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Why don't Australian magpies in Tasmania swoop at people?
I'm currently living in Tasmania (Australia) and I have noticed that Magpies don't swoop at you here, yet they do in other parts of the country.
Just wondering: does anyone know why?

@havefun I reckon he means Tasmania

If it is Tasmania are we talking about Magpie (Pica pica)? (an introduced species). Or Magpie-Lark? Or the Australian Magpie?

@havefun OP is talking about Cracticus tibicen, the Australian Magpie. Indeed, there is no record of swooping in Tassie for 2017, 2016 or 2015. That's a very interesting question. Josh, just a tip when you come back to the mainland: make friends with the magpies. They have a very good memory, and they can recognise a face for years. I'm friends with all the magpies in my street (friendship = food), and I was never attacked.

It appears that there are attacks in Tasmania.There is a different agpie alert page for Tasmania. Still very few though.
https://www.magpiealert.com/SwoopingMagpieMapTAS.php

Tasmania has been inhabited for 40,000 years. Chances are, they used to trap them with nets, hit them with sticks, or throw boomerangs at them. Some genetic factor can also have made them larger and bolder on the mainland, like hybrid vigor from a large population. Different prey and local predators could have also made them swoop less often.

I cannot give you a proved explanation of why magpies don't swoop in Tasmania. Nevertheless, my goal here is corroborating your impression with some data, and indicating a possible cause.
Aussie Magpies and swooping
Australian magpies are not the same species of European magpies (Pica pica). Actually, they are not even corvids. They belong to the Family Artamidae, and their scientific name is Gymnorhina tibicen (synonym: Cracticus tibicen). Here is a male magpie (you can tell he's a male by the white colour in his back):

Australian magpie in Victoria
Magpies are territorial birds and in the breeding season (which is right now, as I write this, in September) a small percentage of the males become quite aggressive towards people approaching the nest.
According to the Wikipedia link above:

These magpies may engage in an escalating series of behaviours to drive off intruders. Least threatening are alarm calls and distant swoops, where birds fly within several metres from behind and perch nearby. Next in intensity are close swoops, where a magpie will swoop in from behind or the side and audibly "snap" their beaks or even peck or bite at the face, neck, ears or eyes. More rarely, a bird may dive-bomb and strike the intruder's (usually a cyclist's) head with its chest.

Cyclists are well known targets:

As a personal and anecdotal note, I have to say that I bike during the breeding season and I was never attacked by a magpie, nor I've ever seen a magpie swooping.
No swooping in Tasmania
Your claim sounded quite incorrect to me when I first read your question. After all, the magpies in Tassie (short for Tasmania) and the magpies in the mainland belong to the same species (G. tibicen).
However, after some research, your claim seems to be correct: there is very few, if any, report of magpies swooping in Tassie.
For instance, this is a chart from the Magpie Alert website:

As you can see, there is no registered attacks in Tassie (TAS) from 2013 to 2017.
And here is a map of the attacks (the online version is here):

Most of the attacks happen in Victoria and New South Wales. However, besides Tasmania, you can see both in the chart and in the map that there is no attack registered in Northern Territory (NT) and New Zealand (NZ) as well.
That data doesn't prove that there is no swooping in Tasmania, but it does show that, somehow, Tasmanian magpies behave differently. Maybe they are more shy, or maybe the males over there perform other behaviours to drive off intruders before swooping. It's also possible that the explanation is completely different: maybe people in Tasmania don't like to go online and complain about magpies.
A possible cause
The Tasmanian magpie (G. tibicen hypoleuca) is the smallest magpies of all in Australia. Besides that, it is the magpie that forms the largest groups (Kaplan, 2004), with as many as 15 individuals.

Tasmanian magpie, also a male
Coincidentally, magpies form smallest groups exactly in the areas of higher incidence of swooping, like Victoria and New South Wales. The possible correlation among those variables (swooping rate, body size and group size) is something that is still to be investigated.
Conclusion
However, regardless the actual explanation, the fact is that the number of registered attacks in Tassie is, indeed, smaller than in the mainland. After doing a lot of research, the explanation for this remains unknown to me. Let's wait for more answers.
PS: as I said in my comment, magpies are not that aggressive: they are very nice birds and very intelligent ones as well. So, one way to avoid attacks from the magpies in your area is becoming friends with them: magpies have a good memory and they can recognise a face after years. So, if you become friends with your local magpies, they probably won't attack you if you get closer to the nest. By the way, the best way to making new friends is with food (that works with humans too).

Source: Kaplan, G. (2004). Australian Magpie: Biology and Behaviour of an Unusual Songbird (Australian natural history series). CSIRO Publishing.

A little late with this response but here goes. My home in Tasmania is a semi rural bush block that is also home to a primary magpie family (3 to 5), and also home to an ever changing peripheral group (upwards of 20) of older juvenile magpies. Although the magpie family make it clear the patch belongs to them, they show their superiority more with irritation, the odd sneaky peck or two, than outright aggression. As long as the other magpies defer to them when they're all in the same vicinity peace reigns.
My theory is the family, who I have a close relationship with, know I wouldn't be happy if they attacked other magpies, so they keep their disdain fairly low key.
They proved this recently when next door's free range chooks were causing a problem. I only had to chase them away for a single day before the 'family' took over and chased them away for me. But, even then, non contact swooping was applied.
Tasmania is filled with low key people who have time to take the time...just a guess, but perhaps this friendship factor is the key to the lack of magpie swooping in the state. Or, more likely, Tasmanian magpies have simply evolved to be a less aggressive breed.

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As someone who moved from WA to Tasmania 18 years ago, I discovered the Tasmanian magpies to be much more wary of humans that others I have met.
They very much kept their distance for many years. Traditionally many Tasmanians have an old fashioned approach to nature. In previous years I suspect a swooping magpie would simply have been shot and the birds have learned to keep away from us.
On the mainland you have large cities, with many parks and open areas. Ideal for magpies and full of humans. You also have lot's of cycleways and people moving about. Tasmania has a lower population, many rural areas and less of the territorial intrusion sort of behaviour that magpies resent.
I was working on a Tasmanian university campus and from my office window I often saw the local magpies swooping cyclists. Open areas, strangers moving about, the birds took exception. I was never swooped because I was recognised.

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I have been a cyclist in Tasmania for decades and until recently had never been swooped by a magpie.
In November 2020 I rode the "Tassie Gift" bike-packing event and was swooped and chased at Caveside on my way to Mole Creek. There were multiple aggressive birds over about a 10km stretch and I was hit on the helmet twice as I tried to outrun them.
Then again a few days later on the trip on my way towards Cressy I was attacked again. They seemed very angry and followed and swooped for a long distance.
So unfortunately I can confirm that they do indeed swoop in Tassie but only in certain places.
They have not swooped me yet on my home trails around Launceston. But sometimes I can see them looking at me intensely and I wonder if they are thinking about it.
I hope they are not all starting to learn this dangerous and disturbing behavior.
A few hours after the second attack I saw one flat on the road that had been squashed by a car. Oh what joy and mirth that bought me, cop that you f^%ker may many of your mates meet a similar fate.

Welcome to Biology.SE! Please take the [tour] and then consult the [help] pages for additional advice on [Answer] effectively on this site and then [edit] or delete your post accordingly. This seems more like a comment on the question rather than an answer, and, while anecdotes are potentially interesting, answers are much more likely to receive a favorable response they include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion and thus not appropriate for this site. Thanks!


