text:
ratio between heat transfer coefficient and thermal conductivity
Consider the Robin boundary condition for the diffusion/heat equation $\mathrm{u_t=a(t)u_{xx}+f(x,t)}$:
$$\mathrm{-k(t)u_x(0,t)=h(t)u(0,t)}$$
or
$$\mathrm{u_x(0,t)+\frac{h(t)}{k(t)}u(0,t)=0}$$
where $\mathrm{k(t)}$ thermal conductivity and $\mathrm{h(t)}$ heat tranfer coefficient.
My Question: Is it possible that the ratio $\mathrm{h(t)/k(t)}$ to be constant? Could anyone please help me? I have really no idea.

This is probably better suited to chemistry stack exchange as it smells like physical chemistry.

I'm voting to close this question as off-topic because it is more suited for physics

Most likely, you can't assume that $h/k$ might be constant. Reason is that those parameters are characteristics of two very separate systems.
Thermal conductivity shows how fast heat can be propagated through material. That is, it answers question: if block of metal has $T_0$ temperature on its surface A, and you apply temperature $T_1$ (higher) to opposite surface B, how long it will take for whole block to get to temperature $T_1$.
Heat transfer coefficient is a characteristic of a system. For example, when you have coolant on one side of metal plate, and heated air on the other. Question is how efficiently heat will be transferred from one side to the other. For more you can check this link. As you can see, transfer coefficient $U$ is a function of conductivity of the metal plate $k$. Hence, generally, relationship is non-linear.


text:
Additive genetic variance with $n$ alleles
The genetic variance of a quantitative trait (the quantitative trait in question is fitness) can be express as the sum of two components, the dominance and additive variance:
$$\sigma_D^2 + \sigma_A^2  = \sigma^2$$
, where $\sigma$ is the genetic variance, $\sigma_D^2$ is the dominance variance and $\sigma_A^2$ is the additive variance. $\sigma_D^2$  and $\sigma_A^2$ are given by
$$\sigma_D^2 = x^2(1-x)^2(2\cdot W_{12} - W_{11} - W_{22})^2$$
$$\sigma_A^2 = 2x(1-x)(xW_{11}+(1-2x)W_{12} - (1-x)W_{22})^2$$
, where $W_{11}$, $W_{12}$ and $W_{22}$ are the fitness of the three possible genotypes and $x$ and $1-x$ give the allele frequencies.
Question
The above definition makes sense for one bi-allelic locus.

How are $\sigma_D^2$, $\sigma_A^2$ and $\sigma^2$ defined for a locus that have $n$ alleles?

Here is a related question

this might be a useful resource for you @Remi.b - I'll read the Falconer and Mackay book tomorrow at work too http://nitro.biosci.arizona.edu/zbook/NewVolume_2/newvol2.html

really like this question, spent some time at the whiteboard today trying to work it out! made good progress!

Chapter 4 of lynch and Walsh seems to deal with this - from around table 4.2

@GriffinEvo At which page is it? I could find table 4.1 at page 11 and table 4.3 at page 22! table 4.2 is probably in between :D

In my copy it is page ~77, I think you should see equation 4.23a and some of the preceeding section on "average excess" - this is Lynch and Walsh Genetics and analysis of quantitative traits. I'm away for the next couple of days but will be trying to write this in an R code with data to test it out next week - perhaps we should move to the chat room to discuss more!

Well, the total genetic variance is just, by the definition of the variance,
$$
\sigma^2 =\sum_{i,j} f_i f_j (w_{ij}-\bar{w})^2
$$
(using $f_i$ and $w_{ij}$ for frequency and fitness, respectively), and
$$\bar{w} = \sum_{i,j} f_i f_j w_{ij}$$ is just the average fitness.
You can calculate the additive genetic variance for different loci by simply assuming that there is no dominance effect, i.e. the alleles are independent. If it helps, think of it as a quantitative trait in a haploid organism. Thus,
$$
\sigma^2_A =\sum_{i,j} f_i f_j (w_iw_j-\bar{w}')^2 = \sum_i f_i(w_i-\bar{w}')^2.
$$
with
$$
f_i=\sum_jf_{ij};  w_i=\sum_j f_{ij}w_{ij}; \bar{w}' = \sum_i f_i w_i;
$$

Thanks a lot for your answer. Could you please help me to develop the formula for $\sigma_A^2$ for a diploid population?

this should be true for a diploid population. The additive genetic variance is defined as the variance in a population where there are no interaction effects between genotypes, so $w_{ij}$ can be written as $w_iw_j$

I'm sorry I might be a bit slow to understand :)… Can you please show the development to find back $\sigma_A^2 = 2x(1-x)(xW_{11}+(1-2x)W_{12} - (1-x)W_{22})^2$ from your equations? Thank you.

source: Stack Exchange

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

sort: votes


text:
What are the costs associated with carrying lots of genetic material
What are the costs (if any) associated with carrying lots of genetic material (Big genome size)?

energy for copying?
raw material for copying?
space in the cell?
Maintenance cost (matter and energy)?
time to copy is a limiting factor for the minimum generation time?
Less robustness?
More likely to evolve a gene that spreads well but has a negative fitness impact on the rest of the genome (selfish gene or outlaw)?

The answer probably depends on the organism. I am interested about any information concerning uni- or multi-cellular eukaryotes, bacteria or viruses.
Do we have any knowledge about how important are these costs or is it pure guesses?

This post comes in reaction to @AlanBoyd comments on this post.

It may also have negative effects due to mutations in genes which are not really needed but develop a negative effect.

What would be the cost of cleaning up this material?

What do you mean "cleaning up this material"?

Related question: http://biology.stackexchange.com/questions/10442/variations-in-genome-sizes

It is generally known that the smaller (or less complex) an organism is, the more "condensed" it's genome is. For example, bacteria (or some eukaryotes) have operons (http://en.wikipedia.org/wiki/Operon) or overlapping genes using different and they don't have introns, which alltogether saves a lot of space.
There are many reasons for that. Available space in the cell is definitely not one if it, however. Energy for copying and maintenance is a good point, but you have to keep in mind how evolution works. Bacteria and unicellular eukaryotes are usually adapted to a very specific environment in which they can reproduce rapidly. This means, they only need a small set of genes, specific for this environment and they have to reproduce very frequent, which means they are very prone to mistakes during DNA-copying. Such a mistake can lead to the death of the cell, which in this case equals the death of the organism.
In higher organisms however, the advantages of a bigger genome outweigh the disadvantages by far. Evolution can happen much faster because and mistake while copying does not necessarily lead to the death of the whole organism. Adaptation to a much greater variety of conditions is also necessary, e.g. when you look at plants: Their genomes are (on avarage) much bigger than the ones we mammals have, because they cannot move if the conditions around them become unpleasent. Instead, they need to find a way to adapt. This means, a big genome is in this case a fitness bonus. More interestingly, plant genoms are highly mutable (http://en.wikipedia.org/wiki/Transposable_element), which was originally thought to be a huge disadvantage.

Plants also often carry a lot more copies of their chromosomes than animals, I've heard of plants with 8 copies of each chromosome, creates a lot of opportunity to carry multiple alleles for a gene and use whatever works best for the current situation.

This answer makes very little sense. First, organism size and complexity are not always that related, (i.e. bull kelp and a shrew). Second, it is false that organismal complexity relates to genome size. This is true for prokaryotes, but less for viruses, and entirely untrue for eukaryotes. In fact, Polychaos dubium is a single-cell amoeba that has a genome ten times larger than humans. Or, for instance, the fact that amphibians lead the animal kingdom in genome sizes. Third, genome size does not correlate with vagility, for instance, worms and fungi have much large genomes than birds.

You clearly have not read my answer very carefully. I never claimed that organismal complexity relates to genome size. In fact, I argued that plants have bigger genomes than mammals, even though you will hopefully agree with me that mammals are much more complex organism. Furthermore, we are talking about generals trends and avarages here. Of course you can find plenty of exceptions - and Polychaos dubium clearly is one of them.

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


text:
Cells "grown in LB broth to an OD600nm"

Cells "grown in LB broth to an OD600nm"

What does the OD stand for in this?

Just a google search would have fetched you the answer.

This phrase in isolation has no meaning, because the value itself is missing: "to OD of X at 600 nm".

OD = Optical Density
As you grow cells in broth, the broth becomes cloudy. The more cells there are, the cloudier it is. After you grow your cells for a while, you can measure their progress by shining a light through your sample. The more light your cell culture absorbs (higher absorbance is equivalent to higher OD) the more cells there are in it.


text:
Blood and hair follicles from 25 people put on the Moon; enough to regenerate a human population?
Discussion on the question Why were blood and hair follicles from 25 people put on the Moon? calls into question whether this is a stunt or might have any basis in science.
There's two parts to my question:

If somehow preserved well, do hair follicles and blood samples from a group of humans provide sufficient coverage alone to reconstruct a human population as far as the DNA content is concerned? Ignoring that you don't have an egg to put it in, is enough DNA present, or would there be key bits of DNA missing that you'd need a germ line sample in order to get? I suppose this can be asked as "can we clone people from blood and hair follicles alone?"
Would 25 individuals be enough to obtain a viable population of clones?

Background from the linked question:
The Wired.com article A Crashed Israeli Lunar Lander Spilled Tardigrades on the Moon says:

Spivack had planned to send DNA samples to the moon in future versions of the lunar library, not on this mission. But a few weeks before Spivack had to deliver the lunar library to the Israelis, however, he decided to include some DNA in the payload anyway. Ha and an engineer on Spivack’s team added a thin layer of epoxy resin between each layer of nickel, a synthetic equivalent of the fossilized tree resin that preserves ancient insects. Into the resin they tucked hair follicles and blood samples from Spivack and 24 others that he says represent a diverse genetic cross-section of human ancestry, in addition to some dehydrated tardigrades and samples from major holy sites, like the Bodhi tree in India. A few thousand extra dehydrated tardigrades were sprinkled onto tape that was attached to the lunar library.

If the 25 human samples were from diverse regions of the world, i'd bet that it would be easy to build a human population with medical supports, although the frailties may not make them viable for wild tribe life.

