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Enzyme kinetics; what happens at the peak of the Gibbs energy graph?

At the very peak, the energy is in a state of activation energy. Here, is the substrate just attaching to the enzyme, or is is substrate already breaking?

Look up transition state.

Enzymes are catalysts that lower a reactions activation energy (Ea), and thus increases the rate of the reaction. The diagram above is a Gibbs-Free energy landscape/pathway, where the top of the diagram is the transition state between the substrate and the product. Enzymes speed up chemical reactions by stabilising the transition state, and in effect, lowers the activation energy (Ea) required to transform the substrate into the product. The active site of enzymes are thus specifically 'designed' to be as energetically favourable as possible for the transition state.

To understand enzyme kinetics it could also be a good idea to look at (understand on a general level) the Arrhenius equation and reaction rate constants (k), to more completely understand what we mean by activation energy and reactions rate.
This whole topic is taught in basic biochemistry, and thus well described by many educational websites, all biochemistry text books, and even found in  educational youtube lectures (which is perfect for a basic understanding before you read more heavy theory). My earlier biology SE question Enzyme kinetics: recommended literature to grasp the concepts better also has some good book recommendations.
Following are also some webpages you can look at.
Khan Academy:

With the catalyst, the activation energy is lower than without. ...
That's because enzymes don't affect the free energy of the reactants
or products. Instead, enzymes lower the energy of the transition
state, an unstable state that products must pass through in order to
become reactant (...)

Chemistry LibreTexts: General transition state stabilisation is also a nice keyword that would give you a lot of information, e.g. from Chemistry LibreTexts:

Linus Pauling postulated long ago that the only thing that a catalyst
must do is bind the transition state more tightly than the substrate.
That this must be the case can be seen from the diagram (...)

Wikipedia: It could also be a good idea to generally read about catalysts, here from the wikipedia page where they use the classical example chymotrypsin and its oxyanion hole (active site that binds the substrate) that contains the Asp-His-Ser catalytic triad:

In the presence of chymotrypsin, (...), a nucleophile is used in the
form of the catalytic triad - Asp 102, His 57, Ser 195 side chains.
Moreover, the oxyanion hole, which consists of the backbone -NH-
groups of Gly 193 and Ser 195 of the enzyme, have the N-H groups
positioned in such a way that they will donate strong hydrogen bonds
to the substrate's C=O oxygen, given that the carbon atom is
tetrahedral as found in the transition state. This strains the bonds
of the trigonal planar C=O of the original substrate, helping the
reaction to proceed to the transition state. The hydrogen bonds also
stabilize the formal negative charge on the oxygen atoms. In this way,
the activation energy of the reaction is lowered and the rate of
reaction thus increases.


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Are there any half-evolved animals alive today?
I know that there are animals that are "simpler" than other animals but are there any that are half-evolved? Are there any animals with half-evolved functions, like arms, legs, etc?
This was part of the original question, but it was incorrect.

Saying that every species on the planet is "transitional" is an unacceptable answer because it only works on the assumption that macro-evolution is true.
Saying that all the transitional animals just died off also doesn't seem quite right. If all the previous transitional  animals just went extinct, then wouldn't we just have a few specialized species alive today? This wouldn't allow for the diversity we see today.

Evolution is a process which has no defined intermediate states and no endpoint. We are all constantly evolving...

Where and how do you define "half"?  Certainly you can find groups of species (e.g. ring species) in which neighboring species grade almost insensibly into one another and interbreed, but widely-separated ones are distinct, and don't interbreed.

If there were any living "half ape half humans" then you'd be asking why there aren't any "half that half humans".

I don't think this question should be closed. It's a legitimate question that simply comes from lack of knowledge in the field of evolution. I'm sure many people (wrongly) think about evolution in the same way. The question is otherwise fairly well written and to the point, and an answer that builds on the current comments will help inform the OP.

@Bryce Could you please clarify what you mean in your second paragraph? I don't follow how "no ultimate or final species" implies "macro-evolution is true".

Humans are half-ape / half-whatever-we'll-be-in-a-few-hundred-thousand-years. What does "half-evolved" mean? We only label things "transitional" (a relative term) as a convenience because they're partway between the origin and our current reference point. In the far future we'll just be identifying current species alive today as "transitional" as well.

Although the question displays some misunderstanding of evolution, it might be possible to reframe and instead think "Have we ever observed speciation in animals?" It's not really right to say "half-evolved" but the answer to that is yes, we have observed speciation, for example see this previous question/answer.