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Sexual reproduction in organisms with 1 parent
An organism that carries out sexual reproduction with itself,  for example a flower with both the anther and stigma,  does it actually contain 2 sets of genes in order to produce genetically dissimilar organisms or do it just leave the offspring to become genetically dissimilar through random crossing over during miosis?

Your second piece is correct: dissimilarity is produced through meiosis.
from The evolution of meiotic sex and its alternatives

Strikingly, almost all forms of uniparental reproduction do maintain
  meiosis, but abandon just outcrossing. Hence, the paradox of sex in
  eukaryotes must focus on the purpose of meiosis.

What do you mean by abondoning outcrossing?

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How to determine the primary Uniprot accession number from a list of accession numbers?
Given a list of UniProt IDs that are linked to an Ensembl ID, is there a way to systematically determine which is the primary accession number with no other information?
According to ExPasy

Researchers who wish to cite entries in their publications should always cite the first accession number. This is commonly referred to as the 'primary accession number'. 'Secondary accession numbers' are sorted alphanumerically.

But what if the order has been jumbled or compiled from a different source and resorted.
For example:
Ensembl:
ENSMUSG00000035642
Uniprot:
Q8R0P4, Q8CF11, D6RJK8, D6RJJ4, D3Z442, D3Z1Q3, D3YZD8, D3YY39, D3YX09, D3YWY5
This question is cross listed on the Bioinformatics stack-exchange.

You might get a better answer to this at the [Bioinformatics.SE] site. Perhaps you should select the curated entry?

I think there is an issue with the terminology. The "primary" accession number, is the first accession number in cases where an entry has more than one accession number, as described in http://www.uniprot.org/help/accession_numbers:

Entries can have more than one accession number. This can be due to
  two distinct mechanisms:
a) When two or more entries are merged, the accession numbers from all entries are kept. The first accession number is referred to as the

‘Primary (citable) accession number’, while the others are referred to
  as ‘Secondary accession numbers’. These are listed in alphanumerical
  order.
b) If an existing entry is split into two or more entries (‘demerged’), new ‘primary’ accession numbers are attributed to all

the split entries while all original accession numbers are retained as
  ‘secondary’ accession numbers.
Example: P29358 which has been ‘demerged’ into P68250 and P68251.

Both reviewed and unreviewed entries can have primary accession numbers.
What you probably mean, as previous posters understood, are accession numbers of reviewed entries as opposed to unreviewed ones.
In that case, you can indeed add "reviewed:yes" to your query, e.g. when you are using the UniProt ID mapping, http://www.uniprot.org/help/uploadlists

Swissprot is the reviewed section of Uniprot's holdings. TrEMBl contains everything else.
Q8R0P4 or Mth938 domain-containing protein (AAMDC_MOUSE) is the reviewed Swissprot, aka reliable, identifier.
When searching in Uniprot you can filter to only see Reviewed/Swissprot identifiers; see the top-left corner of the link above.

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Is this not a moth?
I apologise for the terrible photographs. I tried many times and can not shoot better ones.
I came back from vacation and moths (I assume) came creeping out of two packages containing oatmeal and rice respectively. I bought pheromonic traps for moths attacking food stuffs, but they have not caught a single one, although they are inches from it. So, I wonder, are these no moths:
Here slain:
[]
Here alive:

I notice they don't match the colour of any food stuffs moth mentioned here.
The slain moths wingspan (distorted as it is) equals the width of my thumb.

Well, they are definitely moths of some sort, but I wouldn't dare identifying them from those photos (maybe try in better lighting?). Since they came out of food packages, that makes me think it's likely that they live there. Have you checked for larvae? I'd recommend sealing the packages.

It is a moth.  Width of the thumb is big for a moth that attacks food, at least in the US.  Pheromones are specific to specific species of insects.  Otherwise you would show up ready to mate and find something of a different species waiting.  You could freeze the packages for a day or 2 to kill anything in them.

@Will thanks. Already threw away everything I thought they could reach, but I am still worried


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Stem Cell Replication
Reading from the internet, I've come across quotes that said stem cells have the potential to replicate indefinitely. However, there are other sources that say cells that are specialised will have their telomeres shortened each time the cell undergoes cell division until it renders them unable to reproduce.
I would like to ask if stem cells that replicate in terms of self-renewal will have their telomeres shortened as well to a point where they can only renew themselves a set number of times before they cannot undergo cell division anymore.
Thank you.
[P.S. I'm no biology student, just a curious person seeking answers, hence do forgive me if this is supposedly a basic question. I've tried looking online for answers but it seems quite difficult to get a satisfactory or targeted answer.]

Telomere shortening is intrinsic to the process of replicating linear DNA (termed the end-replication problem). Adult stem cells that rapidly proliferate express the enzyme telomerase which is capable of lengthening shortened telomeres, thus allowing theoretically indefinite replication.
Further reading: Telomeres of Human Chromosomes

On which signal do stem cells replicate? is the presence of telomerase (from external sources) the only signal?


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Do GPCRs have 7TMHs?
I've screened a non-redundant set of GPCRs acquired from UniProt. I found a handful of examples of record IDs that contain more than the 7 TMHs. For example Q89609 and P20905, both of which have been manually reviewed to some extent.
For an idea of the variability in the GPCR family, below is a screenshot from a Clustal Omega alignment comparing P2095 to a bonafide human GPCR. There are ~16 indels of varying length.

Also, when blasting against SwissProt, the 2 hits that appear are also GPCRs with the same function from mammals but they have the expected 7 TMHs.

Is it possible for GPCRs to contain more than 7 TMHs, or is it a case that the annotation is incorrect?

How big is the sequence homology to the GPCR that definitely have 7 tm-domains?

This is from the reference given in the SwissProt entry:  The predicted structure of the 5HT-dro receptor reveals... eight putative transmembrane domains instead of the expected seven I don't have journal access right now, but the paper may be insightful.

@Chris I've compared one to a bona fide GPCR, however, the sequence variation in the GPCR family makes this a tricky question to answer. Also, sequence homology is rife with errors when examining TM proteins.

@canadianer Thanks for this. Evidently, my question is long standing from the 1990s! Originally I suspected SignalP had made an error and the first TMH would be cleaved, but that paper suggests it's the second TMH that is not found in other GPCRs. I'll give this a thorough read.


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The onset of hair loss in men
I've seen men starting to lose hair in almost all ages. Why is the onset of hair loss in men different? Is there a normal distribution?

Mostly it is because of the scalp and a decrease in the hair follicles ability to maintain production of sturdy hair (keratin along with melanin for hair color). In some cases, it is also genetic such as in Male Pattern Boldness.
Hair thickness changes with age. Hair is made of many protein strands and a single hair lasts between 2-7 years on your head. The hair then falls out and is replaced with a new one. How much hair you have on your body and head is also determined by your genes. With age, the rate of hair growth also slows down. Source
I would say however that the major impact-factor ought to be testosterone production especially in the case of MPB. More specifically DHT (Dihydrotestosterone) which is a derivative of testosterone. The amount of DHT is higher in balding scalp than non-balding ones.
In addition, it has been shown that the number of DHT receptors on the hair follicles also increases in balding scalps. Also, blocking the conversion of testosterone to DHT delays progression of hair loss and onset of MPB. That is why DHT is usually held responsible for miniaturization of hair follicles leading to hair loss, and this can happen at any age based on the DHT amount, but usually happens as we get older. Source
Testosterone is mainly found in man, but women certainly do produce it, even though it is present in minuscule amounts. Under normal conditions, women have a very small fraction of the level of testosterone that men have. However, even a low level of it can be converted to DHT and trigger hair loss in women. Source


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How optimal are the distances of voltage-gated ion channels on axons?
In both myelinated and not-myelinated axon segments ("axons" for short) there are theoretically maximal distances of voltage-gated ion channels beyond which propagation of the action potential would break down because the potential arriving at the next ion channel would be too weak to open it. (In myelinated axons it's about the distance between the nodes of Ranvier.)
In not-myelinated axons this distance is smaller, in myelinated axons it is greater.
Compared to these theoretically maximal distances there are the real distances between the ion channels (smaller for non-myelinated axons, greater for myelinated axons), resp. their mean distance along the axon.
My question is: How strongly do the real (mean) distances of ion channels deviate from the theoretically maximal ones? An axon with greater mean distance than the maximal one would not work very well, an axon with a significantly (and unnecessary) smaller mean distance would waste resources and would possibly produce distracting interferences.
Side question: What's "the" standard deviation of the mean distance of ion channels (nodes of Ranvier)? ("The" because there may be differences between types of neurons/axons.) Are there numbers available?