No, because AFAIK you can't just clone a mammal from DNA.  You need a mother from the same or a closely-related species.  Think of it as "blueprints": instructions to a factory that has a lot of highly-specialized CNC machinery.  Without having those machines (or being able to build duplicates), your CNC instructions are useless.

@jamesqf so perhaps the use of the verb "clone" in the question was misguided. There's still the question of the fraction of the genome present in hair follicle and blood being sufficient.

If you had the technology to build a human from the DNA in hair follicles, you'd probably have the technology to synthesize DNA from scratch. So instead of sending up 25 hair follicles, send up an SSD with DNA sequences from thousands of people.

@user137 a little bit like this?

If we assume for a moment that the samples could be successfully cloned, 25 individuals is probably not enough to maintain a stable human population for more than a few hundred year without experiencing severe inbreeding depression and eventual extinction.
In population biology, there's a general rule of 50/500 for minimum viable population sizes. Essentially, a minimum population of 50 is needed to prevent inbreeding depression, and 500 to stabilize genetic drift. Of course that's a generalization used in management situations, and lots of factors go into making a calculation like this with any amount of precision.
One estimate gives a minimum viable human population (for generational space travel and permanent colonization) of ~40,000 humans in order to maintain genetic diversity. But that only applies to a population carefully screened and selected to maximize the effective population size. Another suggests 160 people could be enough for a stable population, as long as they return home to mix it up with the rest of humanity every 200 years or so.

Thank you for your well-supported answer! I was worried about the samples not covering a complete genome, but didn't stop to think about this issue at all!

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


text:
Why exactly are the reflections of sunlight in this dragonfly's eye hexagonal?
I photographed a rather cooperative, large dragonfly today and after getting back to my desk and looking closer at the images I realized that the reflection of the Sun in its eyes produced large hexagonal bright spots that are:

much larger/wider than if the eye surface were smooth specular reflector
relatively uniform in brightness all the way to the edge
have very sharp edges, transition from bright to dull red is very abrupt.

I'm aware that the components of compound eyes are usually at least roughly hexagonally packed, but what is happening here is something more than that.
What is it about a dragonfly's compound eye that can account for all three of these characteristics of reflected sunlight?
Presumably this is the same red dragonfly species as is seen in Identify these two large, colorful dragonflies in Taiwan? It's the same area and time of year.

Two more taken at different angles relative to the Sun. (click for larger)

Here are high res pics if they are of assistance. I can't tell if the reflection is on the concave inside of the lenses or the convex top of the lenses, perhaps even some wall effect in the ommatidia. There are graphs of reflection in ommatidea. https://img.fotokonkurs.ru/cache/comment_image_big/comments/2013/04/26//305186.jpg and... https://www.youtube.com/watch?v=lVqO6gwcVKU

@aliential Oh, I see what you mean I'll try to read further about the lens and what's below it, maybe I can make a model of it in Blender and then try rendering. Thanks!

@aliential update: google suggested this video next, Insect Vision: Ommatidium Structure and Function You mentioned graphs of reflection in ommatidea but I don't see any in your links, was there another?

https://i.pinimg.com/originals/9d/e6/43/9de643a614510e726d3cb48810b4ab2f.jpg and https://www.ephotozine.com/photo/ommatidia-57879669 and https://simple.wikipedia.org/wiki/File:Dragonfly_compound_eyes02.jpg

Yes this can be modeled! lens: n=1.43 to 1.45, crystalline cone: n=1.34 from The properties of the visual system in the Australian desert ant Melophorus bagoti

It would be cool to model the compound eye in blender. perhaps there are some guides to building a hex lattice, that you can copy adding a lens and cone, perhaps do a flax hexagon lattics and then bend it into a hemisphere as a final step. perhaps make the lattice from flat to sphere using a maths mutation equation, in meshlab there is an equation option.

Here is the image in comments. The direction of the sun can be seen from the shadow of the left antenna. I just sketched this image to note some observations, it's the best answer that I can find at this time.

source

Yes I think this provides a lot of insight, thanks!

It's a bit of a steep optics challenge sorry it would be better to demonstrate using a 3D graph. Using blender there is probably an algorithmic option to place many components, so you'd just have to put in one ommatidea and then algoritmically copy it to a geode/spherical group. i don't know if the light comes from  the lens or the cone, although the straight edges which are shorter are giving less reflection.

I think that in Biology SE we can only go as far as identifying the anatomy/morphology. Consider adding the diagram in Figure 5 of the paper linked in this comment so readers can see the anatomy from an optical point of view? The interface between the bottom of the lens material (n=1.43 to 1.45) and the crystalline cone material (n=1.34) below it will also produce a small back-reflection, a bit like retro-reflective glass beads

ok, i'll send you the mesh if you do the light render: i'd send an occluding mesh to wall off all the lenses, and one mesh made of thousands of lenses to be rendered in transparent. I can use 250 vertices per lens and render 10k lenses, and another mesh with cones is fine too. i can render the mesh although i don't do raytrace apps only wavefront.

Thanks, and I appreciate your enthusiasm, but it's outside the scope of what I can do right now, and outside the scope of how we should use Stack Exchange. However if you't like to pursue it then you can take the information here and in the question and try  a "How to model a dragonfly's eye's optics and reproduce this photo" type question in Blender SE and there's a chance someone there will find it interesting to try! They are quite an active, creative bunch!

But it has to be "How can I..." not "Please do this...".

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


text:
Biological origin of shuddering during sleep
What is the biological origin of the following behavior:
Sometimes, during the early, formative phase of sleep (when you have a gradually dimming consciousness of what all is happening around), you feel some kind of a tremor of sorts - a feeling as if you are about to fall off. The body responds by twitching the limbs, so as to "balance", and you end up waking up for a second or two, where you realize that you aren't about to fall and all is fine.
Since Cerebellum is involved with maintaining equilibrium and balance, I have the intuition that this is related to some transient behavior where the Cerebellum is dimming down. When you are in deep sleep, you do not have a sense of balance, so I guess Cerebellum does dim down the sense of equilibrium.
But the apparent flaw in my reasoning is - if this was indeed the origin, one would have experienced these tremors every time one slept. That doesn't happen, it is only occasional (AFAIK).
So, biologically, what is the true origin of this behavior?

FWIW, I am aware of the fact that answers on SE are well-intended to have a broad scope, but still, I feel necessary to point out my familiarity with Biology is quite basic and limited to as much as is taught in a typical high-school (to people who take up Biology as a chosen stream). Hence, I'll request the answerer the please point me towards some introductory literature, in case using more advanced terms is unavoidable. Thanks :)

These are called hypnic jerks, also known as hypnagogic jerks or sleep starts. They are normal part of the wake-to-sleep transition. Hypic jerks consist of non-periodic myoclonic movements, generally involving an isolated limb.
The exact physiologic origin of hypic jerks is unknown. We can say that they correlate with a particular waveform on the EEG known as a K-complex:

Picture from http://en.wikipedia.org/wiki/K-complex
K-complexes are a normal part of Stage II sleep and can evoked using auditory stimuli, even if sleep is not interrupted. In the case of hypnic jerks, the K-complex is usually followed by alpha (wake) activity. To my knowledge, there is no evidence that hypnic jerks originate in or are routed through the cerebellum. K-complexes themselves are related to cross-talk between the cortex and the thalamus, a circuit that doesn’t involve the cerebellum.
In addition to the EEG findings, it has also been shown that the jerks are accompanied by autonomic activation — transiently increased heart rate and respiratory rate. There is also an (unexplained) subjective aspect. You described it as feeling "as if you are about to fall off,” which seems to be consistent with the published literature on this. As mentioned in the review cited below, some people report a sensation of "falling into the void.”1
The clinical implications, in case you were wondering, are summarized well by Vertugno et al.:

Sleep starts are common physiological phenomenon affecting up to 70% of the adult population and their course is benign, resolving without any neurological sequel. Therefore, reassurance and counselling are all that is needed to treat the patient. Though an adequate explanation and reassurance may be sufficient, some patients may require a small dose of clonazepam (0.5–1 mg at bedtime) to ameliorate the symptoms on a short-term basis.

1. Vetrugno R, Montagna P. Sleep-to-wake transition movement disorders. Sleep Med. 2011 Dec;12 Suppl 2:S11-6.

You requested in a comment a reference to introductory material on the topic. What we know about the neuro-physiology of sleep is mostly based on the analysis of EEG (brain-wave) tracings. I therefore refer you to this introduction to sleep polysomnography if you would like to get a better handle on how scientists think about sleep.

Thanks for your response. I have +1'd it and will go through the linked articles a bit later (a bit short on time right now), and get back to you if I need any help in understanding them. I'm deferring the accept for until then, but I'm sure this is only temporary. Thanks again :)

@TheDarkSide Unfortunately, the Vetrugno paper requires access through a library (or paywall) for viewing the full text. It was the only review I found that includes significant discussion of the topic in a relatively recent issue of a top-tier sleep journal. If you're not able to access it, let me know and I can see about finding something else. The PDF of the polysomnography chapter should be viewable in full, though.

I do not think sleep starts are associated with sleep starts. K-complexes are a characteristic of sleep (Stage 2), although they can be seen is deeper stage 3 and 4 sleep as well. Sleep starts tend to occur during the wake-sleep transition. Sleep starts can also be "Hypnagogic hallucinations" which can vary to sensations of falling (common) to loud noises leading to the infamous "exploding head syndrome". Sound is not the defining characteristic of Hypnagogic hallucinations.  ;)  See https://www.sleepassociation.org/patients-general-public/exploding-head-syndrome/

Sleep starts can be exacerbated by caffeine and "stress" . See also - http://www.sleepeducation.com/news/2013/08/22/sleep-starts

@bodhi.zazen Re. your first comment - you’re confusing a lot of things here. 1) Yes, K-complexes are a defining characteristic of Stage 2 sleep, but they are also frequently associated with brief arousals (alpha frequency), i.e. sleep-wake transitions. 2) The literature about auditory-evoked K-complexes within sleep is extensive. 3) Hypnagogic hallucinations are REM-sleep phenomena, most often seen in narcolepsy, sometimes in sleep deprived young healthy people. Totally different deal. 4) Exploding head is different still, a type of HH but likely different mechanism.

