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Has a mammalian species that cannot interbreed with another ever been selectively bred in isolation from it so that it can?
Take two mammalian species that cannot interbreed by any means. Has one ever been selectively bred in isolation from the other so that eventually it can?

Define "cannot". It's quite usual to use techniques like embryo rescue https://en.wikipedia.org/wiki/Embryo_rescue in plant breeding in order to create hybrids between species that otherwise couldn't successfully interbreed in nature.  I think that sometimes the resulting hybrids can be fertile with one or both parent species.

Restating jamesqf comments: What kind of of reproctive isolation barriers are you willing to consider. Two species cannot interbreed if there is a mountain range between them! Two species cannot interbreed if they do not want to mate at the same time of the day (this is a type of pre-zygotic reproductive isolation known in several Diptera species for example).

"Cannot" means "are not able to by any means". I'll amend.

define breed, some viruses can transfer genetic material between species, so thing we are happy to exploit in genetic engineering.

"Breed" means "sexually reproduce to produce offspring". I won't add this, because it is obvious. I will, however, change to specify mammals.

And you are accepting any kind of reproductive barrier? Would moving a species on the other side of a mountain range count?

For the edited question, and just considering biological barriers like different chromosome counts, I'd suggest that the answer is no, simply because it would take a lot of time and effort (and expense!) for no obvious benefit.  That doesn't mean it's not possible, as shown by a number of distant crosses in plants, where there is obvious economic benefit.  E.g. https://en.wikipedia.org/wiki/%C3%97_Chitalpa

I'm assuming that the only way we can know if it "can" interbreed with the other species is if it does, whether in domestication or wherever. @jamesqf - I am not sure about that. There are some mysterious things where canines are concerned. Research paper from 2009.


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Glycosidic bonds
For the glycosidic bond in maltose, why is the glycosidic bond formed between hydroxyl group on C1 in 1 glucose molecule and hydroxyl group on C4 of the other glucose molecule? Why not between, say, hydroxyl group of C2 on one and hydroxyl group of C4 on the other?

In a cyclic molecule of glucose, C1 is the result of the aldehide group linked to C5. This makes C1 a reducing carbon that can share electrons. This is why C1 must always take part in a glycosidic bond.
The other carbon may be C'1, C'2, C'4 etc. That changes the structure and name of the molecule (i.e. two glucoses bound by α 1-4 bond is Maltose and by α 1-6 is Isomaltose)

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The role of atomic theory in biology
Feynman writes, in his Lectures on Physics Vol. 1, Chapter 1:

The most important hypothesis in all of biology, for example, is that everything that animals do, atoms do. In other words, * there is nothing that living things do that cannot be understood from the point of view that they are made of atoms acting according to the laws of physics.* This was not known from the beginning, it took some theorizing to suggest this hypothesis, but now it is accepted and it is the most useful theory for producing new ideas in the field of biology.

He would have written this around 1961-1963. Was he right then and/or is he right now? Is what he says applicable for the entirety of biology (say evolutionary theories) or only for a subset of biology?
Would Feynman have been referring to a few specific advances or to the general state of biology at the time?
Please note that this question comes from an (interested) amateur to both physics and biology, I hope the question is appropriate for this site.
Edit: Perhaps this will clarify the intentions behind my question:
I would be interested to know how much atomic theory actually helps biological research. For instance, it often happens that the specific low level details are not necessarily important for explaining the high level theory. A nice example is abstract algorithms vs implementation in programming languages vs hardware implementation. Is this the case with biology or do the details of atomic theory matter? For instance, have advances in physics led directly to new biological discoveries?

Did the original claim repeated In other words twice or is it a typo?

Yes it is still true for all of biology, of course physics has expanded a bit, and likewise we have discovered cases of biology exploiting these new parts, for instance photosynthesis might involve quantum tunneling.
Feynman's quote basically restating that there is no magic or supernatural aspect to biology, no vital essence or spirit required to explain how it works or seperate living matter from non-living, it is all just chemistry and physics. The most complex chemical process ever discovered but still just chemistry and physics. Of course he does not mention chemistry becasue of course chemistry is just physics as well, the laws of physics control both, so saying it is a result of atoms obeying the laws of physics expresses both.
He is saying biology is still obeys the laws of physics and are made of atoms, this is true for all of biology, but as Feynman points out took some time to be accepted, keep in mind this is the time of the Miller–Urey experiment which showed organic molecules could form through entirely non-biotic means, which was not as widely accepted at the time as many think, especially to a general audience. Many similar discoveries a t the time were showing the same thing, there was nothing special about biological molecules or their interaction. things like evolution is the inevitable result of the interaction of basic properties (reproduction and heredity)just as a salt crystal is the inevitable result of the interaction of charge of sodium and chlorine. Vitalism still hung around in the popular mind and a few corners of academia at the time Feynman was growing up so taking a few moments to help dispel this notion in his lectures makes a lot of sense, especially given how much advancement was done by abandoning it.

Feynman most definitely talks about chemistry. In fact, the title of the section that the quoted text comes from is, "1-4 Chemical reactions". I recommend you actually be familiar with the quoted work before speaking about it. Feyman Lectures, Vol. 1, Ch.1

Also, the idea of being redundant by expressing a phenomenon from both and chemical and physical perspective, most definitely is not congruent with Feynman's mentality. There are literally dozens of video interviews where Feynman expresses the importance of interpreting a single event using several different contexts. He refers to this as "playing around with it".

@charles I have read it actually, and explaining what the quote means is important for understanding its application, you seem to be reading far too much into the quote.

Your last paragraph is the kind of thing I was looking for. I would also be interested to know how much atomic theory actually helps biological research. For instance, it often happens that the specific low level details are not necessarily important for explaining the high level theory. A nice example is abstract algorithms vs implementation in programming languages vs hardware implementation. Is this the case with biology or do the details of atomic theory matter? For instance, have advances in physics led directly to new biological discoveries?

that is two separate questions which would be far better answered as there own formal questions. A formal questions they will also be educational for us all, as I suspect others will have farm more examples that i can provide. .

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What are the advantages of using interphase cells rather than metaphase cells for gene mapping purposes using FISH?
I have been told that interphase cells are better for gene mapping purposes than metaphase cells but don't know why.

Can you give more information about what kind of mapping is being done? Do you have a reference for the claim?

Clones of human DNA were used for FISH. I don't have a reference for the claim, but please could you suggest some advantages of using interphase cells rather than metaphase cells for gene mapping.

Already good to know the question is about FISH. You should edit this info in your question. Have you read the wikipedia on FISH? There seems to have quite a bit of info already that may well help you.

Thanks for your reply. The wiki page describes the process of FISH but doesn't address advantages of using interphase instead of metaphase cells.

In metaphase, chromosomes are at their highest level of condensation. FISH relies on being able to dissociate the two strands of DNA to anneal a sequence-specific probe. So, my guess is that it is technically easier to achieve a good FISH staining in interphase, when chromosomes are much less densely condensed. There might be other reasons I am not aware of (I am not a geneticist).


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Can different Chromobactierum strains have completley different colony morphology?
In the analysis of an unknown bacterial broth I observed a gram negative rod genus. Upon plating I observed small, dark purple and convex colonies; corresponding presumably to Chromobactierum. After then replating the purple colonies I then observed white fillamentous colonies that were gram negative and was subsequently able to make an identification that suggested the organism was either of genus aeromonas, vibrio or Chromobactierum. I found an article showing that Chromobactierum colonies dont have to be purple and can have a range of morphologies (see link). My question is: upon replating, can the morphology of the two colonies change so drastically?( assuming I had two different strains of Chromobacterium present)
Source:http://jb.asm.org/content/66/4/470.full.pdf

This different Gram reaction suggests you have a contaminant.

Sorry error on my part. The purple bacteria observed on the first plate were gram negative

It is not uncommon for bacteria to stop producing pigments when cultivated on artificial media in the lab.

Did you PCR the 16S?? Most phyla are Gram negative and several skin flora bacteria are negative and unpigmented —yes, there will be many bright yellow staphs (+) and red Serratia marcensis (-), but not all. So I agree with the contamination hypothesis.


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Help me to identify this stream insects

this insect I found on a stream in the southern region of Bangladesh. Its dorsal part is fully black and head and thorax is yellowish with black spot. Body size approx. 5-6mm, limbs 8-10mm

Where (what country, what region, what kind of stream, ...) did you find it? What is its approximate size? Was it alive when you got it? What can you tell us about its behaviour?

If I'm interpreting what I'm seeing correctly, you have some sort of Water Strider (Order Hemiptera, Family Gerridae) here; which one will depend on where you found it (and your name suggests that you might not be from the United States -- which means that I at least cannot go further).

Hey I am sorry I didn't give the details... I found it in Bangladesh southern region. Its body length is around 5-6 mm and it limbs are approximately 8-10 mm

Attempt at an answer
I think it is a water strider. There are 1700 species of water strider. Some of them are easy to eliminate (the marine ones typically) but I am not really able to give you more info from your picture.
To make sure, it is a water strider, can you please tell us
- How long are the legs (hard to tell form the picture)?
- If it was alive, was it standing on water? What can you tell us about its behaviour?
What insects live in the water?
If it is a stream insect, it could be...

a mosquito larvea
a mayfly larvea
a odonate (dragonfly or damselfly) larvea
a water strider

Here are my thoughts for each of them

a mosquito larvea

No, mosquito larvea don't any limbs

a mayfly larvea

I can't see the long cerci

a odonate (dragonfly or damselfly) larvea

Again I can't see the cerci
Also, although, it is often hard to see, it does not appear to have a fancy detachable mouth piece.

a water strider

We can't tell the length of the limbs from the picture. Were they really long?
If it was alive, was it standing on the water?