Cool question. I don't know if anybody looked into this. Keep in mind that the variability in the action potential and state of the axon will degrade the reliability if set exactly at the theoretical optimum assuming no such variability.

It is a cool question... but I don't think it's answerable.  We'd have to study a given neuron (potentially in a given species) with a given number of sodium channels per node, a given radius, etc... at which time you could do experiments and/or calculations.  If you fail to take these factors into consideration, each local "spike" will vary in how much it can effect the next node and the "maximum distance" will be subject to a large variation.  For example, in a larger neuron, the sodium has more space to diffuse cross-sectionally, leaving less sodium to diffuse laterally.

@rotaredom It may be answerable if that research has already been done.

@rotaredom: I visited your profile and clicked "This user". Maybe you cannot (or at least did not try to) imagine what complicated psychological effects it may have for a user to surprisingly find him- or herself as someone else's hero. I would suggest not to play with this - it's somehow rude and cruel.


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What predates on cactus in the Atacama desert?
Introduction
Last week, I was in the Atacama desert where I've seen many cacti. Some / many of them were seemingly suffering from predation. Most of predation seemed to be on cardón, often restricted (but not only) at the interface between the woody bottom part and the green spiny part. It looks like a big piece (maybe over 300 $\text{cm}^2$) of the flesh was bitten away. Unfortunately, I do not have a picture.
These cacti have very long spines and it was unclear to me what predator could maintain selection for cactus lineages to produce that many large spines.
In the desert, I have seen rabbits, guanacos, small birds, vultures, large black coleoptera and butterflies.
Question
In the Atacama region,

What species predate on cacti?
Is there a single species that causes most of the predation on cacti?

What does it look like? Are there pieces bitten/picked out, scratches?

In North America, bighorn sheep are known to eat Ferocactus sp (barrel cactus) by "pawing and butting at the cactus" (according to Warrick and Krausman, 1989). Were there any animals around that could do that?

Guanacos probably! I just had a hard time to imagine so few guanacos making so much damage to so many cacti. Also it was surprising to me that guanacos could deal with those spines but I guess that if bighorn sheep can, why guanacos could not!

I agree with @Remi.b. I would just also note that I have seen similar damage on candelabra (Browningia sp.) in northern Chile, where an apparently similar-sized wound was effected by perching raptors (scarred by talons). I am pretty sure that one of them was a variable hawk and another a mountain caracara. Also, you likely saw vizcachas, not rabbits!

Short answer
This type of herbivory is probably from feral livestock, especially donkeys.
Long Answer
There is video footage of guanacos eating flowers off of cacti in the Atacama. For example, an image capture of a Getty Images video:

 Credit: BBC Natural History
This type of florivory has been documented in related species of cacti as well (e.g., see Gomes et al. (2016)1)
However, I could find little evidence about guanacos eating the trunk of these cacti (especially to the degree you describe).
Actual herbivory of Echinopsis cacti has been reported in multiple publications. For example, Peco et al. (2011)2 cite feral livestock as a major source of herbivory in columnar cacti in South America:

Columnar cacti are an important feature of the arid “cardonal” landscape in South America. The predominant columnar cactus in the southern zone is Echinopsis (=Trichocereus) terscheckii. At some sites, the species suffers considerable trunk damage, attributed in previous studies to feral livestock grazing (donkey and cattle).
In a previous study we found that damage intensity on Echinopsis terscheckii trunks correlated with abundance of livestock dung in their surroundings, but not with the abundance of guanaco dung (Lama guanicoe) (Malo et al., 2011; Novillo and Ojeda, 2008). Futhermore, E. terscheckii was found in summer or winter donkey diet but not in guanaco diet in the study area (Reus pers. comm.). Direct observation of donkeys feeding on columnar cacti suggests that this species is the main cause of stem damage

See this National geographic video explaining how camels and other related animals handle eating spiney cacti. (Specifically, they accomplish eating cacti through the use of hardened papillae guiding the spines down the throat vertically).

Works Cited:

 Gomes, V.G.N., Koroiva, R. and Araujo, A.C., 2016. Vertebrate florivory on the short-columnar cactus Echinopsis rhodotricha K. Schum. in the Brazilian Chaco. Plant Ecology, 217(12), pp.1481-1487.

 Peco, B., Borghi, C.E., Malo, J.E., Acebes, P., Almirón, M. and Campos, C.M., 2011. Effects of bark damage by feral herbivores on columnar cactus Echinopsis (= Trichocereus) terscheckii reproductive output. Journal of arid environments, 75(11), pp.981-985.

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How can cancer preventing genes from animals be transferred to humans?
I recently read this non-peer reviewed article that states that the prevalence of cancer in crocodiles or elephants is really low, much lower than humans.  It is said below

A team of researchers in the US looked closer, and found an abundance of a gene called TP53. This gene is known for its ability to repair damaged DNA and thus halt the spread of cancer, and it's some 20 times more common in elephants than it is in human beings. It appears elephants have developed more of these genes as they've evolved, in part to protect calves born to older mothers
"These findings, if replicated, could represent an evolutionary-based approach for understanding mechanisms related to cancer suppression," says the report, published in the Journal of the American Medical Association.
Naked mole rats are even more miraculous - they never develop cancer, even when scientists try and induce it artificially. What appears to be happening, at least according to a recent study, is that the mole rats are using natural mechanisms to clamp down on the spread of cancer and fight back against the mutation.

Question
So why is it that these genes cannot be transferred from animals to humans? Maybe when the baby is at fetus stage?  What are the current problems/limitations and if possible, how would scientists transfer these genes?
My logic is that since mice and elephants are both mammals,  it should not be too hard to achieve this.

The link is https://www.sciencealert.com/these-animals-can-t-get-cancer-and-scientists-think-they-could-hold-a-cure

While this research is interesting and might help curing cancer at some point, it's not a ground breaking revelation.
The gene in question here is TP53, coding for the very-well known tumor supressor protein p53. Humans do have this gene, but apparently elephants hav acquired multiple copies of it (~20) during evolution and that might explain why they don't get cancer so easily.
The problem of testing this is not a technical one. Using modern genetic engineering methods it should be fairly easy to multiply the gene in human or mice embryos, or introduce the additional variants from the elephants. Someone might already be planning to do that in mice.
For use on humans however, this is highly unethical. Without proof that these gene copies actually prevent cancer (and one observational study is not a proof), you can't just use a new medical treatment. Secondly this treatment would require genetic modification of an embryo (because its actually cancer prevention, not acute treatment) and that is illegal almost everywhere on earth (even genetic modification of somatic tissue for cancer treatment is just now becoming an experimental therapy).

