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How is the Energy Systems Language used in ecology?
Is the Energy Systems Language useful in systems ecology? It is developed by Howard T. Odum, "the father of system ecology", to make analogies between ecological systems and electronic circuits. But how far this analogy remains correct? What important results have been found from it? Is it widely used by ecologists in other subfields? If yes, then why isn't it applied to other fields?

Related: What are the branches of system ecology?

Energy systems language is definitely still used in systems ecology, ecosystems ecology, and ecological engineering. It can be used in other aspects of ecology depending on the approach of the ecologist, some ecologists appreciate it more than others. For a broad snapshot of how science is currently building upon Odum's 1983 Intro to Systems Ecology, check out a Google Scholar search for the latest papers citing that text by Odum.
In my experience with it, energy systems language and energy flow diagrams introduced by Odum are used as helpful conceptual tools: understanding and organizing complex systems qualitatively and then potentially quantitatively; putting useful constraints and guidelines on brainstorming the effects of adjustments to complex systems; etc. This can be done in a teaching context, helping students understand systems and bridging the fields of engineering and ecology. It can also be done in a high-level professional context, sorting out the intricacies and potential solutions of very complex environmental problems.
I find that energy systems language is used most wherever the study of complexity and ecology intersect. This is especially true in the study of ecological complex adaptive systems and in studying agro-ecology. Even in those cases it depends on the ecologist in question: those with more of an engineering background tend to appreciate Odum's framework, whereas those without an engineering background may rely on other frameworks.

Can you list some other frameworks? What are the differences between them?

@Ooker Outline of ecology lists various ones, especially Landscape Ecology under "Level of Complexity" and all those under "By technique used for investigation" and "By environmental approach". Those all offer distinct ways of exploring ecology, and the same ecological phenomenon could be explored quite differently using those different approaches & frameworks (systems ecology being one of them). The eco-involved interdiscplinary fields will often have frameworks from the discipline(s) they combine with ecology, e.g. accounting in eco-econ.


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What plant is this? (Found in South Thailand)

Have tried to recognize with PlantSnap App, no results.

It looks like Desert Rose, commonly used for Bonsai plantings.

Good ID.  Adenium obesum, in the Apocynaceae as is Plumeria, but from Africa (I almost had it!).

Looks like a Plumeria but there are several species and many horticultural variants.  It's native to the New World.

source: Stack Exchange

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

sort: votes


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Phylogeny: Hybridization between different species sharing same genus?
I am doing a cross-breeding project with Capsicum chinense x Capsicum baccatum. I'm planning to breed them until 6-8 gen.
My question: What will the completed breed be classified as? Would it be a new species or will it be considered as a strain of chinense or baccatum? Thanks.

Hybrids are not considered named species of either of their progenitors, but classified as hybrids of both. So they would be called Capsicum chinense x baccatum.

Well.... all eukaryotes are hybrids.

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


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why hens determine the sex of the chick?
So, I have an exercise where I have to correct the second part of the sentence. It goes like this:

In hens, the sex of the chicken is determined by hen, because the hen is the heterogametic organism

And I really can't find the mistake, please help.
 Also, I'd like to know why hens determine the sex of the chick.

Outside of small eventual semantic issues about the notion of "determination", there is no mistake in this sentence.

Do you know what the sex determination system is like in birds? Do you know how the XY and ZW sex determination system work?


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What is this frog I found
What type of frog or toad is this? I found him in my backyard in southern Alabama and he is clearly very small. I’m not sure what species it is, it’s mostly brown but has small spots on the top of his mouth and under his eyes and he is completely white on his belly. Anyone have any idea what this little guy is?


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Any volumetric data for areas of the brain?
I was trying to write an overview of AI and wanted to quantify some numerical data about the brain.  It is easy to find many sources quoting 100 billion neurons.  However, I would like to get the number of neurons (obviously approximate) in each area.  Also, while I can find the average number of synapses to neuron, it would be nice to know if there are higher numbers is certain areas of the brain.
This is not my field, it would simply be instructive to generate a table of data.
Is there any source, even approximate volume for different areas of the brain?

Not volume, but number of neurons in distinct coarse areas: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2776484/#B46

For the number of neurons, assuming you are referring to the human brain: https://biology.stackexchange.com/questions/53587


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What is this worm-like creature?
It is on my bed sheet. The hairy part the the rear end. The length is about the diameter of a US dime (~18mm).

I don't know about other uses but I am a bit bothered that so many US users are using their currency as unit of measurement. Please do not measure in US dime, US quarter, foot, banana or beer height but use the metric system!

@Remi.b - Americans don't know what the metric system is. Distance in feet, speed in miles per hour and fuel by the gallon ;-)

The other answer is most certainly incorrect. Silverfish are silver/grey and (like all members of the Zygentoma order) have three distinct, tail-like caudal appendages from their posterior end -- really, two large cerci with a central long filament.
 [Sources: 1, 2, 3].
The OP's specimen resembles the larva of a dermestid carpet beetle of some type; specifically, the location and appearance make me think it might be a black carpet beetle (Attagenus spp) -- for example A. unicolor.

 Source: Univ of California Master Gardener Program of Contra Costa County Blog
Description:
Tell-tale characteristic: the tuft of numerous "hairs" on the posterior end:

The larvae of the black carpet beetle, which may reach 12.7 mm in length, are very different from other carpet beetles’ larvae. They are elongate, carrot-shaped, golden to chocolate brown, and have a tuft of very long, curled, golden-brown hair at the tail end of their body.  [Source: Penn state Dept. of Entomology]

A description from IFAS suggests that larvae develop stiff, bristlelike tails when older.

See bugguide.net for more pictures, such as this one
Pest:
According to many of the sources I've linked to already, the larva is the damaging life stage of this beetle.

It's hard to tell from the image quality, but is it a silverfish? It has roughly the same body shape and size:

(source: umn.edu)


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How to learn and memorize animals classification to get an intuition about them?
I would like to have a good intuition on how close is what animal to which one and how large each group is by number of species and population. I was wondering if there is a good website with good demographics and graphs that could help me memorize it because it's really so hard to make up the tree myself from wikipedia pages!

There is a very good website and application for that. It's called Onezoom tree of life explorer which I believe is for London imperial collage.

OneZoom won't be of much help for sometimes to get a broad vision of the most considered branches of the tree of life. It is too detail for such purpose.

I'm not choosing this answer so as to gain more attention in hope of getting some better alternatives. If I don't get anything better in a few days I will accept it.

Another alternative is the Tree of Life web project, which includes species richness information in the lower levels of the tree and allows reasonably easy navigation of subtrees. You can find the animal portal here.
EDIT -- another alternative, which is in active development, is this integration of Wikipedia and the Open Tree of Life Hyperbolic Tree.

It is very good! but the problem is that it is very slow! with onezoom it's like a map but with this you have to load the page again each time you navigate which becomes frustrating.

@ladybug you may find that open Tree of Life has a smoother browsing interface. Not sure about number of taxa, though.


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difference between trisomy and partial trisomy
Trisomy is having 3 chromosomes but then what is partial trisomy ?. I was reading about Patau syndrome and it is called trisomy 13 ( because instead of usual 2 chromosomes,it has 3 chromosomes). it was also wriiten that 20% cases are PARTIAL TRISOMIC...what is the meaning of partial trisomic?

I assume you checked Google first? The first result looks like it covers this (https://rarediseases.org/rare-diseases/chromosome-6-partial-trisomy-6q/) - are you asking for further explanation of some aspect of this?

no, actually i was reading from the slides given by my professor

Any organism with a partial polyploidy has got some tissues with a different number of chromosome set, unlike the rest of cell tissues.
These situations are often consequences of meiosis error and are more common in plants than in any other organism.

I think the OP's question is "What does it tell about the genetics of an individual if this individual has partial trisomy?". I don't think the question was "What are the health consequences of partial trisomy?" nor "How does partial trisomy comes to exist?"

Partial trisomy is just an example of a partial polyploidy. So actually I think my answer is short but straight to the point.


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Is there any kind of antibiotic effective against fungi?
I know that antibiotics usually have properties affecting specifically bacterial cells, like by inhibiting peptidoglycan synthesis. but do any antibiotics exist affecting eukaryotic cells, like yeast or other fungi? I read in a text that "most" eukaryotic cells are resistant against antibiotics and that confused me.
Regardless of whether it can be used against bacteria or not, is there any kind of antibiotic effective against fungi, or any kind of eukaryotic cell?

Please be more clear. Are you asking if there's any antibiotic usually used against bacteria who's effective also for eucaryotic cells?

No, regardless of whether it is/can be used against bacteria or not. I know that the antibiotics usually have properties affecting specifically bacterial cells like by inhibiting peptidoglycan synthesis. but do any antibiotics exist affecting eukaryotic cells? like yeast? or fungi? I read in a text that "most" eukaryotic cells are resistant against antibiotics. that confused me

The term antibiotic typically refers to chemicals effective against bacteria. There are antimicrobial chemicals effective against fungi, and they are rather aptly called antifungals.
In general, for every organism, there will be a chemical that is toxic to it.

Good answer, but just one suggestion. Wikipedia's definition doesn't match the use of these terms in infectious disease medicine and pharmacology. Antibiotic (like antimicrobial) is a general term (see Goodman and Gilman Chapter 48, General Principles of Antimicrobial therapy). We have more antibacterial antibiotics, in general, since these pathogens are easier to selectively target, so most antibiotics are antibacterial antibiotics. For that reason, yes, it typically refers to chemicals effective against bacteria, but that's just because there are more of them.

Wikipedia can be a good source, but it is particularly weak for infectious disease principles.

@DeNovo Wikipedia was not my source, I just included those links for further reading. In my field, antibiotic and antibacterial are used synonymously. The WHO and ECDC seem to agree on this. That said, I'm not a medical doctor nor a pharmacist. I don't disagree with your points and you're welcome to edit my answer as you see fit, or post your own.

