text:
Are babies cute, or is cute babies?
I have no doubt that the cuteness of babies is an evolutionary advantage. So the 'why' is clear, a bit of research also explains the mechanics, such as babies having certain features that trigger hormonal reactions. Therefore the 'how' is also fairly clear.
However, this leaves the question for which I did not really find an answer:
Did babies evolve to increasingly trigger cuteness in the brains of adults, or did adult brains evolve to increasingly get attractive to what babies look like?!
In most cases the direction of influence in an evolutionary process is quite clear (e.g. if the sun is bright in an area, humans adapt to it by getting a darker skin, the sun itself did not evolve to become brighter in area's where people with darker skin live).
However, as the appearance etc. of babies and how these are percieved is actually both about humans (who typically are first babies and then become parents) I am now doubting if babies are evolving to be cute, or if cuteness is evolving to match babies!
I am very curious if we know if the evolutionary influence is a one way street, bidirectional, or perhaps we (recognized scientists) actually have concluded that we have no idea. In case it was not clear I am mostly interested in humans though I guess the question may apply to other races as well.

I did think about other things that are typically found to be cute by humans (e.g. baby animals), but these roughly have the same features that we currently find cute in human babies (e.g. being small) so I don't think this rules out an influence in either direction.
My personal intuition is that babies will definitely evolve towards the general current standard of cuteness, but I would not be surprised if the standard of cuteness also evolves towards the general current appearance of babies.

Let's please try to be civil as we offer criticisms of questions posted here. Not every question needs to be about everyone's preferred area of biology, I expect that almost everyone who uses this site regularly has some class of questions that they aren't as interested in.

For OP, I think your question will get a better response if you try to frame it in some existing discussion rather than working from the ground up. Have you found biologists who study "cuteness"? What are the issues they discuss?

I don't think there is a natural selection against babies that are not cute or less cute.

On an intimately related topic, neoteny in humans and its evolution are worth investigating.

Sounds a bit like a chicken-egg question and as such is almost certainly unanswerable.

@DKNguyen - I used to deliver babies. The ugliest baby I ever saw, a truly ugly baby, went on to acquire two siblings. So I believe you're correct.

@anongoodnurse That made me lol. On second thought, that might be just within the  past few thousand years (maybe not even the past few hundred). Maybe a million years ago parents did subconsciously neglect less cute babies when times were hard and they were equally healthy. Especially if they became tied with traits associated with fitness and health (things like facial symmetry, etc). I'd guess it goes back even farther. After all, humans, kittens, puppies, and birds diverged long ago and we find them cute.

I did not expect the statement that babies are cute to be so controversial that it needed support in itself, but have added this link as a reference to show that it is not only my perspective. https://psychology.stackexchange.com/questions/16098/why-baby-animals-seem-cute-to-us
Now of course there are more assumptions (the post rougly explains cute as 'expressing the need for care' and surely it is not proving that this also results in babies actually getting that care, but perhaps we can focus on the mechanics of evolution rather than how I worded the question.

Its a lot easier to change how adult brains think than baby anatomy.
Babies are tightly constrained by development, certain things need to grow faster or earlier than other things. This is why most vertebrate young share many of those features. meanwhile evolving a behavior is one of the easiest things to evolve, a huge portion (~80%) of our genome is devoted to the brain and thus behavior.  A classic example of this interplay is that it is nearly impossible to keep babies from puking, so the brains of parents react differently to the puke of babies. It is also worth noting non-cute babies are usually suffering from, what would be in nature, fatal defects. It is also worth noting people find their own babies cuter than other babies, which means cuteness is also partially subjective.
https://onlinelibrary.wiley.com/doi/abs/10.1002/1097-0355(198121)2:1%3C56::AID-IMHJ2280020109%3E3.0.CO;2-G
If you want a more detailed breakdown you are gong to need to ask a series a questions because cuteness covers a lot of behaviors.

Very nice insight, to be fair I was not sure if I would get any insight at all.
Based on the earlier comments I should perhaps keep my mouth shut at a biology seminar, but at the next birthday party where we run out of topics I will definitely pose that it seems likely that cuteness is for a notable part defined by babies, rather than them only evolving towards it!


text:
What are the most intelligent plants?
For intelligence lets adapt the definition from here:

Perception of the surrounding environment
Adaptation to environmental conditions
Communication (in the case of plants, through chemical secretions)
Social interaction (by sending and receiving chemical information) and cooperation for mutual health and safety.

Basically, I'm looking for the spices of plants that demonstrated very high sensitivity and responsivity to their surroundings.
Those intelligent plants are not necessarily the plants that can physically move in seconds like mimosa pudica, rather also those who show any kind of respond even to humans - if we accept some  of the research that have been done in the past years.
Edit: It has been demonstrated conclusively can communicate: i.e., have the ability to send and receive signals. Just, for example, by "Below-ground communication" using chemical cues. Moreover, it has been also demonstrated that plants are aware of their surroundings: the roots can bend to avoid some obstacles. Yet another example of a kind of communication/awareness is the phenomena of Crown_shyness.
There are researchers that are not shy of using the term intelligence here (Some researchers even go further to suggest a kind of memory in plants).
This question adapted the terminology (that is used by some), and provided the reader with the definition and explanation that is too long for the title. I believe the reader should not be deterred here, as ultimately this question is not about semantics. The question basically asks if there is any kind of test or scoring points to distinguish those "intelligence behavior" between plants, as I believe that there are plants that are more "intelligent" than others - but I could not find information about this online.

Welcome to the site. Please take a [tour] and visit the [help]. There you will find lots of good information about what sort of questions to ask, and how you can make a good question/answer. In particular, questions with "most" are likely to be answered as opinion and don't fit the stackexchange format well. We also ask that questions have some evidence of an attempt to answer them by the asker. If you rephrased your title to something like "what is the evidence for communication and intelligence in plants" then you might get a better response.

@bob1, I've taken notice and added some more information. For now, as I explained in the body of the edit, I prefer to keep the title as is. If someone believes he has a better title, he can be free to edit the title.

Users might better give the OP (me) enough time to edit the question after requested before downvoting. or at least explain  why the question was downvoted.

No point in worrying about downvotes, see this main-meta post regarding downvotes and comments. Now you've edited you're much more likely to get upvotes.

there is no evidence plants can perceive their surroundings, plants ae not aware of anything. A plant no more perceives its surroundings then a a TV perceives its remote. individual cells can send an receive signals, adapt and engage in social behaviors, so you have not defined anything the simplest unit of life can do. you are combining several unrelated and basically incomparable metrics and asking us to evaluate their balance, which makes this essentially opinion.

Note that your links are to "popular science" sites or Wikipedia. There is nothing "wrong" with this, but it does suggest that you've done at best a very cursory examination of the available literature. In particular, such sources tend to over-simplify, make extensive use of analogies, and extrapolate well beyond what has actually been shown. This can lead to a (sometimes very) distorted idea of what is known. In your case, you use a lot of terms (e.g.s "intelligence" and "awareness" in a very colloquial fashion — its great that you try to define the former, but I think you will get a  ...

@John what about things like phototropism, geotropism and chemotropism? I think that no perception is a bit strong. Conscious behaviour? no, definitely not, but perception isn't limited to conscious behaviour.

... better response if you determine what terminology is used by people doing this research and use that —  if they do use "intelligence" then tell us exactly how they define it. ——— Also note that even in humans it is quite possible to react without any conscious awareness, which makes your use of "aware" when you appear to mean something more like "responsive" needlessly confusing.

@bob1 again all things single celled organism can do, perceive means being consciously aware of something, which you can't do without a brain.

My vote would be for the aspen. The entire thing. One stand. Communicative, yes. Perceptive, yes. But intelligent? For a plant, maybe.

@John - your comment is dead wrong. Not only can plants respond to temperature, day length, gravity, position of the sun, moisture, etc., there is scientific evidence that they can do more. Your comment is faulty to the degree of harm to science. Any gardener knows plants much better than you do. Biologists should know more, not less, than a hobbiest in the field.

@anongoodnurse, again all things single cells can do, there is no evidence plants are consciously aware of any of this. there is a difference between sensation and perception, plants can sense all those things they perceive nothing. please read my statements with care before you  declare them in error.

@John - I didn’t say anything about consciousness. I said your comment was dead wrong, and it was.

@John- it should not surprise me in the least when people assume that a disagreement is based on lack of careful reading, but… it still does.

@anongoodnurse am curious what statement of mine you think is dead wrong that does not have to do with consciousness? As I said perceive means "consciously aware of"

I’m voting to close this question because: 1) it is asking for something that seems impossible to answer objectively ("most intelligent" is controversial even within humans where we at least roughly agree that "intelligence" is a meaningful concept); and 2) it remains unclear what is meant by "intelligence" in this context and the edits so far have not helped. Please see the [tour], [ask], and other [help] for details.

@tyersome, That's okay if this forum thinks and votes the question is off to close it. But I want to offer my take as to why - by your two points - the question should stay open. (1) It is possible to answer objectively by offering appropriate tests (see my answer); it  simply not possible to answer uniquely. that's was I used plants in the plural. (2) If it is unclear - though it was defined (before the edits) - please explain what is not clear.