Putting All moral issues aside, what would be the answer to by question?

There may be pleiotropic effects of these genes that are damaging to humans.  So, for that reason, it is a technical issue.  It is an ethical issue largely because it is still a technical issue and would require experimentation (on mice).

@user35897: Have a look at this article: http://www.nature.com/news/2009/090520/full/news.2009.493.html. Cancer suppression might be just one effect.


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Cloning problem. Digestion test at the end of the cloning is always negative
I have a problem with my cloning, I'm trying to clone a 483 pb in a pSecTag vector with restriction sites HindIII and BamHI. Here are the procedures I'm doing:
•   I introduce the restriction sites BamHI and HindIII into my insert by PCR with Pfu (blunt end polymerase) and gel purified it.
•   I clone my insert in a pJET1.2/blunt vector. I get enough colonies and I tested few of them with an internal insert primer and a vector prime via PCR. The results are positive.
The problem came when I digest my insert from pJET and try to clone it in a pSecTag vector.
•   I digest my insert and the vector with HindIII and BamHI in Buffer Red during 1.5h at 37ºC (fermentas). I purify the insert and the vector from the gel and checked that all fragments run at the correct size on a gel. All correct.
•   I do the ligation (T4 DNA ligase) using a 5:1 Insert:vector and less tham 100ng of total DNA. The ligation (20ul) is performance at 22ºC for 30 minutes.
I get few or not transformant colonies. When I get colonies, I tested them by PCR:
**
•   With internal primers, the result are positive

With a primer for the vector the result is negative.
The strangest thing is that when I use pJET primers that do not anneal in the pSecTag I get positive results.**

For transformation i'm using chemocompetent DH5-alpha, with a heat-shock of 42°C at 45 seconds. I tested the bacteria with a plasmid before using them.
I change condition several times but always obtain the same result. I follow all the protocols but I don’t get my construction.
Anybody knows where the problem is? Thank you.

It sounds like the insert is still in pJET doesn't it? Is there any chance you mixed the two vectors somewhere in your purification step after the digest? Instead of PCR you could try doing a restriction map.

Thanks for your answers Yes, the insert is still in the pJET. One of the times that this happened to me, I digested it and the bands corresponded with my insert and the pJET. I sent it in sequence and the result was the same. There is no possibility of having mixed the vectors, given the problems I have had I have been doing the steps on different days to avoid any kind of misunderstanding in the manipulation.

Why are you blunt cloning it in to pJET first?

I can't digest my PCR insert directly, the RE can't cut.

Even minute amounts of undigested vector will contaminate your transformation. You could PCR amplify your insert from the pJet cloning plasmid and then digest the PCR product with BamHI and HindIII. In order to get rid of the pJet template either gel purify the digested insert, digest pJet with some times which cuts it multiple times (less preferable) or put everything on a column and hope that pJet is diluted enough (less time consuming but a bit risky).
The other thing you could exploit is that pJet is ampicillin resistant while your target vector is also Zeocin resistant. If you add Zeocin to your E. Coli it will kill a pJet positive clones while sparing the pSecTag positive clones.
Your insert is fairly small so using a bit more DNA than usual won't hurt.
If you can post some pictures of your gels this might be helpful as well.

Thank you very much. I was thinking of doing that, amplifying by PCR, digesting and purifying it from gel. Or also try sequential digestion. I must have some contamination but it is difficult to know where.
I would upload some photo of the gels but I do not know how.


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Could a horse-sized duck fly?
The more general question would be whether or not one can scale an animal to some other size and preserve its properties. The method of scaling is by volume, scaling all dimensions by the same factor. The mass is scaled so that the mass/body ratio is constant.
Some factors I thought about:

How does muscle strength scale with muscle size?
Could the joints support the new mass?
If ducks rely on aerodynamics/wind to fly, how does the size change influence those factors?

You weren't by any chance inspired by this song to ask yourself that question? http://www.the-burgenland-bunch.org/Songbook/Fing-mir-eine-Muecke/Fing-mir-eine-Muecke.htm

Why a duck? Is a duck the most aerodynamic bird?

Horses can only gallop for 15 minutes before being exhausted, and can only canter for fairly short periods of time.  It would flap it's wings very slowly and there would be insane energy demands on a single wing flap. to lift and maintain 300 kilos by 10 meters takes horse muscles about 5 minutes at maximum output and then the horse is very exhausted.

I don't know why a duck.

The largest flying bird ever was probably Argentavis, which weighed about 70 kg, far smaller than a horse but still pretty impressive:

A duck scaled even to 70 kg wouldn't be able to fly since it wouldn't have the same relative wingspan.  A 1 kg duck has a wingspan less than 100 cm; volume (and weight) increase as the cube of dimensions, so a 70 kg duck would have maybe a 4-meter wingspan, whereas Argentavis was nearly double that (around 7 m).
The largest flying animal we know of was probably Quetzalcoatlus, or perhaps one of the other Azhdarchid pterosaurs, which were definitely horse-sized depending how you measure:

These pterosaurs were comfortably over 250 kg, which puts them into small-horse range, so something that is "horse-sized" could definitely fly.  However, these are very differently shaped and scaled from ducks, as you can see.
One important difference is probably that pterosaurs launched from the ground using their wing muscles -- quadrapedal launching -- whereas birds use their legs; heavier leg muscles needed to launch a big bird are wasted weight in flight, while heavier wing muscles needed to launch a big pterosaur remained functional in flight. That re-emphasizes that big things are not just scaled-up small things, but need to reshape their bodies to cope with their size; the square-cube law is just part of it.

One response to your first question: Muscle strength depends on the cross-sectional area of the muscle, as it depends on the number of fibers. Therefore, it is increased by the square of the muscle diameter. On the other hand, the mass of the muscle increases in the third power when the diameter increases. So, a large muscle has less effect per kg than a small.

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


text:
Determining water movement in Cells with Same DPD
A cell has OP=10bars and TP =5bars .other cell has OP =15 bars and TP =10bars. DPD of both is same ie.5bars. So how do we determine in which direction water will move?
OP is osmotic pressure. TP is turgor pressure. DPD is Dossusion Pressure Deficient.

Please type the full form of those abbreviations.

@JM97 Done. All Full Forms Added.


text:
How is "firing together" detected in Hebbian learning?
I assume, that the signal that forces a synaptic receptor/ion channel complex to change its behaviour (i.e. strengthening in the course of upregulation) must be the combination of the state of the complex ("occupied" or "open" or any other state except the ground or rest state) and an extraordinarily high membrane potential at the complex (caused by a retrograded action potential).
The not-ground state indicates that the presynaptic neuron recently has fired, the potential indicates that the postsynaptic neuron recently has fired. According to the rule "fire together, wire together", both conditions must be fulfilled for Hebb-like strengthening to occur.
I assume further that the membrane potential that triggers the upregulation of the complex must be significantly higher than the typical post-synaptic potential generated by the synapse, otherwise activation of the synapse alone would suffice for strengthening to occur, which violates Hebb's rule.
Is this way of thinking essentially correct? Or is strengthening triggered by other signals than the ones mentioned above?

Are you looking for an explanation of the biology, or something else? It sort of seems like you are trying to derive biology from logic rather than logically understanding biology; that's a good way to generate hypotheses but might not be the best approach for understanding what is already known about biology.

Not from logic, but from what I can imagine: How can a receptor be upregulated but only shortly after (or while it is "active") and shortly after its neuron has created an action potential? (The first it "knows" by its own state, the latter it "knows" from the membrane voltage at its location. So my imagination goes. Both together result in the physical process of upregulation.) But of course, I am looking for an explanation of the biology.