Yes. The antibiotic (general microorganism “targeter”) you’re looking for is an antifungal. There are fewer ways to target fungi as opposed to bacteria, but we can target them nonetheless.
The fungal cell membrane has ergosterol to regulate its permeability whereas the mammalian cell relies on cholesterol. Fungi have cell walls which are not present in mammalian cells and are different in chemical composition to bacterial cell walls. A fungal cell wall is made of chitin whereas, as you mentioned before, a bacterial cell wall is made up of peptidoglycan.
We rely on these differences to target fungi. Some antifungals bind to ergosterol (e.g. Polyenes like Amphotericin-B) whereas other agents inhibit ergosterol synthesis altogether (e.g. Azoles like Triazole). Other antifungal agents target the fungal cell wall by inhibiting the synthesis of chitin (e.g. Echinocandins like Caspofungin).
There are more ways to target fungi, like introducing nucleotide analogues (“look alikes” that don’t work) to disrupt their nucleic acid synthesis (e.g. Fluorocytosine 5-FC). Another method is to disrupt the fungal microtubule’s aggregation during mitosis (e.g. Griseofulvin), thus “arresting” the fungal cells in metaphase.
Recommended Textbooks:

Hugo & Russell’s Pharmaceutical Microbiology 8th edition, Wiley- Blackwell. Edited by S.P. Denyer et al.
ISBN 9781444330632
Essential Microbiology for Pharmacy and Pharmaceutical Science, Wiley- Blackwell. By Geoffrey Hanlon and Norman Hodges
ISBN 978-0-470-66534-3 (pbk.)

Yes, there is. The Azole class of drugs, for example, are used to treat (eukaryotic) fungal infections. One such drug is clotrimazole which targets cytochrome p450 which is responsible for the synthesis of ergosterol (a mimetic of cholesterol; not found in humans), ultimately leading to excessive fluidity in fungal membranes and their lysis.
https://www.ncbi.nlm.nih.gov/pubmed/3288361
Its not that eukaryotes are inherently resistant to antibiotics; rather, its often difficult to treat serious eukaryotic infections because humans are also eukaryotes and share similar biochemistries. See below.
The problem with clotrimazole is that, although ergosterol is not found in human, the cytochrome p450 is (i.e. in the ETC) and it serves other functions which may be affected.


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Help identifying tiny jumping bug
I've found a few of these bugs hanging out on my desk. There aren't many. Maybe 5-10 at any given time. Are they a type of springtail? I couldn't find an image in searching that made me say, "That's it!"
Any help is appreciated!
Thanks!

Welcome to SE Biology. Could you edit your question to include a location? It may help with the identification.

Related to: Bug Identification: Tiny Bugs in Fairport NY, What are these tiny, swarming, jumping bugs?, Can Anyone Identify This Insect?, Taxonomy: Categorising Collembola, What kind of small insect is this?, Unknown aquatic larvae

Those are springtails. Order Collembola. You can find yours here on BugGuide. https://bugguide.net/node/view/258362

Thanks for confirming. Now to figure out how to get rid of them! :-)

@Mattaton do you have a plant that you water frequently nearby your desk? They probably come from that. They're not harmful and if it really annoys you, just water less frequently.

@tox123 Nope, no plant and no moisture that I can find. My office is in a basement, but there's no noticeable humidity. Might see about getting a dehumidifier, just in case. Not really sure WHY they're hanging out here.

@Mattaton they might just be lost. They live in soil and dark conditions, so it's possible that there may just be a way into your basement from surrounding soil.


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How does evolution eliminate problems that only cause diseases late in life?
Humans are vulnerable to heart attacks and strokes. Our modern diet leads to atherosclerosis, this already starts at a young age but it doesn't cause symptoms until an important artery is almost completely blocked or if a piece of plaque ruptures and causes a sudden shutdown of the blood supply to parts of the heart or brain.
However, if people eat like many indigenous people such as the Tsimané do, then they get far less atherosclerosis:

“Most of the Tsimané are able to live their entire life without developing any coronary atherosclerosis. This has never been seen in any prior research. While difficult to achieve in the industrialized world, we can adopt some aspects of their lifestyle to potentially forestall a condition we thought would eventually effect almost all of us.”

Similar results had been found previously, but this then relates to coronary heart disease not merely the presence of atherosclerosis, see e.g. here:

Williams and Jack Davies had shown clinically and pathologically that coronary heart disease was almost non-existent among the African population in Uganda, although Hugh Trowell had reported a single case of coronary heart disease in an African judge. In the Asian community of Uganda, on the other hand, coronary heart disease was extremely common, accounting for almost half of the male deaths in Kampala in 1956–1958.

The question is then how we could have evolved to be almost free of atherosclerosis when sticking to such a lifestyle, given that atherosclerosis doesn't cause symptoms until it has progressed quite a lot, which is typically late in life and that then in the developed world. For indigenous people like the Tsimané it's even less relevant, because they have a much lower life expectancy due to infections.
Nevertheless it does look like our ancestors did evolve such that they didn't get atherosclerosis.

"It does look like our ancestors did evolve such that they didn't get atherosclerosis" Do you have anything to support this peculiar statement?

@David If not, then it would be a massive coincidence that the diet that these indigenous people stick to just happens to yield extremely low levels of atherosclerosis. Note here that it's not just the Tsimané, we can read here: "In the African population of Uganda coronary heart disease is almost non-existent. This statement is confirmed by adequate necropsy evidence. In the Asian community, on the other hand, coronary heart disease is a major problem."

I don't think early man lived long enough to get atherosclerosis, even assuming his diet predisposed him towards this, which I doubt. We get it after reproductive age if our diet disposes us to it. I don't understand what you are on about.

@David The question is precisely about this problem. One the one hand they didn't live ling enough to get atherosclerosis. On the other hand, we now have evidence that sticking to their lifestyle prevents atherosclerosis, if you do live long enough.

I really don't understand you. Are you saying that the diet of native peoples (= prehistoric man) "evolved" to prevent atherosclerosis and you can't understand how selective pressures produced this? Because that's like saying that prehistoric man evolved to have an alcohol-free diet so that he didn't suffer from cirrhosis of the liver. You could argue that prehistoric man evolved to survive on the diet available to him (hence post-weaning lactose tolerance), but that has no relevance how a modern diet affects health.

Is atherosclerosis a specific interest, or just an example? If it's the latter, then Huntington's Disease seems like a good testament to the fact that crippling late-life diseases can definitely persist.

Please read The Blind Watchmaker by Richard Dawkins, it will give you the basic understanding how evolution works. That a certain diet protects against certain diseases does not have to do anything with evolution - it can be (and most probably is) just a random fact. It is possible that tomorrow we invent a completely new diet which by accident will make us highly resistant against let's say the encephalitis - and it will not be the result of evolution.

@HonzaZidek  How do you explain the astronomically low probability that the diet and lifestyle of these indigenous people (not just the Tsimané, also many tribes in Africa) who didn't choose their diet and lifestyles based on any scientific research, just happens to protect them against  atherosclerosis much better than the Mediterranean diet, which is the best scientifically designed diet? This is clearly not a random fact.

@HarrisWeinstein Not per se just atherosclerosis, it's simply that there is now a rigorous result about that. There were strong hints about low levels of atherosclerosis in indigenous populations who survive mainly on a plant-based diet supplemented by only small amounts of meat. Such a diet is likely also protective against bowel cancer, and colorectal cancer. There will of course be many diseases that do occur frequently, but the typical killers of Western people, things like cardiovascular problems, bowel cancer etc. can be prevented by sticking to an indigenous lifestyle.

@David Cirrhosis of the liver is not something that the medical community thought was something most people in old age would get. Atherosclerosis, on the other hand, is something that many doctors still believe is a normal part of a aging process. The Mediterranean diet yields good results compared to other diets, but it doesn't get you close to the results observed in the Tsimané population. And based on other results it would not be a surprise to see similar results in other indigenous groups, it's just a matter of bringing mobile CT scanners to other remote locations.

I am not interested in a discussion of the effect of diet on health, nor is that the purpose of comments on SE. I used the comment feature for what it explicitly says it is for, to try to get you to clarify your question. You did not respond directly to my enquiry, so I have voted to close your question as unclear.

@David Without evolution to not get atherosclerosis, the observation that indigenous lifestyles lead to extremely low levels of atherosclerosis, much lower than what most doctors would have thought possible using any lifestyle choice, would be a massive coincidence.

@CountIblis Just accept that if a diet has good influence on some potential disease, it is not necessarily related to evolution. Your premise is wrong. So your question "How does evolution eliminate problems..." is a nonsense from the beginning. The answer is simple: the evolution has (most probably) nothing to do with your topic.

@HonzaZidek Not necessarily, but that's extremely unlikely. I don't understand how you get to your "most probably" conclusion, given the typical nature of these plant-based indigenous diets. It's not that one has shifted through many thousands of different diets to find one that has good results against one of the many thousands of different illnesses. A typical result in that case would be some weird diet that would have a whole host of side effects that would have good results against a particular disease. Take e.g. the 500 Kcal diet designed to cure type-2 diabetes.

I guess the base question: "How does evolution eliminate problems that only cause diseases late in life?" is very good in general. However the specifics have problems, can you approach your general question with other less controversial example?

Heart attacks and strokes, and any other diseases that afflict humans after age 35 or so have absolutely no influence on natural selection because for the vast majority of our history, these diseases affect only post-reproductives. Evolution is not a state of advancement toward an ideal, but rather, a mechanism to put genes into the next generation. These genes lag behind our current situation by thousands of years because evolution acts slowly. So evolution still favors characteristics that would have been good for our Stone Age ancestors, who did not live long enough to be weeded out by diseases of old age.

Many of our stone age ancestors didn't survive long enough to reproduce. Those who did could live longer than more recent civilizations.