@bodhi.zazen Re your second comment - agreed. The review cited above mentioned triggers: fatigue, stress, sleep deprivation, vigorous exercise, and stimulants like caffeine and nicotine.

Most K-complexs are not associated with arousals and not all alpha activity is awake. An awake rhythm is low amplitude mixed frequencies and the "alpha rhythm" is a relaxed rhythm with eyes closed. The alpha frequency seen with K-complexes has a completely different distribution as K complexes are over the central head regions and thus completely different from the posterior dominant alpha rhythm.

K-complexes can be evoked, but they are not a defining characteristic of sleep starts and it is not clear if the K-complex is the cause or the result of the sleep start, ie, just as they can be evoked by auditory stimuli, they can also be evoked by internal stimuli or the arousal of sleep starts.

Hypnagogic hallucinations are not always associated with Narcolepsy and the hypnagogic hallucinations seen in Narcolepsy are not really Hypnagogic hallucinations, they are REM sleep intrusions into either wake or light sleep and are detailed visual "dream" imagery. See http://www.sleepeducation.com/sleep-disorders-by-category/parasomnias/sleep-hallucinations/overview-facts . The main difference with Narcolepsy, other the the type of hallucination, is that the HH occur when Narcoleptic patients are AWAKE where in "normal" people they occur when transitioning into sleep.

Hypnagogic hallucinations is thus a non-specific term. In Narcoleptic patients they are intrusions of REM sleep physiology into wake or light sleep . In "normal people" they occur in light sleep, during the transition to sleep, and not associated with REM sleep or REM sleep physiology at all. There no evidence to support or refute that exploding head syndrome is or is not different from sleep starts. And I am not confused, I happen to know quite a bit about sleep ;)

Thanks very much for these inputs. I am accepting your answer since you pointed out a nice 'correlation'. However, I feel that the graph is not representing a correlation, but rather a direct response to the (unknown) source. That kick in the graph is the EEG equivalent of the kick we feel physically (rather an EEG representation of the same). That sentence "The exact physiologic origin of hypic jerks is unknown" seems overwhelming, but if that correctly represents the current understanding, there isn't any more I can expect from the answer. Many thanks again :)


text:
Finding intensity of selection against dominant homozygotes
I was looking at some Olympiad questions and came across the following:

If the frequency of a completely recessive allele is $0.2$ and it remains unchanged from generation to generation due to superior fitness of heterozygotes, then find the intensity of selection against the dominant homozygotes.

As far as I know, selection intensity is a quantitative measure of the superiority of the individuals selected for breeding. However, I am not really aware of how to compute its numerical value.
The best I could do was to assume that the frequency would be a ratio of the selection coefficient of recessive homozygotes ($s$) to that of the sum of selection coefficients of both recessive ($s$)and dominant homozygotes ($t$), i.e. $\frac{s}{s+t}$, but that doesn't seem to lead me anywhere. Also, I can't think of a concrete reason as to why the frequency would be of this form if it is actually.
Any suggestions/pointers would be much appreciated.


text:
Searching for comprehensive textbook
I am extremely interested in science in general and in particular biology. Due to a different choice of career-path I probably will not be learning any more biology anytime soon.
So I would love to get my hands on a comprehensive textbook biology which hopefully will enable a goal in lifelong learning of biology.
What are some good recommendations? I looked up biology textbooks on Google and found candidates such as Campbell Biology by Reece and Biology by Brooker. But as there are so many of them, I have no clue which one to get.
So, biologists of stackexchange, can you help me out?

Hello and welcome to SE Biology! A simple search in the SE would have revealed many similar questions! Please look at this link (http://biology.stackexchange.com/search?q=biology+textbook)

Is the there a specific area of biology you're interested in, or just general?

Try Campbell biology.....it covers almost all the topics under biology in a lucid way...also the book has packed quite a volume of info in it ranging from a beginner level to a fairly advanced level....excellent book also in matters of presentation & writing style so that one won't feel bored....

Pros:

Genetics ( both classical and modern)
Ecology (including ethology)
Evolutionary biology
Animal classification
Immunology

Cons:

Biochemistry ( it somewhat feels short)
Plant anatomy ( not adequately covered)
Plant classification ( same as above)

& the rest of the chapters are like animal physiology etc. they are mixed...like some
principles they have gone thoroughly...some others not...but it's acceptable as they have to cover everything in one book...
But of course it's my personal opinion...so before considering it I would rather recommend downloading the book in pdf format & have a look at it yourself...but I feel you won't be disappointed....


text:
Are these little white fuzzy insects "scale"? What species and what is their lifecycle like?

These appeared on three small, similar houseplants I bought about a month earlier at a nursery. There were dozens. I physically removed a few and just pruned stems that had many, and put the clippings in a plastic container with some water to keep an eye on them.
I noticed that they moved around each day and saw one moving in real time. Included are some top-side closeups and some from below through the wall of the plastic container.
Location is northern Taiwan in April, but since the source is a nursery they could be from elsewhere perhaps.
They're about 3 to 4 mm long, and all white. They are white, fuzzy and "pill-shaped" with little fuzzy extensions around their edges. From below they have six (short?) brown legs that are hidden when looking from above.
Question(s):

Are these little white fuzzy insects "scale"?
If so, what species and what is their lifecycle like? (should I be looking in the soil for the next generation?)

@JakobTougaard Wow I think you've nailed it! :-) https://www.alamy.com/close-up-view-of-female-cochineals-dactylopius-coccus-scale-insects-in-the-suborder-sternorrhyncha-image356065881.html

@JakobTougaard just asked Do cochineals ("scale bugs") form aluminium complexes themselves? Where do they get such large quantities so quickly and how do they handle it safely?

@JakobTougaard I have a lot better photos, some through a microscope, I'll upload a some in a few hours.

Mealybugs. They're small, sap sucking insects related to aphids, cicadas, stink bugs and assassin bugs. The name come from the coating of distasteful, powdery white wax they secrete as an antipredator defence. Squash them, as they reproduce and their feeding weakens the plant and can introduce plant viruses. These things are particularly damaging to fleshy, slow-growing plants like cacti and succulent euphorbias. Since your plant appears to be a poinsettia(Euphorbia pulcherrima), I'm not surprised.

This is great, thank you! Yes mealybugs seems to be the right call. I have some additional photos I need to upload that I took through a microscope but I'm sure it won't change the answer though it may make it easier to address "...and what is their life cycle like?" Generally Stack Exchange answers should include links to at least one or two supporting sources. Thanks!

Glad I could be of some help. Their lifecycle is similar to most other true bugs, being egg>nymph>adult


text:
Can some bacteria eat soap molecules in soapy water rather than get killed by it? How do they hang on to their surface lipids? Evolutionary advantage?
In my Chemistry SE question Quantifying soapiness; there's pH, pKa and pO2, is there a p_soap or p_surfactance? I explained that when I am too lazy or too much in a hurry to do my dishes right away I leave them full of soapy water so that stuff doesn't grow in/on the remainder of the food.
I was "yelled at" for not doing my dishes, yes even in Stack Exchange I get yelled at for not doing the dishes!
One reason forwarded in comments is that there is (or may be) bacteria that can eat soap molecules.
Is this true?
How do they not die in soapy water from having their precious membrane lipids removed?
Is it just a question of the level of soapiness being sufficiently low? Do they have unusually robust surface lipids or hang on to them more tightly?
Question(s):

Can some bacteria eat soap molecules in soapy water rather than get killed by it?
If so, how do they hang on to their surface lipids?
If so, did this offer some evolutionary advantage? ("bonus points")

Detergents are not disinfectants. They can kill bacteria but they aren't really designed to. They're designed to wash stuff away. Soaking dishes is probably better than leaving them dry and will probably slow the growth of many things, but it doesn't mean it's going to sterilize anything that is soaking in it. "How do they not die in soapy water from having their precious membrane lipids removed?" It might be false to assume they all have membrane lipids to remove.

The traditional, 1000's of years old soaps (sodium or potassium salts of fatty acids, used at least as early as ancient Egypt) are perfectly eddible not only for bacteria, but for mammals as well. Ever had your dog eat your soap?
Well, they may be too much alkaline for anyone's taste (or homeostatic equilibrium), but this can be compensated or in some cases lived with. The soaps used in the household or for hygiene purposes are never alkaline enough to burn your skin, so they are safe-ish for microorganisms as well.
Given enough water, these substance pretty much hydrolyse by themselves. The thin, barely visible layer the soap leaves over the water surface is pretty much the pure acid (the sodium ions are happy to dissolve to the bulk of water).
Other detergents (sulfonates, phosphates, etc...) have different compositions, but their common characteristic is the large non-polar part of their molecule that is still separable as a fatty acid. Om-nom-nom. The polar part of the molecule may be itself useful for microorganisms in one way or another (e.g. phosphates are of particular interest because they fertilize the open water bodies and algae grows more than it is acceptable).
Major detergent markets (EU, USA) even require biodegradability of the household detergents. The economy of scale means that you will get biodegradable detergents even outside of these markets. Nothing stops bacteria from starting biodegradation right in your kitchen sink (the osmotic pressure may slow them down, but only that much).

On the other hand, these microorganisms that can eat detergents cannot be really blamed for being pathogen for humans. If you are really lazy, leaving the dishes soaked can even help you do them later. The only real problems are the messy look, the smell and your life choices.

What happens to the microorganism's precious lipids? Given enough concentration of the detergent, the lipid layer will decompose. This is (one of the mechanisms of) how your skin dries when you do too much dishes. On the other hand, the outer cellular borders are not only lipids. There are proteins, glycans and other things that together with lipids make the cell not so much vulnerable.
The main factor one may expect to act on microorganisms subjected to common detergents is the osmotic pressure. The cells simply lose water. This slows down all the processes inside.