The dynamics of Hebbian or associative synaptic plasticity are thought to be governed primarily through the function of the NMDA glutamate receptor. The short answer is that you are basically right on all counts.

Figure of the NMDA receptor present the nervous system.
By Blanca Piedrafita [CC BY-SA 1.0 or CC BY-SA 2.5], via Wikimedia Commons
The NMDA receptor is a non-selective cation ionotropic receptor. The reversal potential of the NMDA receptor is around 0 mV, in contrast to the resting membrane potential of a 'typical' excitatory neuron which is around -70 mV. This means that a pretty strong stimulus is required in order for the NMDA receptor to be activated. Whereas some current can pass through the channel upon binding of its preferred ligands (glutamate or glycine), the pore is normally blocked by a magnesium ion. This mechanism confers some degree of voltage-dependent regulation of ion flow through the channel. When a strong stimulus raises the membrane potential at sufficient levels the magnesium block is lifted, allowing more current to pass through. The slow kinetics of the NMDA receptor allow the temporal integration of incoming signals. This makes the NMDA receptor function as a coincidence detector or AND gate. There are many more known details about the mechanisms involved but the above should suffice to answer your specific question.
Further reading: https://en.wikipedia.org/wiki/NMDA_receptor

At first glance I am not quite sure, if your answer covers (subjectively) the details of my question, but I am confident and will have a closer look. Thanks anyway!

If you feel that you need more info, let me know and I will update my answer.

Thanks for the offer, but it will take some time to formulate my concerns. Let me first digest your answer.


text:
Which enzyme curdles milk in human infants?
Following, this question -
Do humans produce rennin?
Rennin does not exist.
And
What inactivates pepsin in infants?
Rennin exist.
What do I know is-
Rennin is found in calves and acts on milk to curdle it.
Pepsin acts as rennin at pH of 6-6.5 and curdles milk.
Humans have pepsin, in infants as well as adults. Pepsin can perform both functions in humans.
So, in infants, is curdling of milk done by rennin or the rennin like activity of pepsin?

@JM97 I read that answer before, but it says rennin exist in infants while in my question I am following a link which advocates, it does not. In, this post I wish to culminate both these, link together what really perform this function.

@David Please dont make this post duplicate to 2 posts that advocate 2 opposite things..

@Anubhav Please see the EDIT in another homo sapiens answer.

@AnubhavGoel — The two posts that between them certainly cover your question do not advocate anything. They ask questions. The answers may express different opinions or assumptions, but that is par for the course. It would perhaps be better if those two questions were merged to provide a more useful single resource, but that may be difficult to do now. You are asking for a clear cut answer when the answers to the other questions indicate there isn't one. I suggest you read them carefully and take from them what you can. Then it hardly matters which your post is classed as a duplicate of.


text:
Can photorespiration do any good?
When CO2-levels are to low plants start to photorespirate instead of photosynthesise. This cost them losses in energy, and adds CO2 to the atmosphere instead of O2.
I wonder if the photorespiration is entirely "bad" for the plant or is there any beneficial outcome as well?

Honestly, I do believe that photorespiration has hidden advantages for plants. Yet, the answers to this question will most likely be primarily opinion-based.


text:
Plants and Specialised Cells
Would the number of specialised cells in a leaf decrease if the plant was located in a shadier area? I thought it would decrease as there would be no need to store as much food in the plant and that the plants usually take nutrients from the surrounding environment. However, I don't know if this is correct; it would be nice if someone could provide a better/correct deduction or explanation defining the difference in the number of specialised cells in the leaf in shadier areas.


text:
Why do some yeast flocculate on top an other at bottom?
When fermenting beer normally after the fermentation has completed the yeast flocculate and drop to the bottom. However occationally they form a foamy layer on top of the beer.
The difference is maybe strain dependent. But exactly what is it that makes the yeast drop to the bottom or raise to the top of the beer?


text:
What's the difference in roles of GATA-2 and BMI-1 in guiding Hematopietic cells?
I've discovered that hematopoietic cells become lineage-positive (Lin+) and go down the path of becoming lymphoblasts and myeloblasts, and that both BMI-1 and GATA-2 are transcription factors that play a role in that.
What is the specific difference in the role of BMI-1 and GATA-2 in guiding a hematopoietic cell down either of those lineages?


text:
Which predator raises its tail to signal no threat?
A guy in a bar once told me that there is some animal which raises its tail when at a watering area in order to signal to the other animals that it's not going to attack. He told me this as an argument to justify humans eating other animals.
Is this true that some animals do this? If so which ones? Links to video evidence would be extra appreciated.
Cheers,
Steve

Hmm.. it could just be me, but that sounds slightly unusual -- that a predator would be inclined to tell other animals "don't worry, I won't attack you". There could however be a stance of the predator that prey interpret to be the most relaxed, comfortable position of the predator, and therefore is least likely to attack while in that position (a position where the tail would be oriented upwards). Anyone agree? Disagree?


text:
Do humans secrete and detect pheremones?
Many animal species are capapble of secreting and also detecting pheremones from members of the same species, which relay messages and signals such as indicating sexual readiness.
Do humans do the same thing? Are humans capable of communicating in this subconscious fashion?

Yes, humans can secrete and sense pheromones, e.g. female tears dampen male sexual arousal.
Science 2011, 331(6014), 226-230
But then on the other hand, a key gene in mouse sex specific behavior (TRPC2) is a pseudogene, i.e. it is inactive, in humans.
Nature 2007, 448, 1009-1014
If you look at the references in those papers you will probably find a lot more examples.


text:
Excitability of neurons
[The following includes a) two specific questions (at the end), b) an attempt to capture a dispositional concept (excitability) in geometric and physical terms.]
I assume that "excitability of a neuron" is a reasonable concept (and measure) to distinguish neurons: there are (as will be seen) neurons that are more or less excitable (in a quantifiable way).
What does "excitability" mean?
Excitability $E$ may be operationally defined as the sensitivity of a neuron to excitatory synaptical inputs. Mathematically stated: as the (decimal logarithm of the reciprocal of the) proportion of excitatory synapses that must be simultaneously active (i.e. generate an excitatory postsynaptic potential, EPSP) in order to collectively evoke an action potential.
Let $N$ be the number of all excitatory synapses of the neuron, $n$ be the the minimal number of simultaneously active synapses that is needed to evoke an action potential:
$$E = \log \frac{N}{n}$$
If the proportion is 100% (all excitatory synapses must be active), $E =  \log (1) = 0$, if it's only 10%, $E=1$ (higher excitability), if it's 1%, $E = 2$, and so on.
How to determine $E$ for a given neuron? With the operational definition given above:

Count the actual number $N$ of excitatory synapses.
Estimate the minimal number $n$ of simultaneously active synapses that is needed to evoke an action potential (by repeated experiments).

Especially the second number $n$ will be quite hard to achieve experimentally. But there is an alternative way to estimate this number, given a simplified model of the neuron:

All synapses have equal (mean) distance $r$ to the axon hillock
(where the action potential is generated).
The EPSP generated at a synapse is $u$.
The EPSPs travelling from
the synapse to the axon hillock have a constant decay constant
$\alpha$.
The threshold value for action potential generation is $\theta$.