Heart disease, heart attacks and strokes do not only affect "post-reproductives". They have been known to affect young people too.

Yes, I agree. "Known to" is correct. How many heart attacks do you think happen before age 35? These are due to other problems. Evolution does not act on the elderly.

So, how then did we get adapted to not get atherosclerosis if we stick to the lifestyle of the indigenous people like the Tsimané people, as pointed out here?

Our ancestors did not evolve to not have atherosclerosis. The study you cited in the Lancet stated that it was the diet and lifestyle that protected the Tsimané from hardening of the arteries. Not adaptation, selection or evolution.

I have to disagree slightly about diseases after 35 or so not affecting selection.  There's what we might call social selection.  (Don't know if that's the proper term.)  That is, someone of reproductive age who has healthy older relatives to share the burden of child-raising is more likely to have surviving offspring.

The Lancet article also says that the levels atherosclerosis observed are much lower than the previous record low. Without evolution to not get atherosclerosis, the observation that certain indigenous lifestyles lead to extremely low levels of atherosclerosis, that are much lower than what most doctors would have thought possible using any lifestyle choice, would be a massive coincidence.

@jamesqf. Yes, I agree. The idea that grandparents can help their children and grandchildren survive makes sense. However, this phenomenon may not yet have had time to be fully imprinted on our genes.

How does evolution eliminate problems that only cause diseases late in life?

This is a fantastic question, which still is the subject of intense research. One possibility might be that we age because there is no or little evolutionary selection against diseases late in life (as old people are less likely to produce offspring). As for any active area of research there are several subtleties. You might enjoy starting with the corresponding section on wikipedia: https://en.wikipedia.org/wiki/Evolution_of_ageing#Mutation_accumulation

If people eat like many indigenous people such as the Tsimané do, then
  they get far less atherosclerosis

This refers to another current research domain, which has only been published in the (really good) medical journal Lancet, where the authors themselves state that several questions remain open, see Kaplan et al. 2017.
Yet their paper already reaches to an important conclusion. While one could hypothesize that the difference in atherosclerosis was due to some genetically inherited property, the authors find support for (and hence favor) the alternative hypothesis, that those people generally live a very healthy lifestyle (e.g. normal BMI, no smoking, ...) which reduces the chance of some diseases.

Similar results had been found previously, but this then relates to
  coronary heart disease not merely the presence of atherosclerosis

Though it would be tempting that this observation could come from a healthy lifestyle, there could also be several alternate explanations (for instance one could hypothesize their genome contains something that only is under selective pressure within the region where they live, and that this something just happens to also help against coronary heart disease).

The question is then how we could have evolved to be free of atherosclerosis when sticking to such a lifestyle.

If this is really is your question, here is the answer. The answer is not biological, it can be answered just by anyone educated in the basic logic.

It is not necessarily true that "we have evolved to be free of atherosclerosis when sticking to such a lifestyle".

The only fact which might be true (supposed the data are correctly interpreted) is that when sticking to such a lifestyle (and maybe also doing something else? or maybe having some enzymes which other population does not have?), these people are free of atherosclerosis. (There are still a lot of questions, e.g. taking into account that they do not live long and atherosclerosis usually does not occur in young age.)

Hence the question is based on an unproven assumption.
Hence the question does not make sense from the beginning.

The question should have been like this:

Is it caused by evolution, that sticking to a certain diet makes an animal free of a disease? How is it in the case of this specific disease and this specific diet?

Such a question would really be a valid question. However yours already assumes something which is not a proved fact and manipulates the answer.
It just sounds to me as one of the weird "arguments" of vegetarians that "humans are vegetarians by nature".

Ok. And I agree with your new answer, although I have no idea whether you are right about the poster's agenda.

1: Straw man, not literally 100% free but I gave the link where the details are given, and these details are non-trivial as also pointed out in the Lancet article. 2 Follows from 1, therefore based on your Straw Man argument therefore False and 3 does not even follow from 2 and/or 1, so it is totally wrong. Sounds like the argument that "humans are vegetarians by nature"? That's another rhetorical trick to smuggle in a Straw Man argument.

@CountIblis See my edit, straw man!

Important to note that a social species like ours has other sophisticated ways to ensure that its genes survive in the next generation alongside the obvious way of "passing down".
Even after our reproductive phase we can teach our children or even take care of their children, which highly rises their chance to thrive and reproduce.
It is also possible to ensure that some of your genes are safely passed, by helping your brothers and sisters to raise their children while sacrificing your direct reproduction, since you have similar genomes.
So even genes carried by infertile people can greatly affect how their identical or very similar instances in their blood relatives will pass through via advantageous social interactions.
Other:
That the Tsimané people have a low life expectancy now does not imply that it was always true. Maybe those infectious diseases were carried in by Western European explorers and conquerors.
You can research the grandmother hypothesis.
Here is a good paper to start.
Update:
The fact that the average life expectancy was low in the past, doesn't mean that nobody lived long. The infant mortality was very high, so relying solely on a average is not wise. Here is good publication on the subject. Mind the first table which shows the life expectancy of the ancient and medieval elite was close to the common life expectancy of the UK in the mid-20 century.

One of the ways a disease X that typically occur after reproduction can be eliminated is via individuals inheriting some other disease Y that cause health problems much earlier in life that interacts with X. Suppose that the vast majority of the population is genetically susceptible to X. Also, suppose that a small fraction of the population is prone to getting Y at a young age and that Y becomes a lot more severe if you are genetically susceptible to X.
Natural selection then already has led to Y to be suppressed via the genes that are directly responsible for that disease. It may that you only get that disease by inheriting the wrong gene from both parents. But the genes for X are also a factor, and mutations in the genes responsible for X would further lower the impact of Y on the population.
In case of X = atherosclerosis, Y could be familial hypercholesterolemia which can cause cardiovascular disease between the ages of 30 and 40 if one gene in inherited (in the modern Western population where almost virtually everyone eats an extremely unhealthy diet),  while it cause cardiovascular disease at childhood when two genes are inherited.


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Can anyone identify this?
Found on Cape Cod MA near a fresh water pond with a muddy bottom. Strange looking creature with a suction cup single "foot" with a mouth opening on opposite end, no limbs, mouth ridges inside mouth, spiral rings of tissue up entire body. Any idea what it is? I thought it might be a tunicate of some kind but I can't find a match anywhere.

It is a artificial fishing lure.specifically a soft worm T-tail, there are hundreds of variations.

Really, just wow on this one.

This may be a mimic but what I have is NOT plastic,

Okay, now we may BOTH be right. This thing I have is not plastic but I finally cut in to it an VIOLA! It is a colony of mud worms that probably took up residence in one and the plastic is long gone, the outside is a mud shell, the inside is a mess of worms...............

Not all lures are plastic many are latex


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Daphnis Nerii not moving
Its been quite a while since my Daphnis Nerii has passed its eating phase, now its just a sort of recluse and is curled up in one corner and sleeps the whole day. It's a bit brownish in colour now. Although when I check on it, by lifting the container and moving it about, it starts jumping oddly. Like a jumpstart,  everytime it gets provoked. It maybe is the last phase of its instar period. Is it getting ready to pupate? Or is it not well?

Wikipedia tells us the following about the larva of the oleander hawk-moth (Daphnis Nerii):

Just before it pupates, the oleander hawk-moth larva becomes browner in color. The pupa of this species measures around 5.5 to 7.5 centimeters in length, and is light brown with black spots and a black line down the middle

The stage your critter is in probably resembles Fig. 1. It's probably fine.

Fig. 1. Caterpillar just before pupating. source: wikipedia

But the problem is that its quite inactive. Do caterpillars tend to stay inactive in pre-pupation?


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Square-cubed law and health
Does the square-cubed law lead to possible health detriments for taller people?
I'm not sure what the optimum height is for humans (e.g. due to their cross-sectional bone density constraints), but given the square-cubed law at some greater height wouldn't a human begin to experience health detriments, whether small or large? For example, lets say that the optimum height is 175cm for a male (I don't know what the actual optimum height), wouldn't each marginal increase in height add excessive pressures to the body?
Or is there any sort of allometric plasticity that humans possess to take into account the physical pressures of being taller, making a range of height being optimal?
Any thoughts, opinions, papers on this would be much appreciated.

Can you please clarify why the question is phrased as specific to humans? Would you expect that smaller is always better in all species?

Well it can be applied to any species, but I phrased it specifically to humans because I was curious of any evidence for health implications in the biomedical field.
I should have given moire detail to my question, I'm sorry! I wouldn't expect that smaller is always better in all species, since it would be costly for a species to have a cross-sectional bone density higher than it needs to support its small relative mass determined by its size. I don't know what the optimum height would be to match bone density in humans, but I was hoping that the 150/180cm example got across the question.

here is a paper linking body size and longevity, but it is not something that can easily be applied to humanity as a whole. http://manoa.hawaii.edu/news/article.php?aId=6515

The question is unclear. However, think about it this way: imagine an extreme case, a human who is 2.5 meters tall. I imagine there would be multiple health issues involved, many which would be 'physical' in nature. In fact, this is the case with people with gigantism. Joints would be under strains they were not 'designed for', cardiovascular issues would present too. Things are not linear, which is the crux of the square-cubed law. A heart of diameter of 20cm grows less rapidly than the appendages and circulatory volume of a super lanky person. It would be a simple plumbing/pumping issue.
There are other corollaries: lung surface area increases much more slowly than its volume. This is why lungs have different structures, and indeed, why lungs look as crumpled as they are. A balloon-shaped lung would not do for any large animal.
Also, taller people have a significantly shorter life expectancy. There are very many easily-accessible resources upon querying the Google machine.


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How does a neuron know to which one of the next neurons to pass the signal
Looking into how neural networks are build in the brain, here are a couple of facts followed by some questions:

The neuron receives the signal through its dendrites and passes it to the terminal at the end of the axon.
A neuron can have as much as 1000 connections to other neurons.

