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Ideal examples of Magnoliophyta Lilianae
What are the ideal examples of Magnoliophyta (Lilianae-to be precise) for a teacher to show students?
And, does anybody know exact name of this flower? Picture


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Aging: Only humans have grey hair?
I am not sure if I ever saw a monkey or a bird age and lose hair pigment as it grows. It maybe due to my lack of information. But it appears to be a general presumption that only humans age and lose hair pigment (hence developing grey hair).
If this is true, then I am curious why only humans?

I don't think it is restricted to humans. Dogs lose hair pigment as well, usually around the muzzle.
This work used graying of hair to discriminate senior dogs.
I don't know which other mammals lose hair pigment, though, nor why.

We also see this in big apes.

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sort: votes


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Why do we develop addiction?
Recently, while on the train, I saw a person not holding the handrails on purpose. He decided that playing a game with no outcome whatsoever was more important than his safety. In fact, he bumped into the overhead luggage carrier several times. Twice he almost stumbled and fell, with a possibly very negative outcome for him.
Once he stumbled and bumped so hard into the carrier, it left a red mark on his face, even after facing it earlier.
Still he refused to hold a handrail as that would have prevented him from playing the game.
Clearly his addiction to the game won over any sense of self protection.
Now thinking about it, I think this is the case with most addictions. At the end, they are to some degree, harmful to the addicted person(imho).
Taking this to the time when we were still facing predators, it must have been careless just to think of getting delicious berries whilst not considering the exposure to predators it came with.
These individuals that are addicted (in a way) and don't care of the dangers associated with a problem, are harmed more often.
Thus, making addiction an evolutionary disadvantage.
Therefore, being easily addicted, as a trait, shouldn't have developed much.
Yet addiction is one of the worst problems of humanity and has been so for a long time.
So how could it develop?
Are my conclusions wrong?
Is addiction just a modern phenomenon?
Or are there evolutionary benefits of being addicted?

You are born with several addictions, to food, air, water, sleep, social interaction, reproduction, ect. Being alive is a struggle between desires and self preservation, everything has risks. You could never leave your house and starve to death.

Sorry this is no philosophical question

You misunderstand, a brain that could not function with addiction could not get you to seek food or water or a dozen other things, Addiction is built into how the brain works.

See that's why I say this isn't philosophical. I don't want to discuss if basic needs to survive are an addiction as well...

@steros John's point isn't philosophical, the point is that the behaviors of addiction are the same as the behaviors for obtaining "normal" needs, just taken to a higher degree.

@John has already shown that without a tighter definition, "addiction" includes breathing and eating. I'm slightly less pedantic than that, but I'm struggling with your question all the same. Are you asking why we developed an ability to take a risk and is this linked with addiction? Are you asking if other species have evolved to be susceptible to addictive behaviours? Are you asking for a biologically relevant definition of addiction?

I thought I made it pretty clear that I'm not talking about satisfying basic needs. But when an addiction becomes a danger for the individual. There's clearly a difference to having basic needs to survive and risking your life for something unnecessary. I didn't want to discuss what can still be called addiction though.

You are talking about healthy normal states and aren't talking about clinical addiction. You use a child playing as an example of being "addicted". This is a very soft definition which makes this so hard to answer.

The supposed duplicate doesn't answer the question at all

So how could it [addiction] develop?

Children need to play in order to understand the structure and behaviour of the world around them.
Bumping into things is a byproduct of this.
This behaviour is distinct from clinical addiction.
See this NHS page which covers some examples of addiction

Are my conclusions wrong?

As I understand it, your conclusion is that addiction shouldn't have evolved.
Asking how/why bad traits evolve is a really common question.
Here is the communities answer to why bad traits evolve and good ones don't.

Is addiction just a modern phenomenon?

Clinical addiction is becoming more recognised and diagnosable all the time.
Recently, the WHO started to cover gaming disorder as a form of addiction.
Alcohol abuse has been around since the ancients (Carr, 2011), and I would assume earlier than that.
Animals can exhibit pathological behavious in captivity, but this would be difficult to describe as addiction (see this Bio.SE question linked in comments by @WYSIWYG).

Or are there evolutionary benefits of being addicted?

Addiction is a condition where the normal brain feedback goes wrong and the brain prioritises a task that feels good in the short term at a huge long term cost.
The "reward" system that encourages us to eat and have sex has been hijacked.
Addiction is an advanced neural reward system rewarding itself for behaviours that can be destructive.
Without that same reward system, our drive for survival by means of food and sex may not have been so great.

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Why do people sing?
I was wondering the why people sing, but from a biological point of view.
Is it necessary for our body? If it is so, then why can't everyone sing well?
Is it in direct relation with neurotransmitter secretion, like the adrenaline? Or is it only a way to express our emotions?

is singing necessary for our bodies, No, but then neither is sex or making tools, That does not mean there is not an evolutionary advantage to doing them.

Nice question, I'll answer it in parts:

Is it necessary for our body?

Well, there can be many perspectives for why humans like singing. Let's talk about the evolutionary perspective first. I found three theories about why singing was evolutionarily beneficial for humans.

The Shakespearean theory, that music is at least one of the foods of love, has a strong claim to be true. The more mellifluous the singer, the more dexterous the harpist, the more mates he attracts. In simple words, whom would you like to marry: a singer + hunter or just a hunter?
A second idea that is widely touted is that music binds groups of people together. The resulting solidarity, its supporters suggest, might have helped bands of early humans to thrive at the expense of those that were less musical.
The third hypothesis, however, is that music is a cross between an accident and an invention. It is an accident because it is the consequence of abilities that evolved for other purposes. And it is an invention because, having thus come into existence, people have bent it to their will and made something they like from it.

Anither perspective is the biological one. According to a Chicago Tribune article people who sing live longer than those who do not. Why? Singing stimulates better blood flow by increasing the efficiency of chest wall muscles in air exchange. Whenever you'd have tried to sing a nice song, you must have felt that you need to regulate your breathing in order to get nice tones. At one moment, have a huge breath-in, and the very next moment, release it slowly. All these help in increasing blood flow and thus, if you keep singing when you grow old, you would live longer!

If it is so, then why isn't everyone able to sing?

This has a very simple answer. The element that makes people sing poorly is problems with pitch accuracy, which is also called intonation. (Pitch can be understood as the ‘sharpness’ of a voice; female voices are typically higher pitched than male voices.)
Why Does This Happen?
It all comes down to those tricky activities of the brain. The problem with the brain lies in not being able to adjust its activities against a particular target (which, in this case, is a particular tone). That may be a bit confusing, so let’s break it down a little further.
When you hear a tone, your brain has a perception of its various parameters, such as loudness, pitch, tone and so on. It turns out that human brains are pretty good at perceiving the right tone, which means that the possibility of an error in our brain’s perception of the tone is ruled out. Hence, the ‘input’ component in this case is alright; the problem occurs at the ‘output’. After hearing the tone, the brain maps out an output tone to match the one it heard, but sadly, it’s not in tune.
It’s not that you don’t realize when you are singing off-key; ears do register that you’re not quite producing the tone that you intended to, so the vocal cords ask for instructions from the brain. However, the brain still sends the same instructions, and you simply can’t get the tone right. It’s almost as though the vocal cords have locked themselves in a particular position to produce the same erroneous tone every time, even after knowing better!
source

Is it in direct relation with neurotransmitter secretion like adrenaline?

Let me clear out some things here first. First of all, adrenaline is not a neurotransmitter, its a hormone (unless you're talking about adrenergic neurons). You can see the differences between neurotransmitters and hormones here.
Second, singing is a complex process and cannot be totally dependent on neurotransmitter (though singing isn't even possible without neurotransmitters!).
Back to the question, serotonin might have an effect on singing. Serotonin is regarded by some researchers as a chemical that is responsible for maintaining mood balance, and that a deficit of serotonin leads to depression. However, its effect on singing is not known yet (at least I can't find a reference for such a study).
EDIT: Another neurotransmitter (which I forgot to mention ;) that plays some (if not all) role here is dopamine. Dopamine is considered as reward and pleasure chemical because it is released in areas of brain (like nucleus accumbens) to give a feeling of reward and pleasure. It has been suggested that dopamine, through the mesocorticolimbic pathway, gives a feeling of pleasure after singing. That is probably why we feel so nice when we hit the perfect tone in a song.

Mesocorticolimbic pathway: a dopaminergic pathway in the brain consisting of the mesolimbic and mesocortical pathways. The mesolimbic dopaminergic pathway originates in the ventral tegmental area (VTA) of the midbrain and connects to the limbic system via the nucleus accumbens (NAc), amygdala, the hippocampus, and medial prefrontal cortex; it plays a critical role in reward related behaviors and reinforcement learning. The closely related mesocortical dopaminergic pathway connects the VTA to the frontal lobes.

References:

Human evolution: why music?
Why do we sing?
Why some people just can't sing well, no matter how hard they try!
Neurotransmitters vs hormones
Serotonin: facts, what does serotonin do?
The neurochemistry of music; Mona Lisa Chanda and Daniel J. Levitin

Adrenaline (epinephrine) is a neurotransmitter. There are many adrenergic neurons.