"...soaps used in the household or for hygiene purposes are never alkaline enough to burn your skin, so they are safe-ish for microorganisms as well." I don't believe that this is so conclusive. If I spill a jar of pickle juice or gin on my skin it is not burned, partly because my outer layer of skin is already dead, yet most bacteria will not survive those. Your answer is interesting but it has a lot of speculation and inference and zero supporting links. Can you support at least some of the most critical assertions of your answer somehow? Thanks!


text:
What type of spider is this? VA, USA
Spider found in Richmond, VA. Can anyone identify?


text:
Can 12 mitotic divisions produce 6000 nuclei?
The following quote is from "Principles of Development" by Tickle & Wolpert:

"After fertilization and fusion of the sperm and egg nuclei, the zygote nucleus undergoes a series of rapid mitotic divisions [...] The result after 12 nuclear divisions is a syncytium in which around 6000 nuclei are present in a common cytoplasm"

12 divisions (starting from 1 zygote nucleus) should produce no more than 212=4096 nuclei, not 6000. Is this just a simple error in the textbook? Alternatively, is there a biological explanation that makes the 212 estimation invalid?


text:
response elements in transcription regulation
I'm studying eukaryotic gene regulation and I want to know whether there are some instances where transcription factors don't need to bind to response elements to initiate transcription. RNA polymerase can directly bind to the DNA.
I can't find any evidence for this. Does anyone know of a case that exhibits this?


text:
DNA methylation in different positions
I'm trying to understand how does  DNA methylation and histone methylation status of promoters differs given their position in a gene? Does position affect whether they are repressive or activating?

For histone methylation , whether the marks are activating or repressive is determined predominately by which histone tail is modified at which position. DNA methylation by itself however is position dependent; in regulatory regions such as enhancers and promoters methylation tends to be repressive (at enhancers this is mostly mediated by being anticorrelated with the activation mark H3k27Ac) whereas within gene bodies DNA methylation is associated with increased transcription (Ref - http://www.cell.com/cancer-cell/fulltext/S1535-6108(14)00316-X )


text:
Confirming exon shuffling in a gene
I'm trying to confirm that the sequence of a novel gene is derived by exon shuffling between several different genes. I have the promoter sequence, gene sequence, and mRNA (with defined exon/intro boundaries). I've tried performing several database searches with the sequences, but each search produces a set of different unrelated hits. How would one go about using this info to confirm the exon shuffling hypothesis? Any tips are appreciated. Thanks!

please avoid cross-posting across Stack Exchange platforms: https://bioinformatics.stackexchange.com/questions/2323/how-to-confirm-exon-shuffling-in-a-gene

It's not clear what is 'several database searches with the sequences'. The most obvious solution is blasting your sequence so you can see which part can't be aligned and then blasting the rest. You can choose different implementations (megablast of blastn) and play with algorithm parameters because it may not work for you as-is. But it will work as-is if you'll blast exons separately. This way you can identify origin genes.


text:
Non-cumbersome respiration sensor for sleep study?
I'm working on a project where I collect ECG signal from multiple volunteers, derive ECG derived respiration(EDR) from the timestamped ECG signal and calculate the cross correlation between EDR and Respiration signals collected from NeuLog device which is treated as reference respiration signal. The problem is that the NeuLog moniter, although widely in use for monitoring respiration, is very cumbersome and uncomfortable for the volunteers to wear and restricts breathing. Is there any alternative respiration monitering devices which doesn't have to be strapped around the chest and less cumbersome to wear?
The following are the other requirements.

Respiration signal should be time stamped(to synchronize with ECG signal).
Minimum Sampling rate of atleast 5sps.
Should collect data offline for atleast 10 hours in single charge of the battery.

I found this device which seems to be more comfortable than NeuLog but it is not clear whether it measures only respiration rate or can also log Respiration signals along with timestamps.
If anyone knows any alternative products meeting the above requirements, please do share the details.


text:
Will bacterial promoter without either -10 or -35 sequence allow no transcription?
I have a strong constitutive promoter on a plasmid inside of E.Coli, which expresses a gene. Having either -10 or -35 sequence modified to random sequence, will it ensure zero transcription from that promoter?
Thanks.


text:
When do plasmids replicate relative to its host cell cycle?
For plasmids is so much shorter than their host cell's genome (about 1/1000 in my case), it will take only 1/1000 time for it to replicate.
With respect to cell cycle, when will that replication occur?

Description of the situation I'm facing:
I have a low copy number plasmids (pSC101) in E.coli, and I'm measuring a fluorescence protein expression level. The problem is, even if the plasmid copy number is known (N), depending on when it is replicated, the number of plasmid in my cell can vary. Therefore, I cannot directly infer expression level per plasmid. Higher expression level might just result from higher number of plasmids.
For instance, if it is replicated right after cell division, I will have 2N plasmids for the most of my cell cycle.
If on the other hand, it gets replicated right before cell division (and partitioning machinery delivers exactly half the number to each daughter cell), I will have N plasmids per cell for the most my my cell cycle.

So, when do plasmids get replicated?
I could not find a similar question here with search.
Thank you very much in advance.

I've found a nice review that has many details on plasmid replication in general, and several papers about pSC101 in detail, and I'll try to extract the key information from these papers.
First of all your plasmid as an ori region that contains so called iteron:

In many cases, the origin of replication contains directly repeated sequences, termed iterons, which are the binding sites for the plasmid-encoded Rep proteins and which have control properties. (...)iterons have been described for several replicons like P1, F, pSC101 (...).

pSC101 plasmid has three of these iterons present, along with a protein called rep that is necessary for replication. Besides these there are sequences that provide binding sites for host proteins such as DnaA and integration host factor (IHF).
Details of these can be found in this and this paper, both provides details on replication and the function of ori region in your plasmid.
As stated in this other paper, plasmid copy number is controlled by the plasmids themselves, that may vary on host type and growth conditions but:

At steady state, the 1 number of replications per plasmid copy is exactly
  one per cell generation. This defines the steady state as shown in Figure 1. It should be stressed that while this is true for the population, it is not for individual plasmids-these are selected randomly for replication.

So not all plasmid copies are replicated once per cell cycle rather random ones are selected and they replicate to maintain the desired number.
When your plasmid has reached its target copy number it will adjust its replication frequency to maintain this number. This is achieved by negative control loops. There are many ways to do this (repressor proteins, anti-sense RNA) or in your case iterons. These sequence along with the rep protein may inhibit replication if too much plasmid is present by a phenomenon called  “steric hindrance" or “handcuffing”. This happens because the rep protein is capable to bind two iteron, simultaneously.
At low copy numbers saturation of iteron sequences by rep proteins initiate replication, but at high copy number rep proteins tend to interact with each other and plasmids pair up through rep-rep interactions therefore cannot replicate. See figure below:

So, long story short: plasmid replication in part depends on host factors but plasmids have means to control their copy number, and once target has been reached they maintain this number in a stable form. I know this answer does not provide solution to the when part of your question, but it provides an answer to the practical part of your problem namely: plasmid numbers are quite stable after the target number has been reached. I hope this helps
EDIT: I've found this article http://www.ncbi.nlm.nih.gov/pmc/articles/PMC210920/pdf/jbacter00181-0364.pdf that says:

In all experiments, plasmids pSG21 (oriS only), F'lac (oriS oriV),pBR322,
  and pSC101 were capable of replicating at all stages of the division cycle,
  with no detectable differences in the patterns.

So bad news for you, because according to the paper above you cannot tell when your plasmid actually replicates. Yet still as the average copy number is quite stable due to reasons described above this may not pose a big problem. Keep in mind even if you have an extra plasmid for a short time that may still not cause problem, because transcription of your riporter gene, folding, etc takes time under which previously synthesized proteins might degrade.
However this paper says the F+ plasmid replication is cell-cycle specific, you may wan to give it a try.

Thank you so much for this help! Great to know the detailed mechanism of copy number control of pSC101 plasmids (iterons). Great papers, too. It will be great if I can also know when the replication happens, too. I have to estimate expression level per cell per plasmid and when I see twice as much fluorescence, I'd like to know whether expression level per plasmid actually went up or it's staying the same while there's just another copy of that plasmid. But thank you so much for this nice explanations!

@Neil - I did some editing, does this help you?

Yes, it is helping me greatly! Thank you so much. I'm trying my best to understand the new paper better to see if I should conclude the thought here or not.


text:
How much heme is in cooked pork and beef; why is cooked pork ("the other white meat") not red?
The new video See how Impossible Pork will make you forget about pig meat includes a very short discussion of

the addition of heme to the product to make it taste like beef
the deep red color of a heme solution
that pork is not nearly as red as beef, (after cooking it's essentially off-white)

Does pork (pig/swine muscle tissue) have substantially less heme content than beef (steer/bovine muscle tissue)? If heme is contributing to the flavor of cooked meats (rather than raw) such as pork and beef, why do they no longer have a red color after cooking?

Note that the muscle composition of farm pigs and wild swines will be very different.

Yes.
Pork has substantially less heme than beef (Cross et al. 2013).

As to why the red colour is lost, it is due to the Maillard reaction, by which the iron in the myglobin is oxidized from Fe(II) to Fe(III).  This results in a colour change in the meat (Tamanna & Mahmood 2015).

Sources:

Cross AJ, Harnly JM, Ferrucci LM, Risch A, Mayne ST, Sinha R. 2013. Developing a heme iron database for meats according to meat type, cooking method and doneness level. Food Nutr Sci 3(7): 905–913.

Tamanna N, Mahmood N. 2015. Food Processing and Maillard Reaction Products: Effect on Human Health and Nutrition. International journal of food science 2015: 526762. doi:10.1155/2015/526762

Thank you for the concise yet complete and well-sourced answer!

Sorry for being so concise; in a bit of a hurry.  :)  The papers referenced are really pretty good reads if you want more info.

I'll definitely check them out tomorrow; this turns out to be pretty interesting!


text:
Would chimpanzees and humans normally be in the same genus if we weren't so sensitive about it?
Listening to the BBC's radio program The Why Factor particularly poignant episode What Can Chimps Teach us About Politics? hosted by Professor James Tilley, I heard Professor Frans de Waal of Emory University's Yerkes Primate Research Center, and author of Chimpanzee Politics say:

The differences are so small; normally we would put humans and chimpanzees in the same genus, but because of sensitivities in the human species we’ve not done that.