As I understand the dendrites can be connected to multiple neurons, so the neuron we are talking about can receive signals from multiple cells.
Now the questions:

The terminals at the axons can be connected to just one or to multiple neurons?
If the axon terminals can be connected to multiple neurons, how does the neuron transmitting the signal knows to which of the further neurons to pass the signal next? Is it passing to all of them at once?
If the axon's terminal can be connected to only one other neuron (for the single axon neurons), how are the two-axon neurons working? How do they know to which axon to pass the signal next?

The neuron that sends the signal does not know which neuron to send the info to. The job of the neurons getting the signal is to identify whether it is their turn to get activated by the signal.
This is controlled by a protein. Depending on how often the neuron is used, a number of channels are formed on the surface of the dendrites. The activation happens at an optimal level of the protein present in the cell depending on the number of channels on the surface.. Each time the cell receives the signal, this some of this protein is created.
First, the neurons with most channels is activated, but if the organism does not get the memory that is wants, the earlier neuron will continue with sending more signals. Then receiving-neuron-number-1 stops activating (because peak concentration has passed) and the next one starts. This continues for all neurons.
In layman's terms, from info-1 to info-2, info-2 is chosen in the order of thoughts most associated with info-1 to least associated.


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Does the sun light have to have *direct access* to fruits to make them sweet?
I understand that sun light is needed for fruits to ripen. In the years with less sun light, the fruits are usually not so sweet. So the sun light is needed to make the fruits sweet.
Where and how does the sweetening process occur? Does the sugar in the fruits come from the photosynthesis occurring in the green parts of the plant (leaves) and is then conducted to the fruits, or is the sugar produced in the fruits themselves? Does it matter whether the sun shines directly to the fruits, or is it enough if just the leaves have enough sun light and the fruits become equally sweet even if they are hidden under the leaves?

It would depend if the fruit has the ability to sense or capture light. This depends on chlorophyll mostly, found in cellular organelles called chloroplasts. If the fruit is incapable of capturing light, the light can still have an indirect impact by being captures on leaves, since plants circulate nutrients - this is why roots can grow without having access to sunlight.
Here's a few excerpts from the following paper (https://www.ncbi.nlm.nih.gov/pubmed/11337414):
"To date, molecular regulation of the role of light in fruit ripening has been studied most thoroughly in tomato, and available evidence suggests that light has its greatest impact on pigmentation, with apparently little effect on additional ripening phenomena."
"The green to red color transition typical of ripening tomato fruit is largely due to the developmental transition of chloroplasts to chromoplasts; as photosynthetic membranes are degraded, chlorophyll is metabolized, and carotenoids, including β-carotene and lycopene, accumulate."
In plain English, the pigment that captures and absorbs sunlight for metabolic reasons (photosynthesis) gets transformed into a pigment which absorbs sunlight for other reasons, such as 'looking tasty' or protection from ionizing radiation. Essentially the same thing happens to leaves in autumn - the green chlorophyll pigment, which absorbs the energy of the sun for the plant to grow, becomes the orange carotene, and the leaf slowly dies off.
Interesting sidenote: biological pigments are very important molecules in ecology and in cell biology. Take a closer look: https://en.wikipedia.org/wiki/Biological_pigment
As for your question about how ripening occurs... Google would do a better job than most.

"tomato... light has its greatest impact on pigmentation, with apparently little effect on additional ripening phenomena."
Does this mean that if you shaded the tomato fruits agains the sunlight, but left the leaves uncovered, the fruits would become sweet, but remain green?

Yes. That would be the experiment!


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Size of Mamenchisaurus sinocanadorum
In most books the size of long-necked sauropod Mamenchisaurus is stated as about 26 meters. Recently, a huge specimen of Mamenchisaurus sinocanadorum was discovered.
However, Gregory S. Paul estimates its size in length of 35 meters and weight of more than 65,000 kg, rivaling Argentinosaurus and Patagotitan, the largest known dinosaurs. However, many doubt these estimates and say they are exaggerated. What are the current and most reliable esimates of the size of Mamenchisaurus sinocanadorum?

The holotype specimen originally discovered in 1993 is described as being 26m in length:

An articulated neck of a large, mature sauropod, with enormously elongated cervical ribs, was discovered in strata of Late Jurassic age in the eastern Junggar Basin, Xinjiang, People's Republic of China. The animal is estimated to have originally measured 26 m in length, but was lightly proportioned relative to Brachiosaurus and Apatosaurus.
...
In the present specimen, one rib from the midregion of the neck was seen to be at least 3540 mm long in the field, and after preparation measures 4100 mm in length.

"A large mamenchisaurid from the Junggar Basin, Xinjiang, People Republic of China", Russell, D.A., Zheng, Z. (1993) Canadian Journal of Earth Sciences

The larger measurements come from additional remains attributed to this species, but not yet formally described. Here is the relevant section from Paul's book:

The Princeton Field Guide to Dinosaurs, Paul, G.S. (2010), Princeton University Press.

Paul's figures are echoed in the following papers:

2006 年，中科院古脊椎所在新疆昌吉奇台（原中加马门溪龙标本发现地附近）发
  掘出一具巨型蜥脚类恐龙，经初步鉴定应归入马门溪龙。从发现的部分颈椎长度推测，
  这具马门溪龙长度可达 35 m 以上，成为了中国乃至亚洲目前发现的个体最大的恐龙。

[Google Translate]
In the year, the ancient spine of the Chinese Academy of Sciences was located in Changjiqitai, Xinjiang (near the original site of the discovery of the Jiamamen brook specimen).
A giant sauropod dinosaur was excavated and the initial identification should be attributed to Mamenchisaurus. From the length of the cervical spine found,
    This [Mamenchisaurid] can reach a length of more than 35 m, becoming the largest individual dinosaur ever discovered in China and Asia.

马门溪龙化石研究综述, (2008)

Mamenchisaurus sinocanadorum (体长26~35 m)

Advances in research on dinosaur gigantism, X XU, Q ZHAO (2016)

Though the first paper does not cite a source, and the second paper cites only Russel and Zheng's original paper describing the 26m specimen.

This is known. The question is if there is other estimation other than Paul's who is known to be unorthodox in dinosaurs taxonomy and size estimations?

@Dr.Evenor As I said, the specimen is "not yet formally described", so as of yet there are no other figures to compare with. Nonetheless I've found another couple of papers which quote the same figure as Paul, but haven't been able to locate the source of this "35m".


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Does natural selection in humans work out in "best outcomes" or do e.g. subjective biases affect it?
Does natural selection in humans work out in "best outcomes" or do subjective biases affect it? That is, how much is natural selection "guided by nature" and "guided by humans"?
E.g. given "fully rational" reproducers, then would the gene pool get increasingly better and produce better and better humans over time? Or is this somehow "independent" of "reasoning"? Such as that the natural selection does not follow all kinds of rationalizations.

What do you mean by "bad traits" ?

@Shred Low-worth to community, low-skill and learn-ability, low physical fitness, unattractive physical features, sicknesses.

What do you mean by "better"? And how did you come to the conclusion that evolution produces "the best"? Evolution only produces that which is able to survive, reproduce, escape the predators (sufficiently enough) - and all of this better then those competing within the same niche (https://en.wikipedia.org/wiki/Ecological_niche). If the evolution "optimizes" something, it optimizes only those traits for which there is pressure of natural or sexual selection.I recommend you to read The Blind Watchmaker by Richard Dawkins. The book is popular, but gives the understanding of the basic principles.

@HonzaZidek I think that one could hold as an abstract ideal that evolution could be altered to lead to better, improved humans. If it doesn't do it on its own. And the reason is that better humans would be even more successful? Isn't science pretty much about improving humans? But there's the difference as to up to how much can humans affect evolution, and how much of it is beyond control by humans?

I completely do not understand the term "better improved humans". All this "better" and "improved" is based only on anyone's biased view. Evolution does not operates with these terms. Evolutionary good = able to pass the genes forward. Evolutionary better = able to pass the genes forward for more generations, able to reproduce in larger scale (and still survive). Evolution-wise, our euro-american (= science-based) civilisation is not very "good", taking into account the decreasing fertility rate (http://worldpopulationreview.com/countries/total-fertility-rate/).

@HonzaZidek So then you're sort of at the center of this question. Because I'm asking whether asking for better, improved makes sense from evolutionary perspective. And up to how much. I'm not sure if improved, better are entirely useless concepts, because humans e.g. have a strong tendency towards improvement of their environment, they build tools etc. But as to whether it's through evolution or something else. E.g. what's the relationship between what each subject decides to do and evolution?

And as for your "evolution could be altered to lead to better, improved humans", this already has a name: eugenics (https://en.wikipedia.org/wiki/Eugenics), very much popularised by Adolf Hitler (https://en.wikipedia.org/wiki/Nazi_eugenics).

@HonzaZidek I would count normal human life that involves development, progress to belong to that, not just eugenics.

That is, given "fully rational" reproducers, the gene pool would get increasingly better and produce better and better humans over time.
Environmental conditions change over time. What may once have been an advantageous trait in a human population may become deleterious in some form at a later time or different environment (i.e. by spatial migration).
Case in point: Central Africa is plagued with malaria, a disease caused by a parasite of the Plasmodium genus which infects red-blood cells (RBC). Sickle cell anemia (SCA) is a hereditary disease which can be deadly, unrelated in its cause and prognosis to the Plasmodium infection, BUT, it confers a resistance to Plasmodium infections due to the RBC of SCA-patients having an aberration in the shape of their RBC's. Here is a selective pressure caused by malaria that "promotes" the profileration of SCA in the local population. As a result, what you have is a large section of Central Africans that are Sickle Cell Anemics, whom have better survival rates than non-anemics in that environment. But if you take these anemics to northern Europe or North America, where malaria is virtually non-existent (spatial, environmental change), the anemics have a higher mortality rate than the rest of the local population.
You get what I'm saying?
Natural selection doesn't produce better and better humans over time - it produces humans that are better able to survive in that era, in that place.