I thought adrenergic neurons work only on noradrenaline & dopamine. Thanks for telling @WYSIWYG :)

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Recommendations for an intro level virology textbook?
I'm a college sophomore, and I was just accepted into a research lab that works with retroviruses. Since I haven't taken any classes on the topic yet, does anyone have recommendations for good, intro-level virology textbooks I could work through to learn some background information?

You can ask the head of the lab or your supervisor, they might have targeted ideas for your research.

Have you taken any molecular biology or biochemistry? They seem like a prereq to virology.

Have a look at the tag wiki on [tag:book-recommendation]. You should provide more details in your question, otherwise it seems broad and tends to generate opinion-based answers.

http://as.wiley.com/WileyCDA/WileyTitle/productCd-EHEP001462.html This book is good enough to guide through the course.

Understanding Viruses, 2nd ED by Shors is the current recommended text at my university for the undergraduate virology course. If you're interested in the area, as suggested in the comments, I'd recommend some reading in cell and molecular biology to really get a sense of the host dynamics. Alberts' Molecular Biology of the Cell, and Watson's Molecular Biology of the Gene are standard core texts. Really, though, the only prereq to our virology course is the upper-level microbiology course.

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How does decreasing surface tension of lipids help to emulsify them?
According to my chemistry book, water has higher surface tension than lipids. But in my biology book it is written that "the gall forms an emulsion of water and lipids by lowering the lipid's surface tension". This will increase the difference between the two substances even more. How can this be beneficial?

Edited to "surface tension" as the original phrase appeared meaningless in context. If I have missed something, please do revert it.

This is essentially a physical chemistry question.

lipids have surface tension - and that's a good thing since it helps hold the cells together!  - that seems like biology to me.  its not clear to me what the 'gall' is but i imagine a non polar or amphipathic (polar and non polar) additive to the mixture will increase the solubility of the lipids in the mix

@shigeta I believe the "gall" means bile. https://en.wikipedia.org/wiki/Gall_%28disambiguation%29

Yes, gall is bile . I am not a native english speaker.

There appears to be either a typo or transcription error in your textbook.
According to this Nuffield Foundation and Royal Society of Chemistry article

Molecules of most detergents and soaps are long chain hydrocarbon
  molecules with an ionic group at one end, usually carrying a negative
  charge, thus making it an anion. This charge is balanced by the
  opposite charge of a soluble cation, for example Na+. The long
  hydrocarbon chains do not interact well with water molecules, and many
  of them are effectively ‘squeezed out’ to the interfaces between the
  water and the air or the glass sides of the beaker. The effect of
  these molecules on the water surface is to considerably weaken the
  forces between water molecules there, thus lowering the surface
  tension.

Soaps, detergents, and bile (all examples of amphiphilic compounds) act to reduce the surface tension of water, not the lipids.

Now it makes sense to me! Thank you for help!

That is why they are called "surfactants"

Surface tension is about how much energy you need to create new surface between not mixing materials e.g. water and lipids. Surfactants like bile makes this easier (lowers the energy required). So they can form small bubbles of lipids: micelles, which can be handled much easier by the digestive system. Another usage of surfactants to make foams, creams, etc... physical-chemistry / surface rheology is all about them.


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Could tumor cells have normal genomic profiles?
I have thawed primary tumor cells and performed FACS. They were EpCAM positive cells. Then, I expanded them as organoids in 3D and did another FACS analysis. Again, they were EpCAM positive. I also sent organoids to pathology for IHC. Results showed they expressed EpCAM, EGFR, and panCK. But to my surprise, the Ampli LowPass sequencing results showed they had a balanced profile like normal cells. How could that be explained? Any help (comments, papers, ...) is appreciated.
Thank you.

I think this is the paper about the Ampli LowPass sequencing technique. Although, I didn't read it thoroughly but from the abstract and result section titles, it appears that this technique is designed for detecting CNVs. Since it is low pass (i.e. low coverage), it may not detect substitutions and small indels accurately.
Your cells may have mutations but not big chromosomal rearrangements. It is not necessary for tumour cells to have such chromosomal aberrations. In fact a simple overexpression of an oncogene or a point mutation causing reduced/loss of activity of a tumor supressor (for e.g. p53) is enough for tumorigenesis.


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How can twins be born months apart?
How can twins be born months apart? What is the science behind it?

Well once the womb is open... But just google it and you'll see that it's very rare but it happens that there are a few days of interval !

In vitro fertilization creates twin embryos.  One is implanted & carried to term, the other is frozen, and later thawed and implanted.


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3D Cellular Model
I'm learning biology on my own and it's pretty hard to understand all processes inside a cell from the side of chemistry and physics and in some cases pointless to bring a complexity instead of abstraction.
I just curious to know if we have some open-source projects that provide 3D
program models of a cell? I mean not just like study model that shows cell organelles and their names but I want something that shows real cellular processes like (1x1 or close to it) real model of a living (in program) cell with some types of abstraction levels.

I don't know of such resources but certainly there are good animated videos of different cellular processes. Khan Academy would be a nice place to look for video tutorials. I also would want to add that a full computational model of an entire cell would be quite complex and I haven't come across any (the closest to complete was that of M.genitalium and it was not intended as an educational resource but a research project instead).

Not of a complete cell, that would seriously overload even most powerful animation software/hardware you could build, not to mention there are gaps in our understanding of the cell. Understanding a cell purely through chemistry is possible if a bit masochistic, sooner or later you are going to need to approach it from a different direction to get the whole picture. There is so much complexity in a modern cell that sooner or later you have to start looking at the emergent characteristics. Don't believe me check out this chart of just the common metabolic pathways in a human cell, you are looking a 3.5 billions years of kluges, breathtaking elegance, rube goldberg monstrosities, and duck tape solutions all layered and tangled into each other, messy doesn't begin to describe it.
But there is several places creating models of individual processes, modeling each individual atom. These will let you at least understand hte chemistry of the components.
www.dnalc.org is focused on nucleic acids and their interactions.
Their work is related to Harvard's biovisions program which uses XVIVO. which is a much rougher but larger scale approach and may be the closest to what you want.
Cambridge MRC has a more diverse selection with better visualization of the actual chemical interactions.
Swissmodel by the Swiss Institute of bioinformatics focuses on protein modeling and has a free to use program and database.
There is even a wikipedia database Protepedia
Image from www.dnalc.org animation

I'm sure others on the site could list a dozen other such programs/databases.

@user237650 Thank you, that should have fixed it.

The complete function of a cell is something which is still quite beyond our current knowledge and understanding. Many gaps remain that prevent us from building such a complete model, and also from engineering an artificial object that would reproduce some basic function of a living cell.


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What is this spiky fruit/cone?
I am trying to identify an unusual cone or fruit found today on Tayside in Scotland. Here is an image. Can you help?

Welcome to SE Biology!  Please insert images rather than making them links — this is for both the security and convenience of other users.  For details on how to use this site, please check out the tour: biology.stackexchange.com/tour and then the help pages on how to ask questions on this site: biology.stackexchange.com/help/how-to-ask.  Thanks!

Sorry it won’t let me upload photos. Will try another website. Thanks anyway

What happened when you tried clicking on the image icon?  Assuming you have copies of the images you should be able to use the "Browse" option to upload copies of your images ...

You have to reduce the file size (by reducing quality). You can use any photo editor to do that. I'll do that for now. Please take care in future.


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Transcription by RNA polymerase in absence of inducer and activator
Does the presence of activator(CAP-cAMP complex) and inducer(lactose) only increase the likelihood that a particular gene(here operon) gets transcribed, i.e increases the rate of transcription of that gene?And transcription of some(assumption) genes always happen?
Because as I know basal level transcription is something that happens always,even without an inducer.

Some genes have basal transcriptional activity whereas some may not at all. Are you asking whether all genes have some basal activity in the absence of an activator?

@WYSIWYG No. I'm asking what is the role of inducer and activator for e.g in lac operon. Do they solely increase the rate of transcription of the operon increases? Is it same for all genes (It mustn't be because you said that not all genes have basal level transcription)? For some set of genes then transcription factors (activators) and inducers solely switch on the gene.


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What is regulatory promoter?
I came across this term in University question paper.

What is the difference between core promoter and regulatory promoter?

I have googled (Web, Scholar and Books) it but couldn't find any information from any authentic source.

I don't understand this. Promoters are regulatory per se, so this doesn't male sense to me.

@Chris I don't know, may be it has something to do with Proximal and Distal promoters.I've edited the post with the question I found.


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Concept and analysis of Pedigree
Pedigree analysis is a process of establishing a virtually correct inheritance pattern of a genetic condition in a proband's family. I call it virtually correct because in many a cases we assume the genotype of a parent to be something by weighing the genotypes of the offsprings.
Now in a given problem like in this one where the trait follows autosomal dominant inheritance pattern I have problem deciding the genotype of I-3.