Thanks a lot. I think the above information will help me to find out the species

Although you may be right about it being a water strider, your answer is incomplete. There are a lot more water insects. Coleoptera, Trichoptera, other Hemiptera than water striders, other Diptera than mosquitos, etc.

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Request for an ID of two spider species found in Australia, NT
These two spiders were found in the Northern Territory in Australia in July (winter time). Both arachnids were shot during the night (I suspect them to be nocturnal), and both were found close to the ground. They do not build webs I think (way too big).
The upper spider is quite big, pretty much hand-sized, and about as big as a bird-eating spider. I think the guy with us told us it was a species of wolf spider (if I recall correctly - I'm unsure). The bottom hairy spider with its nice camouflage is somewhat smaller (if I recall correctly), but still well sized.
I have been searching for their names, but the amount of spider species is overwhelming and Australians tend to focus online resources on the poisonous ones. I'm fairly sure these two are harmless.

The bottom one is most certainly a Huntsman. Something akin to a Holconia immanis, aka the Sydney Huntsman. The picture is difficult but a characteristic Huntsman typically has 2 front legs that are longer than the back legs. And of course they tend to be larger spiders.

 Holconia immanis. source: Wikipedia
The top one looks like a type of brushed trapdoor spider (family Barychelidae), typically composed of such species as Idiommata scintillans, which are known as silverbacks or goldbacks depending on the color of the hair on their head (ref).

Idiommata sp., the 'Silverback'. source: Archne.org.au

I've taken the liberty to add some sources and pictures. Please feel free to undo. Thanks!!!


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Are we "more evolved" than present-day bacteria?
The common ancestor of humans and modern bacteria was most likely a prehistoric bacterium. Does this mean that humans are "more evolved" than today's bacteria?

To be precise, the last common unified ancestor was likely closer related to archaea than to bacteria: https://doi.org/10.1038%2FNMICROBIOL.2016.116

@NoOne that's an impressive misunderstanding of pretty much everything in biology you've got there.

"More evolved" doesn't mean anything in biology.

This is a standard question. The whole problem boils down to what you mean by "more evolved"? Below I am answering the question considering a number of possible definitions. If you have other ("clearly defined") definitions in mind, let us know.

Are [humans] "more evolved" than present-day bacteria?

If "more evolved" == "more evolution time"
Then, both bacteria and humans are exactly as evolved!
As all life on earth shares a common ancestor, all currently living creature has evolved for exactly the same amount of time (about 3.8 billion years).
If "more evolved" == "more generations"
Then, bacteria are more evolved.
Bacteria typically have a much shorter generation time than humans do, so with this metric, bacteria would be more evolved.
If "more evolved" == "more fixed mutations since the MRCA"
Then, it is a little more complicated and may depend upon which bacteria lineage you are considering.
If the genome-wide mutation rate is $\mu$ and the haploid population size is $N$, then there are $N\mu$ new mutations every generation. Given that each one of these mutations has a probability of fixing (fixing = reaching a frequency of 1 in the population) is $\frac{1}{N}$, the rate at which mutations fix is $\mu N \frac{1}{N} = \mu$ at each generation. If a species has $g$ generations per year, then over $t$ years, $\mu g t$ mutations would have accumulated.
The genome of bacteria is typically much smaller than the one of humans, but their mutation rate per nucleotide is much higher. Overall, the genome-wide mutation rate is rather higher in humans but that might well differ from species to species. However, again, bacteria have had more generations per year than humans and therefore bacteria species likely have fixed more mutations than humans have. So from this metric, bacteria are rather more evolved than humans.
If "more evolved" == "able to resist higher acceleration"
Then, bacteria are more evolved although that might among bacteria lineages
Some bacteria have been grown under 400,000 g (National Geographic), while a typical human can only tolerate about 5 g and for only a short period of time!
If "more evolved == more impact on the environment"
The term impact is a little hard to define but I think it is of interest to highlight that, even here, bacteria would probably win because cyanobacteria caused the great oxygenation event which is probably the largest planet-wide environmental change caused by biological organisms.
(thanks @Thawn for this definition he gave in the comments)
If "more evolved" == "having more lungs"
Then, humans are more evolved.
Bacteria have no lungs, humans have two.
If "more evolved" == "bigger genomes"
Then, humans are more evolved. Note also that corn would be more evolved than humans with this metric!
If "more evolved" == "higher fraction of the genome that is encoding for proteins"
Then, bacteria are more evolved.
If "more evolved" == "more protein coding sequences"
Then, humans are more evolved.
If "more evolved" == "more phenotypically different from the MRCA"
You would have to list specific phenotypes of interest. So, here the term "more evolved" still remained a little undefined.
Also, we do not have much information about the MRCA of these two highly distantly related lineages. The question could be more easily answered for more closely related lineages. For example, in mammals, if you consider the following traits and always ask what species is (likely) most different from the MRCA of all mammals

body mass -> blue whale
brain mass -> sperm whale (yes, sperm whales have a very big brain)
lips shape -> platypus (they have a beak)
time taken to type Hello\nWorld on a computer keyboard -> humans

Related posts

What is meant in biology by the term “evolved”?
Why have humans evolved much more quickly than other animals?

+1, wouldn't you reckon this question to be a duplicate, as you state in your answer?

@AliceD Good point. I posted two related posts. The post 'What is meant in biology by the term “evolved”?' kinda make a similar point than the one I am making here. By listing potential definitions, I am hoping to make the naive reader realize that it is not that easy to come up with a good definition that would give us a good intuition about what more evolved mean.

I think the phrase more evolved implies the notion of more valuable information, more sophistication and less genetic junk being encoded inside the genetic material of the organism. If there was ever anything worth of being called genetic junk to begin with, that is... It might be good to add this to the list of interpretations, since that's the most obvious one.

Your definition is unclear though. What do you mean by valuable information, sophistication and genetic junk? All of these terms are very undefined. Try to think of a way to measure these things. If you can come up to way to measure these concepts, then I'll happily add it to the list and try to answer who is more evolved if I can. I added If "more evolved" == "bigger genomes" and If "more evolved" == "higher fraction of the genome that is encoding for a protein" though in reaction to your comment. Thanks

@Remi.b Valuable information and genetic junk are related to what portion of the genome is required to be preserved in order for the organism not to loose any functionality or features. Sophistication is indeed a vague concept, but it is clearly distinguishable between e.g. mammals and prokaryotes. I guess you can say that it is a measure of the complexity of the non-junk genetic material of the organism - if we ever manage to fully understand its functions.

non-junk genetic material does not mean much. You are maybe trying to refer to the concept of junk DNA. I already have "the fraction of junk DNA" as possible definition.

Re "genetic junk", please try to understand that there's a difference between "we don't understand what this DNA does" and "we don't understand what this DNA does, therefore it must be junk".

junk DNA was actually first defined as a synonym of noncoding DNA, so it does not even imply that we don't know what it does. It might be a well known regulatory sequence that is being called junk DNA. But the term "junk" became very popular, took a number of weird definitions and is today onlny very rarely used in the scientific literature.

more evolved == more impact on the environment even here bacteria win because cyanobacteria likely caused the great oxygenation event which is the largest planetwide environmental change caused by biological organisms

I think it's pretty obvious to every thinking person that the objectively correct definition of "more evolved" is "able to resist higher acceleration". (More seriously, this is a fantastic answer, thank you.)

While I believe that all the definitions given by Remi.b are very valuable and have merit, I would like to add one definition which I think is closest to what is commonly understood under the term "more evolved":
"more evolved" == "more genetically complex" (Edit: more specific definition as suggested by Bryan and Remi)
To be more precise I define "more genetically complex" as:

more different protein-coding genes (different being important here because some plants have extremely large genomes due to polyploidy. But this is not adding complexity because polyploidy means that they have many copies of the same genes)
more expressed gene variants
more posttranslational modifications
more genetic control mechanisms

Under this definition, humans are clearly more evolved than bacteria:

Humans have close to 20.000 protein coding genes, while bacteria have somewhere between 1500 and 7500
Humans have RNA splicing, enabling the expression of several different protein variants from the same gene. Bacteria do not have RNA splicing.
Humans use a wide variety of post-translational modifications of proteins to tune protein activity and for signalling cascades. This point is not as clear as the points above because the entire biological domain of bacteria has developed many post-translational modifications, and the exact number of modifications used in the entire bacterial domain is much less well understood than the post-translational modifications in humans. However, it is safe to say that each individual species of bacteria uses much fewer post-translational modifications than the human species (and comparing a single species to an entire domain would be quite unfair).
Humans use a wide variety of very complex interlinked genetic control mechanisms which span from expression control by cell signaling via expression control and gene silencing during embryonic development to heritable epigenetics (Lamarck was not that wrong after all). Like the post-translational modifications this is a very active field of research and more and more expression control mechanisms are being discovered both for bacteria and humans all the time. But again, there is no argument that humans have a more wide variety of genetic control mechanisms than any individual bacterial species.

I think it's quite a stretch to say "more evolved" == "more complex". I mean, certainly you an assert this just due to flexibility of language, but there's zero reason to throw the word "evolved" in there: If you mean more complex, just say more complex (and then get ready to defend your definition of complexity...). Although over time evolution will produce some more complex organisms than started, evolution need not result in higher complexity in all cases.

I think it is a good add +1. I would just note that definition "evolved" based on "complex" and then defining complex is a little of a work around that may lead a naive reader to just retain that "human are more complex" without understanding what this means. I would rather have 4 categories and drop the term complex. I am not sure my criticism is the same as @Bryan's

@BryanKrause; @Remi.b I changed the definition to "more genetically complex". This is more specific and hopefully more clear. What do you think?

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Menstrual cycle and luteinizing hormone (LH)
What is the effect of increased concentration of LH on the follicle at the start of the menstrual cycle?
I know that increased levels of FSH at the beginning causes follicles to mature and release estrogen, but I cannot seem to be able to find what the effect of increased levels of Luteinizing Hormone at the beginning of the cycle would have.