I'm wondering if this is an opinion, or arguably correct. I understand that taxonomy is an "evolving" discipline, but are there scientific arguments or viewpoints that would suggest that chimps and humans would be in the same genus if not for public, social or individual sensitivity to the idea?

To the silent, anonymous "primarily opinion-based" close-voter; I've specifically asked for "scientific arguments or viewpoints" that chips and humans would normally be in the same genus in order to rule out individual opinions. The source of the quote is obviously someone with academic standing in primatology, I'm now asking for the scientific basis behind it, ergo, only answers that are not primarily opinion-based would be appropriate. Let's first wait for the science-based answer instead of invoking the insta-close option.

I'm not the "opinion close-voter" but it seems to me assignment to a particular taxon level, such as genus, is usually (always?) a matter of opinion, and not something with a firm scientific, factual basis.  That two species are related by common ancestry is subject to scientific assessment, but whether you designate  that relationship as being within or outside a particular an arbitrary taxon level like genus is simply an issue of opinion and judgement and not of real-world fact.

The designation might not be a simple, bright line demarkaction, but the data might exist to allow one to say "In these branches of the animal kingdom, species with the same degree of genetic difference are indeed classified as the same genus".  There might be enough examples to strongly suggest that human and chimps are treated in an exceptional manner.

@mgkrebbs If I posted the question "is assignment of an organism to a given genus purely a matter of personal opinion, or is there some well defined science behind it, albeit somewhat subjective?" would you be interested in posting an answer and seeing how it flies? Or I could ask something like "Is the advent of fast, cheap whole genome sequencing turning traditional taxonomy on its head?" I like stackexchange's question and answer format, allowing for multiple answers as well as comments and voting on those answers.

@swbarnes2: But how would a genetic criterion deal with extinct species, for which there isn't any genetic info?  Also, if humans and chimpanzees were to share a genus, why shouldn't gorillas and orangutans be included?

taxonomy-related: What’s in a Name? Taxonomy Problems Vex Biologists


text:
Any examples of a group of micro-organism that continuously spans two or more species classifications?
Are there any examples of a group of micro-organisms where two different, established species are designated and these two groups meet all aspects of the definition of species (perhaps can not reproduce with each other?), but it turns out that there is a continuous distribution of occurences of this group such that they can reproduce "locally" with nearby members?
I lack the sophistication in biology to know the best possible words to use here so some guidance is welcome, and since the concept of species classification has been around much longer than genome sequencing and analysis, the topic itself draws on concepts from several different centuries.
So I've draw a simple diagram with a 1-D simplified "spectrum" of genetic difference, whereas of course it would likely be multi-dimensional.

I think the biggest problem for this question is that most microorganisms only reproduce asexually (by copying themselves). At that point the definition of where one species ends and the next begins has to be done one either observable characteristics or on a sequence basis. At least for sequence based species classification a 'spectrum' is possible, but then the classical species definition doesn't make sense anymore.

@Nicolai It seems that I've seen too many Gary Larson cartoons; yes of course most do reproduce asexually. I wonder how to proceed — do you think the question is answerable as-is in some way, or should I modify the question? If you can expand on your comment a bit as an answer, that might be enough, especially if you touch on species classification in microorganisms. Or, I could just ask "how was species classification done for microorganisms before DNA sequencing?" separately.

For those who learned about biology sans Larson: (e.g. 1, 2, 3, 4)


text:
How many teeth can "African wild dogs" have?
The New York Times article In Mozambique, a Living Laboratory for Nature’s Renewal discusses reintroduction of what the article calls only "African wild dogs" into Gorongosa National Park in Mozambique.
I was taken aback by the "smile" of one of the dogs shown below. Though I'm not particularly familiar with canine dental situations, this looks like an awfully large number of teeth. Is there a known limit to the number of teeth wild African dogs (or any canine) can have?

above: "A wild dog in Gorongosa. One pack has been reintroduced, and a second will be brought in next year.CreditBrett Kuxhausen/Gorongosa Media, via Associated Press" Cropped, from NYTimes.

above: "Wild dogs, apex predators missing from Gorongosa National Park for decades, have been reintroduced and are slowly making a comeback, part of an ongoing experiment in reviving the park ecosystem after years of devastating war.CreditBrett Kuxhausen/Gorongosa Media, via Associated Press" From NYTimes.

I found conflicting information on different websites with a humanima article stating that they have 4 toes and 40 teeth (reference). However, multiple sources state that they have 42 teeth (reference 1, reference 2 and reference 3) with the different teeth being (i= 3/3; c=1/1; p=4/4; m=2/3) x2. I did search for official journal publications but could not find any.
However, since more sources state that there are 42 teeth, I am led to believe that 42 is the right number rather than 40.

Wow, thank you for the thorough and well-supported answer! Viewed top-down, human molars are roughly squarish. I'm having difficulty understanding from the photo in the question how each half of each jaw could only have ten to twelve teeth, unless some of them are extremely elongated along the jaw (front-to-back). Is that what's going on here?

@uhoh That seems to be the case. Here are some images of the skull. http://skullbase.info/skulls/mammals/african_wild_dog.php

Super, and yikes! Thank you for the additional info.


text:
PCR processes number of amplicons produced
Beginning with 600 template DNA molecules after 25 cycles of PCR how many amplicons will be produced?

This is a homework question, right? These are off-topic unless you show some effort solving them yourself.

yes it is . I thought the answer should be 2^26 based on the equation 2^N where N is number of cycles

This is a theoretical consideration, as PCR depends on a number of factors as optimal priming, salt concentration, enzyme activity, available dNTPs and so on. Ideally the number of DNA molecules is doubled with every cycle. So the general formula to calculate the number is:
$ n \times 2^{cycles} = $ number of DNA molecules at the end of the PCR
n is the number of molecules set into the reaction
So for our 600 DNA molecules with 25 cycles this would give:
$600 \times 2^{25} = 20.132.659.200$ or roughly 20.1 billion molecules of DNA.


text:
What is the difference between tonic and phasic firing?
I am reading about dopamine, and I have realized that dopaminergic neurons can fire phasically or tonically. What is the difference between these two modes of firing?

Tonic firing typically occurs without presynaptic input and can be viewed at as background activity. Tonic activity is often characterized by a steady action potential firing at a constant frequency. Note that not all neurons may have tonic activity at rest. It may serve as keeping a steady background level of a certain neurotransmitter or it can serve as a mechanism where both an inhibition or increase in presynaptic input can be transmitted. When a neuron is silent at rest, only an increase in presynaptic activity can be transmitted postsynaptically.
In contrast, phasic firing occurs after a neuron is activated due to presynaptic activity and it incurs activity on top of any background activity a neuron may have. It is typically restricted to one, a few, or a short burst of action potentials, whereafter the activity quickly returns to the resting state.
Reference
Tsai et al., Science (2017); 324: 1080-4

Could you please explain what causes tonic firing? I.e. how can a neuron depolarize itself?

@VivekSubramanian: cyclic changes in restig membrane potential or inputs from other neurons

@AliceD , from the paper you reference, both tonic and phasic activity seem evoked, instead of tonic activity being passive background activity. The definition I would extract from that paper is instead that phasic activity consists of faster firing, maybe only bursting, and tonic firing is lower-frequency firing:   Caption figure 2: "(D) Whole-cell recording of DA neurons showing spontaneous activity and tonic and
phasic firing evoked by 1-Hz and 50-Hz light flash trains, respectively". Or: "low-frequency tonic activity and phasic bursts of action potentials" (first page)

Maybe tonic = constant for a longer duration (like muscle tone), whereas phasic = in phases ?


text:
Where is pollenkitt secreted?
Where is the pollenkitt material secreted? I think the tapetum would be a good candidate, since it provides nutrition to the pollen grains.

This question may be closed, but I can't find the answer on Google Scholar. If it is closed as homework it seems to be difficult homework! I think this question deserves attention.

Thanks for paying attention towards my question. I really think it's tapetum but yeah I couldn't find any statement in support of this.

Pollen kit is secreted by tapetum

You'll find it in University Botany by Reddy shows up on first Google web search.

Yes it's Tapetum.Pollen Kit is made up of Hydrophobic pollen attractant and tryphine(A mixture of hydrophilic substances)

Hi Welcome to BIO.SE. We ask that all answers on this site provide support /references (from reputable sources). See here for a guide to writing good answers


text:
why are malarial parasites specific for anopheles
why are malarial parasites specific for anopheles mosquito. why do they need only anopheles, they just need lower temperature to complete their life cycle. all mosquitoes are cold blooded, so they can get a suitable environment in any of them, why only anopheles?

Did you look this up - research it - in any way? Can you provide some of the information you found? People (myself included) are happy to answer if the poster shows the research they've done. Thanks.

I looked this up but didn't get any satisfactory answer. I just want to know why their is specific relationship for their sexual cycle to complete. All they need is lower temperature because when they are inside human body the temperature is not suitable for the syngamy to occur that's the reason they go into anopheles' body but every other mosquito is cold blooded and is capable of providing the atmosphere for the process to occur

One major factor to consider: not all mosquitoes feed on humans. The malaria-carrying mosquitoes must. That's only one factor. There are many more. Saying you researched it and showing your research are two different things.

@anongoodnurse The Plasmodium falsciparium carrying mosquitoes must feed on humans, but there are other forms of (rodent) malaria. They still are carried by anopheles.

This isn't actually a bad question, although I agree it needs to show some effort. Short answer, though: they aren't. Avian malaria (Plasmodium relictum) is transmitted by Culex mosquitoes (and possibly by Culicoides biting midges, although there are some issues with that study). The reverse question is also interesting; why do arboviruses seem to be almost-exclusively transmitted by everything else? The only arbovirus transmitted by Anopheles is O N'yong N'yong virus (ONNV). Alain Kohl's group published a nice paper on this recently (http://www.ncbi.nlm.nih.gov/pubmed/25548172).


text:
Difference between taking tissue of cancer from secondary place or primary place
Are there any differences when a surgeon takes tissue from secondary place (for example from metastasis) rather then from primary place (from an organ where cancer is) for morphological research?

Are you thinking about differences between a primary tumor and one which has already spreaded? I am not sure if I understand your question.