My opinion:
The genotype of II-6 is AA'. (Obtained from a calculation which I have decided to not to mention as it will make it lengthy and complicated)
(here A=Normal allele on autosome and A'=Mutant allele on autosome)
II-6 receives allele A from mother I-4 (who is obviously AA) and allele A' from father I-3. Now the genotype of the father could be either AA' or A'A'.Since the probability of having a AA' female child becomes 100% if we assume the genotype of the father to be A'A' so the genotype of the father I-3 is A'A'.
But one of my instructor says that it cannot have a genotype A'A' because it is fatal and I am not convinced with his reasoning.
In Huntington's disease presence of one HTT gene is enough to cause death of the person. It is a dominant lethal allele. While in achondroplasia, an autosomal dominant disorder the mutant allele when present in two copies is fatal.It is a recessive lethal allele. A heterozygous person survives with symptoms of Achondroplasia.
So death is not always caused by two copies of a mutant gene of a dominant autosomal trait. It may be caused by only one copy of gene as in Huntington's disease or may not be caused at all(I've no proof of this. Its my assumption).
So in a pedigree where nothing has been mentioned about the lethality of the genes concerned we shouldn't assume them being recessive lethals. This is all I think. Am I correct?
Finally: Should the genotype of I-3 be A'A'?

I-3 can be either A'A' or AA'. In Huntington's disease or Achondroplasia, the father could still survive to adulthood and reproduce. If the father had a chromosomal disorder such as Kallman's syndrome, he would be unable to reproduce. However, this is not a simple mutation, and it is not heritable. You should ask your instructor to clearly define the problem.

Could you cite an authentic reference to your answer ?
I have been reading about lethal alleles from wikipedia:
https://en.wikipedia.org/wiki/Lethal_allele#Types_of_lethal_alleles


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Problem in understanding Operon
Is there a good book that explains operons: lac operon and trp operon in details.
I was reading  the functioning of the trp repressor protein from 'Principles of genetics-by Snustard and Simmons',they have mentioned that the binding of the repressor-corepressor complex to O$_t$$_r$$_p$ prevents the transcription of the structural genes. But they don't explain how.
Khan academy says that the repressor-corepressor complex physically comes in the way of the RNA polymerase. They have used this diagram below which shows that the large RNA polymerase cannot bind to the promoter site due to steric hindrance.

I'm looking for a more authentic source to study exactly how this RNA polymerase is being prevented from transcribing the DNA in both the operons.

Chapter 31 in the Voet and Voet biochemistry book (I have the 4th edition) link has a rather extensive explanation on this subject. It is rather pricey but you can find a copy of this one in nearly every university library. It generally is a good resource if you want to know more about the DNA or Protein structure of a basic process


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What's the name of this spider?
Recently, I was taking a walk down by a riverbank and saw this spider:
Here's all the info I think would be useful

Where? Missoula Montana, United States of America. Specifically, Greenough Park, on the riverbank (as mentioned earlier)
When? today, May 28, 2019
Behavior? They were hard to approach and scuttled away fairly speedily whenever I approached.
Population? They were everywhere, everywhere I looked they seemed to be there, occasionally, I found them in pairs, but never in groups of three.
Additional Info: they were passive until approached, moving rarely if observed from a distance, but when they did move it seemed that their movements were somewhat sporadic, with quick bursts of speed and then stopping and resuming (if they found that necessary)


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Aquatic Snail Identification
I can’t for the life of me find an identification of these snails. They’re thriving in brackish water, but may be freshwater naturally. They’re about .8cm long at their largest. I believe they have live birth due to the lack of eggs but presence of baby snails over the year and a half that I’ve had them.

Hi, Please try to be more specific like where you found this animal. Check the list of the additional info in the species-identification tag: One or more clear Photos.
A Location where the specimen was found (city/region and/or habitat).
An approximate Size (or photo indicating size).
Additional useful info (e.g., behavior, time of day/year, etc...)
Indication of prior research performed by the asker.
A tag for a specific taxanomic group (e.g., botany, entomology, arachnology, ornithology, ichthyology, etc...).

Looks like a Malayan Live Bearing snail , fairly common in the US aquarium trade. I have inadvertently gotten them into all my tanks. Common aquarium fish can't eat them ( unless you crush them on the glass). I did not know they can tolerate brackish water. Yhey will get to 1.5 mm.


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Coagulation of protiens of different products
Protein of egg coagulates on 60 degree but proteins of milk do not coagulate at high temperatures..why?
What is the main reason behind all this?

Milk coagulates at a temperature below 18 degrees is what I do know.

I'll look into it for you.


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Movement of the Thoracic Cage During Movements of the Thoracic Spine
Just for a bit of context: I am trying to create a 3D digital model of the human skeleton as the first step towards computer generated muscle simulation, and as such I want the skeleton to be as anatomically and biomechanically correct as possible. However, I am currently struggling with the movement of the ribcage. I am quite capable in the 3D side of things, but without any medical background I've essentially had to learn everything about the skeleton so far from the ground up.
Whilst there is plenty of information on the internet about the movement of the ribs and sternum during inspiration and expiration, I haven't been able to find any detailed descriptions/diagrams/animations of how the various movements of the thoracic spine (lateral flexion, sagittal flexion and extension, and axial rotation) influence the positioning of the ribs, including in scientific papers (however I can't see that this topic hasn't come up before?).
The only thing I've found for this are three diagrams from this website http://body-disease.com/movements-in-the-thoracic-region/ (bottom right hand corner in each case):

Whilst these diagrams are definitely helpful in showing the general movements and shape, they don't really have the detail that I am looking for: for example the movement of the sternum isn't specified or the exact movements of the ribs and costal cartilage. These diagrams are a good starting point but I can't really work with them - as really I need to understand the four movements of each rib (torsion, calliper, bucket handle and pump handle) where they connect to the thoracic spine in order to create an accurate 3D model.
I would most like an accurate diagram or (even better) an animation of the spine movements with a complete rib cage; however X-ray images, sketches or anything that might provide more information would be useful. Descriptions are also great but as I'm not very experienced with anatomy I may not be able to glean as much information from text as I would from images. Essentially I am not trying to understand the concept of how the rib cage changes, but the specifics of this complex movement.
I know this might be quite a specialist topic (especially given the lack of online information) however I thought I would ask anyway in case anyone knew. Thanks for any information you can give me!
(Also let me know if I've made an error - this is my first forum question)
Edit: after some more digging I've found this image (from http://www.orthotech.ethz.ch/research/musculoskeletal-biomechanics/sarcopenia--implications-of-age-related-muscle-loss-for-spinal-p.html) showing thoracic flexion and extension, which may help in understanding the sorts of thing I'm after. the issue with this image is the fact that the movement of the sternum and costal cartilage is still very unclear:

What benefit can one have from such 3D digital model?

@Jan I want to use the skeletal system as the basis for simulating muscles, fascia and other tissues present in the body to create a photorealistic human which can be used for CGI. The idea is to adjust the different settings of the model (such as muscle definition or amount of fat) to quickly create a vast range of realistic 'humans'. The advantage to conventional 3D modelling would be accuracy (see Weta Digital's 'Tissue' software as a good example). I'm using the open source software "Blender" and I hope to make the system free to use for all if I get it to a point where I'm happy with it.


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How do I identify the different stages of meiosis under microscope?
This is a question I'm troubled with as my exams are knocking at the door. I need help so I decided to post this here.
Here's what I know and understand about meiotic stages:
Specimen: Grasshopper (Gesonula punctifrons) testis whose 2n= 23
Note: The character in bold and italics is the identifying feature of the concerned stage.
Prophase:
Leptotene

The uncondensed chromosomes are visible as a cloud of thin threads.
Each chromosome consist of two chromatids which are not visible.
The single darkly stained X chromosome is found at the periphery of the nucleus.
Late in this stage the chromosomes attach themselves by telomeres to the inner membrane of the nuclear envelope forming a bouquet.
Nuceolus and nuclear membrane are present.(not visible under compound
microscope)

Zygotene

The uncondensed chromosomes are visible as a cloud of threads.
Homologous chromosomes undergo synapsis  forming bivalent.
The single darkly stained X chromosome is present slightly off the periphery of the nucleus.
Nucleolus and nuclear membrane are present.(not visible)

Pachytene

The chromosomes show some degree of condensation.
The sister chromatids separate to form tetrad a structure with four chromatids.
Crossing over between non sister chromatids of homologous chromosomes occur leading to formation of X shaped chiasmata.
Nucleolus and nuclear membrane are present.(not visible)

Diplotene

The chromosomes are thick and darkly stained.
The chromosomes are wooly in appearance.
The paired chromosomes separate from each other except for the chiasmata.
Nucleolus and nuclear membrane begin to diappear.(can't be detected)

Diakinesis

The chromosomes are thick and darkly stained.
Terminalisation of chiasmata initiates.
The bivalents appear rod, diamond or oval shaped.
The nucleus and nuclear membrane disappear completely.