Take a look at the Monotremata that albeit being mammals show some sauropsid ("reptiles" + birds) features, the most characteristic perhaps that they lay eggs. They are most basal in the mammal tree and are thought to have been widespread but now comprise only three species.

I've heard one fairly well-known species described as half-ape, half-angel... :)

@theforestecologist you are actually correct. I am somewhat ignorant when it comes to evolution.

@Bryce and please know that I did not mean that in a negative or accusing way. You just can't know something until you learn it. Kudos to you for trying to learn :).

You can say that some thing is just half the way when you have a standard for it.  Like "the beaker is half filled" you can say this when you know the volume of the beaker and the volume of the water that you poured has just reached half the limit.  But in case of evolution we do not have any standard limit. It is not standardized that any given animal would evolve 'this much' or 'that much'  nor it is written that all animals should evolve into a standard super-animal. So thus we cannot say that something has just half evolved, while others are fully evolved.

I know that there are animals that are "simpler" than other animals but are there any that are half-evolved? Why aren't there living half ape and half humans?

Oh come on. You know if Australopithecines or Homo habilis still existed you would be asking "Why aren't there living half Homo habilis and half humans"? And when the other Great Apes go extinct you'll be wondering why there are no transitional forms between humans and monkeys. The answer to that question is, humans are apes; chimpanzees and we are pretty much as close as two species can be; we could have closer forms that survived but we could also have a much bigger gap between us and our closest relatives than we currently do. In other words, any ape is a valid example of something "half-human half-ape". It's like asking for a vehicle that's half-car, half-volvo.

Are there animals that are just starting to evolve arms and legs?

You mean, modifying fins into limbs in a general movement from water-living to land-living, like the first tetrapods are thought to have done? I like mudskippers.

Saying that every species on the planet is "transitional" because there are no ultimate or final species is an unacceptable answer because it only works on the assumption that macro-evolution is true.

Not quite, it is an explanation of what "macro-evolution" is and what things it predicts.
There are two aspects to the theory of evolution that are often confused; one is how it works to generate diversity and change in living organisms, and the other is how it works to adapt living organisms to their environment and create what we humans see as "design", "function". Both things are results of evolution, but the latter is much less important than we'd think, which leads people who explain evolution to de-emphasize it, which then leads people to be confused as to how it can happen at all.
The thing is, both "design" and "goals/purposes" are concepts that are meaningful in considering evolution, it's just that the words are dangerous because they imply an conscious intention that isn't there. You could replace "design" with "optimization"; random mutation combined with natural selection can form an optimizing process, i.e. a process that will over time generate forms that have specific properties. In the case of life, whatever properties promote the spread of the organism we're looking at.
As for "goal", that's just the physical fact of the world that some arrangements of matter have different effects from other arrangements of matter; meaning that if some arrangements of matter will lead organisms to reproduce better, the optimizing process of evolution will predictably lead to organisms having that arrangement of matter. So we can talk about, say, eyes being "designed" by evolution "for seeing"; the difference between that and a rock "being designed" "for having its shape" is that "seeing" (i.e. that organisms ancestors surviving and reproducing based on how well they interpreted light signals) had a causal influence on the organism's eye's structure.
So in that sense we can think there are "goals" in evolution; seeing, flying, swimming, breathing... and many lineages can be retrospectively seen as evolving "in the direction" of those goals. But the important thing is that those "goals" are completely dependent on the environment; as long as there's selective pressure for improved sight a lineage will evolve to have better eyes, but the second the selective pressure disappears or reverses, the lineage will evolve to maintain its current eyes or to lose them. And of course different lineages may have different selective pressures on them and "evolve in different directions". That's why there isn't a single overriding goal in evolution, just millions of lineages under different selective pressures that might change tomorrow.
That's why we can say every species is "transitional" (because they'll all be something different tomorrow, or not) and at the same time not be able to say transitional towards what (because the environment is complicated and we usually can't tell under what sustained selective pressure a given organism is under, and even if we could we couldn't be sure it remained the same over the next thousand or million years).
Having said that, when our human brains say "half-evolved" we often have specific goals and images in mind - like "halfway towards flight", "halfway towards eyes", "halfway towards limbs", "halfway towards dolphinhood". And there are plenty of "transitionals" by that definition - I brought up the mudskipper; there are also plenty of gliding animals, a plethora of eyes (or "eyes") at every point on the "good at seeing" continuum (more of a state space than a continuum really), aquatic mammals that may remind one of what the ancestors of cetaceans were like and might evolve to be more aquatic in the future...

Saying that all the transitional animals just died off also doesn't seem quite right. If all the previous transitional animals just went extinct, then wouldn't we just have a few specialized species alive today? This wouldn't allow for the diversity we see today.