Do you mean the preovulatory LH surge?

If the preovulatory LH surge occurs at the beginning of the menstrual cycle, then yes that may be what the question is referring ro.

Luteinizing hormone (LH): A hormone released by the pituitary gland in response to luteinizing hormone- releasing hormone. It controls the length and sequence of the female menstrual cycle, including ovulation, preparation of the uterus for implantation of a fertilized egg, and ovarian production of both estrogen and progesterone. Theca cells in the ovary respond to LH stimulation by secretion of testosterone, which is converted into estrogen by adjacent granulosa cells. In women, ovulation of mature follicles on the ovary is induced by a large burst of LH secretion - the preovulatory LH surge. Residual cells within ovulated follicles proliferate to form corpora lutea, which secrete the steroid hormones - progesterone and estradiol. Progesterone is necessary for the maintenance of pregnancy, and, in most mammals, LH is required for continued development and function of corpora lutea.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3136063/


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Definitions of hermaphroditism, dioecious and monoecious?
What is the difference between these terms "monoecious","Hermaphrodite".
my lecturer says hermaphrodite is a zoological term and monoecious is botanical term, but in contrary to it, in my textbook both of these terms are used both botany and zoology.
So what is the actual difference?

Below are definitions that I've seen; there may be less strict definitions under which monoecy (the noun form of 'monoecious'). and hermaphroditism would be the same thing.
Dioecious: Although rarely used for animals, one could say that human are dioecious because each individual produces only one type of gamete. In a dioecious species, some individuals are males and others are females.
Monoecious: In monoecious plants, individuals carry both males and female flowers but not flowers that can produce both female and male gametes.
Hermaphrodite: Hermaphroditic plants have flowers that can produce both male and female gametes.
Then, there are many other fancy terms such as dichogamous, gynomonoecious, subandroecious, heterostyly or androgynomonoecious! Plant mating systems are fantastically diverse and complex!
More information
Some of these terms are defined in The Evolution of Sex Determination, which is very pleasant to read. For shorter articles, consider Barrett 2002 or just Wikipedia > plant reproductive morphology or Wikipedia > dioecy (the noun form of 'dioecious').

According to "Plant Identification Terminology: An Illustrated Glossary" (Harris & Harris, 2001):
The main difference is the frame of reference. "Monoecious" refers to a whole plant having both male and female parts, while "hermpahroditic" refers to an individual flower having both male and female parts.
Hermaphroditic:

With pistils and stamens in the same flower; bisexual; monoclinous; perfect

Note: "Perfect" = with both male and female reproductive organs (stamens and pistils).

Monoecious:

Flowers imperfect; the staminate and pistillate flowers borne on the same plant

I will caution you that different sources use "bisexual" inconsistently to refer to either instance.


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Should corn be considered an invasive species in the Midwest?
Per the United States Department of Agriculture (USDA) an invasive species is defined as:

non-native (or alien) to the ecosystem under consideration

whose introduction causes or is likely to cause economic or
  environmental harm or harm to human health

Corn in the Midwest, USA (often referred to as the Corn Belt) would seem to satisfy the first requirement as an invasive species as it is not native to this area.  Regarding the second requirement, it could be argued that corn in the Midwest causes environmental harm because it is in place of many indigenous plants that many other animals rely on to survive.  For example, habitat loss is considered a cause in the decline of the regal fritillary (Speyeria idalia) butterfly.
A Google search brought me to this Q&A site where many argued that corn is not an invasive species because it cannot survive or spread by itself without human intervention.  I tend to agree with this logic but it does not seem to be within the scope of the USDA definition.
Should corn be considered an invasive species in the Midwest?

I'm voting to close as opinion-based, because there isn't really any biology in this question.

A q for sustainability?

You answered your own question. It does not survive in the wild. Corn IS native to the ecosystem in which it exists, which is an agricultural corn monoculture.

@Karl Kjer.  What seemed to be confusing me is that the agricultural corn monoculture ecosystem is not the native, predominately tall grass prairie, ecosystem for this area.  After reviewing the first part of the definition I do see it says non-native to the ecosystem under consideration (not the native ecosystem) which would mean it's not an invasive species to the Midwest.  Thank you for the explanation.

This list does not exist to consider USDA directives or semantics. Please someone else vote to close this.

OMG i never realized that humans are an invasive species.

Having observed several invasive plants in my yard , I would certainly not consider corn ( or soybeans ) to be invasive.

I’m voting to close this question because it is fundamentally opinion-based and falls outside the remit of this site. That this is opinion is reinforced by the links to a regulatory definition and a non-scientific Q&A.

Should corn be considered an invasive species in the Midwest?

I agree with commenter Bryan Krause in that this question requires opinion -- but I think it only requires opinion as to the definition of what we consider "invasive".
The concept of an "invasive" species is highly contested among biologists. It is often used interchangeably with the terms non-native, non-indigenous, and alien.
Some people think we should consider a species as 'invasive' even if it is native to the region but is causing "economic or environmental harm or harm to human health". For example, the USDA considers Juniperus virginia a native species, despite its spread from plantings and its economic and ecological impacts in 'invaded' regions.

Species are only considered invasive if they become widely established in sustaining, wild populations. If the species is widely cultivated, but rarely or never escapes cultivation, it is not invasive. Even if it widely escapes cultivation, it may not necessarily be invasive because it might not be vigorous enough in the wild.
Corn has escaped and formed wild sustaining populations in North America, including in the Midwest. Here is BONAP's range map:
http://bonap.net/MapGallery/County/Zea%20mays.png
It shows that it is established in all lower 48 states as well as many of the Canadian provinces that border the US. However, if you look at the county-level distribution, you will see that it is spotty.
Given how widely it is cultivated in many of those states (it covers much of Iowa and Illinois, for instance) yet how sparsely it is established there (it only shows up as established in the wild in isolated counties in both states, this provides pretty strong evidence that it's not really that vigorous in the wild.
I have also observed corn plants growing in the wild in the US. They aren't particularly vigorous: there will be one plant here or there, and it never dominates or forms large monocultures. Those highlighted counties are where corn has formed some sustaining population. Not necessarily where it is vigorous, common, or abundant.
Want to see what a map of an invasive species looks like? Here is BONAP's map on garlic mustard, Alliaria petiolata, widely agreed to be invasive:
http://bonap.net/MapGallery/County/Alliaria%20petiolata.png
In spite of the fact that it is not cultivated, it is found in nearly all counties of broad regions from Wisconsin/Illinois east through New England. Furthermore, if you examine it in the wild, you find it forming huge monocultures, shutting out all sorts of other plants.
But back to corn:
The ecological damage caused by corn in North America is not caused by wild corn, i.e. not caused by corn as an invasive species. Rather, it is caused by the agriculture itself, specifically, by vast monocultures of corn and other crops, and various other aspects (fertilizer and other chemical applications) of yield-intensive agriculture.
So I think the answer here, even accounting for the high level of subjectivity in the definitions of "invasive", is definitively no.

Welcome to Biology.SE. First, while this looks like a good answer, it is to a question that is off-topic for this site (because it is asking for opinions) and it would be better to leave such questions unanswered. Second, for future posts where possible please provide references (with full citations) since links can (and do) break. ——— You may also wish to take the [tour] and then consult the [help] pages for additional advice on [ask] and [Answer] effectively on this site.


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Is "Monophyly" context dependent?
I am thinking about this thought experiment: Suppose we have three taxa which are grouped into the following tree: {{A,B},C}, clearly {B,C} is a paraphyletic group. But if A go extinct in the near future, we are left with {B,C} only, then can the group be called monophyletic?

As long as you don't say A is OUT of the BC group, This is a monophyletic group yes.

To expand on Remi.b's answer, groups are defined based on all the species we know about. This includes extinct species. So in your example, the group {B,C} is paraphyletic regardless of whether A goes extinct or not.
But what if A went extinct ages ago and we don't know about it at all? In that case we would only have B and C to base a group on, and they are the only descendants of their common ancestor that we know about, so we would indeed define {B,C} as monophyletic.
The question comes when we discover A's existence, and that it is more closely related to B than to C. At that point we have a choice: expand the definition of group {B,C} to include A, in which case the group becomes {{A,B},C} and is monophyletic, or keep the group {B,C} and accept that we were wrong about it being monophyletic, it was really paraphyletic all along.
You can see these processes happen as paleontology and cladistics advance. Birds used to be classified differently from dinosaurs, but as our knowledge of how birds are descended from dinosaurs increased paleontologists chose to classify them as a subset of dinosaurs, keeping the group "dinosaurs" monophyletic.
On the other hand as our understanding of how mammals/birds are descended from reptiles and tetrapods are descended from fish increased, making both of those groups paraphyletic, the attempts to redefine them as clades have largely failed, so they are now considered paraphyletic groups. "Amniotes" has replaced "reptiles" as the name of the clade containing reptiles, mammals and birds, and "Craniata" is the monophyletic group containing various fish and tetrapods.

To be strict about the definition, a monophyletic group is a group that contains the common ancestor and all of its descendant. This means {{A,B},C} is a monophyletic group only if you consider all of the shared ancestors until the MRCA of them all.
If A get extinct, it still remain in that {{A,B},C} (and their common ancestors) are a monophyletic group. You do not remove A from the group because it is extinct.
Of course, this means that to have a monophyletic group we should be able to name every single species (or even every single individual given how messy is the concept of species; see here) that is descendant from an ancestor but we never do that. The most important is to not willingly ignore or include a species that should not be ignored/included. Here you would ignore A under the excuse that it is extinct and that would be wrong.