Metaphase-I

The chromosomes are thick and darkly stained.
Presence of twelve chromosomal elements (11 tetrad + X chromosome).
The chromosomes are aligned at the equitorial plate.
Terminalisation of chiasmata completes.

Anaphase-I

Two groups of chromosome are in the act of separation.
One group is with 11 autosomes and the other group with 11 autosomes and a X chromosome.
The chromosomes are T or V shaped.
Each chromosome is in dyad state.
The centromere is undivided.

Metaphase-II

There is 11-12 dyads present.
The chromosomes are thick and darkly stained.
The dyads are arranged in circle or flower like fashion.
The chromosomes are rod like

Anaphase-II

The sister chromatids of a dyad separate due to splitting of centromere.
Two groups of chromosome are in the act of separation.
One group is with 11 autosomes and the other group with 11 autosomes and a X chromosome.
The chromosomes are rod like

Here's an image which has nearly all the stages except telophase.Can someone label the stages?

Here's what I feel about them:

Finally am I correct? How do I identify them correctly? Could you site some authentic references?

ID characteristics that can help you recognize diplotene  better:
diplotene :
the only difference between this phase and Diakinesis is that The centrosomes reach the poles.
you can see the photos of diplotene and diakinesis here :
http://www1.biologie.uni-hamburg.de/b-online/e09/meiosea.htm

(a) polyploid nutri-tive cells with many heteropicnotic chromatin bodies; (b) leptotene-zygotene; (c) pachytene; (d) diffuse stage; (e) di-plotene; (f) diakinesis; (g) metaphase I; (h, i) anaphase I; (j) telophase I;. (k) metaphase II; (l) anaphase II; (m) telophase II; (n) round spermatids; (o) elongating spermatids; (p) head of sper-matozoas. Big arrows indicate sex chromosomes, small arrows point to nucleoli and arrowheads indicate m-chromosomes
You can see all the phases clear and perfectly separated here :
http://biology.about.com/od/meiosis/ss/meiosisstep.htm#step1
by the way , try to adjust microscope as best as you can & don't put much  oil immersion .

long answer for this Question ?! there is no other thing to explain .
Sanjukta Ghosh asks how to identify different phases of meiosis under microscope and I provided a link that show all 10 phases perfectly clear . I could upload every single photo by my self on the answer if you are asking for it   . why should I put some additional content and confuse the questioner ?

The images you have linked are not light microscopic views. They are far too clear for light microscope. Besides it lacks the substages of prophase I. I was also looking for an answer that specifies the key identifying characters. It will be helpful if you could improve the answer. Moreover I have attached an unedited image of meiotic stages. Could you label the stages there and explain how you are identifying them.

They are light microscopic view of course the background is white for better contrast they've been coloring very good and adjust very well . that's how it's gonna be in the exams as far as I've seen . but don worry I will improve the answer by specifying the key id characters . but you should know it's a tricky skill some times no one can say what the phase is as it is really unclear  ... these cases are not gonna be on the exams or so .


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Sexing spotted doves
I recently took pictures of Spotted doves (Spilopelia chinensis) during their courtship. The one on the right, is large with a off-white breast and the one on the left is comparatively small with dingy reddish white breast.
My professor and I presumed that the one on the right is the male and the other is the female. The larger one mounted the other during cloacal kiss.
I've checked Wikipedia and other sites which seem to copy Wikipedia, they say that the species does not show sexual dimorphism. On the other hand, this website claims that there is a difference.
Does it show sexual dimorphism?
Location: West Bengal, India

First I think that is a Western Spotted Dove (Spilopelia suratensis), now splitted from the Eastern spotted Dove (Spilopelia chinensis). In your area there should be both species but the red iris and eye-ring should indicate the Western. Sexes are alike so there are no signs you characteristics you can check (source, handbook of the bird of the world, which is the most updated and reliable source in many occasions). Males sing much more often than females (so you can observe this behaviour) and in many species, but I dunno about this one, is the male providing food to the female...so I think your guess is right!
All the best,
Have fun

I am sorry I think there is not much more information that the one provided by wikipedia. Also this specialized website, which I trust, http://www.birdforum.net/opus/Spotted_Dove  repeats the same information.

I took the liberty of adding hbw links to the two species.

I currently have a pair of spotted dove visiting my backyard regularly for feeding.  I noticed one of them has got a more blueish head top than the other, still trying to figure out which one is male.  The one with blueish head top is comparatively smaller in size, and less courageous when it comes to having me around. My best guess is that the more blueish head is female and the bigger, more reddish head is male.  In any case, this is just my best guess.

Welcome to Biology.SE. While anecdotes are potentially interesting, your answer is much more likely to receive a favorable response if you [edit] it to include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion and thus is inappropriate for this site. ——— Please take the [tour] and then consult the [help] pages for additional advice on [Answer] and [Ask] effectively on this site and then edit or delete your answer accordingly.


text:
What are the differences between Signaler and Primer pheromones?
I have searched few authentic books and have found the following difference between them.
Signaler pheromone induces fast reaction in the recipient and the Primer induces slow reaction.
But I did not find any book that discriminates their function.
P.S. I have read Wikipedia and I'm not counting on it.

A good example of a primer and a signaler pheromone could be in the recently discovered pheromone system in pennate diatoms (unicellular algae). When diatoms reach a certain size as a result of successive divisions (they get smaller with each vegetative division) both mating types start to produce a first pheromone that provokes cellular responses in their mates: 1) to stop dividing vegetatively and 2) to produce either another pheromone (a cell attractant, by one of the mating types) or to induce a sensing system to locate their mates. So, the 'Primer' pheromone would be the first, and the 'Signaler' the second pheromone, i.e. the attractant. A similar system exists in fungi. The evolutionary explanation is likely that organisms don't need to invest in pheromones and their associated repertoire of sex genes when mates are not present.
References:

Metabolomics Enables the Structure Elucidation of a Diatom Sex
Pheromone
Pheromone signaling during sexual reproduction in algae


text:
How's idiotype different from paratope?
What I understand of these two terms is that:
Paratope is a portion of antibody that recognises and binds to specific antigen.
Idiotype is an antigenic determinant of antibody formed of CDRs that have specificity for a particular epitope. Some authors call the antibodies recognising a particular epitope an idiotype.
Well the CDRs, they actually form the paratope so is it right to say the CDR that acts as an paratope also forms the idiotypic determinant/ idiotype ?

I have read that the unique amino acid sequence of the VH and VL domains of a given antibody can function not only as an antigen-binding site but also as a set of antigenic determinants. the idiotypic determinants are generated by the confomation of the heavy- and light-chain variable region. Each individual antigenic determinant of the variable region is referred to as an idiotope. In some cases an idiotope may be the actual antigen-binding site (The paratope), and in some cases an idiotope may comprise variable region sequences OUTSIDE of the antigen-binding site. Therefore, each antibody will present multiple idiotopes, and the sum of the individual idiotopes is called the IDIOTYPE of the antibody.
I hope that had been helpful

Could you add your reference?

Kuby Immunology, 4th Edition, Chapter: Immunoglobulins: Structure and Function (83-113)

The following was a reply by an expert from assignmentexpert.com :

Paratope is only the part of Ab that binds to the epitope of an antigen. But this does not mean that every amino acid in the CDR should bind to epitope – it is possible that only 1-2 AAs per CDR bind directly to epitope.
  Therefore, paratope is the part of the idiotype that binds to the epitope.


text:
Kin selection Vs altruism (social biology)
I know that this is a contentious topic and I found conflicting explanations online which is what prompted me to put his question up. In some papers, Kin selection is mentioned based off the concept of inclusive fitness (sum of direct and indirect fitness). However, Kin selection is said to be an altruistic characteristic. That being said, altruistic genes only propagate through indirect selection (since an actor gives up its own fitness and do not generally reproduce). In that case, isn't Kin selection based off just indirect fitness and not inclusive fitness as a whole?
In a webpage, it is mentioned that "Kin selection is the evolutionary mechanism that selects for those behaviors that increase the inclusive fitness of the donor.". In that case, how can kin selection be altruistic? Can someone shed some light on what Kin selection is exactly? Also, a proper definition for indirect selection would be good as well. Thank you.

how can kin selection be altruistic?

Part of you confusion is purely semantic.
Kin selection cannot be altruistic. Kin selection is an evolutionary process. Altruism is a behaviour. Saying "kin selection is altruistic" is like saying "natural selection is flying" (when thinking of selection for flying abilities in, say, flying squirrels).
Altruism
Altruism is a behaviour in which increases another individual fitness at the expense of its own fitness. However, this definition lead to confusion of whether one is talking to lifetime fitness or only to a contribution to one's fitness that will eventually be returned. For this reason people talk about True Altruism and False Altruism
True Altruism
True altruism is a behaviour in which the actors's (the one performing the altruistic behaviour) life time fitness is decreased while the recipient (the one benefitting from the altruistic behaviour) is increased.
True Altruism can only evolve via kin selection (or group selection for the few who still view these two processes as different).
It is the indirect component of the inclusive fitness that selects for altruism indeed.
False Altruism
False altruism refers to cases where the actor performs the behaviour because he is expecting (not necessarily consciously) a return later in life. False altruism can be seen as an investment.
Such false altruism can be selected by natural selection (no need to consider indirect fitness). "Return on investment" can be caused by direct reciprocity or indirect reciprocity. In case of indirect reciprocity, some populations can use a system of reputation, where individuals are more likely to help individuals that they have seen being helpful to others before.
Game theory
All types of interaction between individuals can be modelled in game theory. One can also investigate specific type of strategy in response to a a specific game. For example, Tit-for-Tat is one type of strategy in a multiple encounter between two individuals game.