The plant genus Cuscuta (dodder, amarbel) might be the most 'intelligent' plant(s). It is based on an agreed definition of intelligence, observations on the plant and what the plant can achieve compared to other plants and without a neural network; although this is not a scientific fact and there isn't a scientific consensus on plant intelligence. They are parasitic plants that can attach themselves on a variety of different plants to hijack them for nutrition and can spread plant diseases as well. They appear to use different senses like smell, taste, touch to be able to interact with their environment and to find other plants/food.
Here is a study from PubMed Central titled The foundations of plant intelligence and I'm including some relevant excerpts that provide a summary, the definition of intelligence and some observations on the dodder plant:

Intelligence is defined for wild plants and its role in fitness identified. Intelligent behaviour exhibited by single cells and systems similarity between the interactome and connectome indicates neural systems are not necessary for intelligent capabilities. Plants sense and respond to many environmental signals that are assessed to competitively optimize acquisition of patchily distributed resources.
I consider that intelligence in most animals and plants is concerned with improved survival in the wild and thus in turn fitness.
Perhaps, the most useful summary is that of Legg & Hunter. They collected some 70 different definitions of intelligence and summarized them as follows:
Intelligence:
(1) is a property that an individual has as it interacts with its environment or environments;
(2) is related to the agent's ability to succeed or profit with respect to some goal or objective; and
(3) depends on how able the agent is to adapt to different objectives or environments.
Observations on the parasitic behaviour of Cuscuta (dodder), indicates it performs analogous behaviour to Lymnea but without the need for control by a simple nervous system. Dodder is a typical parasitic plant in that it searches and locates host plants which in due course it exploits. Some 4500 angiosperm species exhibit varying degrees of parasitism.
The dodder seedling lacks a root. Consequently, it must find water quickly on germination. In this condition, it is clearly in a motivational state of search. The shoot circumnavigates and locates nearby hosts from the volatile organic compounds the host emits, as shown by time lapse.
Kelly offered numerous suitable hosts to dodder by tying them together and found a rejection rate of 50% within a few hours, indicated by the parasite branch growing away. The assessment period is thus completed in this short time and since contact is only surface in character, assessment is probably made of the volatile chemical signature of the host. Dodder is using taste like Lymnea and changing search strategy when the source is not satisfactory.
There is little doubt that a primary problem some biologists have with the concept of plant intelligence is the assumption that intelligence is limited to organisms with some sort of neural network. The observations above show that dodder is capable of equivalent behaviour in the absence of a neural network. Alternative methods of assessment exist in plants. Intelligent behaviour is not dependent on neural activity.
Trewavas A. The foundations of plant intelligence. Interface Focus. 2017 Jun 6;7(3):20160098. doi: 10.1098/rsfs.2016.0098. Epub 2017 Apr 21. PMID: 28479977; PMCID: PMC5413888. - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5413888/

Further sources:

Detection of Different Hosts From a Distance Alters the Behaviour and Bioelectrical Activity of Cuscuta racemosa - https://www.frontiersin.org/articles/10.3389/fpls.2021.594195/full
Understanding interdisciplinary perspectives of plant intelligence: Is it a matter of science, language, or subjectivity? - https://ethnobiomed.biomedcentral.com/articles/10.1186/s13002-022-00539-3
Book: Plant Behaviour and Intelligence By Anthony Trewavas

dodder grows in the direction of certain chemical compounds and away from others and can habituate to signals, which all plants and indeed all cells do, so what makes dodder more "intelligent" the paper offer nothing that all know organisms cannot do. It essentially argue all life is intelligent.

Thanks for your answer and suggestion about tags edit which I've adapted. This is a long article and I intend to read later this week. As I said some researchers prefer to use the term intelligence - I agree - but some might disagree and that's completely fine. The problem starts when people turn away from the given definition of the term (and rather focus on the title) - then the discussion is not fruitful for the actual issue at hand.

@discipulus I think it's wrong to think you can redefine a term without pushback; however you change the definition, terms used in an existing way will always carry baggage. The definition given is so far from the use of "intelligence" in context of animals. By that definition, almost all of biology becomes "intelligence", and therefore the term becomes useless.

@BryanKrause, (1/n) what you and others seem to be missing is that I'm not trying define a term for the sake of the definition. I care not about the term. if it helps, one might replace the word intelligence with the term "fjhdsfjhkds" and reread my question. That's for one. For two, and this follows if one says that this can be applied to all biology -- I won't object and will be tolerative - not necessary because I agree or not, but because it is not the point of the discussion.

@BryanKrause, (2/n) Now, if we want to enter the discussion. First, bear in mind, that however strongly one resists the term intelligence - this precise term was used and is used by more than one researcher. So, we have to accept that at least part of the scientific community believes this term is appropriate.  I have not seen appreciation for this fact here.

@BryanKrause, (3/n) Now, the term intellegence was not born out of void. it makes perfect sense (to me at least) to use this term, if one view things in context. the context clearly was the apparent display of function in plants that wes previously hidden to humans. This is a kind of higher function - like communication. in this sense the plant is indeed intelligent.

@BryanKrause, (4/n) I also think it is wrong to think of perception/sensation only in terms of brain and nervous system. those term (intelegece also) predates the human understanding of the mechanism in the animal kingdom (i.e., nervous system) - hence I see no reason to restrict the terms to nervous system. For 5 year old the plant is aware and perceives no less than humans are. YOu can teach the child the plant has nervous system and the child won't object.

@BryanKrause (5/5) Finally, I don't think it is easy to define intelligence in a way that would match humans and animals and not plants (nor even cells or "all biology" if you will).  without restricting the term and thus - effectively - render it very limited and essentially meaningless.

source: Stack Exchange

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

sort: votes


text:
Examples of animals with different number of chromosomes that can interbreed?
When I was first started to write this question, I wanted to know how species evolve to have a different chromosomal arrangement, such as having two pairs of chromosomes instead of one? However, I think I have resolved my misunderstanding by reading:
http://scienceblogs.com/pharyngula/2008/04/21/basics-how-can-chromosome-numb/
My basic misunderstanding was that I thought animals with a different number of chromosomes couldn't reproduce, which appears to be wrong. My question is now, are there examples of animals that can interbreed that have a different number of chromosomes (particularly offspring that are not sterile)? Is there a species that is known to have a variation in the number of chromosomes (yet, somehow, hasn't yet resulted in complete speciation); or are there two species that can be interbred and result in fertile offspring?

Such examples are not that rare: multiple species are polymorphic for supernumerary (B-chromosomes), others are known to show intra-specific Robertsonian polymorphism (fusions of acrocentric/separation of metacentric chromosomes).
One very well studied example, which covers both intra- and inter-specific crossings, are isopod crustaceans from the Jaera albifrons complex. They show Robertsonian variation (and additionally sometimes B-chromosomes):

different species in the same location normally have different chromosomal numbers;
on the macrogeographical level at least some species show certain gradients in chromosomal numbers;
sometimes the same variation can be observed on the level of local populations.

Hybrids between species are viable and not sterile, but rare in nature. Fecundity of hybrids is lower than that of the parental species, and this seems to serve as an additional post-zygotic mechanism of species isolation.
Crossings between specimens of the same species with different numbers of chromosomes do occur in mixed populations and are also possible for parents coming from different extremities of the above mentioned chromosomal cline. In the case of mixed populations frequency of these hetezygotes is less than expected by Hardy-Weinberg. Such offspring is fertile, and its lowered frequency is associated with higher incidence of abnormal meiosis.
On the cytological level (normal) meiosis in a heterozygote individual is remarkable in showing trivalents instead of bivalents for the polymorphic chromosomes:

(a metaphase with a trivalent in the center and two bivalents) (from Staiger & Bocquet 1956)
In addition, in four out of five species of the complex chromosomal sex determination is of the following uncommon type: males are homogametic with sex chromosomes ZZ, while females are heterogametic with ZW1W2 chromosomes. So, females normally have in total an odd number of chromosomes and in their meiosis one observes a trivalent similar to the one shown above: the metacentric Z-chromosome conjugates with the two acrocentrix W-chromosomes.
Some references available on-line:

Lécher & Prunus 1971 (in French)
Solignac 1981 (English, on isolating mechanisms in general)
Lécher et al 1995 (a review in English)
Kappas et al 2013 (a review in English - see pages 23-26)

These are highly relevant to the question, but not accessible on the web:

Lécher 1967 (Cytogénétique de l'hybridation expérimentale et naturelle chez l'Isopode Jaera (albifrons) syei Bocquet)
Lécher 1967 (Polysomie autosomique chez l'Isopode Jaera albifrons syei Bocquet)
Staiger & Bocquet 1956 (Les chromosomes de la super-espèce Jaera marina (Fabr.) et de quelques autres Janiridae (Isopodes Asellotes))

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


text:
What is this insect found in a shower?
I hope the picture is clear enough, I've found a worm like insect like the one below a little while ago in my shower, and today I found another one. I've never seen something like this. I would say it is slightly bigger than a centimeter.
Location: Netherlands

Why do they come in my shower ?

It is a species of silverfish such as Ctenolepisma longicaudata or Lepisma saccharina for examples (thanks @RHA for correction in comments).
Silvefish are well known very resistant pest typically found in washrooms and sometimes in kitchens. They are not directly dangerous but can cause property damage. Here is a webpage giving advice on how to get rid of them

It might be a silverfish or a paperfish. And getting rid of them is, at least in the Dutch climate, virtually impossible. I speak from expierence here. Unless maybe, if you convince all your neighbours to do the same...

What is a paperfish? I could not find a wikipedia entry for paperfish except for a fish species. Yes, silverfish are really resistant and it can be really hard to get rid of them esp. in apartment building.

Sorry. It is Ctenolepisma longicaudata, called gray silverfish in English. Paperfish is my bad translation of the Dutch 'papiervisje'. It eats books...

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


text:
How long is one generation for a mosquito?
For instance, humans are said to have an average generation time of 20 years. I've heard that mosquitos go through 10 generations in a year. Is that information correct?

This  http://www.mosquito.org/life-cycle  is the first hit if you google "mosquito generation time".  14 days, apparently.

it's variable depending on the species, temperature, and feeding.

@Roland I think you can make an answer out of your comment. There will probably be no need to further the answer much more than what the comments currently say.

I feel the need to add that there are thousands of different mosquito species, but I'm guessing you're mostly interested in the ones that cause humans problems? (These should be the ones that the American Mosquito Control Association talk about, too.)

According to this information page from the American Mosquito Control Association, the generation time for a mosquito at 70${}^\circ$ F is about 14 days. The precise generation time depends on temperature and access to nutrients, but yes, it seems reasonable that mosquitos can go through 10 generations or more in a year.

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


text:
Which is the best results for Plasmid dna extraction on gel electrophoresis?