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What are the meaning the nomenclature in high cell density cultivation for the production of a protein?
I'd like to know the meaning of these terms in a HCDC studies of a modified strain.
Max specific yield (mg/g DCW)
Max volumetric product yield (g/l)
Specific product formation rate Qp (mg/g DCW/h)

I wanted only the definitions of each

Maximum specific yield = milligram product per gram dry cell weight (DCW).
Maximum volumetric yield = gram product per liter culture.
Specific product formation rate Qp = milligram product per gram dry cell weight per hour.


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Bird identification from Nepal
I just stumbeld across a picture and wonder which species it is?
I took the below picture of a bird, probably a raptor, in mid-January 2011, 7 pm, on the Annapurna Trek in Nepal. My altitude was around 2000 m.
Since I took the picture a long time ago I cannot recall any information about the size.

Your image does not depict a predator, instead it's a scavenger. It's definitely a vulture, and by the looks of it a Griffon Vulture, which are a common siting in India.
The picture you provide is a bit grainy, and the apparently low-set sun colors the image somewhat yellow, but it does appear similar to below image of a Griffon vulture.

Griffon vulture. source: Vulture conservation in India and Nepal


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How does DNA still work after recombination?
If you take two computer programs and randomly swapped pieces from each of them. The result is not going to work. It will just be garbage. If you take two novels and randomly swapped chapters the result will be garbage too.
How is it than DNA (which is infinitely more complicated) can be combined, some from the father and some from the mother and yet it still somehow works?
Can you give a simple example?

Actually computer programmers can be made by randomly swapping bits of their programs around if it's set up properly, this is called genetic programming https://en.wikipedia.org/wiki/Genetic_programming

How exactly is DNA infinitely more complicated? It's only got a 4-character alphabet? You may argue that it is more complicated in some specific aspect, but not significantly so, let alone infinitely.

@Thijser. Yeah but genetic programming has never really worked that well as far as I understand for that very reason.

@orangedog computer programs (for the computer POV) has a 2-letter alphabet. The claim that it is infinitely more complicated is a fallacy, but the amount of sigils in an alphabet is not a measurement of complexity.

@OrangeDog Although you might say all genes are separate and generate different proteins. All the proteins must work together. The system it encodes, i.e. a human being is a very complicated interconnected system I think you'd agree.

@zooby I didn't say it wasn't very complicated, I simply contest that human language and computer programs are in fact comparable in complexity to DNA.

@Mindwin yes I know, that's why I was asking what measure zooby thinks they're using

@zooby there are indeed a few ways I can think of where DNA is measurably simpler (as far as current understanding goes). For example the order that genes appear on a chromosome is usually not important, and you can usually pad them with meaningless junk. The only immediate complexity is the feedback loops where some genes express proteins that effect the expression of other genes, but you can write a computer program that does the same thing (dynamically re-writing its own execution, or "machine learning") and it will be similarly hard to understand what it's going to do.

You can juggle around things in a computer program too. Some languages lets you define functions and classes in arbitrary order, for instance. You can also pad with useless junk (as long as it's syntactically correct), like defining functions that no one will ever use, or performing the calculation 5+5 without storing the value anywhere.

If you're a computer programmer, this page on computer analogies to DNA might provide you some inspiration.

For an example, homologous recombination is like swapping chapters between different editions of the same book; it would still make sense.

I'm voting to close this question as off-topic because it is based on the false premise that DNA is comparable to a computer program.

Homologous DNA recombination does not swap parts randomly in the sense that any two bits of DNA can swap places. DNA recombination is random in the sense that it may or may not occur. In fact DNA homologous recombination is highly specific and its specificity is what it makes a great tool to study genetics in organisms like yeast by swapping a gene of interest with something else.
In your example of meiotic recombination between the sister chromatids can swap  DNA between different alleles. Alleles are genes that encode for a protein with the same general function, but have some variability in sequence that gives them slightly different properties. The reason why it only occurs between alleles, is because homologous recombination requires regions of homology, in a laboratory experiment this can occur with 20 to 40 base pairs in length and the low likelihood that a 20 base pair sequence is found anywhere else in the genome is why you don't get a chaotic mix and match of genes that you suggested would happen.

Very interesting - and to extend the software analogy this sounds very similar to how patches/diffs work. They also require an identical section before and after the piece of code that is to be swapped with an updated version.

The definition of allele here is a little misleading. An allele is a variant at a locus. Most often people consider loci that are genes but this is not necessarily the case. A sentence like "it only occurs between alleles" is a bit misleading. It would be better to say "it only occurs between variable regions". Also, just to avoid that the reader gets mislead, there are other things that affect variation in recombination rate than polymorphism.

Another software analogy might be something like taking some program with hundreds of shared library dependencies and randomly swapping some of the library versions with versions used in a different release of the overall software. It might make certain things start crashing, or it might make that mysterious bug you started seeing in the latest version go away. ;-)

One must always be careful not to stretch an analogy further than it can withstand, but since you started these analogies, I will follow up on them and explain the small mistake you've done in their representations.
The two books are not as different as you have in mind. You are not pasting the beginning of Uncle Tom's Cabin with the ending of Harry Potter but only the beginning of Harry Potter with the ending of another Harry Potter in which Ravenclaw is renamed Eagleclaw.
Also, unlike in books, there is no beginning-to-end reading frame for the entire chromosome. There are just genes randomly placed along chromosomes. The reality is that the placing is actually not that random but assuming it is can give you a sense of why it can often be fine to recombine two chromosomes and end up with still functional chromosomes.
For the computer program analogy, it would be like swapping files between branches of the same project (thanks @IronSean for his comment).

But what I don't understand is if the genes encode for proteins, how is it that if you have different genes the proteins still all work together? Well I guess then those genes would die out quite quickly unless they worked well with all the other proteins.

Yes, selection does its job at ensuring that only alleles which phenotypic effects are well integrated within the actions of the other genes remain. Also, while there is a level of interdependence, it does not mean you cannot just modify things. In fact, you can often add a new gene in an organism and this organism may well just do fine. We might be more resilient than you would assume at first.

Hmm.. I guess that's why most animals have the same basic layout because that's hard to change whereas eye colour is easy to change without affecting too much else. It sounds like the more complicated we get the harder it is too evolve.

Let's not forget that even after successful fertilization (merging of egg and sperm), many embryos die because of incompatibilities in the genomes.

@Thawn that's a good point. That would `weed out' a lot of unsuccessful combinations.

In the Computer Program example it would be more accurate to say swapping files between branches in the same project, not randomly mixing and matching lines of code. In most cases, swapping some files between branches won't break the whole program.

@IronSean Ah nice. I could not find a good analogy for the computer programs. The one you're giving is perfect and I've added it in the post.

It's also key that unlike most examples of computer code you might look at, DNA is not executed in order but all of it in parallel. So long as your DNA contains the full string for a single protein in tact, it doesn't matter much where in your chromosomes it is. And for some genes, you might have several copies in your genome and losing or gaining a single copy might only have minor affects such as making a dog's nose just a little bit shorter or longer.

Also adding to the book anology, it is more like an library where you exchange, add or remove books. At first glance, it does not change much, but essentially it can change the structure (order) of the books and as library you want all 'important' writework, for it to work.

Can you give a simple example?

Yes. A mother is an entire codebase of Android OS, that boots with a dark blue background and where initial language is set to English (US).
A father is an entire codebase of Andoroid OS, that boots with a dark green background and where initial language is set to English (UK).
Other than that their codebases are exactly identical line-to-line. Recombination: each code line has a chance to be swapped to the code line at the same position.
A child might have a dark green background and English (US) and it will work mostly flawlessly.
You grossly overestimate how different the humans are from each other. (You're biased because you are a human.) Any single species is a group of nearly identical individuals. If the codebases are not very much identical, yes, the result will be garbage, both in programming and in biology. Exactly the same as trying to recombine rabbit's DNA with ant's DNA.
Rabbit and ant are considered different species not because they look differently; but because the codebases after recombination do not work at all.
(Another thing - the codebases over the generations evolved "programming patterns" that made them vastly more tolerant to glitches that typically happen during the recombination. A very very defensive kind of programming, that is really ugly and nearly impossible for a human to read or understand.)

I'd also add that large swaths of the code is functions that are dead and non-functional.  So if the flip-flop happens in them (and they make up the majority of the file), the working functions are intact.

The English language has 26 letters which can be rearranged in combinations of open-ended length, giving colossal variability. According to the Oxford English Dictionary, there are about 170,000 words in current use.
Programming languages are based very loosely on human language structures. Although the pool of "words" is much smaller, they are also open-ended in the sense that the programmer is free to create words or function names.
Both are also sequential - if you do anything other than follow them in the order they were designed to work, you will get gibberish.
Although DNA can be understood as a language it is much simpler than your other examples. It has four letters and all of its words are 3 letters long. That gives you a hard maximum of 64 words. In point of fact, nature only uses 21 of these words, and there is a great deal of redundancy built in.
A "book" in DNA sense is a single gene. The length of a gene varies enormously but the average is about 480 "words". Although the DNA in a book does need to be read sequentially, all the "books" in a chromosome or a genome do not. So long as each "book" is read in order, the "books" themselves can be read individually and still make sense.
So: all recombination needs to do is ensure that the combination occurs in a break between two "books", and everything will work fine. As @user40949 mentioned above, there are processes to ensure that recombination does indeed occur within specific regions between "books". And even if it didn't, a failure would only invalidate a single "book".

perhaps the analogy would be improved by having gene = paragraph, chromosome = chapter, and genome = book?

@JCRM I went with book = gene because the OP was specifically making a comparison about rearranging a book and it making sense. You can't rearrange a gene and have it make sense, but you can certainly rearrange genes on a chromosome and have them still readable, providing there aren't multiple reading frames.

you're absolutely right, I'd forgotten the precise question by the time I'd finished your answer.

Genomic structure, gene structure, and the structure of human culture are quite plastic, and when parts of it get messed up there is usually excess capacity somewhere that keeps the system operating.