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What kind of creature is this?

I saw this on Facebook today and have tried researching it myself, but I have had no luck.

This actually looks like a Gaudy Sphinx caterpillar (Eumorpha labruscae). It only mimics the appearance of a snake!

You can find more information about this species here.

Range: Argentina north through Central America, Mexico, and the West Indies to Florida, Mississippi, South Texas, and Arizona. Strays to Missouri, southern Michigan, Pennsylvania, Maine, and southern Saskatchewan.

You can find more pictures here or videos here and here. Also the below gif (see whole video here) demonstrates the ability of this caterpillar to vibrate its tail end to -- as far as I can tell -- imitate a snake's rattle:

Below is a picture of an adult moth from UC Berkeley:

Wow that is freaking awesomeness!! That first pic is truly amazing. +1

@AliceD Right?!  Google "snake mimic caterpillar" to see some other really cool species!

Here is one of the cooler examples of snake mimicry! It even has a wiggling tail!!


text:
Optimal carbon dioxide concentration range for the human body
Previously I had thought the maximum concentration of  CO2 for human health to be given by the ‘Pettenkofer CO2 level’ with a maximum of 1000 ppm.
But according to this post

a growing body of research suggests CO2 levels as low as 1,000 ppm
  could cause health problems, even if exposure only lasts for a few
  hours.

Therefore it looks like a lower value than 1000 ppm would be healthier for the human body. Is that so?
What would be the target CO2 level inside a passive house? Since outside it is in the range 3-400 ppm. So with more ventillation we could get closer to 3-400ppm, which is Nature’s default (which shouldn’t be bad?)
Perhaps 750 ppm would be ideal — is there any research on that, either cognitive or related to blood vessels.

What suggests that any $\ce{CO_2}$ concentration is beneficial, let alone a concentration between $400\ \mathrm{ppm}$ and $1000\ \mathrm{ppm}$?

well, outside, in the nature, there is 3-400ppm.
AND:
that x>1000 is bad = Pettenkofer advise

Just cause something's in our natural habitat doesn't make it beneficial for us. We've evolved to tolerate starving and fighting too.

oh, hokay. Thanks :) good idea. but maybe this is not a well-researched topic, since I cannot find some exact facts, what would be the most healthy for the human-body.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7575229/  Little researched is a good comment in this time of hysteria.  It is known that the flora starts to die at 180ppm but finding the level the human body can tolerate is difficult.  I would GUESS that 500ppm would be the highest we should generate in order to level out the temperature differentials between the solar minimums and maximums.  We could allow the level to rise at the beginning of minimums like we are currently entering and lower it as we approach maximums.  Again I would guess guess 300ppm would be a satisfactory cooling level of atmospheric CO2.  The plant life would love a higher level and we would love a lower level.  We cannot live without the flora remember.  Both flora and fauna must be accommodated as we control the climate.  Weather cannot be controlled but we can do something about climate.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7575229/

Last time the volcanic action of the young earth brought it out of the snowball phase.    It's a balancing act between the two, flora and fauna.  I am GUESSING that the present level is acceptable and perhaps as high as 500ppm to help keep us warm during the Solar minimum phases of sun activity.  As low as three hundred during the maximums would surely be satisfactory as I would worry about the plant life if we take it any lower.   I doubt 1000ppm is the highest the human body could tolerate but perhaps you know of an authoritative source for that comment?  Climate control is interesting.

1000ppm has adverse health effects.https://www.nature.com/articles/s41893-019-0323-1.epdf?sharing_token=HEcz83zLgH4k3DMFFe7vp9RgN0jAjWel9jnR3ZoTv0Nmh56_6v6IG1wyUXiF6sNTHAt-0vDDZqKRyKQg__8_oxrm08uvJsMrDK8PUmvmArmz1HVHliC8Mpo0GJqILaz6LpL37FyuByZK0Mj9OreAXxduBL57CuuvxRjInYDsFqHubn5AHYm8XcGGeMzeIztQxbm3YUJS9Kiqx4m9QO2EcDdAmX7pTXsQa8hV-iVPEB4%3D&tracking_referrer=www.theguardian.com  Why would we want to approach that? Humans evolved over the past million years with a CO2 level around 300ppm. I think that's probably what our bodies are designed to function at.

The question isn't about "What's good for humankind broadly?" such as effects on flora, it's asking about the "human body" and inspiration for human animals specifically.

I figured controlling the climate for the comfort and better breeding conditions of the flora and the fauna was a good thing.  I don't really understand what else could be good for mankind.  As the planet thrives, so do we.  Higher CO2 benefits the flora and during minimums it benefits us.  The reverse is true during maximums and this offers us a way to tailor the climate for the benefit of everyone.  If we understand what we're doing controlling the level of Co2 is a good thing, No?  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7575229/

Your answer could be improved with additional supporting information. Please [edit] to add further details, such as citations or documentation, so that others can confirm that your answer is correct. You can find more information on how to write good answers in the help center.


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Are your finger muscles and tendons interconnected?
Are finger muscles and tendons interconnected? If they are interconnected, then if i exercise one finger will it train the other fingers since they are interconnected and share the same muscles in the forearm? (correct me if im wrong)
I have done some research but i cant find the answer for example(if your thumb joint is injured you should avoid using stress balls to exercise the other fingers, why?)

Welcome to SE Biology.  It is expected that you will demonstrate that you have done some research on your own before asking questions here.  For details, please check out the tour: https://biology.stackexchange.com/tour and then this help page on how to ask questions on this site: https://biology.stackexchange.com/help/how-to-ask.  ------ For example, have you tried searching for "hand anatomy muscles and tendons"?

That's a really interesting question!  What might help you the most is reviewing hand and forearm muscle anatomy.  I have some examples that could help.  The flexor digitorum profundus and flexor digitorum superficialis are hand muscles that originate in the forearm region.  At the wrist they split into four tendons (so FDP has 4, FDP has 4) one for each non-thumb finger.  They help make a fist.  Then there are the intrinsic hand muscles.  One interesting example is the lumbricals, which originate at the FDP tendon and have a very specific action.
To answer your question, I don't see any reason why exercising the four non-thumb fingers is recommended against, other than the possibility that you could be inadvertently moving/stressing the thumb.  I don't believe there is any connection between muscles of the thumb and non-thumb fingers, other than proximity of muscle/tendons.


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How Plausible is Restoration of Cryonically Preserved People?
I fear death (so much that I'll prefer a year/few of torture over death), and plan to sign up for cryonics. I would like to know how plausible it is, why the answer would be so, and if possible how many years away would revival be.
Thanks.
I have read a lot of articles on Alcor, and done several hours of research since yesterday. Mainstream Science seems to assign infinitesimal probabilities against, it, but the guys at Alcor (and other Cryonic institutes like Cryonics.org think they've got a case). It seems theoretically possible to me, but I don't want to but into too much hype—so how plausible is it?

Not even the "world's leading cryonics company" wants to give any kind of estimate. http://www.alcor.org/FAQs/faq01.html#patients

I've browsed their FAQs; I want information from a non biased source.

I think @skymningen's point is that if even the biased source isn't promising anything, the plausibility is vanishingly small.

You browsed their FAQ, was there any data? Have they accomplished a successful freeze/thaw? Do they have stability data? Safety data?

Vitrification of a Rabbit brain and devitrification was done, and the brain was successfully preserved in perfect condition (they didn't bother reviving it though.

Largely implausible, mainly due to damage from freezing. This type of damage even happens when food is frozen (although flash-freezing decreases it).
More feasible approaches for avoiding death would include machine-replacement parts, lab-grown transplants, neural backups, and regenerative gene modifications. I'm surprised no one has considered studying hibernation and how to add similar genes to humans that would enable hibernation.

They don't freeze people—they vitrify. Freezing damage doesn't happen. Downvoting for not bothering to acquaint yourself with the process before condemning it.


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Can mRNA be used by ribosomes more than once?
Can mRNA be used by ribosomes more than once? I mean can mRNA be translated more than one time? If not what will happen to it after translation?

Have you looked for an answer on your own?

Welcome to SE Biology. Before asking a question we expect you to have done some work yourself. This is a very basic question the answer to which you can find in Wikipedia or in the online editions of textbooks like Berg on NCBI Bookshelf.