I did plasmid dna extraction and uploaded on the gel.
Well 1: marker
Well 2: nicked,circular,and supercoiled bands
Well 3: linear,circular,and supercoiled bands
Well 4: circular and supercoiled bands.
Which one is the best result?

What do you mean by "Best"?

Best extraction

You still have not explained what you mean by “best”. Do you mean “highest yield”, “most un-nicked” or what? Do you know what the different bands represent? If, as I suspect, you do not then you need to find out for yourself. You could even search this site to find a photo I included in an answer to a previous question. But we expect posters to provide context to their questions, and evidence of their own attempts to find an answer.

My professor asked me this one, and I’m not sure what do we mean by the best here. I’ll check and edit then the question. Thank you

This is very obviously homework. Please see the [help] for the homework policy.


text:
Is synesthesia caused by crossing the circuitry of different sensory inputs?
I have a question about human perception. After reading the book "Sensory Perceptual Issues in Autism and Asperger Syndrome" and knowing about synesthesia (https://en.wikipedia.org/wiki/Synesthesia) something occurred to me.
If unique circuits of neurons are responsible for each of our senses, and the circuits can cross with each other (synesthesia), and given that autistic people can switch off a sense or may have problems filtering inputs, and all impulses are of one kind, how can the brain know where these inputs are coming from? For example if input is coming only from the eye, can a person think that it is coming from the ear? Can we see with our ears, or hear with our eyes, through some sort of circuit-crossing?

Thank you i highly aprreciate all feedbacks, because english is not my mother language and i am glad to learn more about it to improve my skills.

You can write a thesis about that topic. You should rephrase it a bit, perhaps: At what stage in the circuits of neurons can sense perceptions of synesthesiacs become confused? What prevents ordinary people from seeing sounds and hearing what we see, if the circuits are eventually merged? Because subconcious perception is very fascinating that's an awesome topic to learn from, I donno if i will find a resonable response though, you need a pscyhologist/neurologist experience.

I think you are confused about what is happening we can all filter out information (Sensory gating), we take in vastly more information than we pay attention to, autism reduces or removes the ability to filter out incoming signals. https://en.wikipedia.org/wiki/Sensory_gating

Good question; I tried to rewrite your title to be more of a question format rather than a topic heading - feel free to edit it if this wasn't quite the question you meant to ask.

i think you didnt change the meaning. I even love that format !! :D thank you very much

Short Answer
Synesthesia happens at a point during processing where we are not dealing with "raw visual input" or "raw auditory input" anymore, but already with more abstract constructs such as "colors" or "sounds".
Full Answer
Your question seems to consider sensory perception as a matter of "inputs" and the brain detecting those inputs, such that for example the only difference, from the brain's point of view, between visual inputs and auditory inputs is that one comes from the ear and the other from the eye.
A more accurate way of seeing it is that our sensory perceptions are really the brain constructing a coherent reality from the information it got from our senses. And I do mean "information" in the most abstract, computer-sciency sense possible. It's not like our eye is a photographic plate that contains "what we see", and the brain just has to reconstruct that. The processing of visual information, by which I mean picking out various features from the light received and deriving meaning from them, starts right in the retina. Some examples from the "14.5 Visual Processing in the Retina" section in this page:
http://nba.uth.tmc.edu/neuroscience/s2/chapter14.html
On bipolar cells:

The two bipolar cell types have different functional properties.

The off bipolar cells function to detect dark objects in a lighter background.

The on bipolar cells function to detect light objects in a darker background.

On horizontal cells:

The surround effect, produced by the horizontal cells, enhances brightness contrasts to produce sharper images, to make an object appear brighter or darker depending on the background and to maintain these contrasts under different illumination levels.

On the retinal ganglion cells:

The retinal ganglion cells provide information important for detecting the shape and movement of objects.
Type P retinal ganglion cells are color-sensitive object detectors.
Type M retinal ganglion cells are color-insensitive motion detectors.

On amacrine cells:

There are 20 or more types of amacrine cells based on their morphology and neurochemistry. The roles of three types have been identified. One type

is responsible for producing the movement sensitive (rapidly adapting) response of the Type M ganglion cells.

enhances the center-surround effect in ganglion cell receptive fields.

connects rod bipolar cells to cone bipolar cells, thus allowing ganglion cells to respond to the entire range of light levels, from scotopic to photopic.

Similarly in our ears, the cilia cells that vibrate in response to sound are frequency-dependent, and it is information about those frequencies that gets transmitted to the rest of the brain for processing. In other words the very organ that detects sound also performs a kind of Fourier transform on the sound waves it detects before anything else.
See for example:
https://psychology.stackexchange.com/questions/15274/how-does-the-inner-ear-encode-sound-intensity
This parsing, combining and interpreting of information continues throughout the perceptual circuits of the brain, and not in a straightforward way either - it is hypothesized that there are two independent or semi-independent processing streams for visual information, the ventral and dorsal streams, one which is for identifying objects and the other for guiding actions:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4678292/
There is also information flowing the other way, where more "advanced" brain regions draw conclusions about what's actually there and feed those conclusions back into the more "basic perception" parts to ensure that that's what we see. I.e. perception has both "feedforward" and "feedback" processes, or "bottom-up" and "top-down".
All of this is to say, there is absolutely no way for the brain to confuse information from the retina and information from the ear; the early processing in both of those is too tightly linked to the organ itself, and perception as a whole is inextricably linked to cognition. It's not like a mouse and keyboard that you can plug into different sockets; the retina technically is part of the brain in the first place!
This is not to say visual and auditory senses cannot be confused, obviously synesthesia happens, but it likely happens at a point in the processing where we're not dealing with "raw visual input" or "raw auditory input" anymore, but already more abstract constructs such as "colors" or "sounds".
For example this paper (gotten from the Wikipedia page https://en.wikipedia.org/wiki/Neural_basis_of_synesthesia) :
https://web.archive.org/web/20060527085838/http://psy.ucsd.edu/~edhubbard/papers/JCS.pdf
Hypothesizes that the synaesthetic association of letters with colors is caused by cross-wiring between the area of the visual cortex that processes letters and the one that processes colors.
This paper from the same source:
https://academic.oup.com/brain/article-abstract/118/3/661/321747?redirectedFrom=fulltext
Finds that color-word synaesthetes had, when told words the associated with colors, activation in the language and "advanced" visual processing areas but not in more basic visual processing areas.
Similarly for autism, given that sensory perception happens at every level in the brain, including conscious thought, those perceptions can be blocked or filtered (or not) by the brain at any stage. No need to assume it is at the "raw input" stage.

Nice answer, I hope you don't mind my edit to bring the punchline up to the top.


text:
about lipid oxidation, does acid fatty transforms in glucose?
Lipid oxidation generates fatty acid and glycerol going into the bloodstream.
Can they be converted into glucose by gluconeogenesis or are they turnd into ketone bodies?

Welcome to SE Biology. Please take the tour and read how to ask questions before posting.  You will see that you are required to demonstrate the attempt you have made to answer the question yourself. This question has been asked and answered before on this list and generally on the internet.

My english is very bad. Can't you give me the article?


text:
Can a person be infected with Polio even after vaccination in childhood?
We know that a person develops antibodies by active immunisation after the administration of vaccines (either in dead form / live attenuated form). Is there any chance of developing the same disease in immuno compromised persons after reaching adulthood?

Short answer: Yes.
Slightly longer answer:
Recall how a vaccine works - it introduces an antigen to the body, which provokes the body to produce antibodies towards that antigen.
Antibodies, simply explained, call upon the remainder of the immune system to fight off a potential infection of foreign body. If there is no immune system to mobilize, the infection would most likely run its course. However, the immune system would have to be sufficiently weakened in order to not be able to fight the infection.

While I don't know about polio specifically, some diseases do require "booster shots" as the initial immunity can be "forgotten" by the immune system*.  For instance, it's recommended to get a tetanus booster shot every 10 years or so.  But with other diseases, immunity apparently lasts for life.  https://en.wikipedia.org/wiki/Booster_dose
*This is different than getting annual flu vaccines.  In this case, it's the virus that tends to mutate, so that previous vaccines are no longer effective.


text:
What is the probablity that SARS-CoV-2 will mutate?
In many epidemic/pandemic situations, a lot of time the pathogen in question will mutate. For reference, this is the definition of mutation taken from Wiki:-

A mutation is an alteration in the nucleotide sequence of the genome of an organism, virus, or extrachromosomal DNA. Mutations result from errors during DNA replication, mitosis, and meiosis or other types of damage to DNA (such as pyrimidine dimers that may be caused by exposure to radiation or carcinogens), which then may undergo error-prone repair (especially microhomology-mediated end joining) or cause an error during other forms of repair or else may cause an error during replication

So my question is,
1》What is the probablity of SARS-CoV-2 mutating?
2》 How can we predict, in advance the mutation of the virus? (Maybe by studying the environmental factors of a specific place)
3》Lastly (something that makes the biologist cringe) is there any way to prevent mutation? Any way at all to somehow limit the mutations which can be used widely?

BTW I am not a biologist, only a person among the millions out there, trying to find a way to help prevent the spread of the disease. My aim is to somehow use ML with Covid data to predict mutations (if possible...)

Please use the correct terminology: Covid is the disease caused by the virus, which is correctly named SARS-CoV-2. The disease itself cannot mutate.

@Chris Agreed. I thought the terminology was used so widely that I forgot that they weren't inter-replacable...

HIV is a virus. AIDS is the disease caused by HIV. No one says AIDS mutates. Not to be a jerk about it, but the terminology you choose is important.

https://biology.stackexchange.com/a/92213/5075

Although @Chris has sorted out the misconceptions you have as a non-biologist, I would point you to authoritative sources of information about the virus and epidemic that are listed on Meta, in case you did not see the banner. We would all like to do our bit in the current circumstances, but you should realize that there are thousands of elite experienced professional scientists of all types working in this area. You might wish to find out what they are doing.