When $m$ synapses simultaneously generate an EPSP of size $u$, these EPSPs will sum up at the axon hillock to
$$ U = m\times u\times 10^{-\alpha r}$$
Only if $U \geq \theta$ an action potential will be generated, that is, the minimal number of simultaneously active synapses to generate an action potential is
$$ n = 10^{\alpha r}\ \frac{\theta}{u}$$
With this we can estimate the excitability $E = \log\frac{N}{n} = \log 10^{-\alpha r}\frac{N\ u}{\theta}$ by
$$E = -\alpha r + \log(N) + \log \frac{u}{\theta} $$
$\alpha$, $u$ and $\theta$ are more physical constants (more or less the same for all types of neurons?), $r$ and $N$ depend heavily on the arbitrary geometry/morphology of the neuron (especially do longer and more strongly branched dendrites have more synapses).
My specific questions are (please feel free to answer only with "yes" or "no"):

Has the property of excitability (in the operational sense above) been investigated a) for single neurons, b) for morphological types of
  neurons?
Is there an observed significant correlation between morphological type and excitability? Note that larger dendritic trees have larger
  $r$ (decreasing $E$) but also larger $N$ (increasing $E$).

(Final remark: The relation between $r$ and $N$ of a neuron is partially reflected in the structure – especially the degree of branching – of its dendritic tree.)

Excitability has definitely been tested and measured, but I'm not sure about your exact definition (sort of hard to prove a negative).
For differences in "excitability" across neuron types, I can think of two general approaches.
1) You could simply consider the firing rate and define cells as more "excitable" simply if they fire more or have a lower current threshold (though one must be careful in interpreting the actual "mV" value of threshold, because resting potential and input resistance are crucial and thresholds are dynamic).
These parameters have nothing to do with the number of synapses on them or the number of synapses it takes to fire; if you focus too much on these parameters you risk making a comparison that isn't all that helpful (see the analogy below). This approach is most suited to comparisons across cell types.
2) The second type of excitability concerns the intrinsic properties of a cell: what is it's input resistance, spike threshold, how much current do you need to inject at the soma to evoke a spike, etc. These properties can indeed vary across cell types, but you really have to think about it in the context of (1) to avoid the same problems with the analogy below. A cell might be near threshold but receives very small inputs; should that cell be considered more excitable than another?
Instead, it makes more sense to think about changes of excitability: "how does Manipulation X affect the excitability of Cell K?" If it changes the amount of current you need to inject to the soma to evoke a spike by depolarizing the cell or increasing the input resistance, you would say it increases excitability. This is, in my experience, by far the primary way in which "excitability" is discussed in neuroscience, rather than as a factor that varies across neurons. I did a search on Google Scholar for "neuron excitability": every one of the first 20 results was using it in the context of a change in excitability from one condition or manipulation to another.
A tangential analogy (the problem with your proposed definition of excitability):
Your proposed definition of excitability is a bit like measuring income based on paycheck frequency or number of digits on the check. You could certainly do comparisons between jobs on those merits, and in some cases they might be valid for what you'd normally think of as "income", but as soon as you move between countries (i.e., brain regions or cell types) currency changes, and suddenly the number of digits doesn't help because you don't know if you are talking about British pounds, US dollars, or Brazilian real. And even within a population, if the paychecks come weekly rather than monthly, the same face value of a check means a totally different annual income (i.e., if a cell has synapses that are rarely active, they contribute less to depolarizing it than synapses that are active all the time).
Contributions to excitability
Your question proposes that morphology is a defining characteristic of excitability. In a previous question you asked, I directed you to a review by Magee, J. C. (2000). Dendritic integration of excitatory synaptic input. Nature reviews. Neuroscience, 1(3), 181. - this review is applicable here, too. Active conductances in the dendrites and variation of synaptic properties with distance from the soma (larger, faster EPSPs the further from the soma you go) act to regularize the influence of EPSPs with distance, so you cannot rely only on passive properties. That also means you can't simply assume that a cell with lots of synapses far from the soma is not excitable.
However, there are definitely differences in firing rates and firing thresholds across neuronal subtypes, and you can take these to mean differences in excitability. There are many papers that talk about the diversity of intrinsic properties or firing rates of cells. I'll list a couple here for further reading:
Llinás, R. R. (1988). The intrinsic electrophysiological properties of mammalian neurons: insights into central nervous system function. Science, 242(4886), 1654-1664.
Izhikevich, E. M., & Edelman, G. M. (2008). Large-scale model of mammalian thalamocortical systems. Proceedings of the national academy of sciences, 105(9), 3593-3598.
It's also important to recognize that excitability is dynamic and cells that are highly excitable in one state may not be as excitable in another state, even though their morphology does not change.

I am glad you mention Llinas: I just started reading his I of a vortex.

Thanks for your demanding answer, anyway. I'll try to make the best out of it.

Careful with Llinas, I link to him with caution. He's a good scientist and easy to read, but in his reviews and books he is definitely writing from a persuasive angle. I don't mean that in some nefarious way, but he definitely has an opinion in mind that he's trying to convince you about; not everyone in the field would agree with everything he tries to convey.

I am careful, and know what you mean - but he is not the only one. Do you know of one prominent author to which your precautions don't apply?

Getting off topic here, but I think the distinction is more of writing style; some write like they are telling you the truth and don't really give away that there is another way. Such writing is often the most compelling. Others write intending to relate the state of the field, including the controversy, and make their opinions more obviously opinions. Of course caution is always warranted, but I mean to suggest that, at least in my experience and opinion, Llinas likes to start with the premise that his thinking is correct without much service to the possibility he is not.

(again I'm talking in terms of books, not necessarily his science)

I (believe to) understand what you mean, completely and in every respect.

And I totally agree with your (hidden) criticism.

Let us continue this discussion in chat.


text:
Help id-ing creature
I know. This is going to be extremely difficult without a picture. But bear with me here, because I haven't seen it afterwards. I hope somebody can give me a list of possibles.
I was taking a stroll down the street when I saw this creature. Maybe two feet long. It was black, with a tail about the size of the tail of a cat. It had catlike paws, which were not that big. Its face was pointy, with a reddish nose and brown eyes, with a whitish area of fur above the eyes. Ears were small and curved at the end. It was hiding in a bush, and did not seem to run away when I checked it out. When I got up, it made a sharp screech and ran away.
I'm from Kerala, South India. Thanks in advance.

Sorry, bit I think that this is more or less impossible without an image.

sounds like a mongoose or a civet, which species is hard to guess there are several species of both in India, and they come in a variety of colors and sizes. In the mongooses the color can vary a lot even in the same species. One easy way to tell the difference is civets have cat like ears while mongoose have short rounded ears.
But here is a picture one at least one species of each, since their body plant does not vary much even if their color and size does.
Indian Brown Mongoose,

Sri-Lanka Mongoose

Asian Palm Civet

Yes! That's it! I think I saw an Asian Palm Civet.

Indian tree shrew

Is that the guy?

Nope, this is not it,


text:
Why do retroviruses go through a DNA stage to replicate their RNA genome?
Why do retroviruses (e.g.HIV) convert their RNA genome to DNA (using reverse transcriptase) and then transcribe it back into viral RNA (and translate that into viral proteins). Surely to replicate their genome it would be simpler to use RNA-dependent RNA polymerases as RNA viruses like Measles Virus do.

Biology isn't as stringent as quantum physics, but still, "everything which is not forbidden is allowed." Retroviruses use reverse transcriptase because a) they can and b) it works. You can get into complex evolutionary arguments about comparative benefits, but ultimately retroviruses stick around because reverse transcriptase works well enough for them to continue to survive. Evolution isn't goal oriented - it doesn't seek simplicity just for simplicity's sake. What works, works, and what doesn't, doesn't.