Ah, but what diversity do we see today? What we observe in the fossil record is the constant extinction of some forms and diversification of others, that nevertheless remain more like each other in important ways than they were to their earlier aunts and uncles - meaning while at some point you might have forms A, B, and C, a million years later you have A1, A2, A3 and A4. To illustrate, the earliest tetrapods had a wide variety of number of digits on their limbs. Of course they all basically looked like fish. Most of those early tetrapods went extinct; the only line that survived had five digits. And millions of years later we have a stunning variety of organisms descended from that lineage, most of which look nothing like fish or each other, yet they all follow the same basic skeletal plan, down to the five digits. So which is more diverse?
Basically your question accurately describes the biosphere as the fossil record shows it, you just missed one thing: diversification. Meaning the "few specialized species" are actually a "few specialized families/orders/classes/phyla that themselves contain many species".
When thinking of evolutionary change it's better not to think of a line from A to B, but something like self-spawning fireworks. One group expands, a lot of its elements fizzling out but some of them spawning their own subgroups that expand in turn while still being recognizably part of the original group, and so on so forth with the fizzling of the most and spawning of the few, at some point the older groups might be so large and full of different subgroups that they start losing their definition, and basically at some point you realize the whole big mass of elements that now cover the sky includes both A and B, meaning if you roll back the tape you can certainly track how something that looked like A changed over time into something that looked like B, but it's really a very small part of the whole show.

Re "...animals that are just starting to evolve arms and legs", you might consider otters and seals as partly-evolved whales.  That is, they're at different points along the evolutionary path from a terrestrial animal with legs to a fully aquatic animal with fins.

source: Stack Exchange

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

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Why does Fallopia Japonica not cause issues in Japan to where it is native unlike other countries?
Fallopia Japonica (also known as Japanese Knotweed), is currently causing a huge issue in the English countryside where it was introduced. This is due to the fact that it spreads and grows rather quickly, its roots go roughly about 3m into the ground and are quite hard to dig up as there are so many of them interconnected and they are so firm. The only really absolute way of getting rid of them is chemical treatment for the soil which is obviously not so good for the environment nor that soil. This treatment is necessary due to the fact that even if one is to leave a very small amount of the root there, the plant is likely to still grow back quickly. All roots have to be fully removed for it to go.
However, in Japan, to where it is native, there is no such issue as there is in England and other countries where is it causing a mass problem.
This is probably due to the fact that the ecosystem is different and thus it will be balanced out and controlled by other plants in the ecosystem which aren't present here.
However, I have not yet come across proper research on this matter, so I was wondering if it is known why it isn't such a problem in Japan and how it is controlled and balanced out by what is naturally there, but isn't in the countries where it is causing an issue? Is there a specific plant which controls it? Perhaps an animal that eats it?

native herbivores that evolved to eat it + viruses & other pathogens that evolved to attack/infect it are present in Japan but likely not elsewhere. I can't imagine that Japanese Knotweed is any different from most invasive non-native species. You'd best do some research on invasive and non-native species in general.

Hi there is info out there. Try these 2 links to start with and there will be references to follow from these
Regards Jo http://www2.le.ac.uk/departments/genetics/people/bailey/res/hab
http://www.cabi.org/Uploads/CABI/Japanese%20Knotweed%20Alliance/Info%20pack.pdf

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


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What are the effects on hearing of in ear headphones?
I have been told many times by my teachers and grandparents that using in ear headphones will ruin my hearing, but I was unsure of these claims. So of course I turned to stack exchange to help me.
So really I'd like to know the effect on hearing from frequent earphone use (particularly as I listen to quite a lot of loud rock music)?
Thanks.

The main effect on hearing is the volume of the sound. Both the intensity and duration matter. However, it seems like hearing loss from personal music players is not as prevalent as from other causes like gunfire or occupational noise exposure (see also here).
The specific problem with in-ear headphones is people tend to listen to them louder than other types of headphones, here is an example study that shows this result.
So, in summary, there isn't anything wrong with in-ear headphones if you listen at a low volume, but be wary that peoples' tendency is to listen louder with in-ear headphones, and you already mentioned liking loud music. The volume is going to be your problem.
Be very wary with your hearing though: once you have lost hearing, there is no way to get it back at this time. Hearing aids only temporarily compensate for the loss. You might be okay now but regret a lifetime of noise exposure by the time you are an older adult.
References:
Clark, W. W. (1991). Noise exposure from leisure activities: a review. The Journal of the Acoustical Society of America, 90(1), 175-181.
Hodgetts, W. E., Rieger, J. M., & Szarko, R. A. (2007). The effects of listening environment and earphone style on preferred listening levels of normal hearing adults using an MP3 player. Ear and hearing, 28(3), 290-297.
Mostafapour, S. P., Lahargoue, K., & Gates, G. A. (1998). Noise‐induced hearing loss in young adults: The role of personal listening devices and other sources of leisure noise. The Laryngoscope, 108(12), 1832-1839.

why this answer is not pinned to the billboards, streets, whole internet and TV's? We need to shout out this to all.