There are a few cases in translation that I can think of where an mRNA is translated more than once: the closed loop model of mRNA translation, translation reinitiation, and translation by polysomes.
Closed-loop model
Here's an interesting paper to get you started: ncbi
Essentially, the theory is that mRNA can form a closed loop with the 3' end held to the 5' end by various factors. The ribosome assembles near the start, runs through the mRNA, translating the polypeptide sequence, then dissociates at the STOP codon. Since the "end" of the mRNA is near the "start" of the mRNA, the ribosome can reassemble soon after dissociation.
Translation reinitiation
See this.
The ribosome dissociates incompletely at the STOP codon, the small subunit keeps moving on the mRNA, then the large subunit reattaches at a downstream start site. This happens when the mRNA has multiple ORFs.
Polysomes
(See the wikipedia article on Polysomes for more details)
This basically means that you have a ribosome train moving along an mRNA. The same protein is being translated multiple times, but by different ribosomes. One really cool thing about this is that it's actually been observed by electron microscopy!

(source: bioninja.com.au)
To answer the 2nd part of your question...
wikipedia
mRNA gets degraded in a process called RNA interference (RNAi). Small interfering RNAs (siRNAs) are also transcribed that are incorporated into a ribonucleoprotein complex (RISC) that has an mRNA cleaving activity. The siRNAs are complementary to segments of mRNAs in order to give specificity to RISC.

You should not have answered this question but waited until the poster had shown some evidence of effort himself. As it happens your answer is unduly complicated for a novice and incorrect as regards RNA degradation.

I agree with everything @David said. I'd also add that translation reinitiation is not "reusing" the mRNA, it's simply translating multiple ORFs in succession. The closed loop model is interesting, but the authors say directly in the abstract that it's a part of polysome processing, which is the section you should have focused on. Additionally, as David said, this question should not have been answered. From How do I write a good answer? in the [help], Answer well-asked questions. Not all questions can or should be answered here.

Since you are new here, I strongly suggest you take the [tour] and carefully read through the entire [help] to learn more about the site, including what is on-topic and what is not.


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How can a drink contain 1.8 kcal energy while 0 g fat/carbs/protein?
How is it possible that the Red Bull Zero contains 0 gramms of fat, carbs and protein, but it still has 1.8 kcal of "energy".
I always thought that the human body can gain energy only from 3 kinds of nutrients: fat, carbs and protein. Is there a 4th kind? Or they just display an energy value that's not accessible to the body?

This is slightly off-topic, since it's very unlikely to be related to your question - but yes, humans can gain energy from many more things than just sugar, fat and protein; it's just that those three are dominant in the food we eat. One example would be alcohol (ethanol); we can also process polyols and organic acids. Even fiber, which is often considered empty (and useful, mind) filler can be partially digested for about 2 kcal/g - so a single gram of fiber would be enough for that energy value (while being both a carbohydrate and a (poly)sacharide, it's usually listed separately).

@Luaan Exactly, I wanted to mention ethanol too. It was a big surprise to me and I actually had asked a question to find out how is it possible.

@Luaan I thought that alcohol is a carbohydrate.

@CrouchingKitten Nope. It does have carbon, oxygen and hydrogen atoms in the molecule, but that doesn't mean it's a carbohydrate, just like fats aren't. Especially in food context, "carbohydrate" essentially means "sugar", usually including some non-sweet saccharides like cellulose (in your photo, that would be in "Kohlenhydrate" but not under "davon Zucker"). Really, alcohol is closer to fats than carbohydrates, but even that isn't really all that useful. It's not commonly included in either group.

@Luaan Thanks. So this means that the body can't convert it to glucose? So the only way the brain can make use of alcohol is if it's first converted to fat, and then to ketons?

@CrouchingKitten The body does convert it to fats (if you're well fed), but I don't think there's any specifics dealing with the brain - after all, ethanol goes through the blood-brain barrier with no trouble. It has long been thought that ethanol doesn't cause the well known CNS symptoms on its own - it's the intermediate products of ethanol metabolism that do, probably mostly acetaldehyde. Assuming this is true, ethanol must be metabolised in the brain (and thus provide energy, as outlined in Tomáš's link), since acetaldehyde doesn't cross the blood-brain barrier.

@CrouchingKitten I doubt anyone would recommend it as a food source for the brain, unlike sugars and ketons, though; for obvious reasons :)

The list of ingredients on the can mentions "Zuckerkulör," which is caramel colour, which can have 2 kcal/g, according to one producer.
Next, there is "Citronensäure," which is citric acid, which can, as other organic acids, have 2-3 kcal/g, according to this source.
There is also taurine, which is an amino acid-like compound, so it could, like proteins, have 4 kcal/g, but is, according to Taurine Metabolism in Man (Journal of Nutrition), poorly metabolized and probably has less than 0.2 kcal/g.
It is sometimes allowed, at least by U.S. Food and Drug Administration, to round the amounts of macronutrients (carbs, proteins, fats) smaller than 0.5 g per serving to zero, which is what they obviously did in this case, but they decided to keep the summary of calorie values of all ingredients exact.
It is usually said that only 3 types of nutrients contain energy: carbohydrates, proteins and fats.
Digestible carbohydrates (sugars and starch) provide 4 kcal/g. Undigestible, but fermentable, carbohydrates, such as soluble dietary fiber, sugar alcohols or polyols (maltitol, mannitol, sorbitol, xylitol, isomalt) and organic acids (citric, acetic acid, etc.), can provide 2 kcal/g of energy in average. On the other hand, some carbohydrates (such as "Sucralose" from the ingredient list) are neither digestible nor fermentable, so they do not provide any calories.
The "fourth" nutrient that can provide energy (7 kcal/g) is alcohol (ethanol), but is not considered a nutrient by some authors.
According to Food Label Accuracy of Common Snack Foods
 article (Obesity, 2014), the calories on the food labels should represent usable calories (metabolizable energy):

Of note, it is important to distinguish that food label calories
  actually represent metabolizable energy, which is total caloric
  content minus calories that are presumably not absorbed by the body
  and excreted as waste.

This article says that ~95% of ingested taurine is excreted. KEGG also says that taurine is not converted into any energy molecule in humans.

Could it be Zuckerkulör (caramel colour)? It's just caramelized sugar.

@AkselA -- answer should be edited to include your comment as that is almost certainly the answer. If not then it is that plus some of the other ingredients -- Aromen e.g. or anything else that constitutes a fraction of a caloric intake as, total, they only need to add up to <2 Calories.

This reminds me of a "zero calorie" recipe I once saw which involved ten squirts of cooking oil. Somebody had calculated the calorie count of one squirt, rounded to zero, and then multiplied that by ten...

@AkselA There's very little caramel colour and, also, I'm not sure it has much energy in it: it's essentially already been partially burnt.

@DavidRicherby: I don't think there's much energy in a couple of drops of caramel colour either, but then again we are only looking for a very small amount of energy.

@AkselA Oh, good point. I'd not noticed the actual numbers. Since the question is, essentially, "How is there more energy than I expected?", I didn't stop to think that "more than I expected" could still be "almost none."

@GeoffreyBrent Reminds me of how TicTacs have 0g of sugar per serving (1 mint), while they're probably mostly made of sugar.

@WYSIWYG, I checked that article and it really seems it is not taurine that provides calories.

@AkselA, it's quite likely that it is caramel colour and citric acid that provide calories.

@DavidRicherby: Why do you think all the sugar in the caramel is burnt? Ingredient design is an art nowadays. Listing sugar as an ingredient is actively avoided nowadays. Burning just 1% of the sugar and labeling the whole as "caramel colour" would be a sneaky way to put sugar in the recipe without explicitly listing it as such. And it's certainly a whole lot cheaper than putting in honey (another common "non-sugar" ingredient)

@MSalters 1kcal of sugar is a tiny tiny amount and not really detectable as sweet in a volume like this, so what you describe probably doesn't apply here.


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Is DNA from more parents (than two) better for the fitness of the offspring?
I'm designing a system (a computer system actually) and (a whole while ago) I spoke with a friend about it and he had this opinion:

If you combine DNA of more parents (than 2) it's better for the
  offspring.

It's a bit of a theoretical question but is this true?
I'm using genetic algorithms where you can choose the number of parents,
if this were to be true I'd take 4 parents, if not I'd stick to 2.
I saw here a question about the occurrence in nature but it remains unanswered.
(2 parents are easier - in this system - so maybe that's the reason it is not observed in nature)
About the system: it needs to produce 'fit' offspring (as fit as possible and as fast as possible), where fitness is measurable (this part is already covered...) and the most fit individuals in the population are selected to pair.
The only limitation set on this kind of systems is that the offspring has to have a chance to be fitter than the parents (so children are allowed to be less fit than parents (being it 4 or 2).
(Of course this lowers the importance of the question but still: does offspring of more than 2 parents have a higher chance to be fit? (my friend mentioned: the more diversity in the DNA the better...))
If you need more information about this bit I'll try to answer comments (if I do know the answer or can give more information about it).