Stories, books, tales, songs, etc. are both mutable and recombinable.  From the party game of "telephone" to the creation of new works of art, sections of one work are replaced intentionally or by accident either with original contributions or with pieces from other works. These new works are then selected for fitness for the intended purpose by the creator or by other social mechanisms. The only ones you ever observe are not complete failures by those criteria. This is a pretty good analogy for the type of recombination you are talking about.
If a genetic recombination event ends up making a gene that no longer serves its original function, that is usually OK and the organism will have another way to survive. It may even be more fit (always in a particular context) without the working gene. The non-functional gene may acquire a new function (by further recombination or mutation) over generations. [a paper of mine where we show, that many genes reduce fitness https://www.ncbi.nlm.nih.gov/pubmed/23990803 in particular environments]
You absolutely can "rearrange a gene", some genes anyway, and have it make sense. One example: many genes can be "circularly permuted", the beginning (N-terminus) of the protein can be moved to various positions. [a paper of mine where we do that: https://www.ncbi.nlm.nih.gov/pubmed/12149462]


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Can acetylcholine leak away from the synapse and cause spasms?
I am currently studying Pharmacology and a question came to mind. We know that Acetylcholine is used as a neurotransmitter in the neuromuscular junction, both Sympathetic as Parasympathetic, but as I understand, correct me if I am wrong, they don't interfere with each other because of their locations being physically separated. My question is, could somehow occur the incomplete absorption of Acetylcholine in the receptor of the organ, let's say for a Parasympathetic response and it "leaked" to a nearby muscle or even into a Sympathetic receptor and create a involuntary movement for example?

The enzyme responsible for the breakdown of acetylcholine (Ach), i.e., acetylcholinesterase, rapidly degrades, and inactivates Ach in the synaptic cleft after release. This process is particularly fast, as the synapse has to be cleared of neurotransmitter for a next action potential to occur (Čolović et al., 2013). So no, Ach does not leak away under physiologiocal conditions (Fig. 1).
In fact, common cholinesterase inhibitors that lead to Ach buildup by inhibiting its degradation, do not cause involuntary muscle twitches (spasms) as side effect. However, they do evoke muscle cramps, but that is easily explained by the increased retention of Ach in the synaptic cleft, leading to prolonged muscle contraction.

Fig. 1. Cholinesterase is active in the synaptic cleft. source: Health & Fitness.
Reference
- Čolović et al., Curr Neuropharmacol (2013); 11(3): 315–35

"So no, Ach does not leak away under physiologiocal conditions "
I beg to differ. During times of  psychological stress, after a physical injury or infection, these can interfere with mitochondrial biogenesis and acetylcholine  leak from the neuromuscular junction damaging the sarcoplasmic reticulum and creating a feed forward loop.
Even though the pathophysiology of myofascial trigger points is not fully understood, the hypothesis of acetylcholine leakage is mostly accepted. Indeed, leakage of acetylcholine leads to impairment of sarcoplasmic reticulum with following extensive calcium release, as well as secondary sarcomere contraction and cell membrane damage. It results in local vasoconstriction leading to ischemia and hypoxia [3, 4]. That is why acetylcholine leakage at the neuromuscular junction may be significant in the context of thermal imaging.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7053472/
Myofascial Trigger Points Therapy Modifies Thermal Map of Gluteal Region
Grzegorz Onik, Teresa Kasprzyk, [...], and Karolina Sieroń
Zhuang X, Tan S, Huang Q. Understanding of myofascial trigger points. Chin Med J 2014;127:4271–7.
Bron C, Dommerholt JD. Etiology of myofascial trigger points. Curr Pain Headache Rep 2012;16:439–44.


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Reading an amino acid physicochemical properties diagram
I want to know if I am reading the venn diagram correctly and why there are discrepancies in the diagrams.
I'm trying to determine which amino acids are considered hydrophobic and I am using this diagram suggested by my teacher from Amino acid properties and consequences of subsitutions.

From the diagram I've determined that A, G, C, T, V, I, L, F, W, Y, H, K, M are hydrophobic.
My problem is when I visit other sources I do not get the same results. Using Amino Acid Table I determines that A, G, I, L, M, F, P, W, Y, V were hydrophobic:

Furthermore, there is even another different venn diagram from Decoding the Building Blocks of Life from the Perspective of Quantum Information

Polarity and hydrophobicity are not discrete phenomena and, therefore, categorizing amino acids as such has some measure of arbitrariness, especially at edge cases. It all depends on one’s definition.
Other properties have similar problems. Charge depends on pH. And what is the cut-off between “large” and “medium” sides chains?
What is, in my opinion, more important than memorizing charts/diagrams/etc (unless you have an exam) is understanding why different amino acids have these properties. For example, why can threonine or tyrosine be classified as both hydrophobic and polar? Why can cysteine or serine, which are classified as uncharged, act as strong nucleophiles in enzymatic reactions?

What search terms should I use to research which amino acids can be classified into multiple properties?

@JohnnyJohnston — You don't seem to understand the remark in the answer about "understanding why different amino acids have these properties". You need to look at the structures, look at the classifications, and then use your knowledge of chemistry to see how they apply. If your chemistry is inadequate for this, you need to remedy that deficiency before you can proceed further. Let us know and we can recommend some reading.

@David Thanks for the reply. My knowledge in chemistry is very limited and close to zero.

@JohnnyJohnston — You might try The Biochemical Society's "Essential Chemistry for Biochemists" or The Royal Society of Chemistry's "Chemistry for Biologists".


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Are nosebleeds unique to humans?
Are there other species that get nosebleeds? If so, do they occur for the same reasons that humans get nosebleeds? How would an animal stop a nosebleed?

Cats, dogs and other animals can suffer from epistaxis.  The causes differ depending on the animal.

foreign things in the nose, abscess, cancerous growth, snake bite, some poisonings and diseases especially in the trachea and lungs and anthrax. Sometimes excessive sneezing or coughing can result in nose bleeding as well. All animals are susceptible to get nose bleeding.

They would need to see their vet or owner to get it treated.
https://www.thevillager.com.na/articles/7474/Dealing-With-an-Animal-Bleeding-From-the-Nose/

Nose bleeding (or epistaxis, as Graham rightly termed it) is common to many species, such as dogs, cats, pigs, and many other animals.  As for the causes, like Graham pointed out, it really varies from species to species.
To take dogs for an example, the leading causes of spontaneous nose bleeding are leishmaniasis (a tropical / subtropical disease transmitted by sandflies) and other bacterial infections, such as CME (canine monocytic ehrlichiosis, a disease spread by ticks).
As you can imagine, minor trauma to the nasal region can also cause nose bleeding, not just in dogs, but in many other animal kinds.
That said, I feel sorry for the elephant who gets a nose bleed.

Sources:

A retrospective study of 61 cases of spontaneous canine epistaxis, . Mylonakis, M. N. Saridomichelakis, V. Lazaridis, L. S. Leontides, P. Kostoulas, A. F. Koutinas, 2007
Leishmaniasis, Wikipedia
Monocytic ehrlichiosis in dogs, Procajło A1, Skupień EM, Bladowski M, Lew S.
A Porcine Epistaxis Model: Hemostatic Effects of Octylcyanoacrylate, Adam J. Singer, MD, Steve A. McClain, MD, Arnold Katz, MD, 2004


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Minimum hardware and knowledge to study effects on live cells
I'm very interested to study the effects (or reactions) of different forces (magnetic fields, electric fields, etc) on living tissues/cells.
I know I have to have a living cell, the force applied and a microscope to study this but I do not know what kind of microscope will do and what kind of living organism to use (and how).
Any help to get me started will be of a tremendous help.

This is too broad of a question. You might wish to research first and come back when you have a specific question. Basically you are asking how to study cellular responses to physical stimuli - much broader than that in the field of cell biology is next to impossible. You might wish to visit our help center. Note that each stack has its own unique help center.

Quite contrary - this is a very beginner question in a vast domain. All I need is a simple/basic guidance for it. If every time you ask a question in a new field you are invited to take a walk (aka "search the internet") then we will never advance or start to become cautious with the people from that field.

A beginner question, yes, and that's fine. It's just too broad. It's an open-ended question and pob

I want to start with magnetic and electric fields only to see if it works and then to move to the more mysterious "qi" energy field....but I need to start from something...

The "minimum hardware" you need consists of, at least:

a microscope, as you said (which one exactly depends on what you want to do with it);
whatever device you need to apply physical stimuli to cells (again, it depends on what you want to do exactly);
a cell culture incubator;
a cell culture hood to be able to work under sterile conditions;
a dedicated cell culture room where to put the previous two items;
a cell line to perform experiments on (actually, more likely several different cell lines).

Your question sounds like you are thinking about a personal project, but consider that none of these items is cheap. Add them up, and this project is really not affordable with the finances of an average individual.
The "minimum knowledge" you need consists of, at least:

knowing how to do cell culture (mostly working under sterile conditions, which not only requires proper equipment but also very specialized technical skills);
knowing (at least some of) the scientific literature about cellular responses to physical stimuli, because no lab is going to hire you as an intern if the project you have in mind has already been done and its results published years ago. You can search the biological scientific literature using PubMed.

So, to me it seems that your best chance of starting this project is to find a cell biology lab with this equipment and expertise, and do an internship there. You can start by looking this up on the website of the university closest to you.

Thank you for your comment - at least you split the problem into many more manageable ones. I think the basic start for me is to get the "basic kit" for this kind of experiments. For example minimum microscope specs, most basic cells (that are easy to grow and handle) and easy to observe.


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Is there a statistical analysis test I can perform that will give me a estimate of total population from my own smaller data sets?
Doing my dissertation on the long term trends in moth populations. I am looking at the trends of specific species. Is there a method to obtain an estimate of total population from smaller samples?

Do you mean estimate of population size? From what kind of samples? Do you have genetic data? do you have capture-recapture data, ...?