Yes @Chris i'm thinking about that.

I would disagree a bit with the previous answer. There are absolutely differences between the metastasis and the primary tumor. One result of this is that people very rarely die of primary tumors, but rather from the metastases of those tumors. The primary tumors will be quite heterogeneous and contain largely cells that have not undergone steps necessary for migration like epithelial to mesenchymal transition. After cells have metastasized they will be separate from the original primary tumor, and contain unique genomes. Because this is the more 'progressed' group of cancer cells, these are often the cells that need to be targeted. So, determination of the proper treatment strategy should be done on the metastasized cells.

I'm not talking about treatment. I'm talking about taking metastasis for research to determine property of cancer. I mean determine whether cancer is malignant or not.

Then you might be getting a little confused with terminology, if the cancer has metastasized it is malignant.

By definition, a cancer which has spread to another site via the circulatory or the lymphatic system (called metastasis) is malignant. If a surgeon takes it from a secondary site, it is malignant.
In the past, there were times that a cancer was so undifferentiated that to determine it's source was not possible. As science (particularly genetics) and technology continue to advance, tissue of origin is more easily determined.

Are there any differences when a surgeon takes tissue from secondary place rather then from primary place for morphological research?

Theoretically, it seems as it shouldn't, but it can happen at times, because, for example, a carcinoma may contain a mixed population of cancer cells, while the metastatic tumor may be of only one type.
For research purposes - which is different from diagnostics - it depends on the features most desired for research purposes.
In the past, there were times that a cancer was so undifferentiated that to determine it's source was not possible. As science (particularly genetics) and technology continue to advance, tissue of origin
NCI Dictionary of Cancer Terms
Multicenter Validation of a 1,550-Gene Expression Profile for Identification of Tumor Tissue of Origin

I would ask this on Biology.SE, where there are many researchers. Shall I migrate it there?

@AlekoGharibashvili - Will do. Might take me a while because I'm a new mod. :)


text:
Why does the blend of many cicadas sound lower-pitched than individual nearby ones?
In the last emergence of Brood XIX, I noticed that the nearby cicadas made individual chittering sounds that you could hear against a more distant background of a warbling "flying saucer" sound. The flying saucer sound was fairly high pitched (around the C# an octave above middle C), but the individual cicada sounds weren't the same pitch - they seemed to mainly have a higher pitch but with lots of white noise.
Obviously, the more distant sound was the combined sound of all the chittering noises, but I'm curious if anyone has done an analysis of how the lower-pitched ambient sound is derived from the higher-pitched chittering sounds.
My guess is that the higher frequencies somehow dissipate more or are filtered out by the trees, but I would be really curious to know if someone has worked this out in detail. I realize this may be more of a physics question than a biology question, but I thought I would start here.
(Another reason I find it interesting is that I don't notice the same sonic phenomenon when the dog day cicadas come out every year later in the summer. I just hear the chittering sounds.)


text:
Which is better against genetic mutations? Asexual or Sexual Reproduction?
In terms of genetics, which type of reproduction is better against adverse mutations? I understand a bit of Muller's Ratchet—in which asexual organisms accumulate a number of deleterious mutations in their genomes. However, doesn't the crossover process and corresponding genetic diversity in sexual-reproducing organisms make them more susceptible to these mutations?

Mutations can be caused by much more than just recombinatory events--polymerase fidelity, DNA damage repair, even environmental factors can have a huge impact on DNA damage. While most DNA polymerases have an error rate of around one mutation per billion, there are different levels of fidelity among different polymerases (McCulloch and Kunkel, 2008).
Regarding the fidelity of crossover/recombination events, it is true that these events increase the likelihood of a lethal or detrimental mutation. However, recombination is not a random process. Recombination hotspots are chromosomal locations where the rate of recombination can be hundreds of times higher than other locations. These hotspots are generally in "safe" locations, not in the middle of a crucial gene, etc. There are also recombinase enzymes specific to certain sites of recombination.
As to "which is better", I don't think the answer is as straightforward as you might think. You might think a sexually-reproducing eukaryote with a very high-fidelity DNA polymerase and safe, specific recombination hotspots would be ideal. That situation is generally what we find in nature, so you're (probably) correct. However, at the other extreme, think of a virus*. Viruses have a much, much, much higher rate of mutation than eukaryotes--orders of magnitude higher. This is how a virus survives, basically out-evolving the host's defenses. A high rate of mutation works for a virus, and a low rate of mutation works for a multicellular eukaryote.
*Of course, there is always debate about whether or not viruses are alive. However, they definitely reproduce.


text:
What is 'independent assortment'?
What is the definition of 'independent assortment'. I tried researching this term but came back with two results:

alleles assort themselves independently of different alleles
the alignment of homologous chromosomes is random along the metaphase plate; resulting in the daughter cell inheriting either maternal or paternal chromosome based on 50:50

Which is the correct term?

The term was pioneered by Mendel, who had no knowledge of chromosomes, so definition 1 would perhaps be the best answer. However, we now know that definition 1 arises from definition 2 (chromosomes are inherited independently of each other) and from the fact that chromosomes recombine (cross-over).
That said, independent assortment does not apply to linked genes, which tend to be inherited together. That is, they are not independently assorted.


text:
What are some difficulties animals had to overcome to reproduce on land?
This is for AP Biology, but the assigned textbook chapter doesn't contain any information about the question.

What are some difficulties animals had to overcome to reproduce on land?

Some disadvantages I brainstormed are

the formation of bones—need for vertical structure and support against gravity (?)
development of lungs

Are there any more?
Thanks,

Are you asking about specifically reproduction or land-survival in general?

Are you thinking of vertebrates specifically? Or animals more generally (including insects, mollusks, etc.)?

Just reproduction. Hm, no really specifics—any animals.

I would have thought finding a way to get away from spraying a bunch of eggs on the water bottom, and then spraying them with a bunch of sperm and hoping for the best would have been the initial problem. Sea creatures that carry the developed eggs around would have been one approach (sea horse does that?)  Impregnating females to carry around eggs would have another approach (reptiles, then snakes on land for example). Eventually leading to live birth, and the mammals that returned to the sea? (dolphins, whales).

The disadvantages you mention have not much to do with reproduction, but with locomotion and oxygen absorption.
Difficulties to reproduce on land are the fact that aquatic egg-producing creatures typically lay soft eggs with porous shells to promote exchange of water and waste products with the surrounding water. Water is essential for growth as a typical creature consists for some 70% of water. Soft-shelled porous eggs when laid on on land dry out very quickly and are prone to predation.
The main adaptation to reproduce on land instead of water has been the development of the amnion. The amnion is basically a membrane filled with water (the amniotic sac) in which the embryo is immersed during development. Hence, you could argue that the transition to land in terms of embryonic development has never taken place, as the embryos develop in a protected aqueous environment contained within the amnion! The early amniotes laid eggs on land where the embryos develop, while the later ones such as humans carry their embryos/fetuses around. But early as well as late amniotes are characterized by a developing embryo immersed in a watery environment contained in the amnion. Other structures that aided the transition to land were eggs with hard shells, and the allantois. A hard outer shell in amniotes that lay their eggs on land  helps to protect them against drying out, the harsh terrestrial environment and predators. The allantois helps to exchange and store waste products produced by the embryo, a structure not needed when eggs are immersed in water and waste products can diffuse freely through a weak and porous shell.


text:
Testing monophyly from per site log-likelihoods without optimising branch lengths
How can I obtain per site log-likelihoods for a topology against an alignment without optimising branch lengths? (which software can I use to do this)
Per site log-likelihoods can be used for various tests of whether a topology fits the data in a multiple sequence alignment well using e.g. the Shimodaira-Hasagawa test, the AU test etc.
RAxML, Garli and FastTree and other software packages can calculate per site log-likelihoods given a tree, alignment and substitution model but all will automatically optimise branch lengths first.
I would like to test a tree in which a pair of sequences (A and B) are monophyletic, where in the maximum likelihood topology they are not. My problem is that when I infer a tree with a constraint requiring A and B to be monophyletic, the edge length is set to the minimum within the allowed precision. But having an edge length so close to zero does not make biological sense if the tree is describing a monophyletic clade for A and B: the minimum length of the edge must be equivalent to one substitution or character change, else A and B are in a polytomy containing clade with other sequences which is not the biological scenario I'd like to test (in that case there would be ambiguity regarding the relationship of A and B to other groups emerging from that polytomy).
So . . . I'd like to edit my constrained tree and increase the edge length to the A and B clade to the minimum one substitution length, then perform the AU test against the per site log likelihoods for that topology. But the above software optimises the edge lengths, resetting the edge length to A and B to effectively 0!
thanks

If you have the budget for it, I highly recommend Geneious for topology work.  It was a real saver for me on an epi paper last year.
Anyway, they allow for testing per-log likelihood without adjusting edge length.  If you want to throw up some dummy data somewhere I can throw up an example.
I have no connection or stake with the company, just happy with it.

It turns out the tests I mentioned (SH, AU) are strictly tests of topology, not branch length. So choosing arbitrary branch lengths as I proposed would bias the test (according to Prof Alexandros Stamatakis; I'm assuming choosing an arbitrary topology does not cause a similar bias, because that is what the test is designed to assess). Thanks for answering the question though.

Yep, that's why I mentioned without "adjusting" or scaling edge length.  I don't think you would ever want assign an arbitrary branch length, or at least I can't think of a reason to.

Because a bunch of adjacent internal edges of length zero makes a polytomy but a bunch of adjacent internal edges of non-zero length does not make a polytomy - it makes a series clades with events between them that may be inferred from the sequence data in the same way a particular topology can be. These are different biological hypotheses that you might want to test, in the same way assigning arbitrary topologies are different biological hypotheses.


text:
How to compare a camera and an eye
How could I compare what a normal eye can see to a camera lens?
I just went through a very comprehensive article @ CambridgeInColor, but I'm still not really clear.
When I take a picture with a SLR camera from an object about 30m from me: what focal length do I need to use, how should I present this picture to truly capture what the eye can see (because of the 40-60° that we see 100% everything)? And how should I print it to scale?
Are there any options so I can put a ruler, or a human being at a certain point to be able to show the differences?
I hope I'm clear here, but if not, please comment and I'll try to explain better!
What I'm aiming for is that I need a picture, but not a picture in itself, but more like what the eye will see at that position. Not what the camera registers.
Thanks

There are many questions similar to this posted on the SE Biology page (http://biology.stackexchange.com/search?q=camera+eye).

