to eat twice as much of that
  protein (for example rice or peanuts).
In your case, if beef is making you recover fastest, you'd need to eat
  30*0.92/0.70 = 39g of peas for the same effect.
You could get around this by combining different sources of protein.
  For example grains are limited in lysine, while beans are limited in
  cysteine/methionine.

thanks for the answer, but could you explain the calculus 30*0.92/0.70 ?

It's from this link: https://en.wikipedia.org/wiki/Protein_Digestibility_Corrected_Amino_Acid_Score. The questioner wanted to know how much pea-protein they needed to eat to get the equivalent of 30g of beef protein. Beef has a "quality factor" of 0.92, pea has 0.70.

Mm I don't know then if that calculus is correct. If you eat 30g of soy protein you get all the essential amino acids. To have the same result with beef you have to eat 30/0.92=32.6g of beef protein, and with pea you have to eat 30/0.7=42.9g of pea protein. This is what I understood from reading about PDCAAS.

You're correct, but the poster was talking about the consumption of 30g beef protein.

Ah I understand now

Firstly, here are many types of proteins in both peanuts and chicken, so it is a little ambiguous to say "peanut proteins" or "chicken proteins". Secondly, proteins are proteins. "Complete" and "incomplete" are simply nonsensical terms for describing these macromolecules. Each protein performs a certain task, be it structural, like keratin, or functional, like enzymes. The purposes, as well as the abundances and characteristics of the proteins in say, a piece of chicken define its traits. The amino acid content, though related to these things about proteins, do not imply them. Proteins in different food items are simply made up differently.
To answer the question, no, there is no inert limiting factor on the synthesis of proteins in peanuts, and yes, these proteins are "complete".
I hope this helps!

I think sound wave is talking about nutrition, and the use of protein as a food. In nutrition, the terms complete and incomplete protein are widely used.

Ah ok I was unaware of that

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