The point of a statistical test is not give you an estimate, it is to test a null hypothesis.

@Remi.b I disagree with the statement that statistical tests are used only to test null hypotheses. Statistical tests can be used to estimate population parameters, of which population size is one.

@kmm IMO, one might use the statistic that the test returns when you use a given package, but per say, a test means that you want to "test" a hypothesis for the sake of testing it. If the OP is trying to estimate a parameter, (s)he does not need to make any test. If (s)he has a hypothesis he wants to test (like the population size is equal to 2000), then (s)he needs a test. Asking "Was statistical test estimate this parameter?" sounds wrong to me (it should either be "How to estimate this parameter?" or "How to test to the null that the parameter is 2000?").

Why is this "too broad"? This is a very specific question on which there is a large and relevant literature. Just because you're not familiar with the topic doesn't mean it's off topic.

@iayork I agree, this should be reopened. The Q could show more effort and background, but I dont find it too broad.

I'm assuming you're asking how to estimate population size based on numbers of individuals you capture. Yes, there are many approaches to this. The R library SPECIES-R offers a number of methods of calculating this. They are described in the manuscript SPECIES: An R Package for Species Richness Estimation. Some of the methods described are:

Chao, A. (1984), Nonparametric Estimation of the Number of Classes in a Population, Scandinavian Journal of Statistics, 11, 265-270.
Norris, J. L. I., and Pollock, K. H.(1998), Non-Parametric MLE for Poisson Species Abundance Models Allowing for Heterogeneity Between Species, Environmental and Ecological Statistics, 5, 391-402.
Chao, A., and Bunge, J. (2002), Estimating the Number of Species in a Stochastic Abundance Model, Biometrics, 58, 531-539.

and many more.

±1 for your well referenced answer. My motto still is that a good answer can make the question. Perhaps you could add a little background in the question post.


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Why has the term "natural history" been used to denote the study of nature, and more recently, of life?
The term "natural history" is a translation of the Latin phrase historia naturalis meaning "the story of nature". Nowadays denoting the study of life, it originally also covered astronomy.
Why has there been the notion of "story" here, even in studies that by themselves have taken the form of the classification of collections using a principally synchronic approach that has paid little attention either to changes that organisms experience during their lifetimes or to evolution?

Interesting question, might it be better over at https://hsm.stackexchange.com/ ?

This is two questions. SE prefers just one. I suspect the linguistic asumptions in the first question may be over-simplistic, and that question better put (after some research) to SE English Language and Usage. For the second (recent usage in astronomy) it may be better follow @gilleain suggestion.  Neither are questions of biology.

I'm voting to close this question as off-topic because it is not about biology. It may be appropriate for the History of Science and Mathematics StackExchange site.

Argh, the annoyance of button-selected "reasons". @gilleain has a point. I'm not sure which is best, but I think probably here because it's mainly about biology insofar as "natural history" mainly covers topics within biology nowadays, and even if you take something like the Natural History Museum in London, it's all about living species, biology. I do accept that you can say well at some point for a few writers the term encompassed astronomy as well, which isn't in biology, which is a fair argument. Maybe offer your thoughts, mgkrebbs, before clicking a button?

I think the question is better combined, because it could get an answer from someone who can write at length about the history of the term and it's not as if the two parts can sensibly be considered totally separately. "Why has the term 'natural history' been used recently to denote the study of life?" would obviously be about biology, @David, and equally obviously neither part of the question is principally about English language and usage - see the reference to Latin in the question.

I am afraid what is "obviously about biology" and what are valid topics for this question and answer site about biology are two different things. As an aside, I haven't ever heard the term Natural History used in a modern scientific context, and if indeed it is used today in Astronomy, that is no concern of this site. I repeat that if you want to understand the history of the word you'd be better on EL&U. There are people there who actually know how the word scientia was used in Latin, and are aware how late the word science entered the English language. Have you researched this yourself?


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what is the classification of this stream insect?

This insect I found from Southers region of Bangladesh. Its limbs are larger than its body.and the picture shows its dorsal part.

This is a Water Strider (Order Hemiptera, Family Gerridae); the end of the abdomen is not in focus, so it's impossible to say if you have an apterous adult (of a subfamily other than Gerrinae) or a nymph; if the latter is the case a species-level identification will likely not be possible.

Most probably it is Trepobates sp.


text:
How is (Insect) population control through male sterilization effective
This is no doubt a simple question.
I was reading about Sterile Insect Technique where sterile males out-compete non-sterile ones to mate with females and thus reduce the population.
My question is - why don't the females just re-mate after they don't reproduce?
I'm assuming that the number of sterile males will be much less than the existing male population.
Is it because my assumption is incorrect and there are more sterile males?  Or my assumption is correct and given the life-cycle of the organism, the females have only once chance to mate?  Or something else?

Sterile insects are typically produced by radiation. A sufficient dose is used to cause substantial DNA damage in the gametes of the males. However, this doesn't mean the sperm are completely non-functional.
In fact, it is important that the sperm are functional and simply contain dominant-lethal mutations at a sufficient probability (Robinson, 2005 describes this in detail as well as the dosing strategies to optimize the desired outcome).
The males still mate and fertilize the eggs of the female; it is only later that the eggs will eventually fail to develop, but there is no way for the females to be aware of this (nor much that can be done even if they were - once the eggs are fertilized they cannot be fertilized again).
It is also important to release a sufficient population of sterile males to impact the population. Depending on the species, it may or may not be necessary to completely overwhelm the existing population, but a typical goal seems to be 10-100x the native population. By raising males in laboratory conditions, it may be possible to produce a larger population than would typically survive to mating age in the wild.

References:
Cockburn, A. F., Howells, A. J., & Whitten, M. J. (1984). Recombinant DNA technology and genetic control of pest insects. Biotechnology and genetic engineering reviews, 2(1), 68-99.
Klassen, W., & Curtis, C. F. (2005). History of the sterile insect technique. In Sterile insect technique (pp. 3-36). Springer Netherlands.
Robinson, A. S. (2005). Genetic basis of the sterile insect technique. In Sterile Insect Technique (pp. 95-114). Springer, Dordrecht.

Finally some quality content. What a relief. +1

@AliceD Haha I've been trying where the questions warrant it. Unfortunately it seems most of my answers have gone unnoticed lately, based on the very low total view counts in the 30-40 range even after several days. Just not much of a voting population around lately.

Excellent answer @BryanKrause.  As to your dilemma, perhaps this is due to the rise of pseudo-science.

Yes, voting is a hitting rock bottom. I'm trying to spend more time here again. I've been investing my spare time over at Psych mostly.

Good answer, but "In the cases I am aware of, this technique is used with species that only produce one batch of offspring" - the main case I'm familiar with is mosquitoes, where this isn't true.

@arboviral Thanks - I'll remove the statement. Although from some brief research it looks like mosquitoes still only mate once? Can you confirm that?

@BryanKrause As far as I know females have one receptive period, and normally mating is inhibited once sperm are transferred (hence mate once), but you sometimes get incomplete sperm transfer and therefore multiple mating (https://www.cambridge.org/core/journals/bulletin-of-entomological-research/article/multiple-mating-in-female-mosquitoesevidence-from-a-field-population-of-anopheles-freeborni-diptera-culicidae/1CA5BD9936FA474774B638280CC5DD03). Males can mate with several females.

@Bryan it's fine as a first approximation though - the vast majority will only mate once. So it makes virtually no difference to your original statement now I think about it - sorry :)

No worries. I'll leave it removed. I think if anything it distracts from the main point of my answer, which is that these sterilization strategies are predicated on making sterile embryos rather than males completely incapable of mating.


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What is the precise mechanism by which exercise reduces chance of cancer?
Sources like this: http://www.cancerresearchuk.org/about-cancer/causes-of-cancer/physical-activity-and-cancer/how-physical-activity-prevents-cancer point out that we can reduce our risk of some cancers by exercising.
But it seems to just be hypothetical, like "scientists think insulin can turn on signals that tell cells to multiply", and
"This can lead to the cells multiplying much more frequently than usual, to replace dead and damaged cells, increasing the chances of mistakes that could lead to cancer"
But human metabolism significantly increases during and after exercise, implying high rate of cellular division! Therefore, these 'hypotheses' seem questionable in their attempt at saying, "cells don't divide as much". I believe that these may be contributing factors, but I don't believe they're the main cause of most cancers in general. I am deeply skeptical that muscle inflammation requires less cell division than colon inflammation.
I have a hypothesis that exercise simply reduces cancer in the following manner: increase cellular movement, which increases the probability of the following:
1) t-cells tag foreign pathogens
2) white blood-cells capture foreign pathogens
3) damaged cells are repaired/found/killed faster
Statistically, increasing the entropy of a system would allow the individual components to cover a larger area in a shorter amount of time. Since the number of pathogens introduced into the system remains relatively constant while the interal system speeds up, it's like running a high-pressure jet stream of water and soap through pipes to clean them out. The soap (t-cells) and pressure (contractions of heart/blood vessels) together help clean the system effectively.
I'm having trouble finding evidence/support for this hypothesis, so if someone could point out the flaws in my hypothesis or point me to some sources to find out more, I'd be deeply appreciative.

Check mTor downregulation during exercise.

I think the only answer here is "nobody really knows why, it's something that's been discovered through statistical studies".

Come on, comments aren't for answers, people...

No one knows, it's just a line of research

Can you cite any evidence at all that exercise does any of the list you have?

Vigorous exercise (even for five minutes) causes increased DNA damage http://www.ncbi.nlm.nih.gov/pubmed/20839226. The increased DNA damage would stimulate the defenses including the immune system (e.g. natural killer cells) http://www.ncbi.nlm.nih.gov/pubmed/16618710, and the boosted immune system would eliminate cancer cells, reducing cancers based on the immune suppression model of cancer http://www.ncbi.nlm.nih.gov/pubmed/27928220. The reduction of cancers with increased exercise (physical activity) has indeed been observed http://www.ncbi.nlm.nih.gov/pubmed/18506190.