I don't see how you want to prevent mutations - and these don't have to be a bad thing as the mutation of SARS (the original one from 2003) shows, here the mutation (or better the deletion of a part of the viral genome) led to an antenuated pathogenic virus. Since this mutation happened in the early phase of the spreading, it became the major virus. See reference 1.
Mutations are a statistical process which happens all the time, especially for RNA viruse due to errors in the polymerases (see reference 2). So the answer to your first question would be: 100%. It is mutating, which can also be seen in the sequences which have been published so far. The differences are only minimal with a sequence homology between 99.91 and 100% (see reference 3), but this can already lead to changes in the amino acid sequence. You can see this in the screenshot from phylogenetic tree of all sequenced SARS-CoV-2 viruses on [Nextstrain] (see the site for the actual development):

To your question 2: You cannot really predict where mutations happen and which will come through in the long time, as this is a statistical process and the sheer number of viruses around in each infected patient. But there are positions which are more prone to mutations, while mutations at other parts of the sequence will lead to much less fit virus. There is not so much data available yet (remember that this virus is only around since the end of last year), but reference 3 has some data on it (figure 3):

Question 3: I don't see how this should happen, as this involves the polymerases which are involved in replication.
References:

Attenuation of replication by a 29 nucleotide deletion in
SARS-coronavirus acquired during the early stages of human-to-human
transmission
Why are RNA virus mutation rates so damn high?
The establishment of reference sequence for SARS‐CoV‐2 and variation
analysis
On the origin and continuing evolution of SARS-CoV-2

@reuns Good idea, I missed that site. Thanks for the notification.


text:
How to analyze phosphorylation shift by western blot?
I want to see the phosphorylation shift in my protein of interest.
I have created a point mutation in my protein. so that it will not able to go for the phosphorylation compare to my control. i want to check by western analysis.
i can see a very small shift. is it possible to get a better shift?
Another important thing is my protein size is ~150 kDa.
can you please share any suggestions on this

Are you dealing with phosphorylation of tyrosine, threonine, or serine? 2) What is the difference between the control vs. WT? 3) Why do you want to do this — there may be alternative techniques that could be more reliable ...

Exactly serine to alanine. Fine, actually one allele is knocked out, another allele is mutated. Wt is a parental cell line. control is a single knockout without a mutation. I know there are other methods available but i wanted to verify by western analysis

Why is there an apparent size difference between the WT and control?

Did you do SDS-Page or a native gel?

Why is there an apparent size difference between the WT and control? For this Wt i used a different tag (smaller size). Control and my experiment i used the same tag (bigger in size)                                                                                Did you do SDS-Page or a native gel?     SDS- Page

Please [edit] your post to include all the relevant information from these comments. Comments are ephemeral and thus should not contain material essential for understanding the question. Thanks!

The run length of bands in an SDS-PAGE (which your western is probably based on) depends - at least in theory - only on the size of the protein: SDS binds to proteins with a fixed size ratio and thereby provides a negative charge based only on size. Unless you have reason to believe that your protein is an exception from the usual (which might be indicated by things like not running at the expected size) you will very likely not be able to see a band shift (change in run length) based on presence or absence of phosphorylation in a standard western blot.
Things you could try to detect the phosphorylation:

Use phospho-specific antibodies. These are often expensive, tricky to use or just not available, but this is the only ting I can think of working with a standard western blot setup
run a native-PAGE, that way your run length depends on shape, size & charge of the protein. I still wouldn't expect a single phosphorylation to be cause a visible shift for a 150kDa protein, but you can try. This might require using longer run-time of the gel to get really high resolution for the size you are looking for

I agree that observing a shift for a 150 kDa protein may be difficult, but shifts due to phosphorylation can be seen for some proteins on SDS-PAGE gels. See for example this paper.

@tyersome I guess it is possible in some cases even though it normally shouldn't happen - I edited the answer. Also note that the authors of that paper were "using a modified acrylamide/bisacrylamide ratio" for the gels to get a visible separation of the two bands.

Yeah, it will take 15 to 20 hrs to complete the run. sometimes the gel gets a small break. i


text:
Question on kilobase - packaging of genomic material in viruses
I have been looking up some information of SARS. Wikipedia says it is 29.7kb in length while 1kb is around 300nm. However, the microscope image on wiki shows the virus size <100nm. It doesn't make sense mathematically so that think I missed some knowledge. I hope this question qualifies to be posted on stackexchange. Thanks in advance.

This value is only true for linear DNA. However, DNA in cells is not linear, it is folded, which makes it ways more compact (otherwise the DNA in our own cells would be around 2 meters long).
See the figure from reference 1 for a schematic view how this works in higher cells:

The table below (from reference 2, either klick on the picture or the link below for a bigger version) shows how the length of a piece of DNA is influenced by packaging:

There is another caveat in this question, Corona viruses (as the SARS virus) are singlestranded RNA viruses. The RNA of viruses contains packaging signal sequences, where special proteins bind, before the virus is assembled around the bound genetic information. See reference 3 for a general overview and reference 4 for the packaging of the SARS virus in special.

DNA Packaging: Nucleosomes and Chromatin
DNA, chromatin and genome numbers
Genome packaging in viruses.
Assembly of severe acute respiratory syndrome coronavirus RNA
packaging signal into virus-like particles is nucleocapsid
dependent.


text:
Why is glucose used in oral rehydration therapy?
What is mechanism of action of glucose in the intestine to reduce the watery and electrolyte secretion?

Oral Rehydration Therapy uses electrolyte solution containing some glucose. It is because, the absorption of electrolytes is more efficient when glucose is added. Sodium uptake from intestine is carried out by sodium glucose co-transporters.


text:
What is the difference between pluripotent and totipotent cells?
Both develop into specialized cells.Then how are they different?

@GerardoFurtado You can easily correct such spelling mistakes. That's why we have the edit function. And it is not seen as offensive here, as it helps to improve the question/answer.

Expending on Gerando Furtado link
Totipotent cells can differentiate into three germ layers (endoderm, mesoderm, or ectoderm), into cells of the cytotrophoblast layer or syncytiotrophoblast layer of the placenta.
Pluripotent cells can differentiate into the three germ layers (endoderm, mesoderm, or ectoderm).
So totipotent cells develop into the all the cells of the embryonic body and fetal side of the placenta. While pluripotent cells can only develop into cells of the embryonic body.


text:
Converting unit/mg or unit/ml into ng/ml, or vice-versa
I am working with the enzyme Cu/Zn Superoxide (SOD1) and i am quantifying them in ng/ml.
However, most past studies has SOD1 quantified in unit/mg or unit/ml, and i need to compare the SOD1 level of my study with those past studies. Is there a way to standardize these units?
Thank you!

You need a value for the specific activity of the purified enzyme, in units/ mg (or similar). Also you need to check on the definition of a unit of activity for your enzyme since this is empirically defined.

There is no archaism in measuring enzyme amounts in units. Unit definition for SOD and a protocol can be found here (from Sigma): https://www.safcglobal.com/technical-documents/protocols/biology/enzymatic-assay-of-superoxide-dismutase.html :
"One unit will inhibit the rate of reduction of cytochrome c by 50% in a coupled system, using xanthine and xanthine oxidase ..."
I don't think, there is a good way to convert ng's to units, since one measures either mass or enzymatic activity, and the correlation between them is not always consistent. Units should be much more reliable in terms of comparisons with other studies, if you are not considering your enzyme as, e.g., a nutritious substance.

Quantification is a measure of your protein quantity and units/ml or mg is a unit of protein quantity. These are two different things. You need to set a rxn of SOD with its substrate and get activity which is proportional to your consumption of substrate. Then u will get the activity of your protein which will be in units/mg or ml

But: This is only valid for a certain batch, since the activity of protein preparations varies between batches. Thats why we have this units, which is not a very good thing. But better than nothing.

Right sir....:)


text:
Do local potentials always precede action potential?
Do all stimuli change the membrane potential to a value lower than threshold potential first, and then by summating end up in an action potential?
How do voltage-gated ion channels detect this change in voltage and respond adequately by opening?

I have to admit that I have never thought about if lower potential stimuli can add up. I have done some research though and you are correct. If there is multiple stimuli that don't reach threshold potential it is possible that those sum up. Summation is possible due to stimuli that are directly after another or that are at the same location after another.
-> Spatial summation
-> Temporal summation
Do all stimuli have the same effects?
No - some inhibit a reaction, some provoke one.
How do channels react?
Voltage-gated ion channel contain proteins that react to changes in electrical fields .
At first the sodium channels open up when the stimuli reached treshold potential. That causes the sodium ions to rush into the cell, making it more postive. They start to close before the overshoot.
The potassium channels then start to open and repolarize the membrane.
Single shots doesn't have a huge effect on the membrane.
Na+/K+ ATPase keeps the settings for action potential alive.


text:
Why hasn't evolution gotten rid of the appendix yet?
A figure I have recently stumbled upon suggests that about 7% of the world population will, or have, had appendicitis in their lifetime. Cutting out the appendix was impossible until very recently. Even if the appendix only just started, in evolutionary terms, being infectable, it would still be capable of wiping out an entire population in no time at all, meaning some other population would adopt an alternative. No matter what the benefits, the costs would be detrimental and most definitely outweigh the former. We've had at least a million years (correct me here if I'm wrong) to get rid of the appendix, but we didn't, even though it kept on killing. It seems very counterintuitive that it's still here. Can anyone explain, please?
Edit: I recognise that an appendix serves some purpose to the body. My question is: aren't the benefits much less significant than the costs?

Do you really think that appendicitis has been one of the major causes of death in the history of mankind?

The appendix still serves multiple purposes, you may be interested in these questions, https://biology.stackexchange.com/questions/1502/is-the-appendix-a-vestigial-structure-in-all-vertebrates and https://biology.stackexchange.com/questions/55796/is-vermiform-appendix-no-more-a-vestigial-organ

Also you misunderstand something, appendicitis are not random, so there is no way they could wipe out the human population, that's like thinking heart attacks could eventually wipe out humanity.

Does appendicitis even ever appear in pre industrial diets? I suspect not.