@Bez I of course did a search first before posting. But the only 2 closest related articles were something about sighted Ness and my question. So I believe the question is relevant. Please correct me if not.

What exactly do you wish to achieve here? I mean, what is the practical purpose of this question? As of now the question is kind of vague and a purpose-driven approach may yield more answers to this interesting question.


text:
Immortality Gene? Really?
I read somewhere in the internet and wondered if human genes have deactivated immortality genes locked somewhere in the DNA strand. Is this statement true? What does it mean for human lifespan?

"I read somewhere in the internet" -- please link to the specific claim, because this clearly doesn't have a shred of truth to it.  It will help those answering explain why it's not true.

The original article i was referring is unavailable but here is one claim.It could be a conspiracy theory, but one could never be sure with genetic engineering. http://www.livescience.com/6967-hang-25-year-wait-immortality.html

Honestly, I understand you are asking this question in earnest, but everything in that interview screams that that person is a crackpot.  Ten years into his research and I've never heard anything, so he's behind schedule!

I remember De Grey, he gave a TED talk 10 years ago http://www.ted.com/talks/aubrey_de_grey_says_we_can_avoid_aging?language=en. I don't recall him talking about specifically a gene for immortality but I guess this is the telomerase gene and in this case well it's very simplistic to say it's locked somewhere... If I remember well overexpressing this gene allowed to reconstruct the chromosome telomeres and a study in mice showed they would live longer. The problem is that telomerase only will not make any organisms immortal...

I looked up the subject of the interview you linked at livescience.com on PubMed, and looked back to about 2010 before giving up. There are 121 citations in that search, and nearly all of them are in Rejuvenation Research, a journal that he just happens to be the editor of. All of the references I looked up were quite obviously editorials, so it looks like this guy is just playing at being a scientist. Maybe he's good at synthesizing current research, but he sure isn't contributing anything original.

-1: You should add more information. At this moment it is difficult to predict what internet source you are talking about and therefore its authenticity cannot be verified. In general you should put in some effort before asking a question.

In tissue culture and cell engineering fields, the word "immortal" is often used to express something else instead of human or animal life spun. When you take cells from human tissues and grow them in test tubes--although flasks or dishes are used in reality--, cells stop growing after long term culture. They say it is cellular senescence. Several genes actually regulate this cellular senescence, and inactivation of these genes causes infinite cell proliferation. This is immortalization of cells. Then, cells in a human bodies are immortalized, do they get immortal? Probably, not. Cellular senescence partially explains senescence of bodies, but these two are different things. In human bodies, cellular immortalizaion occasionally occur. It is tumor pathologically.

The article probably had a scrap of truth to it. Ageing is not plastic and longevity can be altered in a variety of ways. Although caloric restriction seems to affect longevity the most, there are also longevity genes from a range of cellular processes that have been identified in yeast and mice, indicating that ageing is a whole system process. But none of those genes are "immortality genes". Finding and testing their effects in humans is difficult.
Here is a video on the background on ageing.
Related answer that you might find interesting.

I think you read about the telomerase: https://en.wikipedia.org/wiki/Telomerase
The chromosomes while duplicating, they loose some of the DNA segments from their ends, from the telomer. This is believed to have a direct effect on senescence.
The telomerase reproduces the end DNA strip of the chromosomes. This enzyme is found in active form in stem cells and in white blood cells.
The DNA sequence coding this enzyme is found in every cell, but in an inactivated form. Probably the article you are referring to, was talking about the telomerase, because it can be activated in almost every cell in our body. But this can lead to uncontrolled growth of the cells, and when this happens we talk about cancer.
More information at: https://en.wikipedia.org/wiki/Telomere#Structure.2C_function_and_evolutionary_biology


text:
Would biotechnology in agriculture actually decrease biodiversity, as many people say? Does it have to?
I've heard the claim that because farmers would be using the same seed, you would end up with an entire crop population that could be susceptible to a disease. Like if you had a diverse population of potatoes, not many of them could become blighted, but if you have only one kind of potato on your farm and that kind is susceptible to Phytophthora infestans, then all your potatoes would become blighted.
I was wondering:

Is this really how it works? Like once a seed with a desired characteristic is found, is it cloned? Or would they implement the same gene into many different crops?
If they do clone them, why couldn't they implement the same gene into a diversity of crops? Is it too costly?
Could one use mutagenesis to create diversity? If the seeds are cloned, could a certain number of the seeds be modified to try to account for natural diversity?


text:
A few questions regarding immunology
I know that there is a variable region on antibodies which can recognize a wide variety of antigens, and that germinal centers create more "fit" antibodies to respond to an infection.
So I was just wondering:

Does this process itself evolve? Only vertebrates have this type of immune system if I understand correctly, do we actually get better (faster/more efficient) at responding to disease?
Is there any antigen which antibodies don't recognize?
Can an organism be so efficient at this process of immune response, that it essentially never gets sick or dies of disease?
There are cases where organisms contain viruses which do not harm them. Could an organism have this relationship with all viruses? As in, no virus is actually a disease to them?

Your question(s) is too broad. You should narrow down to a specific point.

This is a pretty broad question, but I will try to give an answer:
This process will undergo further evolution over time, no question. It has evolved into the current state and there is no reason to assume that this ended. When there are mutations which prove advantageous, they will evolve. This may also involve a faster response time for example, but we can of course make not definite claims about it.
There are antigens which are not recognized by the immune system, the process is called molecular mimicry. In it, microorganisms mimic molecules or structures which are found inside the body of the infected person and which are therefore not recognized by the immune system (if the immune system recognized self-antigens, this leads to autoimmune diseases). Have a look at the references 1 and 2 for more details.
This is a rather theoretical question. Our immune system is really efficient in clearing potential threats before you get a real infection. You can see the difference when you compare healthy individuals with persons which are immuno suppressed because of a transplantation. These persons need to be very careful about their environment in avoiding the exposure to potential pathogens. And they easily get infections. Additionally microbes evolve to evade our immune system. So I think the answer here is no.
These are viruses which co-evolved with the organism, an example would be the ebola virus in certain fruit bats. Here it does no harm, while it is a big problem for humans. As there is a really, really big number of viruses available in nature, it is quite unlikely that we learn to tolerate all of them. Additionally viruses mutate and change over time, so we would have to learn again to live with them.
References:

Molecular mimicry
Molecular mimicry and immune-mediated diseases.


text:
Can you Transfer Cancer Between People via Saliva or other Bodily Fluids?
This may sound like a strange question. But could a Cancerous cell be transferred from one person to another from Oral contact e.g. Through Saliva, or other exchange of bodily fluids?
I know that other diseases from Bacteria / Viral can be transferred in this way, but does the same apply to Cancerous cells? - or would the recipient's body just breakdown and destroy the cancerous cells?

have you done any research on the topic on your own? simple googling might give an answer

Possible only if they share the exactly same HLA types. In other words, it is almost impossible.  It is taboo that researchers culture cells from their own tissues and experimentally transform the cells to get cancer phenotype. Such transformed cells could grow when the researchers accidentally contact them because rejection would not occur. But, I think oral contact would be safer than wounds.

Although transmissible cancer has been found in some species, such as Tasmanian Devils and clams, it is quite rare in most species. Certain viral and bacterial agents that cause cancer, however, can be transmitted. One example is HPV, which can cause cervical cancer

Cancer is successful at killing it's victims because it is genetically still very similar to the host.  The immune system does not respond to it sufficiently to eradicate the mutated cells and this allows it to grow out of control.
When dealing with any kind of transmittal this would be close to an organ donation.  Without a very close match, and Immunosuppressants the body will "reject" any cancer cells, and wipe them out.  Saying this here have been freak incidents where in an organ transplant scenario, cancer was transmitted.


text:
How can cane sugar sucrose be different from beet sugar in regard to carbon-13 content?
According to an article in SCIENZA IN CUCINA, by Dario Bressanini, le Scienze Blog content of $^{13}C$ differs in sucrose in beet sugar compared to cane sugar. What is this due to? Are there any similar examples?
Is the difference in synthesis enough to explain the difference?
One could guess that the weight of the carbon molecule is more critical in one of the synthesis chains.

@user438383 That looks like an answer, but you've posted it as a comment.

@user1136 I just asked another user to not answer in the comments, why are you now doing the same?

Hi, I don't think anyone is critiquing your question. Two different people have posted comments (now deleted) that started to answer your question, instead of answers, which is against policy at https://biology.stackexchange.com/help/privileges/comment . We're just asking them to move that to the Answer box instead, I think your question is good as is.

The differential uptake of different isotopes of carbon is covered well at:
https://en.m.wikipedia.org/wiki/Fractionation_of_carbon_isotopes_in_oxygenic_photosynthesis
Plants have a lower proportion of C-13 than atmospheric CO2.
The two mechanisms that cause this are the reduced diffusion speed of the heavier C-13, and an energetic difference in the chemical reactions that favours C-12.
In sugar cane (C4 photosynthesis) the carbon dioxide is captured in an additional step compared with sugar beet (C3 plant).
This capture step in C4 plants (using phosphoenolpyruvate carboxylase) is less exclusive toward C-13, so the carbon in these plants has detectably more C-13 than C3 plants.
This subsequently affects the isotopic proportion of all the carbon in the plant


text:
Isn't biological immortality strictly speaking impossible?
This question relates to both immortal cells such as cancers and organisms like the Hydra genus. Isn't it technically impossible for these "immortal" biological systems to live forever, even disregarding accidents and disease?
I am aware that they are considered immortal because they do not exhibit the usual degradation of functionality as they chronologically age. In cancer's case an up regulation of telomerase prevents the usual gradual depletion of DNA at the chromosomal ends limiting a cell's lifespan. But at the same time cancer cells and immortal organisms still undergo DNA damage and thus mutation (cancer cells even mutate faster as far as I know), wouldn't the stacking of these mutations at some point kill off the cancer cell line/immortal organism as some vital part of their metabolism is inevitably damaged?
Wouldn't true biological immortality require an organism with DNA that is either impossible to damage or if it could would always be perfectly repaired? (creating an evolutionary dead-end as well)

It sounds like you're actually defining immortality as perfect self-replication. With that definition, yes, it's practically impossible, as no DNA replication machinery is perfect. Is it a rhetorical question?  :)

@Roland It wasn't intended as a rhetorical question hahah, I'm just wondering if I'm missing something obvious. I read about achieving human biological immortality by engineering up regulation of telomerase and this question popped in my head as a caveat to human immortality.