You did notice that your last link offers a completely different MOA then the one you put together?

Welcome. It's good practice to give the full citations, just in case the link goes down. Nice referenced answer +1

This answer gives good information, but doesn't really answer the question because if individual organisms could just stimulate the immune system without an adverse effect, why would they need exercise to do it?


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Emulsifying action of bile salts
n my book, It is given that the action of Bile salts (a part of Bile juice) is similar to the emulsifying action of soaps on dirt. The role of bile salts is to break down the fat into smaller globules.
I don't understand this and cannot find it on the internet. Can someone help me with this?

The Wikipedia entry on Bile says it all:

Bile acts to some extent as a surfactant, helping to emulsify the lipids in food. Bile salt anions are hydrophilic on one side and hydrophobic on the other side; consequently, they tend to aggregate around droplets of lipids (triglycerides and phospholipids) to form micelles, with the hydrophobic sides towards the fat and hydrophilic sides facing outwards. The hydrophilic sides are negatively charged, and this charge prevents fat droplets coated with bile from re-aggregating into larger fat particles.


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Can plants suffer from CO2 poisoning?
Is there a point where too much CO2 is bad for a plant? Basically when there is too much CO2 in the air can a plant get sick?
Since plants photosynthesize and need CO2 to generate glucose and store starch, and since chemical reactions are pushed toward their end product when the reagent concentrations are increased, one would expect that more CO2 would be better, at least lead to increased growth and survival rates.
Is there a ceiling where CO2 gets toxic?

I have taken the liberty to add some background. Feel free to roll these changes back.

I'd question whether CO2 availability is really much of a limiting factor in plant growth.  I would think it would be the energy available from sunlight, if growth isn't limited by other factors such as water, temperature, nitrogen & other soil nutrients...

Many trees at Mammoth Mountain have died due to CO2 poisoning. See https://pubs.usgs.gov/fs/fs172-96/ for more info from link: "High CO2 concentrations in the soil kill plants by denying their roots O2 and by interfering with nutrient uptake. In the areas of tree kill at Mammoth Mountain, CO2 makes up about 20 to 95% of the gas content of the soil. "

Short answer
It has been shown that plants may already suffer from doubling the atmospheric CO2 concentration from 340 to 610 ppm, something that might happen during the next hundred years or so based on current emissions.
Background
A popular science website tells us that an excess of carbon dioxide (CO2) reduces the rate of transpiration of some plants. This is so because the stomata, which are the openings of the leaves (Mansfield & Majernik, 1970) and used for exchanging gases as well as water vapor (transpiration) will close when there is too much CO2 in the air, or other polutants such as SO2. As transpiration drops, the water flow from the soil to the leaves also drops, causing a runoff of water.This in turn stalls nutrient uptake. Indeed, doubling the present-day CO2 concentration to 610 ppm does not necessarily lead to increased growth and may in fact inhibit growth due to excess starch formation in the leaves, indicating it's simply stored as backup energy, nothing else (Coviella & Trumble, 1999). It is believed that plants might be near their saturation point and cannot eliminate CO2 faster than they are doing right now.
Somehow plants also become more susceptible to insect foraging when CO2 concentration increases.
Note however, that CO2 tolerances are species dependent. Most research in this arena has focused on common crops. CO2 tolerance in for example cotton plants is low, and starch buildup has been observed in the entire plant, but especially in the root systems and the stem (Hendrix et al., 1994). Other species, such as wheat and rice are less prone to effects of elevated CO2 (source: Nature).
References
- Coviella & Trumble,  Conservation Biology (1999); 13(4): 700–12
- Hendrix et al., Agricult Forest Meteorol (18994); 70(1–4): 153-62
- Mansfield & Majernik, Environmental Pollution (1970); 1(2): 149-54
Source
- Earth untouched

So did plants in the time of the dinosaurs simply carry adaptations to allow for a higher saturation point and thus greater use of CO2?

In case the OP wanted to see an example of CO2 killing plants, there's a place in California where this happens due to volcanic activity:  https://pubs.usgs.gov/dds/dds-81/Intro/facts-sheet/GasKillingTrees.html

@TheEnvironmentalist Ferns have been found to do well at high (3360 ppm, 10 time pre-industrial levels) CO2.  https://link.springer.com/article/10.1023/A:1006805427943

In situations with extreme excess of CO2, plants experience "excess starch formation" because it is "stored as backup energy" and it "inhibits growth"? So... Global Warming makes plants fat?

"... something that might happen during the next hundred years or so due to current global warming." Are you saying that warming increases CO_2 levels?

Good answer, but I think it's missing a critical point - different plants have vastly different tolerance. Many plants benefit from even large increases in CO2 levels (algae love CO2, as do many ferns etc.), while many can be stunted in growth or outright killed by a "mere" doubling. Also, I don't think it's warranted to say the increase in CO2 is "due to global warming" - even if the increase in CO2 levels is due to increases in global temperatures (and not vice versa, for example), it's not something you can just flatly assert without references, and the cause isn't really relevant.

@Luaan thanks for these comments. I have added several lines and additional references.

@jpmc26 - you are right, this was an error in my answer. I have removed it.

@jpmc26 Mind, increasing temperatures certainly do increase CO2 levels. Warmer oceans mean lower solubility of CO2, which means it's released to the atmosphere. Melting permafrost releases tons of CO2. There's plenty other examples, and likely many we have no idea about. Nothing surprising about that. But AliceD's formulation was certainly... tricky.

@Luaan you are right, and carbon release is a vicious circle. However, as you say, my wording was too blunt, but expanding on it is outside the scope of the question. Cheers

It depends upon the plant species.
As explained in Algae thrive under Pure CO2 Nature 227, pages 744–745 (15 August 1970):
Cyanidium caldarium (an algae found in Yellowstone National Park) grows much better in pure carbon dioxide than in air.
However, other plants can suffer from acidification of cell fluids at high carbon dioxide concentrations.
In Elevated Atmospheric Partial Pressure of CO2 and Plant Growth Oecologia (1979) 44: 68, it was shown that increasing CO2 concentration to 640 ppm from then-normal 330 ppm caused increased growth for both cotton (a C3 plant) and maize (a C4 plant), but the increase was much greater (100%) for cotton than for maize (20%).
According to The optimal atmospheric CO2 concentration for the growth of winter wheat (Triticum aestivum) J Plant Physiol. 2015 Jul 20; 184:89-97, photosynthesis at 968 ppm CO2 is optimal.  At 1200 ppm, photosynthesis is less than optimal, but still much higher than at current ambient CO2 levels of about 410ppm.

Since you need water to live, seem you would be peachy dropped on the bottom of the ocean ;)
Organisms usually adapt to specific conditions. In particular, plants need oxygen to actually consume the glucose produced in the process of which oxygen is a byproduct.
Is it possible to imagine an organism adapted to not having oxygen, by storing its own oxygen for reuse later? It sure is, and it might have been what originally happened in the original oxygen-free atmosphere.
But as a matter of fact, in the current oxygen-rich atmosphere this ability would be completely useless, just as it would be for you to bring everywhere a backpack full of air to breathe. As a consequence, no mayor plant does it; and it would take centuries of evolutionary pressure to develop it.

Most animals have anaerobic metabolic pathways. As you scale up, they tend to be progressively less capable of supplying all the metabolic needs of the organism, but they're there. Many plants evolved during a time with much higher CO2 concentrations in air, and some (like the vast family of algae) have essentially no upper limit on its concentration. Lots of plants need oxygen, but not all of them. As it is, your answer isn't very helpful - it would be better to include examples with references, rather than misleading metaphors and arguments from evolution.


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How can census population size be smaller than the effective population size in some species? is that possible?
The only way I can think this could happen is through a recent population bottleneck. Can it be possible though ?

Why are you asking? Have you encountered a case where the census population is considered smaller than the effective pop size?


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How is bad garlic breath eliminated by swalllowing a bit of raw garlic?
Please bear with me, as I am just a poor physicist.
I have learned how to make traditional pastourma  from a recipe given by my late aunt Dora, which is like pastrami except with a very strong garlic contribution and a lot of other spices. This leads, after eating, to strong garlic breath. My daughter complained of the "stink" when she was near me.
I somewhere heard that if one swallows a bit of raw garlic before eating food with strong garlic content, the breath stays fresh. I have tried it several times, and it works (my daughter the detector). It seems magical, or homoeopathic!
As a physicist, I would like to know how is this possible?

Searching the net for "how to avoid garlic breath" some references come up.

Enter Ohio State University to help. Researchers there have evidence suggesting that we can neutralize bad breath naturally before it offends those around us. According to science, here are three ways to do it.

Recommended: raw apples, lemon juice, green tea.

Green tea is very high in antioxidants called polyphenols. As with the enzymes in the apple, polyphenols cover up the odor-causing chemicals in garlic.
Sheryl Barringer, one of the study's lead researchers, said that it’s best to use the bad breath cures at the same time you’re eating garlic. So we’d recommend adding some apples to that salad with garlicky dressing or using some lemon juice in your next garlic dip. Unless you want to squeeze the citrus straight into your mouth, that is.

And in a link found there, the chemical explanation is:

According to the researchers, foods deodorize garlic breath through two mechanisms. First, enzymes in the raw foods help to destroy the odors, and then, phenolic compounds in both the raw and cooked foods destroy the volatiles. This is why raw foods were generally more effective because they contain both the enzymes and the phenolic compounds.

It must be that raw garlic taken just before eating garlicky stuff works the same way. No magic. Maybe the researchers will see this and do a proper experiment :).


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Are all diseases caused by organisms (microorganisms)?
Are there other causes? Or is it correct to say that all diseases are in fact caused by organisms (microorganisms)?