How can we explain what does not exist (your scenario)?

@GrahamChiu - Maybe a source to support that? Galen described "colic passion" below the umbilicus and to the right.

Erasmus JPF. The incidence of appendicitis in the Bantu. S Afr Med J. 1939;13:601-607.

@GrahamChiu So why does it happen then? I thought it just gets infected.

@John if it's not random then what causes it? If not infection, that is.

Almost certainly related to poor dietary fibre, and slow bowel transit times, which aren't seen in primitive diets.  In the same way that diverticulosis is not seen in primitive cultures with lots of plant fibre.

@GrahamChiu Can you post that as an answer and maybe provide a link? I'll tick it.

Possible duplicate of Is the appendix a vestigial structure in all vertebrates?

Appendicitis appears to a fairly modern disease likely caused by refined diets leading to slow bowel transit times resulting from low fibre content.  We have some evidence to suggest that this is the case with no Bantu people recorded having any episodes of hospital admission for appendicitis in [1]

Hospital records from three Johannesburg hospitals were reviewed in Erasmus' study, from 1929-1937. Appendicitis and overall admissions were recorded according to racial groups. Using these figures, 4% of white inpatients were admitted for appendicitis, compared to 1% of coloureds and 0% of black inpatients.17 Although these figures do not represent the true incidence rates in the general population, as hospital access and utilisation patterns are likely to have differed between three racial groups, the important possibility of differential incidences between racial groups was raised. These trends were supported by findings from audits in Cape Town and Upington. [2]

The change in diet in urban african natives has also lead to appearance of diverticular disease, which was previously unknown in that population.  Diverticulitis is also an infection of a colonic pouch. [3]
So, it seems these are both modern diseases of low incidence so both these factors mean little selection pressure exists especially with modern medicine and surgery.

Erasmus JPF. The incidence of appendicitis in the Bantu. S Afr Med J. 1939;13:601-607.
Acute appendicitis in South Africa: 2015 A systematic review
Emergence of Diverticular Disease in the Urban South African Black

Disclaimer: I have had my appendix removed.


text:
Can offspring be less genetically similar to the parent than more distant relatives?
I'd be interested in answers about any sexually reproducing species, but for simplicity I'm going to focus on humans in this question.
If the parents are very genetically different (i.e. the number of alleles they share is much less than the average number of alleles shared by 2 people in a population), is it possible for, say, the father to be less genetically similar to his offspring than he is genetically similar to, say, his cousin? If so, what about an even more distant relative?
Of course anything is "possible", so really I'm asking if it's reasonably likely and if so, how likely is it? If, for example, a genetically east Asian person and a genetically south African person had a child, would that child likely be less similar to either parent than the parents are to their respective cousins or even non-relatives from the same area?
If there are any false assumptions I'm making in the question feel free to point them out, but please provide references.

Provided that a significant percentage of fathers are not biological fathers of their children... ;) More seriously: what is meant by similarity here? Genetic similarity or phenotype? I think clarifying this would already suggest the answer.

I think it's pretty clear I'm talking about genes. Genes determine phenotypes so the questions would have the same answer but the nice thing about genes is theyre quantifiable. You can count the number of alleles.

Gene are not the only thing determining the phenotype. Moreover, one can easily resemble one parent, despite having 50% of the genes inherited from the other.


text:
In an ant (or bee) colony, what is the very approximate ratio of new breeders to workers?
For example, out of every 1000 eggs laid, X mature into drones and/or virgin queens.  That seems impossibly precise but it illustrates the kind of number I want well.  I'll accept answers for any species and any number of species, even one, with any amount of precision or lack thereof, because right now I can't even feel confident saying that there are more workers or more breeders, though I obviously suspect more workers.
I would also be ecstatic to have any live count just before the nuptial flight, i.e. for this colony in this study there were X workers, Y drones, and Z virgin queens just before the nuptial flight, or X workers and (Y+Z) breeders, or X% of the colony was breeders, or for this species on average X% are breeders just before the nuptial flight.
Anything.  Any one thing and I can accept it as an answer.
I can find any number of studies that talk about the sex ratio between drones and virgin queens, so I know someone is counting.  Maybe I'm not reading closely enough, but they always seem to slip away from giving all the numbers I need to figure this out for myself.

My guess is that the answer could be quite different for different species: I would recommend narrowing it down to a specific species so the question doesn't get closed as too broad.

Limiting it to a single species means that the answer can more easily be "We don't know".  I'm trying to avoid that by accepting an answer for any species because the last thing I want is "Oh, I know the answer for this other species but it's not the one you asked for so I'm going to walk away with the knowledge."
I've edited the question in an attempt to make that clearer.  If there is anything I can say to be even more clear, please let me know.

It will vary so drastically that the ratio will be exactly 1 (or 'NA' :D) for solitary species and close to 0 for species that make gigantic colony with a single queen.

I'm interested in the virgin queens that get pushed out of the hive for the nuptial flight, not the one or few laying queens in a colony.  Also, I will accept statistics for any one species, it does not have to be an average across multiple species, although I will accept that too if that is the number that's available.  I will even accept a single study that clearly publishes a number for one particular colony at some particular point in time, even if gathered incidentally while pursuing some other research goal.

So.
This answer is specific to the western honeybee, Apis mellifera, as there are massive amounts of data on them; more, possibly, than any other insect species. There has certainly been more data collected about them than any other hymenopteran.
At around the time of the nuptial flight, there may be as many as 60,000 workers in the hive, though likely number is more like 15,000 - 20,000. There will be either one (virgin) or two (one mated, one virgin) queens (the old queen will stay with the hive, if she is alive). There may be as many as 400 drones from the original colony (though usually the number is less, around 150 is typical; 10 - 50 of them will actually mate with the queen), and an equal number may join in the flight drawn from other colonies, especially in commercial beekeeping operations. Somewhere between 1000 - 6000 workers will take part in the nuptial flight with the virgin queen and the drones.
This means that in honeybees, the nuptial flight contains 1 queen:~5000 workers:~150 drones.
Data is drawn from many years working with bees and beekeepers. Opinions will vary somewhat depending on the beekeeper and the beekeeping methods. These are based, generally, on bees kept for clover and fruit pollination in the western USA.

Thank you!  I'm surprised at the high drone to virgin ratio but there you have it.


text:
How to Scale Metabolic rate and drug dosage according to Mass?
I was reading a book "Biology and evolution of Crocodilians" by Gordon Grigg and David Kirshner.
And I can't understand the part about metabolic scaling no matter which method I tried I can't get the same result as the one in the book.
(Box 1.2 and Box 7.1)
Box 1.2
It is about Lolong immobilization and dosage which has example of 0.5mg for 40kg Croc scaling to 2.4mg for 1075kg Lolong instead of 13mg, however no matter which method I tried I could not get the same number. (exponent for crocodilians is 0.829)
When I tried
(0.5/(40^0.829))×(1075^0.829) for Box 1.2 I got 7.65420145365 instead of 2.4
For Box 7.1
It gave example of 0.1kg to 10 kg mammal oxygen consumption scaling from 116ml/h in 0.1kg animals to 3483 in 10kg animals (as oppose to 11600 ml/h.) (exponent for mammals here use 0.738)
I tried (116/(0.1^0.738))×(10^0.738)
Which get 3471.02697847
Instead of 3483.
I have no background in science at all so it is likely I am doing something wrong.

Welcome user71055. We've an international community here many of whom simply won't have access to that particular textbook. Please quote the relevant text in the body of your question, then show what attempt you've  made to understand it (show your workings). Please also take our [tour] and refer to the [help] for guidance. Enjoy the site.

3471 and 3483 are the same number unless you have at least 3 significant digits of precision in all your estimates.

When I tried the
(0.5/(40^0.829))×(1075^0.829) for Box 1.2 I still can't get 2.4 but instead got 7.65420145365


text:
How can metagenomic analysis be used to determine the native habitat of a bacterial species?
Background
A native habitat refers to the natural environment in which a particular species or organism has evolved and to which it is best adapted.
In the context of bacteria or other microorganisms, a native habitat might include specific soil types, plant surfaces, animal hosts, or aquatic environments where the organism naturally occurs and forms part of the ecosystem.
Metagenomic analysis refers to the study and analysis of genetic material recovered directly from environmental samples, bypassing the need for culturing individual species in a laboratory. This technique allows scientists to explore the diversity of microbial communities, including bacteria, viruses, fungi, and other microorganisms, within a given environment.
Question
How can metagenomic analysis be used to determine the native habitat of a bacterial species?
Prior self-work
Disclaimer: I have been searching for an introductory text on this matter for almost a week now with no hope. All I find is applications in the form of research studies that didn't, as expected, give any introduction on the matter, specifically with satisfactory details.

In biotechnological water treatment assays, it's common to correlate certain species of bacteria or protozoans with a score to determine if the water is safe to drink or not or whether it has to go for further processing, etc...
A similar principle is used in metagenomic analysis but contrasting DNA samples recovered from the environment against known DNA sequences of bacteria/fungi/virus in databases. It's like DNA barcoding. There is the added complexity of also having to log the different physical aspects of each sample collection, and it seems that this review from 2024 concludes that there's still work to be done.

References:
Roy G, Prifti E, Belda E, Zucker JD. Deep learning methods in metagenomics: a review. Microb Genom. 2024 Apr;10(4):001231. doi: 10.1099/mgen.0.001231. PMID: 38630611; PMCID: PMC11092122
National Research Council (US) Committee on Metagenomics: Challenges and Functional Applications. The New Science of Metagenomics: Revealing the Secrets of Our Microbial Planet. Washington (DC): National Academies Press (US); 2007. 1, Why Metagenomics?


text:
Are there any fungi that can digest humic acids?
Humic acids are a complex group of organic substances, that are generally known to be hardly biodegradable. Fungi as agroup are known for breaking down complex organic matter like cellulose or lignin. But are there any that beak down humic acids as a major contributor to their energy needs?