Ignoring the complications that S Pr mentions in their answer below, this would totally depend on the individuals involved. If you could include the DNA from a distant relative (or no relative at all) to the DNA of two siblings, you could easily eliminate the risk of inbred deleterious homozygous recessive traits. However, if just two parents are distantly related and/or would not develop an embryo with deleterious traits, then it shouldn't matter a whole lot.

Can you create an answer with this? (I'd upvote it), also - if you'd like - we could use you in the chat room: https://chat.stackexchange.com/rooms/93100/offspring-from-more-than-2-parents

There are very many details to address in this question. I will try to keep it brief and keep the scope of your question in mind, which is rather narrow. I also think your friend is over-simplifying and misleading you, assuming he is honest about the explanation he gave you.
We are talking about sexual reproduction, correct? Firstly, with 3+ parents:

it's not obvious that you will have "more diversity" in the DNA, nor that
"more diverse" DNA will be a cause for increased fitness.
Additionally, it would take a whole lot of machinery and evolutionary happenstance at the cellular and molecular levels to recombine DNA from 3 or more parents to make a stable, recombined genome, and this itself may introduce more problems than solutions.
More so, you're implying that a sexual organism that requires mating between 3 or more individuals will be fitter than an organism born of fewer parents. This is subject to whether the gain in fitness of having more genetic parents will outweight the cost of maintaining such a system. This would certainly be dependent on the environment, the population, and all the nasty little details of life, such as how mate choice would work, whether a backup for 2-individual mating would exist, etc.

Remember that fitness is a probability of obtaining a number of offspring rather than the number of offspring. I think it is self-evident that the requirement for more parents, rather than less, lowers the probability (i.e. fitness).
This is quite a hypothetical discussion. In nature, for all its ever-experimenting and ever-diverging forms of life in the last 4 billion years, we find no organisms with more than 2 sexual parents. Take this as a sign that the natural occurrence of this kind of system is probably not favorable to survival and reproduction.
And I realize we could discuss this topic on many fronts (I have a few more ideas that I omit here), it's a rich question to digest.

excellent answer, would you like to digest this here or do you have a place that's better suited for this kind of discussions (I have quite some remarks as well and we seem to diverge on the meaning of 'fitness', so - from my part - further digestion would be most welcome :-D

If it's brief, ask here in the comments, otherwise you could make a chat room for it. I recommend making it public!

I created a room: https://chat.stackexchange.com/rooms/93100/offspring-from-more-than-2-parents let's digest :-D


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Improving DNA quality and yield from stool samples
I prepared genomic DNA from pig stools but the concentration was very low — about 3~4 ng/µl, when I measured it using nanodrop. The A260/A280 and A260/A230 values also did not come out very well (0.4~0.5 and 1.0, respectively). I also tried filtering the DNA two times but it didn't improve the quality. Does anyone have experience with DNA extraction from stool samples and suggest me how I can improve the quality and yield?

Expected photometric ratios for pure DNA are around 1.8 (A260/A280) and 2.0-2.2 (A260/A230). For reference, if you are extracting pure RNA, its ratio is ideally 2.0 (A260/A280).
Often, lower ratios usually indicate low purity due to contaminants or simply a very low amount of DNA.
EDTA, carbs and phenol among other chemicals all have absorbance at 230nm. If you used TRIzol reagent to extract DNA, you may also get some absorbance from this reagent at 270nm if you incorrectly pipetted some of the phenol phase (pink stuff) or the interface (white cloudy stuff between the aqueous phase and the pink phase). If you measure a low ratio, like you did, it probably means that in your final DNA extract, you seem to have (a) things that are not DNA in your solution, and/or (b) a very low concentration of DNA.
If you suspect you have enough DNA, you can purify to try to remove non-nucleic acids. However, with ratios that low, I suspect you should extract DNA from scratch; it does not appear that you have enough to rescue simply by purifying again.
Which method did you use to extract your DNA? What do you mean by filtering?

Oh I didn't use trizole reagent. I used a commercial kit. filtering means DNA binding and eluting at column tube during experiment.

You're using spin columns, I'm sure. They contain a silica resin that selectively binds DNA (RNA is also possible), by varying salt conditions. You pass the solution with your DNA by centrifuging, the DNA gets trapped on the resin, and then elute the bound DNA with a second pass of an elution buffer. It's quite a high-quality way of purifying DNA from a solution, in my hands it works better than TRIzol extractions. I have no idea how you obtain an aqueous solution workable with columns from pig stool. In principle, it should work well if the input is good enough. Sorry that's all I got!


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What is 'exhausted buffer' in gel electrophoresis?
For gel electrophoresis of DNA, we use TAE or TBE.
TAE buffer is cheaper than TBE but it has low buffering capacity; it exhausts faster than TBE buffer and there is a need to change the buffer during gel electrophoresis when electrophoresis longer.
but what is 'exhaused' in gel electrophoresis?

Do you have a source saying you need to change buffers during electrophoresis? I have never heard this and never seen any problems running gels longer.

Never heard of having to change the buffer during electrophoresis. When you turn down the voltage, you just throw it away. I would even think that replacing the buffer during the test, could produce errors and affect in a negative way the layers separated into the gel. Right now i do not have my labs notes under hand

OMG I heard about that where BRIC, Korean biologist community. ...I cannot believe there.

Then, what is 'exhausetd buffer' in gel electrophoresis?


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

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


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How to detect specific mRNA dsRNA by Northern analysis?

I silenced a gene by RNAi method, for that i chose the gene and the size of the gene is 1.5kb and my insert size is 500nts. i did the transfection and i want to confirm the silencing by northern analysis. when i did i got the ribosomal RNA instead of my specific mRNA reduction and dsRNA accumulation.
Total RNA was prepared with TRIzol reagent (Sigma), and 20 μg/lane was fractionated on a 1.2% agarose, 2.2 M formaldehyde gel. The RNA was visualized with ethidium bromide. The RNA was transferred to a nylon membrane (Hybond; Amersham Biosciences) for 14 hrs and probed with [α-32P] UTP-labeled used SSC for transfer and Prehybridization at 55 for 2hrs incubation, in the probe for 10hrs and Washing at 60 for 2X SSC 20 mins two times.

In this image you can the samples TET induced and uninduced RNA. but the result was confusing and am getting such a strong ribosomal RNA (2.2 Kb) contamination.

Did you try a dot blot or northern with your pure dsRNA to check if the probe is even working? You can use IVT to produce it. You can even use your plasmid as a proxy for dsRNA for dot blot. How big is the probe?

Not really a constructive comment but nowadays hardly anyone uses northern blot. qRTPCR is commonly used for quantification of RNA: it is fast, clean and sensitive.

Yes, i did IVT to synthesis my probe, its 500nts, in our lab we don't to qRTpcr, we believe in basic biology, i put my insert in tetracycline inducible plasmid..when i induce the cells with TET the dsRNA synthesis and it blocks mRNA production. my question is there any way to reduce the rRNA...if i reduce my rRNA i can get my mRNA specific band, any suggestion?

Since your probe is 500nt long, you can increase the hybridization temperature. You can increase the washes too. You can also check if your probe has any complementarity with rRNAs. If so, you may design a better probe. By dot blot, I meant doing a blot with pure RNA samples instead of total RNA. BTW, you may like and prefer to do northerns for whatever reason but don't justify by saying that it is "basic biology" as if qPCR is something that belongs somewhere else.

Thank you for your suggestion i will do that. sorry for that, I mean to say the qPCR enzymes are too costly as compare to alpha-UTP..

Hi, it does not have any complimentary to rRNA because when i designed the construct i did cross check with the whole genome of my organism of interest to check whether they have any off-target. It is fine. i do prehybridization on 55 degree now i am going to increase to 60 degrees. once i get the result i can update.


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Analysis over single chromosome data
I have no expertise in biology, I'm a data scientist, and I would like to know if it makes sense, from the biological point of view, to analyze data (SNP data) coming from a single chromosome, and not all 22 chromosomes, to predict the risk of a certain disease.
Should I obligatorily use data from all chromosomes? Why?
Thank you very much. And sorry if it is a very basic question, but I really would like to understand this.

You can analyse a single chromosome. All the bioinformatics tools I know, allow that. Consider only the reads that map to the desired chromosome (or any segment of the genome). However, most next-gen sequencing experiments sequence the whole genome and not just a single chromosome. You'll just end up losing information by not considering other chromosomes.

Ok, understood. So you are sying that it finally depends on the final objective of the analysis, right?
In my case, I want to analyse the data (dataset 1: lung cancer individuals, and dataset 2: type 2 diabetes individuals) to create a final prediction model. Also the idea is to perform feature selection and detect relevant/significant SNPs to later identify related genes and see if they are related with the disease or not.
So the ultimate question would be, for complex diseases like lung cancer and type 2 diabetes, should I analyse data from all chromosomes or only some?

Even though tools let the individual analysis of a single chromosome, is it biologically correct? Does it make sense from a biological point of view? Does it depend on the disease being analyzed?
I'm asking because biologists have told me that the conclusions of the analysis I'm doing, can olny come from the analysis of data from all chromosomes, but I would like to know the biological justification of this.
Hope I made my self clear. Thank you!