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How does the body differentiate between sources of good and bad cholesterol?
I keep hearing "good cholesterol, bad cholesterol" everywhere, and how certain food sources of cholesterol raise LDL and certain other raise HDL.
I don't understand how any food can increase specifically HDL or LDL. I just don't understand the mechanism. Cholesterol is cholesterol, regardless of whether it ends up in LDL or HDL, or whether it came from eggs or or dairy. Somebody please explain to me how specific sources of cholesterol raise HDL and why others raise LDL; how does the body differentiate between the source.
As far as I know, all cholesterol and fat digested from the intestines, regardless of the source, are packaged in chylomicrons as 1) phospholipids, 2) triglycerides, 3) cholesteryl esters, and enter circulation from the lymphatic vessels, then deposited as a chylomicron remnant (CR) in the liver.
How does the liver know whether the 3 particles in the CR came from a good source or bad source? And how does this trigger HDL vs LDL synthesis?
[Btw, if im not mistaken, the liver only makes HDL and VLDL, not LDL]
I'm looking for the biochemical pathways behind these claims. I just cannot picture the mechanism.

The body doesn't differentiate between types of cholesterol. It simply does what it does. Cholesterol is cholesterol, that's a fact. You need to read about the difference in HDL and LDL, with emphasis on the "L" (lipoprotein). That's what matters, not the cholesterol. You might want to edit your question.

I know the difference. I'm asking the mechanism behind claims such as: "olive oil raises HDL, butter raises LDL" etc.


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Reference for the bite force for Nile Crocodile
The (maximal) bite force of the Nile Crocodile (Crocodylus niloticus) is estimated around 22,000 Newton (refer to YouTube interview with Ofer Kobi, a crocodile conservation ranger and croc farm owner, time 7:50-8:00, Hebrew , where he estimates the bite force as above 2 metric tons). However, I didn't find a proper reference for this. Dr. Gregory Erickson measured the bite forces of a 5.2 meters long Saltwater Crocodile (Crocodylus porosus) and obtained a value of about 16,000+ Newton and estimated a 6.7 meters long Saltwater Crocodile can exert a bite twice as strong (about 34,000 Newton). See Paper by Gregory Erickson et al. Interesting to note that Erickson measured small Nile Crocodile (total body length < 3 meters) so it does not represent the bite force of a full adult big crocodile.
Remarks on units of force:
1 Newton = 1 kg * 1 meter / sec^2
$1 \ \mathrm{Newton} = \frac{\mathrm{kg} \times \mathrm{meter}}{\mathrm{second}^2}$
1 Newton = 0.224808943 lbf = 0.225 lbf (pound-force)
10,000 Newton is approximately 1 tonne-force (1 tonne = 1 metric ton = 1000 kg)

Where did you get your estimates from?

From an interview with an owner of a crocodile farm.

An interview you've conducted yourself? An interview that has been diffused on TV? Do you have a link to this interview or some document where we can find direct quote or something?

No, an interview on TV. It was held in Hebrew. Since he is not a scientist I am looking for a better reference for the bite force of a Nile Crocodile. It seems strange that no body measured the bite force of a 5+ meters nile croc.

You can still link to the interview (or at least refer to the emission name and date of appearance). It really is always a good habit to link to your sources and it shows that you're not just throwing random number out of the void. You can also link to Erickson's study. Good format will increase your chances of getting people to care about your post. Good luck!

Here it is: YouTube Time: 7:50-8:00

I sent an e-mail regarding this question to Dr. Gregory Erickson. I did not receive an answer yet.

Here is a video by Brady Barr (video in YouTube) measuring 5000 lbf for an adult Nile Crocodile. This is equivalent to 22.24 kN (more than 2.2 tonnes of force). This result is also refered here (Getty Images).
 Source: Gianfranco Gori, Wikipedia


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How taking up plasmids on heat shock evolutionary advantageous to bacteria?
During the transformation protocol we apply heat shock to bacteria to make them take up plasmids from their environment. It is really useful in the lab.
However, it presents an evolutionary paradox in a bigger context, if bacteria begin to take up free floating plasmids on distress, they will most likely acquire genes from the other bacteria, who perished in the same distress, so those genes most likely will not be useful against their adversity.
I am sure there are other factors here to resolve this paradox. What are they?

The simplest one is they didn't. Not everything an organism does or has is an advantage many are side effects of  other mechanisms or the case of heat shock you are purposely creating highly unlikely conditions to break existing mechanisms. In the case of heat shock, high heat coupled with very high calcium levels break down the normal mechanisms that prevent plasmids from entering the cell, after that normal diffusion takes over.  It is like asking why we evolved to absorb material injected into us, we didn't injection is bypassing the normal defense mechanisms. It is similar to using DMSO to carry molecules across the skin, DMSO is so unbelievably unlikely in nature that there has never been a reason to evolve a defense for it.


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Do different transcription factors attract different kind of RNA polymerase?
Initiation step of transcription is simply binding of RNA polymerase on the DNA strand and its activation by addition of a phosphate group onto it.
Different kind of promotors are present close to the transcription starting site and different kind of transcription factors (TFIID ,TFIIB ...) are present binding onto promotors making the RNA polymerase bind onto DNA.
is there different types of RNA polymerase II ? I know that it is
RNA Polymerase II which is responsible for mRNA formation but my question is; is RNA Polymerase II further subdivided according to what kind of protein will be synthesised after translation? otherwise why do different kinds of transcription factors exist?

Why didn't you research RNA polymerases before posting? This would have answered your question and saved you wasting other people's time.

"RNA Polymerase II which is responsible for mRNA formation but my question is; is RNA Polymerase II further subdivided according to what kind of protein will be synthesised after translation" shows clearly that ı researched about the subject and I am asking for a further detail that ı am NOT ABLE TO find an answer for.   It is optional for one to share knowledge or not I think, so I am not wasting anyone's time I think. Your use of language is harsh and irritating.

Please read "how to ask a good question" in the Help. You are required to do research before posting. There are ample articles on Wikipedia and elsewhere that describe the RNA polymerases and transcription factors in eukaryotes, as there are text book chapters in reputable books on biochemistry on NCBI Bookshelf. You cannot find anything about the mistaken idea you have about multiple RNA polymerases for the simple reason it is a misconception. The subject of tissue-specific or stimulus-specific transcription is huge — go read about it.

TFs, the DNA they bind to, and the transcriptional machinery (including the Pol II [RNA polymerase 2] enzyme all form a complicated three-dimensional complex. It depends on the topographic conformation of the DNA, epigenetic factors, a whole bunch of things which are orchestrated. However, once the machinery is activated, the Pol II enzyme is capable of transcribing the DNA regardless of its resulting protein. You can get the enzyme to transcribe nonsense, or functional coding regions which will produce functional proteins.
In epigenomics, it is also commonplace to identify mRNA being transcribed on DNA regions which do not bind a transcription factor. This is because the machinery recruits the polymerase at a transcription initiation site, but there may be nearby DNA (looped, for instance, or on a neighboring nucleosome) which is accidentally transcribed, simply because the polymerase was brought into close proximity and began transcribing the wrong DNA.
Such enzyme reactions are a bit like chopping an onion: the knife is the enzyme, the onion is the target DNA, and your stray finger is the non-target DNA. Usually it is the onion that is chopped.
Biology is never perfect, it follows the laws of chemistry and therefore is a stochastic process.


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What is the recommended culture volume for HeLa cells and seeding number for 384 well plate wells?
For 24 well plate wells, thermofischer recommends to seed 0.05E6 cells with 0.5 to 1 ml of medium. What are recommended numbers for a 384 well plate well?

The Privalsky Lab@ UCDavis writes:
Growth Area of Tissue Culture Plates and Dishes
    Growth Area (cm2)   Media Volume (ml)   Maximum Volume (ml)
Plates
 35 mm            8          1.6- 2.4
 60 mm           21          4.2- 6.3
100 mm           44          11 -16.5
150 mm          148          30 -45
245 mm (square) 500         100-150

Dishes
  6 well        9.5         1.9  -2.0       16.8
 12 well        3.8         0.76 -1.14       6.9
 24 well        1.9         0.38 -0.57       3.4
 48 well        0.95        0.19 -0.28       1.6
 96 well        0.32        0.1  -0.2        0.36
384 well        0.056       0.025-0.05       0.125

Flasks
 T25             25          5- 7.5
 T75             75         15-22.5
T150            150         30-45


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Does a certain tumor type being invasive mean that it is highly metastatic?
Does a certain tumor type being invasive mean that it is highly metastatic?

Oncologists examine the margins of a biopsy for morphology and invasiveness. A tumor that is becoming invasive has a high potential to become metastatic, based on numerous factors. I would be hard pressed to tell you that a tumor is highly metastatic without testing, though. I am not an oncologist, either.

They are different things, metastasis is not the same as invasion.
Highly invasive cancer means that the tumor spreads beyond the layer of tissue in which it developed and is growing into surrounding, healthy tissues.
Highly metastatic tumors cause secondary malignant growths at a distance from a primary site of cancer.
In order for tumors to become metastatic, they must move and grow beyond their initial location and reach the circulatory system in order to travel to another location. During this phase, depending on the tumor, the malignant growth will acquire the ability to escape (tumors cannot do this at first, because it requires genetic mutations in genes responsible for cell adhesion). There are many other known factors which co-occur in cancer development - it is a rich field of research.
Here is an informative website for you to browse about the medical side of it: http://edcan.org.au/edcan-learning-resources/supporting-resources/biology-of-cancer/defining-cancer/invasion-metastasis


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Gypsy Moth Caterpillar Behavior
I have recently done a fair amount of online research about gypsy moth caterpillars and sources I looked at say that older caterpillars feed on the trees primarily during the night and drop down and hide in dark sheltered areas during the day.
I work for someone who had a severe gypsy moth infestation last year and we tied burlap around several isolated trees to see if we could reduce the damage. At the height of the infestation we noticed that there were, at any given time during the day, 20-40 caterpillars circling the base of the burlap and sometimes successfully crawling over it. It looked like they were actively trying to climb up into the trees during the day, which seems to contradict everything I've read.
Can anyone offer any insight into this behavior?