According to Wikipedia, humic acid (HA) is a product of the biodegradation of dead organic matter. Shown below is a representative structure, but it important to understand that humic acid is a name given to a family of loosely related polymers of the products of biodegradation.
Although HA is resistant to further biodegradation, there are indeed fungi that are able to break it down further.

There is evidence that fungi can break down HA:

Grinhut et al (2011) Mechanisms of Humic Acids Degradation by White Rot Fungi Explored Using 1H NMR Spectroscopy and FTICR Mass Spectrometry Env Sci & Technol 45, 2784-2754

This paper reports studies of the mechanism of HA degradation by Trametes and Phanerochaete fungi (Basidiomycetes). This degradative property is attributed to the secretion of non-specific oxidising enzymes: manganese peroxidase, lignin peroxidase and laccase. the authors report evidence for "oxidation, a decrease in the aromatic content, and indication of demethylation of the HA during biodegradation.
The paper is also a source of references to earlier work.
The indications are however that these fungi carry out this degradation in the presence of other nutrients, i.e they cannot utilise HA as a major carbon/energy source.


text:
What bug is this?
Saw this bug on a window in my house. Never saw a bug with antennae like this!
Edit: I live in NY, and saw this bug about 1 PM. Also, I found there were several more on other windows and I think I might have a problem!

Please see here: https://biology.stackexchange.com/tags/species-identification/info

I am not a good naturalist but I would say some kind of Scarabaeidae

Where is your location?

In case anyone finds it relevant: many of these bugs (10-20 it seems) were brought in from outside, nearby the house, with the firewood. Apparently these bugs are drawn to wood.

Sure looks like a Deathwatch Beetle (Ptilinus ruficornis) with pectinate antenae.

Source: https://bugguide.net/node/view/59669
This Encyclopedia of Life site also has some more information.

The antennae are also a sign of the animal's sex: both figures (Q & A) are males (the antennae of a female would be sawtoothed).


text:
What is this spider? Found in garage during May in NY
Stands very flat with its legs very outstretched, doubles-up its front legs (first pic looks like it only has 6 legs). Brownish-dark gray, not quite black. It's alive, but it wasn't particular active or spry when I saw it.

Edit: more pictures, with a quarter for scale

Also, sorry for the cup, but I was under strict orders not to lift it.

yikes! There are a lot of spiders who double-up their front legs for some reason so that at first glance it looks like they only have six. I don't know if that's the case here but it certainly might be. Also see google search spider appears to have six legs Have you seen it move and confirm it walks with six (and that it's actually a living thing and not a prank?) Can you also edit your question and add the approximate size? Thanks!

See also Are there any spider species out there that only have 6 legs? and as mentioned on your previous weird looking insect identification question, refer to https://biology.stackexchange.com/tags/species-identification/info

something for scale had been nice,is that thing 2m or 2mm?

@trondhansen and hopefully before I have to go to sleep tonight :-)

I added more pictures with a quarter for scale. @uhoh I had forgotten I had even asked a question before (it was 4 years ago). Forgot about those little beetles!

@trondhansen it's pretty big and seems to have eight legs after all.

It appears to be an American nursery web spider (Pisaurina mira), a species of spider in the family Pisauridae (Nursery web spiders).
They tend to double up the front legs and they can have the dark median band on the abdomen like the one in the photos. They can be found in New York also and it is listed in the spiders found in New York here:
https://spiderid.com/locations/united-states/new-york/
Some fishing spiders look similar but their size and pattern are different.
We can't see in the photos but you can also confirm by checking its eyes. This species has a unique straight anterior row of eyes where they are arranged in two rows.

Here is a similar one with a more clear photo I've found:

Source: https://www.spiderzrule.com/nursery-web-weaver/


text:
What is this thing that is growing in my yard? And should I get rid ot if?
I live in Wilmington, Delaware (Mid-Atlantic USA).  The north side of my yard is largely shaded by my house and grass is spotty.
Periodically when I go into the yard I will find as many as four pod-like things have opened on the ground.  I almost never notice them before this stage, the one time I did it looked like a patch of dirt until I stepped on it and it sort of shattered.
I'm baffled by it and my wife thinks it's some form of fungus.
We have two children under 4 and we are concerned it could be poisonous.  It certainly doesn't enhance our yard's attractiveness.

With that in mind, I have a handful of related questions:

What is it?
Is it dangerous?
How can I get rid of it, if I so choose?

Addendum:
I believe we have found an unopened example of what we've been seeing:

It may be some type of puffball fungus.  If possible, a photo before it has opened would be helpful with identification.

@Kurt After a couple days of looking, my wife seems to have found an unopened example, I've added the photo to the question.

You might want to ask this in the gardening part of stack exchange.

Likely some kind of "earth star" fungus/mushroom. It is decomposed too much to identify.

Your wife was right--it is a fungus (hard to tell which one). There' probably a lot of organic matter under those bricks, maybe old leaves and dead wood. Location makes sense. While I would not eat it, on account of the difficulty with identification and the fact that mushrooms are often problematic, there is probably no reason to get rid of the caps (unless you have kids). Finally, even if you rip off the cap, most of the rest of the fungus is under ground. The mushroom you see (cap) is just the tip of the proverbial iceberg.

Myriostoma is a fungal genus in the family Geastraceae. The genus is monotypic, containing the single species Myriostoma coliforme. It is an earthstar, so named because the spore-bearing sac's outer wall splits open into the shape of a star. Source: Wikipedia.
But this recent article shows otherwise https://pdfs.semanticscholar.org/08ea/2ee6be93787f2e0034b85222b751a5281167.pdf


text:
How does the inability to produce vitamin C helped weight gain?
I recently wondered how do dogs cope without vitamin C intake like us.
A few Wikipedia pages later, I learned that our dry-nosed ancestors lost about two-thirds of the gene responsible for vitamin C synthesis some 63 millions years ago. And then this passage:

Johnson et al. have hypothesized that the mutation of the GULOP (pseudogene that produces L-gulonolactone oxidase) so that it stopped producing GULO may have been of benefit to early primates by increasing uric acid levels and enhancing fructose effects on weight gain and fat accumulation. With a shortage of food supplies this gave mutants survival advantage.

(Wikipedia: L-gulonolactone oxidase)
I'm curious about the interaction (GULO/uric acid/fructose effects/fat storage) quoted above.

The effect comes indirectly since lower levels of ascorbate increases urate levels, according to

Arthritis Rheum. 2005 Jun;52(6):1843-7.
The effects of vitamin C supplementation on serum concentrations of
  uric acid: results of a randomized controlled trial.
Huang HY1, Appel
  LJ, Choi MJ, Gelber AC, Charleston J, Norkus EP, Miller ER 3rd.

So the direct weight gain effect is due to increased levels of uric acid.
Further in the chain of events is that

Recent studies show that fructose-induced uric acid generation causes
  mitochondrial oxidative stress that stimulates fat accumulation
  independent of excessive caloric intake.

according to

Diabetes 2013 Oct; 62(10): 3307-3315.
Sugar, Uric Acid, and the Etiology of Diabetes and Obesity
Richard J. Johnson1,2⇑, Takahiko Nakagawa1,3, L. Gabriela Sanchez-Lozada4, Mohamed Shafiu5, Shikha Sundaram6, Myphuong Le1, Takuji Ishimoto1, Yuri Y. Sautin7 and Miguel A. Lanaspa1

Thanks. What remains unclear to me is the GULO/uric acid/fructose effects/fat storage interaction, i.e., the how.

Doesn't the article tell? I can't look into it until after several days, although I am interested in this as well. I think the cure is to restore GULO and urate oxidase. It seems to benefit our health.

I haven't accepted before because I haven't seen the Jul 28 edit you've made, we last corresponded on Jul 26. Thanks for the edit and the reminder.


text:
How is convenience sampling used in healthcare-associated infections prevalence studies?
Question
Examples of such studies:

Prevalence, Antimicrobial Drug Resistance and Associated Risk Factors of Streptococcus Pneumoniae Bacteria Infection Among
Under-Five Children With Acute Lower Respiratory Tract Infection
Attending Sheik Hassan Yebere Referral Hospital, Jig-Jiga, Ethiopia:
"The study was conducted at Sheik Hassan Yebere Referral Hospital from
March 1 to April 30, 2021. ...... Then, from pediatric outpatient
department study participants who had symptoms of acute lower
respiratory tract infection were selected by using convenience
sampling method."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10243350/

Multidrug-resistant among Non-Fermenting Gram-negative Bacteria Isolated in the Department of Microbiology of a Tertiary Care
Centre:
A descriptive cross-sectional study was conducted in the Department of
Microbiology of a tertiary care centre from 1 September 2021 to 30
August 2022 after obtaining ethical approval from the Institutional
Review Committee. All samples received in the Microbiology laboratory
for diagnostic purposes were included. A convenience sampling method
was used.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10725231/

Positive Bacterial Culture among Adults with Suspected Urinary Tract Infections Presenting to the Department of Medicine of a Tertiary Care
Centre:
"Data was collected between 1 July 2022 to 31 December 2022...... A
convenience sampling method was used."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10924528/

Self-investigation
What I understand so far:
In such studies, the population consists of all patients present in the study hospital or department throughout the study duration. However, there is a barrier to accessing the entire population due to the factor of time. That's why convenience sampling method is used.
How does the consideration that some of the population might not be available during sample selection, but could become available later during the sampling process, come into play?
What role does the sample size play, particularly if the calculated sample size is, say, 200 patients? These studies mention a "minimum sample size". Could this be considered in part sequential sampling, even if the studies don’t explicitly mention it?
So the overall method is to be "Convenience sequential sampling".
Disclaimer: I have been searching for two weeks for an answer.

It's up to the individual studies to report their sampling methods and criteria for stopping or other justification of the time frame used. If they haven't, that's their fault and the fault of peer reviewers to have not caught what is missing.

We are not talking about one or even the three studies mentioned here, there are a bunch of these. They could be onto something, even if they didn't mention it. Maybe they just know it.

What do you mean "they could be onto something"?

Their studies could be statistically valid for the research purpose.