I now feel my previous comments were based on a misunderstanding of the question. On this basis I have withdrawn them, answered the question, and reversed my close vote. The question is still very basic, but I can see how you might have become confused if the subject was not introduced to you properly.

I have changed your title and question to clarify  it as several people have been confused by it. If this is not what you meant could you please elaborate.

I am going to focus the answer on mainly "why HIV virus has evolved such mechanisms to go from RNA to DNA and back to RNA when it could simply use the first RNA to make its copies". While others have already discussed the broad point, I will discuss more about the details. There are a few points which might support this, all of which basically come down to evolution.

Increased Mutations: the process of conversion of viral RNA to DNA is carried out by the viral enzyme reverse transcriptase. The point here is that this process of reverse transcription is extremely error prone (Zheng et al, 2005), which increase its chances of evolving drug resistance and other abilities.
Recombination: again, the enzyme reverse transcriptase possesses ability to cause recombination of viral DNA. During recombination, the nascent DNA can switch multiple times between the two copies of the viral RNA (Charpentier et al, 2006), known as copy-choice recombination, and can rapidly shuffle the genetic information between the parental and progeny genomes.
Post-transcriptional modifications: after the viral DNA is completely transcribed, it undergoes splicing to form mature mRNA. These mRNAs lead to production of viral proteins Tat and Rev. Accumulationof Rev inside nucleus allowes the full mRNAs to leave the nucleus and form viral genomes or structural proteins Gag and Env (Pollard et al, 1998). Thus, reverse transcription is vital for the virus.

References:

Zheng YH, Lovsin N, Peterlin BM (2005). "Newly identified host factors modulate HIV replication". Immunol. Lett. 97 (2): 225–34.
Charpentier C, Nora T, Tenaillon O, Clavel F, Hance AJ (2006). "Extensive recombination among human immunodeficiency virus type 1 quasispecies makes an important contribution to viral diversity in individual patients". J. Virol. 80 (5): 2472–82.
Pollard VW, Malim MH (1998). "The HIV-1 Rev protein". Annu. Rev. Microbiol. 52: 491–532.

"extremely error prone (Zheng et al, 2005), which increase its chances..." - Do viruses - retroviruses -  have anything better, any proofreading at all? (cp. "what works, works")

I'll assume that "better" here means "better than other RNA viruses". In that case, I don't think so (I haven't looked into it, but coming from the observation that a lack of proofreading is somewhat beneficial for the virus, I think it's safe to deduce that the retroviruses would stay away from things like proofreading. Also, I doubt there would be quantitative studies regarding comparative analysis of proofreading activities of retroviruses and other RNA viruses).

Much later, from DNA back to RNA, there's none, I guess. Thanks!

Interpreting the question
Initially I interpreted the question as little more than “Why one type of virus rather than another?” (dsDNA. ssDNA, ssRNA [+ve v. –ve] etc.), and this (which would be unanswerable) was the way @Taimur seems to have understood it. And I also felt that the poster’s reference to ‘complexity’ reflected more his familiarity with other viruses than any real appreciation of what is complex in a molecular manner.
However I now think I misunderstood the question because of not appreciating the erroneous assumption on which I believe it is based. If I am correct, it could be rephrased in the following manner to make that assumption clear:

“If the only purpose of integrating a DNA copy of the retroviral RNA
  into the host genome is to replicate the RNA in the virion, why is an
  RNA-dependent RNA polymerase not used as in other RNA viruses?"

Answer

This stage of the retroviral life cycle in which a DNA copy is
  integrated into the host genome is not an incidental stage in a
  mechanism to replicate the virion RNA — it is the key element of the
  modus operandi or strategy of existence of the virus.

Explanation
As explained in the first paragraph of the Wikipedia article on retroviruses, once integrated into the host genome it can persist there:

“The host cell then treats the viral DNA as part of its own genome,
  translating and transcribing the viral genes along with the cell's own
  genes…”

One way of thinking of this is as a strategy the virus adopts for ‘hiding’ until circumstances are suitable for it to produce more infectious progeny. One might even regard the form that is integrated into the host DNA as the viral genome — rather than the form that is encapsulated by lipid and protein into virus particles.
This sort of lifestyle is similar in some ways to that of certain DNA bacteriophages that can produce either lytic or lysogenic infections. Such persistence of viral genomes in the host is also seen in some eukaryotic DNA viruses like herpes simplex virus, in which an individual may have what is called a latent infection, which produces occurrences of cold sores (in the case of HSV1) throughout the lifetime of the individual as the virus is activated from time to time by various stimuli.

Is there some intermediate stage before the "DNA stage" where the virus is being translated from its RNA for presentation on MHC? Or, do cells have to wait, always? E.g. HIV Immune Evasion: Disruption of antigen presentation...Elizabeth R. Wonderlich et al. ("Perseverance is no evasion")

There is an excellent freely available account of reverse transciption here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3475395/pdf/cshperspectmed-HIV-a006882.pdf. From which you will see (Fig 1)that reverse transcription takes place on the viral RNA. I don't know whether there is sufficient enzyme in the virion to catalyse this — I imagine some translation has to occur, but this is not for providing a template for reverse transcription. I don't know what relevance presentation for MHC has to this, and in any case it is not an area I know anything about.

Viruses are one of the particles whose evolutionary origin is still a mystery to scientists. Various hypotheses have been presented but none of them have been proven so far.
However, as one of our commenters has said, "What works, works and what doesn't, doesn't." This is the basic concept of the evolutionary theory. All organisms which can survive in an environment using a certain adaptation, whether it takes more time or less time, will survive and continue using the same adaptation.
One more point to consider is that individual organisms never evolve, only populations (organisms of the same species living in the same area at the same time) evolve. This means that a retro virus will not change to adapt to a simpler method just because it takes less time. If conditions arise that do not favour retroviral method of using reverse transcriptase but favours the method of other RNA viruses, then retroviruses will simply then decrease in number until they are zero and RNA viruses will survive.
I hope to have satisfactorily answered your inquiry.

Well, dude! You are not writing a letter. While we do expect formal language in questions and answers here, please don't post "overformal" answers.

@another'Homosapien' I will make sure to avoid that next time. Thank you.

@another'Homosapien' I have made the edits.


text:
What kind of an animal is that?

Found in Austria. At half past nine p.m. in the summer/autumn.

Due to the long legs and the shape of the abdomen, this is probably a crane fly, a dipteran from the Family Tipulidae.
Just for comparisson, here is Holorusia hespera:

Crane flies can be very large. I still remember the first crane fly I saw, in New Zealand: it seemed like a humongous mosquito (mosquitoes are dipterans from a different family, called Culicidae), it was quite impressive. Have a look at the size of this crane fly:

Despite their scary size, do not fear them. Unlike mosquitoes, crane flies are completely harmless: adults have a short life span, only days (just enough to reproduce), and in most species of crane flies adults don't eat at all.
Regarding the exact species of your specimen: the number of species in Europe is huge and, together with the fact that your photo is not the best one, it will be very difficult narrowing this down to Species, or even to Genus. Therefore, a better photo is necessary.

That's more than enough information, thank you! :)


text:
Which spider species is this, and is it dangerous?
Sorry for a quite bad picture. I was afraid to get closer!
Seen in Croatia, inlands, not near sea. As he is on the picture there with the legs stretched out, I'd say he was about 8-10 cm in length.