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Is it true that it is mostly impossible, for any kind of antibiotic, to succeed in killing off every bacteria in a very rich environment?
It is commonly believed that the resistance to antibiotics by micro-organisms is truly evolution at work, and that the recent surge in superbugs may very well be attributed to it.
When we refer to a bacteria's ability to "evolve" into resisting this antibiotic, I assume we mean that when we introduce antibiotics into the environment, a lot of bacteria die but some who by mere chance and luck didn't do so and that these lucky bacteria go on to survive and multiply, thus aiding in the creation of so-called superbugs, or rather, bacterial resistance to sophisticated drugs.
This whole situation already suggests to us, or at least to me, that there's much inherent complexity in these organisms and indeed a certain uniqueness to each.
I have, however, been troubled recently by the following question: is it truly impossible, for any kind of wholly new antibiotic which was not used before (no matter how complex), to succeed in killing off every single bacteria in any rich habitat/environment (no matter how populous)? And that there'll always be some bacteria on whom this shall not work apparently due to uniqueness in something of their structure?

If I am not completely wrong, any kind of single agent drug (this is also true for targeted therapies in cancers for example) eventually leads to resistance. The evolutionary pressure is enormous and you only need one successfull cell.

It is not bacteria surviving by pure luck that leads to resistance.  Rather, they have some variation in their makeup that makes them harder to kill.  They survive, pass this trait on to "offspring", and eventually outnumber the easy to kill variety.

@Chris this will largely be based on how aggressive an antibiotic you use, prolonged immersion in liquid salt will kill all the bacteria but would kill the host as well.

Yes. It is down to mutations. DNA replication is not 100% accurate, there will be mistakes that are not corrected in the progeny produced.
Antibiotics works like a bit of gunk wedging itself into the machine of a bacteria cell but avoids jamming a human cell due to that very same shape. Gunk that wedges into both human and bacteria machines is just a really bad poison. So that gunk has a very special shape.
Resistance can be acquired by recognizing gunk of that particular shape and removing it (not something easy to evolve but very effective when it does) or just change the shape of the machine so the gunk cannot stick. Usually the altered machine doesn't work as efficiently as it can but in an environment polluted by fouling gunk, it works well enough.
And a rich environment means there are many bacteria.
So if your chances of mutating the right part of the bacteria machine to gain resistance is 1 in million, a rich environment with 10 million cells will have 10 such mutates.
Of course in reality we are talking about trillions (a million million) of bacteria cells per human (actually 39 trillion bacteria per human) and we are talking about billions of humans.  And we are not even counting the number of bacteria in the soil and in farm animals.  And it takes a few years for resistance to evolve.
When you look at the numbers involved , it is very difficult not to imagine resistances evolving. Even if the chances of that happening is 1 in hundred of trillions. It just takes a single bacteria cell to mutate and so gain resistance for it to spread and pass that resistance to other bacteria.

The answer is no. The antibiotic will kill all the bacteria it's intended to target, unless a special resistive variant cell(s) exist. What this means is that it is possible that non-resistive cells are not present.
Also bear in mind that it's not the drug that induces the mutation, rather it just isolates and funnels the randomly generated mutant (if present). Also remember that the vast majority of mutations are deleterious or neutral, so the probability of resistant strains even existing in a population are low. [That doesn't mean they cannot exist at all.]


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Are there any animals that maintain white fur year round?
Besides examples of rare albino animals, it seems animals only have white fur during the winter.  Additionally, and not coincidentally, the examples I've found live in the northern latitudes with predicable snow cover and have different colored coats in the summer months.  Are there any examples of animals that maintain a white coat of fur year round, or are there simply no environments that such a trait would be beneficial in?

https://en.wikipedia.org/wiki/Sheep :)

White Cats

Relatedly (but not fur), all-white colouration is not restricted to animals that experience snow. Consider the white tern, a tropical seabird. https://en.wikipedia.org/wiki/White_tern.

Are you asking about only wild animals?  Because there are numerous domestic animal varieties that have breeds that are white.  There's also the white tiger: https://en.wikipedia.org/wiki/White_tiger  And then there's the old argument about the zebra: is it white with black stripes, or vice versa?

@jamesqf: Yes, only wild animals.  Sorry, I should have been more explicit in my question.

Polar bears (Ursus maritimus) have white fur all year long.

There are probably several other examples. @L.Diago gave sheep as example. There are also all white troglodyte species.

This may be splitting hairs so to speak but the fur of a polar bear is actually transparent and gives off a white color due to reflection of snow. https://polarbearfacts.net/why-are-polar-bears-white/

@wanderweeer It is actually a good point. I have never been able to fully understand the polar bear fur but I would note that on the second picture, on a green background, the polar bear still look white.

@wanderweeer: That explanation seems a bit confused. As Remi.b says, a polar bear can have fur that will still look whitish even when there is no snow around. The fur is (more or less) colorless and scatters the ambient light, so it looks whitish. Many "white" objects/substances are built of smaller parts that are somewhat translucent or transparent; e.g. salt and snow

@Remi.b: I think it's closer to being blue and black tbh

@Remi.b & sumelic: I wish I knew more about how the lack of pigmentation in the polar bear hair works optically and I'd agree that it has more to due with scattering the ambient light than it's surroundings.  I don't ever remembering hearing a similar explanation for the white fur of other arctic animals.


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Genotypes of gametes produced by an F1 individual?
I have an urgent question as I have an exam tomorrow. I was skimming some past exam papers and one question came up which has me completely confused.

A cross was made between a pure breeding diploid pea plant with round, yellow seeds and a pure breeding diploid plant with wrinkled, green seeds.
R and r for round and wrinkled respectively, and Y and y for yellow and green respectively. Assume dominant allele of each gene is upper case, and that the two genes are on different chromosomes and so are independently assorting.
a) Give genotypes of two pure breeding parents
RRYY, rryy
b) Give the genotype of resultant F1 progeny
RrYy
c) Give the genotype and respective frequency of the gametes produced by the F1 individual and indicate whether the gametes are parental or recombinant.
This is the question I am having trouble with and confused about

The reason I am confused is primarily I do not understand what is being asked when referring to the "gametes produced". Is this an F1xF1 cross and the question is asking about the F2 generation? I assumed not as the next question is:

Two of the F1 individuals obtained from the above parental cross were crossed to obtain the F2 generation
d) Give the phenotypes of the F2 progeny and their ratios

If someone could please shed some light on this it would be much appreciated

Gamate is a haploid germ cell produced by either male or female parent. In your question,two homozygous dominant and recessive parants produce RY and ry gamates respectively. F1 would have four types of gamates if we think about their genotype.They should have any one of  RY, Ry, rY, ry as their genotype.
RY and ry are parental gamates. They have the genotype of the gamates that F1's homozygous parents produced. Other two are recombinant genotype. Since they behave independently, you can go with mendelian genetics and draw a punnett squre.write RY Ry rY ry horizontally and vertically then get the F2 cross genotypes. Dominant genotypes will determine the phenotype.


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What is Phytogenetics?
What is Phytogenetics? I have searched google without finding a definition. Is it even a defined term? I found it in a reference relating to genetic engineering.

Have you really googled the term? If I google phytogenetics, the first 8 results are 7 definitions and 1 translation.

@Remi.b it turns out that google results can vary dramatically for each person depending on geographic location, language preference, and other things, especially if you are logged in as well. It's always good to remind people to do a search and include what they did find in their search. I get a few definitions, offers of translations into other languages (Spanish, Turkish), and an advertisement and a prospectus for two different companies. start-up

Phytogenetic is

adjective
Botany
      Relating to the origin and evolution of plants.

(Source: Oxford English Living Dictionary)

prefix. Phyto, or phyt, is defined as plant. An example of phyto used as a prefix is in the word phytol, which means an oily alcohol that comes from combining the chlorophyll of plants with other substances and is used to create synthetic vitamins. http://www.yourdictionary.com/phyto
noun. Genetics, the study of heredity and the variation of inherited characteristics. https://www.merriam-webster.com/dictionary/genetics
Try the google machine or visit a local library next time you have trouble with words. It has worked quite well for people in the past!


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Cleaning out Agar from Autoclave Reservoir
I have a Tuttnauer EZ10 autoclave where the previous user poured m-Endo Agar into the reservoir. Using vinegar, we've been able to remove most of it, but there is a thin film of purple residue coating the interior walls. To get the autoclave safely working again, would you recommend I 1) pour water in and do a steam cycle, or 2) buy the Tuttnauer Chamber Brite and use it?
P.S. I can't make an agar, autoclave, reservoir, maintenance, or cleaning tag, so would someone please make those too?
Thanks in Advance!

Did any get down in the water drain pipe?

Hi CKM, yes it's in there too. What next steps would you recommend?
We have got the agar out of the interior walls of the central chamber, but you can see the agar residue in the water reservoir container. Some vinegar we poured into that chamber has gotten a majority of it in the water reservoir, but we are interested in getting it as clean as possible before use.
And thank you so much for taking the time to help use resolve this issue!

So I had a floor-standing Hayama HV-50 autoclave when this happened, so I'm not sure how different the process must be, just to preface. We had to actually lock-out/tag-out our device, take the side covers off and disassemble the copper drain piping. Then we took what was essentially a plumbing snake and snaked the agar out of the drain pipe. Running a hot cycle and things like chemicals and boiling water didn't work well for us because down in the piping, the contact surface area at any given time is the thin diameter of the pipe. You could have 8+ inches of agar noodle in there.