Keep in mind that all living things are the result of an unbroken chain of replications going back to the first cells. If "immortality" is defined to include "the ability of cell lines to replicate indefinitely" (and if we bring in the "immortality" of cancer cells, then it is) then all evidence points to biological immortality being possible - I mean, not really, the heat death of the Universe will get us if nothing else does, but 3-odd billion years isn't a bad run so far. This is different of course from the question of the immortality of any given multicellular organism.

I don't think you're missing something. The word "immortality" is used to describe cell lines that have bypassed the normal replication limit of normal ("mortal") cells, but you're right it's technically not true. If you culture a cancer cell line for a very long time, it will degrade in various ways and at some point it will stop growing and die.

I think part of the confusion between where your question wants to be and a purely rhetorical question is that there are two different types of immortality here: perpetual life of an organism, like a human - who contains many cells that proliferate and die all the time, and immortality when referring to lines of cultured cells: the definition of an immortal cell line is a line which will not stop replicating due to intrinsic mechanisms to limit cell division. (edit: while typing this comment @Roland commented effectively the same exact thing)

Cancer isn't 'human' but more of a 'human-derived organism'. It in essence becomes a unicellular eukaryotic organism growing in the ecosystem of an animal (or a dish). As such consider that a group of cancer cells are just related to one another in the same way a colony of bacteria are and thus are 'immortal' in the same sense that bacteria would be considered immortal. Cancer cells are constantly evolving in the same way as bacteria. Immortality is more of a philosophical concept then a biological one down at the cellular level.

Good question.
There are many organisms that are technically biologically immortal. However, I would like to point out that the definition of biological immortality is this:

...cells that are not limited by the Hayflick limit, where cells no
  longer divide because of DNA damage or shortened telomeres.

(That's from here.)
So biological immortality doesn't really cover disease or physical trauma, which would actually include damage to DNA. I know what you're thinking: But wait, doesn't biological immortality literally mean cells that don't die because of DNA damage? Nope. Close, but no. Look back up at the definition. You probably caught it this time (by the way, it's not listing two different reasons (DNA damage and shortened telomeres), just rewording the Hayflick limit (DNA damage aka. shortened telomeres)). Biological immortality does not mean that the cell will not die because of excessive mutation (which would fall under physical trauma mind you, be it from chemicals, radiation, or just plain mistakes during replication), it means that the cell will not die from excessive programmed mutations, aka. its Hayflick limit, aka. telomere degradation. A molecular biology course summary from Berkeley says:

However cells that express telomerase still undergo cellular senescence in response to DNA damage, oncogenes, etc.

Ok, sidetrack time (go ahead and skip this part if you already know what telomeres are). A telomere is a repeated DNA sequence at the end of a chromosome that protects the coding regions from deletion (the reason for these deletions is complex and off topic, but long story short, RNA primers cannot attach to the very end of a chromosome, so a little of the lagging strand is lost during every replication). So the telomere takes the hit instead of the important coding DNA further up the chromosome (see this article.) As you can imagine, there is only enough telomere to go around, so cellular aging exists unless the organism has active telomerase, which is an enzyme that adds telomeres every time they are lost (see this article).
So, short answer, biological immortality is very possible in its actual definition (see above).
Concerning your definition (immortality regarding all mutations, programmed or otherwise), an organism comes to mind: Physarum polycephalum. It is biologically immortal in the way we have just defined, but also avoids DNA mutation by sharing DNA (constantly comparing and fixing sequences) among thousands to millions of nuclei through homologous recombination, which repairs DNA mutations at a freakishly high efficiency when you include millions of strands bearing what should be the same sequence (see this article). Physarum polycephalum is a slime mold, meaning that when cells meet each other, they fuse. This particular slime mold actually prefers to be a plasmodium, which is a constantly growing mass that is technically a multinucleated single cell but can grow to be potentially infinitely large as far as we can tell. Because of its extreme ability to correct mutations, this organism has been referred to as, exactly like you said, an "evolutionary dead-end." I'm sure it still sustains some mutations over a very long period of time, but you might want to check it out nevertheless.

Nice answer, +1! I recommend that you add some more references in the answer, like about telomeres and Physarum, etc.

Thanks, I do find it a bit weird that aging in this context is solely defined as shortening telomeres instead of overall DNA damage. Also that mold seems fascinating.

@another'Homosapien' Thank you. Done. And thanks for the italics, not sure how I missed that... :)

@KoenvdH My pleasure :) Keep in mind, that's just the definition of cellular senescence (aging). While we're pretty sure it has a lot to do with the aging of the whole organism, we still don't know for sure if that's the entire story. But alas, that is a discussion for a different question. To avoid confusion, slime molds are very inaccurately named; they are actually protists. They were named when we still thought they were fungi... But yes, they are quite fascinating. :)

The whole "science" behind telomeres is rather flaky, for example:
Is Telomere Length a Biomarker of Aging? A Review

Although telomere length is implicated in cellular aging, the evidence suggesting telomere length is a biomarker of aging in humans is equivocal...
They observed that the change in telomere length at follow-up was highly variable with some participants showing an increase in telomere length.

So like most questions in biology, there's no answer.
Also P. Physarum has many strains, it is in no sense an "evolutionary dead end" simply because it can't mutate.
http://www.genetics.org/content/78/4/1051.short

"There is no answer" is not an answer. A more accurate description of your situation would be "I do not know the answer, nor do I care to seek one out." In which case, it would be better to not answer at all. Regarding your links, see my answer. I said nothing of mortality rates, like the article you cited was discussing. Rather, I was speaking purely of cellular senescence, which was the OP's question. The correlation between telomere degradation and mortality rates has so many variables (disease, trauma, lifestyle, etc.) that it is very difficult to substantiate, as we see in that article.


text:
How is Cas9-gRNA-tracrRNA complex lysed in mammalian cells?
I am interested in degradation of Cas9-gRNA-tracrRNA complex. I would like to understand how do the cas9 enzyme, gRNA and tracrRNA degrade in mammalian cells (with references, if possible).

There has not been much research on this part of CRISPR-Cas system, as everybody is interested in geting gene editing done, but very few think about what actually happens to the things we leave inside. So, the mechanism of its degradation is not well understood. But there has been some research on this, which leads to the conclusion that the Cas9-gRNA, being a ribonucleoprotein (RNP), degrades by the normal protein degradation pathways, and is indeed very quick process. See this article:

By contrast, Cas9 RNPs are delivered as intact complexes, are detectable at high levels shortly after transfection, and are quickly cleared from the cell via protein degradation pathways...Second, rapid clearance of Cas9 RNPs from the cell may increase CRISPR specificity by reducing the amount of time that Cas9 is available for off-target cleavage...Cas9 RNPs are active immediately following transfection and are quickly degraded within the cell. These fast degradation kinetics enable Cas9 RNPs to modify target genes with reduced off-target effects.

For more information about RNP degradation, you can have a look at this article. An example of RNP degradation pathway is this too:


text:
How is the protease inhibited by lopinavir different in SARS-CoV-2 compared to SARS-CoV?
The protease inhibitor lopinavir, originally developed as a cure against AIDS and HIV, has been shown efficient against SARS Coronavirus SARS-CoV.

Dayer M R, Taleb-Gassabi S, Dayer M S. Lopinavir; A Potent Drug against Coronavirus Infection: Insight from Molecular Docking Study, Arch Clin Infect Dis. 2017 ; 12(4):e13823. doi: 10.5812/archcid.13823.

Why is Lopinavir not efficient against SARS-CoV-2? Is there a difference in the gene encoding for the protease?

Is there a difference in the gene encoding for the protease?
This paper by Wu et al. annotates the SARS-CoV-2 genome and compares its divergence from other coronaviruses, which may help answer your second question.
This annotation includes 16 genes for non-structural protein ("nsp"). Supplemental materials for this paper indicate that all but two of these proteins (nsp7 and nsp13) have amino acid substitutions between SARS-CoV-2 ("2019-nCoV" in the paper) and SARS-CoV.
The gene nsp5 encodes 3CLpro (chymotrypsin-like cysteine protease), so there are differences there.
Literature suggests nsp5 and other non-structural proteins are potential targets for a number of antiviral therapies.
Another paper suggests further that lopinavir targets nsp3 products, among other proteins, in use against SARS-CoV:

Lopinavir’s possible target is Nsp3b, Nsp3c, helicase, NRBD or E-channel with the mfScores of –158.050, –189.140, –114.018, –171.127, and –221.785, respectively.

The nsp3 gene contains a papain-like protease 2 (PL2pro) domain. Supplemental materials from the first linked paper suggest nsp3 has a different amino acid sequence between SARS-CoV and SARS-CoV-2.
It might be worth digging into the Wu et al. paper and the raw annotation data to look at what those a.a. substitutions are, to see if that might help in determining why lopinavir is not as efficient at inactivating PL2pro and reducing levels of the novel coronavirus.
It may also be worth considering the target itself. Going back to the Nature Biotechnology article:

But Erik De Clercq, of the Rega Institute for Medical Research in Leuven, Belgium, says that in searching for or designing effective drugs against COVID-19: “We should stay away from antivirals known to be acting at targets not playing a role in the replication of coronaviruses.” Such drugs include penciclovir, which is targeted at the herpesvirus DNA polymerase, and lopinavir/ritonavir, which are targeted at the HIV protease. Instead, he would favor targeting a virus-specific protein such as the RNA-dependent RNA polymerase, noting that coronaviruses do not contain or use a reverse transcriptase.