What would make them statistically valid and what would make them statistically invalid? If the methods are not clear, how could someone tell?

I'm not after certain studies per se, but a type of studies which the three studies mentioned belong to, labeled by the research purpose and "Convenience  sampling", even if they didn't describe their methodology fully. Maybe they didn't mention the full statistical methods, there could some other study that did mention the full method. Also, from the research purpose, it should be possible to guess at-least not the exact method they used, but the possible one(s).

I'll reiterate my first comment: "It's up to the individual studies to report their sampling methods and criteria for stopping or other justification of the time frame used. If they haven't, that's their fault and the fault of peer reviewers to have not caught what is missing." - you can't fix what they haven't included by asking third parties here.


text:
How are sewage, sludge and wastewater natural environments?
[1]

Acinetobacter species can be isolated from such natural environments
as surface water, wastewater and sewage, healthy human skin, plant,
animal and food material as well as domestic appliances.

[2]

Table 1. Natural habitat of non-baumannii Acinetobacter species.

[3]

Enterobacter species have been previously isolated from various
natural habitats, including activated sludge, wastewater, soil and
marine environment for various environmental applications

[1] The natural environment as a reservoir
of pathogenic and non-pathogenic Acinetobacter
species
[2] Reservoirs of Non-baumannii Acinetobacter Species
[3] Decolourization of azo dye using a batch bioreactor by an indigenous bacterium Enterobacter aerogenes ES014 from the waste water dye effluent and toxicity analysis
Am I missing something here?

They're "natural" as in not, say, cultured. They're listing places in the world you'd find the species without artificially putting it there. That's it. They're not making some grand statement about human involvement more broadly. I think that's what you're getting at or assuming?

Maybe there is some type of human involvement that is natural and the answer maybe lies in what human action is natural and what's not?

The human animal involvement and The civilized man involvement?

I wouldn't consider it as deep as that. "Natural" does not have intrinsic meaning. It's a human concept, we can choose to use the word for any grouping of things that we want; to be useful in science, it would be necessary to clearly define it for a given purpose, but it need not always have the same meaning. It's fallacious to reason backwards and derive meaning based on a label without an accompanying definition.

Maybe my answer probably works for a non popular definition. I still need to know where did the popular/universal/global/present definition came from.

I meant that I want to know what is the definition of "Natural" in these texts or similar ones.

I think the true answer lies in whether human involvement is an outcome of its animality or their civilized being:

It is evident that modern civilized man disrupts "natural" ecosystems
or "biotic communities" on a vast scale. However, it would be
challenging, if not impossible, to draw a clear line between the
activities of early human tribes that presumably integrated into and
formed parts of "biotic communities" and the destructive activities of
the modern world. Is man part of "nature" or not? Can his existence be
reconciled with the concept of the "complex organism"? Seen as an
exceptionally powerful biotic factor that increasingly disturbs the
equilibrium of preexisting ecosystems, eventually destroying them
while simultaneously creating new ones of a very different nature,
human activity finds its rightful place in ecology. Tansley, A. G. (1935). The Use and Abuse of Vegetational Concepts and Terms. Ecology, 16(3), 284–307. https://doi.org/10.2307/1930070

For sewage, activated sludge, and wastewater, there is a chance that the necessary factors that would lead to such bacteria would be there without the interference of civilized man. It would be in the form of, for example, Stagnant Water Bodies, Animal Dung Accumulations, and Decaying Organic Matter:

As an ecological factor acting on vegetation the effect of grazing
heavy enough to prevent the development of woody plants is essentially
the same effect wherever it occurs. If such grazing exists the grazing
animals are an important factor in the biome actually present whether
they came by themselves or were introduced by man. The dynamic
equilibrium maintained is primarily an equilibrium between the grazing
animals and the grasses and other hemicryptophytes which can exist and
flourish although they are continually eaten back.
Tansley, A. G.(1935). The Use and Abuse of Vegetational Concepts and Terms.
Ecology, 16(3), 284–307. https://doi.org/10.2307/1930070

So it's a matter of possibility not conclusive knowledge that these habitats are native.
For food, it would probably be a matter of the type of processing and refinement that a certain kind of food goes through.

Added a reference that goes very well with my thoughts.


text:
What would happen if nerves didn't have refractory period?
What would happen if nerves didn't have refractory period? And, what part of his nervous system or neurons are not needed?

Who is "his"? Are you talking about a human neurologic system in general?

Yes it is a scenario case.

Is this a homework question? If so, you may want to check this out on the help page... http://biology.stackexchange.com/help/homework

Are you asking about the theoretical implication in terms of the function of neural system? Clearly this is not a biophysically plausible scenario since it will allow infinite number of action potentials in a finite time.

Refractory period returns the repolarization period to the nerve's resting potential . it's the time taken for recovery of a neuron to generate another impulse being excited by another stimulus . so if nerve doesn't have refractory period they wouldn't be able to return to its resting potential & generate new impulse . moreover the repolarization potential further exceeds its value and cause hyperpolarization , so its badly necessary to restore to resting potential by expelling na+ and taking k+ in . unless it would be impossible to restore the resting potential & be ready to get excited to transmit another impulse via the electrochemical pathway . one more benefit of refractory period is that it causes unidirectional impulse conduction.
I didn't get the 2nd part of your question. What are you trying to mean , make it more clear.

Nice answer, but since you are a new user, you should give some source/reference for the answer.


text:
How is insulin transported in vivo in mammals?
What is the mechanism for transport of insulin in mammalian cells?

Do you mean how does insulin get secreted and absorbed? The insulin gene stays in the DNA in the nucleus, just like all other genes. Have you read the Wikipedia article on insulin? It has a lot of information that should help you understand the pathway. If you have more specific questions, please [edit] your question and describe them in detail.

The process is described here. This is my summary, plus a few extra details:
The primary gene product of the INS gene is preproinsulin. As the N-terminal signal sequence (pre-) emerges from the ribosome during polypeptide elongation the signal sequence binds to a signal recognition particle which arrests elongation until the nascent chain has engaged with the translocation apparatus in the membrane of the endoplasmic reticulum (ER). The preproinsulin polypeptide is translocated across the ER membrane in a cotranslational process, and the signal sequence is cleaved off by signal peptidase.
The proinsulin molecule folds in the ER lumen, assisted by various chaperones and, in particular, by protein disulphide isomerase, which ensures that the correct disulphide bonds form. The correctly-folded proinsulin polypeptide is exported from the ER in COPII-coated vesicles which deliver it to the Golgi. At this stage the proinsulin is cleaved by furin-type proteases (pro-hormone convertases; cleave at pairs of basic residues), removing the internal C-peptide (pro-) and after a little C-terminal trimming, leaving the insulin A and B peptides covalently attached via disulphides. This is mature insulin.
The mature insulin leaves the Golgi in secretory vesicles. Since insulin secretion is regulated, these vesicles do not fuse with the cell membrane constitutively, they are stimulated to fuse by a Ca2+-dependent signalling pathway. Vesicle-membrane fusion is mediated by SNARE proteins. At this stage the insulin has been released from the pancreatic β cell. Notice, however, that the insulin has been extracytoplasmic since it was translocated into the ER: all other steps in the transport process are achieved by rounds of vesicle formation and fusion.


text:
Can a cleaved plasmid "close" without exact matching "sticky ends"?
Say if you have a multiple restriction site and use two restriction enzymes on it to cleave a plasmid, can it recombine with ligase?
My concern is that without the small sequence of nucleotides that were in between the two restriction sites, the two ends of the plasmid won't stick and anneal. Would it work if the two sticky ends are almost the same in sequence – two bp off instead of all five?

The plasmid won't religate efficiently if the ends are not compatible.  However, it's possible that very rarely your plasmids may re-ligate, perhaps because of a tiny level of contamination with exonuclease that trims back the ends to be blunt.  Or there may be spontaneous blunt breaks or other strange events.  This may happen in a tiny fraction of the plasmids, one in millions, but since your transformation step selects for circularized plasmid very efficiently you may end up detecting it.
Note that these rescued plasmids are often aberrant since they are unpredictably trimmed at the ends or otherwise followed a non-designed path to circularize; this is not something you want to count on for your cloning, it's an annoying byproduct that you want to avoid.

As I expected and much appreciated


text:
How can you band wheat chromosomes using Giemsa dye?
I am working with wheat chromosomes and trying to stain the chromosomes. However, during staining with Giemsa dye chromosomes appear totally dark. I'm not sure why this might be. Anyone have any ideas?

Plant Science Letters
February 1975, Vol.4(2):85–88, doi:10.1016/0304-4211(75)90252-7
C-banding in wheat evolutionary cytogenetics
G.Y. HadlaczkyA. Belea- first of the articles

The Wright or Giemsa-stains can be influenced by the pH of the rinsing solution after the incubation in the dye-solution. The lower the pH the more pink will be the result. The higher the pH the more blue will be the result. Usually Giemsa-stains are differentiated at an approximately neutral pH. (Weise buffer pH 7,2 or acidified water pH 6,5). To lower the pH you can add few drops of acetic acid. This will also enhance the speed of differentiation.
Giemsa-stains are also sensitive for too long rinsing in diluted ethanol. The color turns blue and more faint.
Also it might be the trypsin that can digest some region rich in C or G. It's not condensed so appears light but the other region is very condensed so the trypsin can't enter and digest this region, which appears dark or the opposite.

Check for C-banding or GTG-banding protocols online to understand the chromosomes. Treatment with mild acid or trypsin gives you various dark and light regions usually light regions begin AT rich regions

can you add some external sources/references to support your answer?


text:
Can the liver prioritize it's metabolizing potential?
Let's assume we have two toxins - one of which is routinely metabolized by the liver, and the other is new to the organism (consider for example alcohol in a heavy drinker and any other drug that is taken for the first time) and they are administered at once.
Does the liver have any way to prioritize metabolizing either of these substances or does it happen simultaneously for both?