It might be prudent to just get field service done on your device so you don't inadvertently void the warranty or permanently damage the device.

Hi CKM, sorry for the late response, thank you for your advice and suggestions! We'll look into doing field service like you recommended. Have a great day!


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Saving lives by "conjoining" people
There are many deaths which occur as a result of a cascade of organ failures triggered by a single event, for example traumatic injuries, severe burns, infections and so on.
Since blood transfusion is a well-tested and established procedure which is safe and helps millions of people every year, would it be possible to treat people by "artificially conjoining" them by merging their circulatory systems with a small group of healthy volunteers? This would of course require them to have compatible blood groups and probably also immune systems to some degree, but it should be possible, at the very least for identical siblings.
Examples of use:

A patient has severe burns on >95% of their body, with severe inhalation burns as well. Their lungs are barely working and doctors give them very low chances of survival. Luckily, there are ten volunteers who are wiling to participate in an effort to save this person. Their circulatory systems are merged, so the injured person does not have to rely on their lungs working properly. They do not have to eat, drink or breathe now. The blood from volunteers helps keep the blood of the patient oxygenated and in optimal composition, their immune systems help the patient's body deal with the possible infections and since they are eating well, the blood supplies the injured body with all the nutrients needed for recovery.
A patient is senescent and suffers from all sorts of aging-associated diseases. They are a very important and rich person, so they pay some people to help them fight old age. This has already been tested to some extent.
A patient is suffering from a nasty case of MRSA. The prognosis is bad, but luckily there are many people from the same group of infectees who have already recovered fully. Their immune systems are still on the lookout for any stray bacteria they could kill. So they are connected, the various blood cells and antibodies find the infection in the patient's body and quickly deal with it.

Could this work? Are there any recorded cases where this has been tried? I am looking for an answer which will address the potential biological challenges this could pose. Let's leave the potential ethical problems aside, they are off topic here.
P.S.: I know what you are thinking. Yes, I know about the movie. My question is serious though.
Edit: I talked to a doctor at the transfusion center and she told me that this approach is very similar to how transfusions were performed in the past. It was problematic because they had no way of knowing just how much blood was transferred between the patient and the donor. She thinks that what I suggest would probably not cause any immediate issues if done properly. However, I think there could be some immunological problems down the line if the people's circulatory systems were joined for a prolonged period of time. I would like to see some information about that.

I voted to close because we don't deal with these sorts of speculative questions here, you could possibly try Worldbuilding.SE. There are massive ethical issues with what you propose that will prevent any real world testing of these ideas, but you may want to learn a bit about organ transplant and how difficult of a problem rejection is for just a single organ from one individual to another.

@BryanKrause I'm sorry you feel this way. I have edited the question to clarify that this is not speculative, I want to find out whether my suggestion has some insurmountable problems. The ethical issues are not universal to all societies (as any libertarians will happily confirm) or countries, and even then it all boils down to the question of whether a small health impact on several volunteers adds up to more than the cost of a single human life. If this is the case, shouldn't blood transfusions be illegal? So let's leave the ethical questions aside and focus on biology.

Pretty sure that one person won't be able to supply enough nutrients for another person from his/her blood though, as they will be used up by the healthier one. And if they are used by the diseased person, the healthy volunteer can suffer from the same if not more disorders leading to more problems.

The problems and possible applications may be close to those of corresponding animal experiments. For an overview see: https://en.m.wikipedia.org/wiki/Parabiosis

As mentioned in other answers, the problems with accomplishing this are manifold but primarily relate to the immune systems of the donors and recipient. While it may seem like anastomatizing the circulatory systems of ten donors to one recipient splits the load, in effect you're creating 2048 different donor-recipient relationships. This is a case where more is definitely not better.
Direct transfusion was first documented December 22nd, 1818. Initial problems with transfusion were primarily related to the treatment of all blood as the same, until in 1901 Karl Landsteiner described the first few blood groups. [1]
These groups classify blood by the antibodies present and, when the matching antigen is encountered by this blood, the antibodies attach to them causing hemolysis and signalling to the potential recipient that there is foreign material in their body. The most significant group is known in the US by its antigens A, B, and Rh (the +/- sign at the end). There are, however, at least 340 different documented antigens, 38 of which are unassigned to blood group systems. [2]
While basically matching blood types may work for a little while, the risk of  sensitization and subsequent hemolytic reaction grows the more foreign antigen containing blood a body is exposed to. Sensitization occurs when the body begins to recognize an antigen in the blood and begin creating antigens for it. This is perhaps best known in pregnancy, technically changing the mother's blood group to include Rh+. [3]
Additionally, graft-versus-host disease occurs when leukocytes encounter tissue that exposes non-self antigens. Thus, blood products are typically irradiated to neutralize the immune cells responsible. [4] The complexity of exposing just one immune system to another for an extended period quickly becomes exponential, as can be seen with multiple organ transplantation. Each organ is reactive in its own way, and thus for each type we know how to transplant there are different criteria to match. [5]
The answer to these problems, it would seem, would be to

Match donor and recipient blood groups.
Suppress the recipient and donor immune systems.
Possibly, irradiate the blood as it passes between them.

Matching immune components is already a difficult problem. Partly due to the number of variables, and partly because the number of willing donors is very limited.
In the case of severe burn trauma, victims of which are already immunosuppressed, this would be a terrible idea as the most prominent risk to survival is the ease with which pathogens can enter through wounds. [6]
The very reason to transfuse for, say, MRSA antibodies is hindered with the array of transfusions occuring. In order to prevent donors from hurting recipients and vice versa, their immune systems must be suppressed.
References

Direct blood transfusions
International society of blood transfusion working party on red cell immunogenetics and terminology: report of the Seoul and London meetings
Significance of Rh-sensitization during Pregnancy: Its Relation to a Preventive Programme
A systematic review of transfusion-associated graft-versus-host disease.
A Review of Organ Transplantation: Heart, Lung, Kidney, Liver, and Simultaneous Liver-Kidney.
Burn Wound Infections

Thanks for the effort, despite the question being rather hated by people.


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Do birds have quadriceps and thighs fused into their hips?
I'm looking at 3D modeling a large bird like an emu or ostrich, but I don't know how the muscles surrounding the femur connect to the hips/back. It seems weird that the entire thigh and quadriceps would be fused into the hip because that would greatly reduce the range of motion of the femur which affects how I animate it, but I can't find any reference that shows it either way.

Is "Ontogenetic scaling patterns and functional anatomy of the pelvic limb musculature in emus (Dromaius novaehollandiae)" not enough?

No it's not....

Have you tried googling avian muscle anatomy.

This is probably WAAAAY to late to be of any use to you but hey...
So the simple answer is:
Kinda.
You were actually correct to intuit that the femora of birds have a limited range of motion, with most of the limb motion being provided from the "knee"-down.
So you shouldn't animate bird legs the same way that you would the legs of other non-bird animals.
That's not to say that the femur doesn't move - it does but not my much (it typically doesn't extend posteriorly beyond the vertical). Much of the thicc thigh musculature is there for support.

Welcome to Biology.SE! Answers are much more likely to receive a favorable response if you include supporting references (primary literature is best) — that allows non-experts to confirm your assertions and learn more. Without that support, your answer is indistinguishable from opinion. This is a good example of how to format references. ——— Please take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site. Thank you!


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What are reciprocal inhibitory synapses?
Quoting Kandel's Principles of Neural Science, 2013,

Amacrine cells generally receive excitatory signals from bipolar cells at glutamatergic synapses. Some amacrine cells feed back directly to the presynaptic bipolar cell at a reciprocal inhibitory synapse. Some amacrine cells are electrically coupled to others of the same
  type, forming an electrical network much like that of the horizontal cells.

(Page 593)
I tried searching for what a reciprocal inhibitory synapse is but could not find any relevant information.

It might be better understood if written with a comma as:

reciprocal, inhibitory synapse

though the rules for this comma usage in English might discourage this because writing "inhibitory reciprocal synapse" doesn't sound quite right. I would say the author wrote it correctly even though it is not perfectly clear.
In this context, they are separate adjectives describing the synapse: inhibitory, because it suppresses firing, and reciprocal because Cell A gives input to Cell B, and Cell B also gives input to Cell A (where Cell A is the amacrine cell and Cell B is the bipolar cell).
The word reciprocal in this context is the adjective definition of the word reciprocal:

given, felt, or done in return.

Note that it isn't the synapse itself that is reciprocal or in both directions, but that the cells have a reciprocal relationship.


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how can I get stronger staining for my lymph node sections
I am using the same protocol and same antibodies that the literature says but still I cannot get good staining for my lymph node sections, I tried to change the fixation method and I am using now acetone instead of PFA, I also tried with acetone plus ethanol, the antibody concentration used worked in previous sections.
How could I increase the signal and/or remove the noise?
It also happened to work in some sections before but not in others even I did exactly the same, why could that be if I am using the same tissue?
Thanks

could you upload example of microscopic image

Is the tissue you are staining now the same age (i.e., time from initial fixation to staining) as the tissue you used before?

yes I do the fixation just before the staining so I treat them in the same way

I attached the picture, thats the pic of the channel for Madcam which is my interest

Did you try a different fluorophore or fresh antibody? What're you using now? And are you getting signal with other markers like DAPI? What does your staining efficiency look like by FACS? Strong separation from negative or weak? Maybe try digesting some lymph node and see if you get good staining.

the antibodies are not fresh but some times work better than other using the same kind of tissue, so I guess is depending of the tissue and age of animal or sections? the stainning efficiency looks okay. I used Dapi, Cy3, FITC 647 and alexa488.

@bio Okay, and your laser/filter setup are appropriate for your fluorophores? If we rule out hardware and reagents, all that's left the the protocol and the slides.

@bio what's your red laser filter setup?