Possible duplicate of What type of spider is this? VA, USA

It is a female, the males of this genus are quite distinct. The genus is Argiope, and the specific epithet most probable is bruennichi. It is not a clinically important spider.


text:
What is this passage trying to say about Darwin's difficulty in explaining variation?
This passage, from the book "How humans evolved" by Robert Boyd, says that one of the problems Darwin had at the time was that he struggled to convincingly explain how variation could be maintained; this was needed to theorize that evolution is the result of cumulative adaptations over many generations. According to the book, there are four problems, one of them being that selection removes variation:

For example, suppose the environment changes so that individuals (finches) with
  small beaks are less likely to die than those with large beaks. The
  average beak size in the population will not decrease because there
  are no small-beaked individuals. Natural selection destroys the variation needed to create adaptations.

I understand the idea, but don't really understand what the example is trying to illustrate. The example seems to be saying if small beak finches survive better, then there would be no small-beaked finches...?
The second difficulty Darwin had was in explaining how animals "might evolve beyond it's range of variation (?)"

Selection can cull away some characters from a population, but how can
  it lead to new types not present in the original population?

The bit above I understood; however, I struggle to see the point of the example that was given for it:

How could elephants, moles, bats and whales all descend from an
  ancient shewlike insectivore unless there were a mechanism for
  creating new variants not present at the beginning?

Please help rephrase or explain again what these two difficulties actually are, or help make sense of the two examples that the book gave.

Sort of related Q: Did darwin ever reach the conclusion that selection will remove variation?

Remember this is all before the rediscovery of Mendel and the understanding of things like recessive traits and inheritance of discrete rather than blended traits. The problem is that, given an environment in which large beaks are beneficial, over geological time selection will tend to eliminate the small beaks. Then, if the geological environment changes such that small beaks are favored, there are no small-beaked individuals to benefit from the change: they would have been eliminated gradually during the long time when long beaks were preferred. The paradox or difficulty Darwin had was explaining how populations could maintain sufficient variability for selection to act to generate new traits.
This issue is similar to the first: the process of natural selection is all about what happens to existing populations. It explains what happens when you have variation existing in a trait. Natural selection by itself does not explain how mutations could occur to produce those new traits.

Darwin was concerned about both of these issues because at the time he saw them as serious threats to his theory (and specifically, like most good scientists, he worried that these things could mean that he was wrong). It seemed like a weakness of exactly the type he saw in prior works on transmutation of species that he was trying to work beyond. It took a few decades and a lot of scientific progress including the rediscovery of Mendel and the Modern synthesis for these problems to be truly worked out. As for Darwin, the best he could come up with was his somewhat-Lamarckian pangenesis idea, which he defended strongly.

You explained point 1 and Darwin's concern in your 3rd paragraph well; I now understand what the book was trying to say. As for the second point, I had to re-read your explanation once or twice, but eventually understood what you're trying to explain. Overall you're answers are good explanations, as I now understand what's being conveyed.


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It is correct to construct tree species-based rarefaction curves for birds?
If I register all the species of birds that uses sp1 tree, then, all the species of birds that use sp2 tree, and so on. With this dataset, I can made a rarefaction curve using "number of tree species" on X axis of the rarefaction graph, instead of using "number of samples"
Is this incorrect? Does anyone knows a paper that made something similar?


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What kind of beetle is this? (Black and yellow)

Found this in my house in Colorado. I took this picture before releasing it. I didn't measure it, but the diameter of the cup it is trapped under is about 5.5 cm, so that makes it about 1.1 cm long. It easily climbed up the side of the glass cup.

This shield bug belongs to the species Perillus bioculatus, and has the nickname "two-spotted stink bug". They're native to the United States, and come in a variety of colors.
You mention that its colors are yellow & black, however, from the image you provide, it seems more of a pale yellow/off white. Because of that, I think it your found insect more closely resembles the first of the following images, whereas you may think it's closer to the second.

And then, a few other colors:

You meant  "two-spotted stink bug" instead of "sting," right?

@PaulParker Oh, hah! Yes, thanks. Edit has been made. :)


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Remove all intestinal bacteria?
I've heard that this has happened to a few people before in extenuating circumstances, but don't know where to search for more information on this.  Is there a name for this?  What are some major symptoms, and how does it affect the body?  How is it identified?

Do you mean E. Coli?

All bacteria.

Are you sure you can prove your statement?  Can you provide some links to your sources ?

It is not possible to do this. You can minimize the number of bacteria by a complete GI cleanse, similar to what you go through before a colonoscopy. The point is to empty the gut of all matter, esp. fecal. But once you're colonized, that's it; you'll never be uncolonized.

This has never happened (at least to my knowledge), since removing all bacteria from a human being would be extremely difficult and also dangerous. And there is a proven relationship between the human microbiome and stress, but "extenuating circumstances" won't remove all bacteria from your body.
However you can look in the Internet for "germ-free animals", "gnotobiotic animal" or "axenic mice". Caesarean section in aseptic conditions is practiced (a fetus in normal conditions has no germs in it) and the "newborn" is immediately put in a sterilized enviroment. There is plenty of research with this kind of animals.
I hope my answer was useful for you! Cheers!


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Please help ID this plant
Can anyone please identify this plant and confirm if the species is Synsepalum dulcificum (Miracle fruit)? Pics were taken near my house in Bangalore. Because the miracle fruit plant is not native to India, I'm guessing it is a different species.

Looks like miracle fruit.

No, I don't think it's an S. dulcificum, the leaves are very different. It might belong to a related species.

Thanks for the comment guys!! really appreciate it! is there anyway to be completely certain of the species. I'll try eating a tiny bit of the fruit today just to see if it works. can anyone who has tried the fruit tell me how it tastes like and whether the effect is seen if a tiny amount is ingested.

Hmm could it be nightshade berries?


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Can PCR duplicates have complementary sequences?
It is common when analyzing paired-end whole-genome shotgun sequencing data to check for and eliminate PCR duplicates. The reasoning is that the probability of sampling a fragment of the genome of the same exact length from the same exact position in the genome multiple times is extremely low. Therefore, if you see multiple read pairs with the same exact sequence in both pairs, these don't represent independent events but are multiple copies of the same event.
My question is whether PCR duplicates can be reverse complements of each other. All the PCR duplicates I've observed myself have been exactly the same sequence on exactly the same strand. Is there a technical reason why this is the case, or is it possible that PCR duplicates could not be on the same strand as each other?

The standard directional Illumina library prep protocols that are used at the facility in my building follow the schematic below:

So, I guess this provides a potential technical explanation for your stranded duplicates, with the broad simple answer being it depends on the protocol used to make the libraries.

Depends exactly where the PCR step is in your library prep.  Usually, there is one that is done after adapters are added, to amplify fragments with intact primers on both sides.  These will of course all be the same orientation.


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Methods for phage separation
How can a mixture of unspecified phages be separated (into singular phage strains)? I.e, what are the main methods?
My research shows it can be done using CsCl centrifugation and affinity chromatography, but both seem laborious, the latter also requiring the phages to be already available in pure form.

Look up "phage purification." Basically, you add your phage solution on top of your host bacteria on a plate and incubate. As the bacteria grow, you should see plaques (clear areas in the bacterial lawn). Each plaque should be the progeny of one original phage, although sometimes two or more phages could be very close to each other on the plate and it will look like one plaque. So you have to take a sample of a plaque, re-plate on another lawn of host bacterium, and repeat this process for several rounds until the plaque morphology seems to indicate that there is only one type of phage present. Here is a good resource for phage protocols: http://phagesdb.org/workflow/

Thanks, excellent link! Any other known way other than manual extraction from plate? Is it perhaps easier to isolate infected bacteria during lytic cycle (or perhaps during induced lysogenic cycle)?