Liver contains thousands of enzymes, thus you should be more specific about the substances you want to compare. If the substances have similar affinity to the specific enzymes their interaction will be equally competitive, otherwise the winner will be the substance with the greater affinity to the most of "receptors" and enzymes.

Aside from "toxins", the liver metabolizes a host of endogenous and exogenous compounds. Endogenous compounds are compounds that are normally present and produced within the body like ammonia and estrogens for example. Exogenous compounds are those like ethanol/alcohol, acetaminophen, and other drugs/etc that are not normally in the body but rather we take a mediations or recreational drugs, etc. Most of the compounds that the liver metabolizes are through a set of enzymes called the cytochrome P450 system, which includes numerous enzymes (too many to list here) that catalyze a number of reactions that help detoxify a substance and/or make it more likely to be excreted in the urine by the kidneys.
If the liver "sees" old and new compounds it doesn't differentiate between which it might metabolize first - that is based on concentrations within the liver. In fact, only if the compounds are metabolized by the same liver enzymes will they compete with one another. If they are metabolized by the same exact P450 enzymes, then the concentrations of each of these substances within the hepatocytes (liver cells) will determine which one gets metabolized more frequently. For example, if the concentration of substance A is much, much higher than substance B, then substance A is going to outcompete the other substance for the enzymes that metabolize it (similar to competitive inhibition in biochemistry). Most of the time, endogenous and exogenous compounds do not necessarily compete at the same P450 enzymes because there are so many different P450 enzymes within the liver.
The liver does not have any way of prioritizing different compounds, however, if the liver is exposed to a particular substance over a long amount of time then it may express more of a particular cytochrome P450 enzyme that metabolizes that particular substance. This is similar to alcoholics being able to metabolize a lot more alcohol than someone who has never drank alcohol previously.


text:
What is the substrate for glycogenesis?
In glycogenesis (i.e. the synthesis of glycogen), are sugar phosphates the direct substrates for glycogen polymerization? I would certainly think so since glucose is phosphorylated and then stuck onto a glycogen chain, but my textbook seems to think no.

What exactly makes you say that your "textbook seems to think no?" What is the textbook? Sugar phosphates are, by definition, substrates of glycogenesis.

It must be a typo then...it's a true or false questions and that is the literal question "In glycogenesis, are sugar phosphates are substrates for polymerization?" and the answer is F

@user2879934 phosphorylated glucose is not the direct substrates for polymerization... for glycogen synthesis UDP-conjugated glucose molecules are used, not glucose-phosphate (maybe this is the distinction that your book is trying to make) UDP-glucose is different than glucose-phosphate (in my opinion a nit-picky question... but these are the sorts of questions found in textbooks all the time - the book is trying to be tricky)

@VanceLAlbaugh so basically phospohrylated glucose + uracil, so it's false because no uracil?

The books wants to say "what is the substrate for glycogen synthase?" You often end up with really vague questions in the more elementary texts, however, so they (the publisher) thinks you know what they mean by "what's the substrate for glycogenesis?" Really, and a quick fact check via Google or what have you would confirm, glycogen synthase is more formally a UDP-glucose-glycogen glucosyltransferase. The substrate for the enzyme is therefore UDP-glucose, and the function is that of a glycosyltransferase, just very specifically utilizing an activated glucose moiety.

@user2879934 I would not consider UDP-glucose a "phosphorylated glucose" - it's a glucose with a UDP moiety on it

A pathway doesn’t have substrates, only a reaction does. And therefore there’s no such thing as a direct or indirect substrate. You can perhaps ask what the precursors are for glycogen (but do you mean immediate or distal), or what the substrates are for the first reaction in the pathway (but only if it is quite clear what the first reaction i).
That’s the trouble with trick questions. They are generally badly worded and tend to lend nothing to biology education.


text:
Why would glucocorticoids promote glycogenesis and not glycogenolysis?
I read in a textbook that glucocorticoids can stimulate the synthesis of glycogen. I do not understand this at all—shouldn’t glucocorticoids try to increase the blood level of glucose? Why would they be storing glucose as glycogen in the liver and muscles like insulin?

Interesting. What is the textbook? Which tissue or cell type does this refer to?

Glucocorticoids have a number of physiologic effects on glucose metabolism, inflammation/stress response, bone metabolism, etc. In general they are called glucocorticoids because they were originally found to be associated with increased blood glucose concentrations. Simply put, glucocorticoids antagonize the actions of insulin and create a state of insulin resistance, as well as increasing the expression of enzymes involved in glucose metabolism. They have a number of effects on all sorts of tissues and biological processes.
With regard to your question specifically, it makes sense that glucocorticoids stimulate glycogen synthesis, because it will allow the body to store more glucose as glycogen and increase the body's capacity for liver glucose production (i.e. glycogenolysis). Remember, at the same time glycogen synthesis is being increased, the glucocorticoids are inducing a peripheral insulin resistance that antagonizes insulin action in skeletal muscle and fat that also leads to increasing glucose concentrations in the blood. Moreover, free fatty acid are released from adipose tissue to be carried via the circulation to the liver so they can be oxidized to produce ATP for gluconeogenesis.
There is an excellent chapter that describes the effects of glucocorticoids on glucose metabolism in the major metabolically-active tissues (e.g. liver, white adipose tissue, skeletal muscle) by Kuo et al from Vol 872 of Advances in Experimental Medicine and Biology (pages 99-126). The book is not open access so I can't paste a picture of any of the figures, but they essentially show what I describe above. Here is another link to a very nice review article in the Journal of Endocrinology that has some great figures showing fuel redistribution in response to glucocorticoids as well.

There is increased insulin/glucagon ratio due to glucocorticoid (increased blood glucose level or insulin resistance) leading to stimulation of glycogen synthase and inhibition of glycogen phosphorylase causing glycogenesis.
2.There is large amount of glucose in liver due to gluconeogenesis. Since Vmax of glucokinase is much higher than that of hexokinase, they are converted to glucose 6-phosphate. Glucose 6-phosphate has allosteric stimulation effect on glycogen synthase so glycogenesis occurs.


text:
Why would growth hormone (somatotropin) cause both lipid AND glucose release?

GH increases lipolysis (lipid breakdown) and the release of fatty
  acids from adipocytes into the blood. Fatty acids then can be used as
  energy sources to drive chemical reactions, including anabolic
  reactions, by other cells. GH also increases glucose synthesis by the
  liver, which releases glucose into the blood. The increased use of
  lipids as an energy source accompanies a decrease in glucose usage.
  Overall, GH activates the use of lipids to promote growth and protein
  synthesis.

(From Seeley’s Anatomy and Physiology, 10th edition.)
That passage has gotten me confused. So more lipids are used by cells instead of glucose, yet the body releases more glucose into the blood in response to GH. What would be the point, or benefit, of this occurring?

The way its stated in the excerpt you have in your question could be a bit clearer. This concept can be found in any basic physiology textbook, and looking at another text may also help clarify it more.

Great question... and an important point about glucose and lipid utilization! The body can't turn fat into sugar, but it can turn sugar into fat. The more technical way to say this is that the body can't convert acetyl-CoA into glucose, but it can convert glucose into acetyl-CoA.
The enzyme that converts glucose to acetyl-CoA, pyruvate dehydrogenase, catalyzes an irreversible chemical reaction. Pyruvate dehydrogenase converts pyruvate into acetyl-CoA, which can be used in the Krebs Cycle, fatty acid synthesis, etc. Once acetyl-CoA is produced it cannot be converted back into glucose (carbohydrate) within the body. This is important because certain cells/tissues can use only glucose for energy production, while other cells/tissues like the liver can use both glucose and lipid for energy production.
This is where your question becomes very important, because the liver is the predominate organ that maintains glucose homeostasis (i.e. maintains blood glucose concentration) in-between meals or during periods of fasting. In periods of fasting, the liver uses free fatty acids released by adipose tissue for energy/ATP production in order to produce glucose through gluconeogenesis, an anabolic process that requires energy.
So, growth hormone increases fatty acid release from adipose tissue stores for uptake by the liver. The liver takes up the fatty acids from the plasma and uses them to produce glucose for release into the circulation for glucose-dependent tissues to use. During this time of fasting, tissues that can use fatty acids and glucose tend to switch to fatty acids as their energy source, while tissues that only can use glucose will continue to rely on glucose production from the liver for their energy source.
Here is a nice summary (open source) from National Library of Medicine explaining in more depth the basis for why fatty acids are oxidized to provide ATP for gluconeogenesis - "Energy Metabolism in the Liver".
Also, George Cahill, a famous physician-scientist at Harvard University who studied metabolism and starvation has an excellent review of fuel flux under fasting and starvation conditions that demonstrates the above mentioned principles as well "Fuel Metabolism in Starvation" - namely that free fatty acids released from adipose tissue are oxidized in the liver and used for anabolic processes in the liver, such as gluconeogenesis that maintains blood glucose concentrations.


text:
qPCR : Cross-contamination while sealing plate
I'm trying to do realtime PCR on a plasmid and I have my positive and negative controls close to each other along with a no-template control. I add 1 ul of my template last into the 96 well plates (on the side wall of the well, to be precise) and I seal the plate with optical adhesive seal (applying pressure with hand) and centrifuge afterwards.
While sealing I have noticed that the template drop I add on the side of the wells is being wicked up and is likely spreading into the neighboring wells. I notice amplification even in wells where I added water instead of the template
Has anybody notice the same or has any suggestions for how to avoid this? Do you add template into the liquid in the well or onto the side wall?

I can't say this happened to me before (but also don't do qPCR all the time).
In principle it should be fine to add the template to the side of the well, since this also lets you visually confirm that you did add the template. However, if you are having problems do consider adding the template to the liquid.
As another way to avoid this problem I would try to first put the adhesive foil lightly on top and then push it down/fix it with something sturdy that has a straight edge (there are special plastic things for this, but a tip-box can also work).

Thanks for the answer. I found a plastic applicator to seal plates in the lab. I will try it and see of it improves the result.

I have tried now sealing with a straight edge and it definitely does not wick the samples or cross-contaminate them. Thanks for the advice!