@mgvaldes it would not be a good idea to restrict yourself to one chromosome unless you have a good reason to do so (for example, X-linked genes). Biological justification for this is that complex traits are dependent on many genes that are scattered across different chromosomes.

Perfect. That's what I wanted to be sure of, since I'm not a biology expert. Thank you very much!

On top of @WYSIWYG's answer, suppose you want to analyze production of certain protein A produced by gene A on some chromosome A. Your data will be like say, luminosity/fluorescence values coming out of tagging this specific protein. But to predict this effect of production (on what period this values might be higher, like in a prediction model), the gene/factor that might be activating gene A might be on some other chromosome B. Until you know the activity of that, you will not be able to accurately predict the production of this.
In a Regression/Tree model, your $X's$ will be categorical/continuous showing the activity of effecting genes(B) while activity of gene A is dependent $Y$.
Hope this helps.

I'm concretly applying ML learning techniques to SNP data from all 22 chromosomes of two separate types of individuals (dataset 1: lung cancer, dataset 2: type 2 diabetes). The final idea is to create a predictive model for each use case and rely on feature selection techniques to identify relevant SNPs realted to the disease. Read the other comments I've given to @WYSIWYG's answer.


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What are the upper and lower sets of teeth are called?
I'd like to know the correct term for the a group of teeth in the skull and jax (mandible) Not the specific types of teeth i.e molars, incisors, carnassials, canines etc but what a set of teeth get referred to. the upper teeth.

Upper teeth: maxillary teeth
Lower teeth: mandibular teeth

The term, "maxillary", is given to teeth in the upper jaw and "mandibular" to those in the lower jaw.

If you search these terms you will find many references.
You can start with wikipedia which has many cross references.


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Do fat people have more chances of developing nitrogen bends?
I was reading some text on deep sea physiology. I got to know that solubility of nitrogen in fat is five times that in water. The exact text from the book animal physiology adaptation and environment by Knut Schmidt-Nielsen, was:-

The body fat, which in a normal lean male constitutes about 15% of body weight, dissolves about five times as much nitrogen per unit weight as does water

I think that having more body fat increases your body's nitrogen saturation capacity, thereby increasing the probability of nitrogen bends.
(Nitrogen bends or aeroembolism is the phenomenon in which nitrogen gas forms bubbles in the blood stream near joints and cause pain)
So can I conclude that fat people (those who have more body fat), are more likely to develop nitrogen bends in their blood stream?
I'd be grateful if anyone out there can help.

Well, you're right! First of all,

Nitrogen Bends or Decompression sickness (DCS) is a disease that arises as a consequence
  of bubbles forming within tissues. Inert gases, such as nitrogen
  and helium, enter the body through the lungs during inspiration.
Increased BMI (Body Mass Index) implies an increased fat content of the body. This
  increased body fat leads to increased nitrogen storage and hence
  possible excessive nitrogen bubble formation and thus increased the
  risk of development of DCS.

Learn more about the relation between Fat and Nitrogen Bends by reading Diving and Hyperbaric Medicine  Volume 36 No. 3 September 2006

Your Welcome, @Anonymous! Please read the link I've attached. It will surely answer your question with some more clarity.


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Photosynthesis: What Powers the Splitting of Water?
The splitting of water is an endergonic (non-spontaneous) reaction, and thus would require energy (chemical work to be done) in order to happen.
In Photosystem II, an enzyme catalyzes this splitting, but where does it get the energy from? Does it use ATP?

@jasonszhao An enzyme never powers a reaction on its own, it requires an energy source by non-spontaneous reactions. Which is usually ATP or NADH. By the current reaction the energy is coming from photons, but it is stored in multiple intermediers before getting near to the water molecule.

Catalysis is about reducing the free energy barrier (aka. activation energy) of a reaction, so it does not require any energy. In photolysis (e.g. splitting water) you get the energy from the absorbed photons.
The exact process is called the Joliot-Kok cycle:

Figure 1 - Joliot-Kok cycle - source

So the photon separates the charges on the P680, after that the activated P680 activates the Yz intermedier, which forces the enzyme to the next step (Sx) in the reaction.

2012 - Transmembrane Electric Potential Difference in the Protein–Pigment Complex of Photosystem 2
2006 - The Manganese-calcium oxide cluster of Photosystem II and its assimilation by the Cyanobacteria

The overall process comprises three types of reaction sequences: (a)
  light-induced charge separation leading to formation of the radical
  ion pair P680+QA(-) ; (b) reduction of plastoquinone to plastoquinol
  at the QB site via a two-step reaction sequence with QA(-) as
  reductant and (c) oxidative water splitting into O2 and four protons
  at a manganese-containing catalytic site via a four-step sequence
  driven by P680+ as oxidant and a redox active tyrosine YZ acting as
  mediator.

2007 - Photosystem II: structure and mechanism of the water:plastoquinone oxidoreductase.

So the process does not involve ATP or NAD or something like that just the "redox active tyrosine YZ". ATP and NADPH are created after the PS2 part of photosynthesis.

Figure 2 - Light-dependent reactions of photosynthesis - electron transport chain - source

The photolysis of water is about storing the energy coming from the photons (light) in ATP and NADPH. In the Calvin cycle the cells use the stored energy to reduce CO2 into carbohydrates. For instance glucose can be delivered to the cells in the root, which can use it as food.

@jasonszhao I think it's clear. It is catalysed by enzymes and powered by light.

Hmm we could connect PSII directly to a proton exchange membrane fuel cell, so we could convert light to electric current probably more efficiently than the current technologies.

The electrones which are generated from splitting water are later used to split CO2.
The general formula is:

The Photosystem II does the first part of the reaction by splitting up water and transferring electrons to plastoquinone and also by generating H+ ions. Water gets oxidized (spends electrons) in this reaction, CO2 in the end is reduced (receives electrons). 4 photons are needed for splitting 1 water molecule and 8 photons to liberate one molecule of oxygen. For green plants the energy for this reaction comes completely from light. In the process the energy of the electrons is also used to generate ATP, not to use it.
A more detailed view can be found in the schematic diagram "Z-scheme" in the Wikipedia page on photosynthesis:

The figure shows the flow of the electrons and the points when they are brought to higher energy levels by light. The energy of the light is then converted in a proton gradient which is then used to generate ATP.
Its also possible to exchange the role of the oxygen with sulphur, the energy source is then usually heat. This is done by sulphur reducing bacteria in the deep sea in the vicinity of black smokers.

@jasonszhao The difference between splitting and liberating are semantics. Chemically you use the energy of the light the split the water molecule in its parts.

Other two of them are describing very details and these are good answers.
Lights are the energy source, activating the enzymes to split $\ce{H_2O}$. When a chlorophyll in photosystem II reaction center absorbs light energy, an electron is released. This is the activated state energized by lights and has enough energy/ability to suck up electrons from $\ce{H_2O}$.
$\ce{2H_2O \rightarrow 4H^+ + 4e^- + O_2}$

Water oxidation chemistry of photosystem II
Light is indeed the energy required for the process to occur! The photosystem chlorophyll involved is P680. The light energy excites an electron to a higher level, and this electron is captured by pheophytin, forming P680+. The redox potential for P680+ is huge, 1.3V, and it becomes a very strong oxidizing agent, regenerating it's lost electron from water during the oxygen-evolving process. The electron that went to pheophytin ends up transferring to QA, then to QB (these are involved elsewhere).
So now, the P680+ oxidizes this redox-active tyrosine residue called Yz by taking an electron. This forces the Yz into a radical state Yz*. As the article goes on to provide, data showed the Yz hydroxyl group pKa to be greater than 9, meaning it should be protonated at physiological pH. As a result, in concert with the electron transfer outlined above, a proton is donated from Yz* to a nearby base: histidine 190. In this manner, Yz* is capable of quickly oxidizing the nearby tetranuclear manganese cluster. An oxygen-evolving complex is formed by Yz, Mn4, Ca, Cl, and a couple of additional amino acids. Yz oxidizes the manganese cluster resulting in transition states denoted S1-S4:

The heavily oxidized Mn cluster then oxidizes water to return to an S0 state, forming O2 as a part of the process.
The authors detail:

We propose
  that O–O bond formation occurs in the S4 state via nucleophilic
  attack on an electron-deficient MnV=O species by
  a Ca2-bound water molecule... O–O bond formation begins by bringing the second
  substrate water closer to the MnV=O in an SN2-like reaction
  (S4 state in figure 2). We propose that this occurs
  through contraction of the Mn–Cl bond upon formation
  of the high-valent MnV=O moiety.

In conclusion, we see light powers the reaction, but it is mediated by protein. The net reaction is an oxidation of a metalloenzyme complex which essentially rips the hydrogens off of water molecules to return to it's standard state. The article used for this answer was the best explanation, with a lot of details, that I could personally find, but it is from 2002. If someone has a more accurate explanation let me know!