I can double check on Monday because I do not remember now, but I checked that time ago with my supervisor and it was fine. I upload now another image (first one) so as you can see, doing the same fixation protocol and staining steps I get very big variations within the same tissue. I also tried different ab incubations, different concentration of the primary and secondary ab and all of them look with a lot of noise so Im not sure now what is real signal and how to avoid this big variation between same kind of tissue.


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FIbroblast vs fibrocyte
After i had been studing for histology examp i tried to solved one nominclature dilema.Its about fibrocytes and fibroblast.
In my histology book is statment, that fibrocytes is special type of cell which can be differentiated to different cell types by specific occasion ( for example exposure to transcript factors).
Then fibroblast is cell of connective tissue. Its differentiated.
Why is differentiated cell named with blast (usually active type) istead fibrocyte (usually the differentiated one)?

If i  misunderstand something i ll be grafull for correction.

See the second part of the answer marked as duplicate: Blast cells may also be cells that produce materials applies to fibroblasts. There isn't anything particularly unique about this example, you've just focused on one but not both of the meanings of the -blast suffix.


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Territorial behavior in humans?
Do humans exhibit territorial behavior like other primates? I have seen people sometimes stare at others -- notably males -- and then physical fights spontaneously turn up. Is this territorial? It seems it either goes two ways: One person looks at another; the other looks back and either looks away or both look away; or they both hold a stare until one or both erupt in to physical blows and try to dominate the other or fight/assault them. Is this a display of human territorial behavior? I know some chicks do it too.
I've also read that in males more so that staring can be an "alpha" or "dominating" gesture to others -- especially if a stare is held at one in response to them either turning away or provoking a fight.
This can be seen in every area, but possibly more so in clubs, bars, or certain social settings.

What you're describing is not territoriality, but dominance/aggression.

From encyclopedia britannica

Territorial behaviour, in zoology, the methods by which an animal, or group of animals, protects its territory from incursions by others of its species.

Following, this definition, yes territorial behaviour exists in humans. Here are three simple examples drawn from different (western) cultures

You seem to be confusing territorial behaviour with general, aggressive behaviour. Whether or not the behaviours you describe qualify as territorial behaviour requires one to make a psychological study to determine whether the individuals had a notion of territory that they wish to defend.

I'd argue that territoriality can be observed on many scales with humans. At the bar, 1-on-1 conversations with a spouse, between homes, between cultures, between parties during war, nations, the list goes on. It is also peculiar that humans seem to extend territoriality into abstract spaces, such as thoughts and ideologies.
I once read the 2010 book Supernormal Stimuli: How Primal Urges Overran Their Evolutionary Purpose by Deirdre Barrett which argues, details and very elegantly describes our instinctual, territorial tendencies in modern humans. I do not doubt that humans today follow instincts we evolved for our time spent in the African savannahs. The book explains other vestigial instincts too, which evolved and now exist in an artificial environment.
Take a look: https://en.wikipedia.org/wiki/Supernormal_Stimuli


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Whats this bug?

My friend found this bug today and we are trying to find out what it is. Long black (about an inch and a half).

Please edit the question and add the location (city/state/country) where you took this image.

Meloid beetle (blister beetle).  Wikipedia images suggest genus Berberomeloe.  This one below, from Spain, is identified on the Wiki page as Berberomeloe majalis. There is at least one other species described from the genus (insignis).


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Is there a biological explanation for a 0.5 difference in allele size with PCR product?
CONTEXT

I am currently working on a set of diversity, this diversity in interspecific (within the same genus). I am using SSR markers, the primers were designed on one species and are working really well within the species (lot of diversity and difference between allele of 1 at least).
When trying them on the other species, I observe the normal non-amplification which could be due to mutation in the primer DNA sequence. But, for some genotypes I have been observing a new allele just between the two older ones (like the new one is 185.5 and the olders were 185 and 186.
QUESTIONS

Is that kind of observation frequent when using primers designed on other species?
I understand how a 1 pb difference could occur CACACA ==> CACCACA, but what could the biological explanations be for a 0.5 pb difference between alleles?

In my experience, working with a similar approach in Campylobacter jejuni, the base pair measurements from these techniques are imprecise and need to be carefully calibrated. I am unsurprised to see 0.5 base pair differences, this can be seen been runs and even, in the worse case situation, between even and odd wells in the same plate(!).
I would use Sanger sequencing to determine the sequence you are getting in one of your isolates, and then use this as a calibration control included in every run.

Thanks for your feedback! I was planning to do a sanger sequencing to understand the problem. The allele though is quite stable (same length on different plates). Usually I see all my alleles in a 0.5 pb variation around the real value depending on genotypes/runs.

@Untitpoi We found that different length targets from the same strain, and the same targets from different strains frequently gave different length results.

@Untitpoi I think it occurs because of differences in the sequence causing sligtht differences in mobility during capillary electrophoresis. If you look at the raw data from a sequencing read, you can see that the peaks appear less regularly than the smoothed processed peak data you usually look at. I would guess there are consistent differences in the progress of sequences based on the physical properties of the nucleotides.


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Does estrogen increase muscular growth in females?
Regarding humans it is said that most psychological effects caused in men by testosterone are caused in women by estrogens. There are many studies on that, particularly regarding temporary shifts of hormone levels: Ovulatory shift hypothesis. Also, there are some studies (and possibly controversial) claiming such differences between individuals.
But this made me think if there are any similar physiological diffences caused by estrogens. It's known that in males testosterone affects muscular growth, which means higher testosterone levels will make it easier to gain muscular weight. So, I ask if higher estrogen levels in females affect muscular growth.
While this question is regarding humans, studies about other primates also can be acceptable.

The article named "Estrogen replacement and skeletal muscle: mechanisms and population health supports this hypothesis, when applied to postmenopausal women:

Evidence suggests that HT will also help maintain or increase muscle mass, improve postatrophy muscle recovery, and enhance muscle strength in aged females.

This particular passage suggests it might not be exclusive to postmenopausal women:

One of the reasons for the relatively new interest in estrogenic effects on skeletal muscle was the identification of estrogen receptors (ER) in this tissue.

Passage containing more specific information:

Although research findings over the past 20 yr have reported conflicting results of HT on muscle mass in postmenopausal women, the preponderance of more recent evidence has “tipped the balance toward a positive and measurable impact of HT” and have highlighted the “proanabolic” effects of HT on skeletal muscle. Several recent studies examining postmenopausal women showed significantly greater muscle mass in women taking HT relative to nonusers.


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qPCR: Huge variation in fold change of genes between biological replicates
I am trying to validate my RNAseq data by doing qpcr for which I am looking at the fold change of few genes across various timepoints of treatment conditions. I am getting huge amount of variation (in thousand folds ) in my biological replicates. I thought may be it is due to genomic DNA contamination so thats why I repeated all my experiment and did DNase treatment twice but still I am having such variations. I am using two reference genes EF and GAPDH and I also have variations in the Ct values of reference genes across various timepoints. I will really appreciate it if you could suggest me with possible problems and solutions.
Thank you, Ambika

How do your technical replicates look?

To clarify, the variation you're seeing in the qPCR isn't being seen in the RNAseq? Do the values correlate? How was the qPCR data normalized?

How are you aliquoting DNA samples into your reaction mix? You can get alot of error just from errors in the pipette. I fine a ECHO liquid dispenser makes all your troubles go away (provided your can find one somewhere) GAPDH is sensitive to metaoblic state (ie oxgyen and glucose levels.) Are you using column purification of RNA with DNAse treatment?

@RoverEye my technical replicates look good, they don't have such variation.

@CKM I made PCA plot to compare my replicates for my RNAseq data. I had 4 replicates for RNAseq in which there was clustering of  1 and 2 together ; and 3 and 4 together. But that might be due to environmental variation since I did that in different time. In qPCR I am seeing the expression of those genes but the fold expression between biological replicates do not match. They have the same trend though. I am having 1000 folds difference in some genes

@JayCkat Yes I am using column purification of RNA with DNAse treatment.And also both EF and GAPDH have 5 to 6 Ct value difference in between the samples.

@ambika Here are some things I would do: Check the data analysis, make sure everything is in FC or logFC (i.e. make sure one isnt logFC and other is linear FC). Check how data were normalized, and whether reference genes were differentially expressed (look for stable expression or lowest CV reference genes). Also note whether the results correlate, is your R2 good if you plot the two on an x-y/scatter plot? Since the two methods measure differently, it may be more important that the trend is the same rather than the result.

@CKM I normalised the data using DDCT method. I am also thinking if my reference genes are not good enough. Thank for your suggestions.

@ambika Maybe you can use your RNAseq data to find a few genes with stable expression across your samples, to use as references in further experiments.

@CKM can you please suggest how can I categorize genes. Any programs or method?

@ambika How do you mean? Like how to categorize them as reference genes? Or something different?

@CKM Now I am trying to calculate stably expressed genes using the RNAseq data. So far I calculated coefficient of variation of all genes based on count data. Now one thing that I am confused about is the list with least CV from all replicates look different. Do I have to calculate CV integrating all the replicates data?

@ambika Calculate the list of stably expressed genes from all the data together. I like to visualize it as if i were working in excel: Columns are samples, rows are genes. Calculate the CV% in a separate column by row (i.e. by gene), and sort low-to-high and pick the ones with the lowest CV%. Just remember if you use them to normalize to drop them from your analysis set.

@CKM thank you so much. I really appreciate your suggestions..

If you have 1000-fold differences between either your biological samples or RNAseq & qPCR there is very likely a problem with your data normalization (if not you need better samples). Ideally you should always use log2 normalised fold change values (qPCR / ddCT directly gives these, they should be somewhat normally distributed around 0 and represent doubling effects which are often biologically relevant).

Also as others have mentioned GAPDH expression levels can be affected by the metabolic state of the cells, so it's not always a good control/reference. Generally a control for qPCR should have similar expression levels to the genes you want to measure (this might be an issue for you, GAPDH & EF can be very high) and of course be stable between the timepoints or conditions you want to compare.