It is not correct to say that all diseases are caused by foreign organisms. Counterexamples are:

Cancer is caused by random genetic mutations in the cells of our body. The mutations can be caused by many factors such as ionizing radiation, smoking, chemical toxins etc.
Diseases such as stroke or heart attack are caused by blood clots blocking the blood flow to essential organs.
Autoimmune diseases are caused by the immune system falsely recognizing cells of the body as foreign and attacking that tissue leading to a wide variety of symptoms.
Alzheimer's disease is caused by chronic neurodegeneration, meaning that the cells in the brain die. The causes are not quite understood but as Alzheimer's usually appears late in life it is likely related to ageing. Also, it is known that some genetic defects can lead to early-onset Alzheimers.
Prion proteins can cause diseases such as Creutzfeldt–Jakob disease also known as mad-cow disease.
Hereditary diseases such as early-onset Alzheimers or ALS are cause by gene defects inherited from the parents.
Toxins can cause chronic diseases such as lead poisoning.

The list probably goes on...
Please note that the first two on the list are the most common cause of death in developed countries.


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Hayflick's limit and cell division
Suppose the Hayflick's limit of a cell is 10 and it divides 10 times.  At this point, it undergoes differentiation.  Is it possible for it to undergo dedifferentiation at this point?

I don't think so naturally. I think the general stream of the progeny goes stem cell => pluripotent cell => progenitor cell => specialised cell.


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Is prokaryotic chromosome really a chromosome?
As far as i know, chromosome is a highly compacted version of chromatin during mitosis. And chromatin is a complex consisting of DNA strand and histones for more effective storage of DNA.
And I'm heard(not actually 'learn' it) that chromatin is only found in eukaryotic cells and prokaryotic cells have a different organization of their DNA.
Taken together, prokaryotes don't have chromatin and don't have chromosome either since chromosome is a upgraded version of chromatin.
But many medium including books and internet sites call prokaryotic organization of DNA chromosome(especially E.coli chromosome)
Hence, my question is:
Is it just a wide use of chromosome term in prokaryotes? or my knowledge of chromatin and chromosome wrong?
*plus, I searched about this problem previously and am heard that the prokaryotic chromosome equivalent is called genophore. How about genophore?

Initially, chromosomes got their name from the ability of eukaryotic metaphase chromosomes to bind certain dyes. The word chromosome is Greek for "colored body".
Nowadays, the term chromosome refers broadly to a single DNA molecule, no matter the organism. Hence the term "E. coli chromosome".


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In humans, are diseases inevitable during old age?
Considering that dying "from old age" actually means that one dies from an illness related with aging, is it inevitable to eventually acquire diseases in old age?

The first part of OP (supposition that dying from old age means that one dies from an illness) isn't required for the very interesting underlying question, whether diseases are inevitable.

There is a thought that aging itself should be considered a disease. In which case, death by disease is inevitable with our current level of medical technology.

During the last 25 years, by targeting the underlying processes of aging biomedical scientists have been able to improve the health and lifespan of model organisms, from worms and flies, to rodents and fish. We can now consistently improve the lifespan of C. elegans by more than ten-fold (Ayyadevara et al., 2008), more than double the lifespan of flies and mice (Bartke et al., 2001; Sun et al., 2002), and improve the lifespan of rats and killifish by 30 and 59%, respectively (Valenzano et al., 2006; Zha et al., 2008) (see Figure Figure11 and Supplementary Table 1). Currently, our treatment options for the underlying processes of aging in humans are limited. However, with current progress in the development of geroprotective drugs, regenerative medicine, and precision medicine interventions, we will soon have the potential to slow down aging (Bulterijs, 2011, 2012).

Aging is not synonymous with disease, and hence it is generalized as such, although vulnerability to diseases does increases over time.
Why is it not a disease? Well biological aging can be defined as:
A process of progressive, intrinsic, and generalized physical deterioration that occurs over time (begins at the age of maturity).
While a disease is:
An abnormal condition of an organism which interrupts the normal bodily functions that often leads to a feeling of pain and weakness, and usually associated with symptoms and signs.
Now let's look as to why we cannot live forever and as to why as we get old our disease susceptibility will be (in general) increased, meaning that yes the majority of the population will be dying from a form of a disease. If not a disease it will be a failure of the body system to maintain life.
I will be looking at this in the form of Natural Selection.
The force of Natural Selection declines with age. For example, a gene that is beneficial during young age, but bad during old age (such as making you susceptible to several diseases) will spread in the population because it will manifest after you've reproduced.
Example#1: A gene that helps achieve good blood coagulation and prevents hemorrhage in young people will spread in the population. However, in old aged people, it will cause an increased risk of stroke. Such associations have been previously found for many genes associated with blood characteristics.
Example#2: Overproduction of sex hormones in young age is beneficial for reproduction but will cause prostate and ovarian cancer later in life.
This is called Antagonistic Pleiotropy
In addition, Natural selection is not concerned with late acting mutations.
So as we age will we be afflicted by a disease? Most likely yes, it depends on the trends in disease prevalence which have changed throughout the years due to preventative medicine. If we do not acquire any death-inflicting (be it slow or fast acting) disease, our body will give up before we do get one.
If you'd like to look at disease prevalence, chronic illnesses throughout the years, or the specific trends in a year, just go over to the CDC's webpage.

"Old age" diseases are fundamentally malfunctions because stuff breaks. Some blame this on shortening telomeres, although an equally big part of the problem is that there are way too many important pieces that are unable to regenerate themselves.
Think of it as a machine where you can't normally get replacement parts. Stuff wears out, goes off warranty, and breaks.
Experimental regenerative medicine is working on fixing that with 3 fundamental approaches:

Adult pluripotent stem cells/regrowth. Researchers are looking for growth/regrowth/cell proliferation and differentiation mechanisms that already exist so they can be leveraged to regrow stuff that normally doesn't regrow. The advantage is that all the parts are grown from your own DNA or cells which means minimal problems with rejection or incompatibility. As an added bonus it could be considered "all natural". The main risk is cancer due to misconfigured cell growth/proliferation.
Lab-grown or 3D-printed replacement. Higher risk of rejection and other problems but simple and cheap compared to the others. Some research includes growing human-cell transplants in animals which raises various ethical and safety concerns.
Cybernetics or machine implants. Probably the most expensive and works out the best... when it works properly. "Robot" parts keep getting better and better, and have the bonus that they are more readily reprogrammable than DNA and biochemistry. A prominent research area includes brain/nerve interfaces with machine parts - expect pieces that either adapt to neural outputs or connect to nerves so you can "learn" how to use them.
The main drawbacks of this approach other than the cost include vulnerability to EMPs (a massive solar flare or EMP attack will fry all unprotected cybernetics/implants/robot parts), being dependent on both electricity and regular food, risk of getting hacked, and general lack of self-repairability short of replacing parts that break (again). Alternately you could argue that the risk of getting hacked through cybernetic implants and robot parts is a fair tradeoff considering they're immune to organic viruses and infections (except if someone invents bacteria that eat through solid metal or plastic pieces)

Thank you for the detailed answer. But I still don't know if it's inevitable to eventually acquire diseases in old age or not. Could you clear this up for me, please?

If you wonder about the downvotes, I assume folks are missing references and sources. Further, you're talking about robots and so forth, while the question is on dinosaurs. And please keep your comments in check. Commenting is encouraged, but not mandatory when downvoting. Downvoting is an integral part of SE.

No one mentioned dinosaurs until AliceD pulled that #FakeFact out of nowhere. As should be obvious from my answer, stuff breaks over time so you're going to get "diseases" in old age if you don't implement any of the regeneration or replacement plans I mentioned. Finally, I refuse to be censored. I'm helping you all out and telling all of you how to avoid "diseases" in old age, the least you can do is post a thank-you. If you don't like it then I can stop contributing.


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Why can't we directly use the DNA instead of the RNA in a DNA microarray analysis?
When proceeding to a DNA microarray analysis, I saw that the molecule that's taken from the cell is the RNA, which is afterwards converted to DNA by a reverse polymerase. But why not taking directly the DNA out of the cell?
EDIT : still about the DNA microarray method, I'd have another question: how can one be sure the DNA strands of the matrix are going to hybridize with the sample that one want to test?

Your second question has little to do with the first one. Please consider opening another dedicated post for this second question.

Before posting a question like this, please stop and think. If you had asked yourself what you are analysing by microarray you would know the answer. I am voting to close this question as it does not show sufficient prior effort.

The context I've heard of that method was exclusively DNA sequencing.I didn't know it finds applications in analysis of RNA - because I'm no professional, you know, which is why I post a question here. Your comment is even more useless than my question.

You guys are so stupid... You're so posh with your little conventions, you think science is a game with precise rules, and the one who's not rigorous enough has lost. Please consider the mortal people like me and their right to access to the sciences.

In each diploid cell, there are exactly 2 copies of every single gene.  No matter what the cell type, no matter what you do to the cell.  (Barring exceptions like some blood cells and cancer)
But RNA expression is what differs between cell types and conditions.  Some cells make some RNA, some make others.  Under some circumstances, a cell might make more of one RNA than at another time.  Changes in RNA are what is worth measuring.  DNA doesn't change.
RNA is converted to DNA because DNA, being double-stranded is more stable, less likely to degrade.

RNA is extracted an analyzed because one possible application of a microarray is to quantify mRNA levels. As with other methods (for example RT-PCR), RNA is first reverse transcribed into DNA to make it compatible with the downstream protocol. Most procedures are indeed optimized for working with DNA, so it is easier to reverse transcribe RNA as the first step than to tweak everything else to make it work with RNA.
You can also start a microarray protocol with genomic DNA, but then you are looking at something completely different than gene expression. A possible application of a microarray in this case is genotyping.
Wikipedia has a lot of information about microarrays.