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Why has malaria only now started to develop resistance against artemisinin?
Why has malaria only now started to develop resistance against artemisinin, considering the compound has been in use for about two millennia in its herbal form in China?
The WHO has reported:

In recent years, parasite resistance to artemisinins has been detected in four countries of the Greater Mekong subregion: Cambodia, Myanmar, Thailand and Viet Nam.

However, the compound artemisinin has been used in its herbal form since at least around 400AD, when it was documented in the well known medical text 肘后方.
What are some reasons that malaria has only begun developing resistance now?
I would imagine that modern artemisinin would be more effective in completely eliminating malaria, as compared to use in its traditional herbal form. This means semi-resistant strains would more likely be killed before they are able to spread or develop resistance any further.

(archived WHO report)

The second source references a blog, which I would not consider a reliable source. However, I have read the actually text here, where the relevant page can be found in page 42 of the pdf. The book itself is quite well known, and its age is not disputed as far as I am aware. I had to post this link in the comments since I don't have enough internet points to include a third link in my post.

Selection pressure (1, 2). One way or the other, there were few enough people taking the drug that it didn't really "matter" to P. falciparum (the deadliest of the malaria-causing parasites) on a population level until recently.
According to the 2014 paper
Spread of Artemisinin Resistance in Plasmodium falciparum Malaria (3), the driver of Artemisinin resistance is a single point mutation (ie a change of a single DNA base pair) in a single gene. The thing to keep in mind is that these single nucleotide mutations happen all the time. You yourself most likely have 3 or 4 of them relative to your parent's genomes. Thus, this particular Artemisinin resistance mutation probably has occurred in the past.
However, as with most drug resistance mutations there is likely some fitness cost paid by the individual in which this mutation occurs. In environments without the drug, wild-type (ie non-mutant) parasites will outcompete the mutants, and the mutation will quickly disappear from the parasite population. It is only when the drug becomes commonplace that the mutant parasites gain the upper hand and the mutation spreads.

Thank you for the answer, it seems a very likely hypothesis. I've given this some thought since as well, would it also be possible that artemisia annua (the 'herbal' form) contains additional active ingredients which also combat the parasite, such that the development of artemisinin resistance provides it no survival/selective advantage? I should clarify that I am suggesting this not as fact but as hypothesis-to-be-tested, since it is starting to sound a little alternative-natural-remedy-ish.


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What bird is this?
Not very good pictures, but saw  this bird I have never seen before out my window
Location: Salem, Oregon, USA

Welcome to Biology Stack Exchange. It would help to have information on where the bird was seen (i.e., what country / state / province), and what the surrounding habitat is like (i.e., rural / urban / wooded / etc.)

Seen in Salem,OR surrounding is urban right in the city.

It's probably a type of heron, thought it's probably going to be difficult to identify definitively with those pictures.

Looks like a great blue heron, but the markings aren't clear enough to be certain. The black cap, shoulders, etc. are good matches.

I agree with @anongoodnurse. Could you tell us a bit about the general area you live and it might narrow things down.

Although the picture is blurry, this almost certainly is a great blue heron (Ardea herodias).

 © Helen Pine, FL, March 2008 (Left)       © Brian Guest, FL, March 2009 (Right)
The coloration and size are what give it away. From All About Birds:

Size: Largest of the North American herons. 97–137 cm long, 167–201 cm wingspan, and weighing 2100–2500 g (up to 6 lbs).
Color: Appear blue-gray from a distance; white in the face with a wide black stripe over the eye.

In flight, the upper side of the wing is two-toned: pale on the forewing and darker on the flight feathers.

That white spot on it's lower neck? That's their built in napkin:

specialized feathers on their chest that continually grow and fray. The herons comb this “powder down” with a fringed claw on their middle toes, using the down like a washcloth to remove fish slime and other oils from their feathers as they preen

Range: The heron is common across much of the US, including as a year-round inhabitant across Oregon.

 Source: All About Birds

Ecology: The heron typically feeds on fish and spend much of its time in marshes, along streams/lakes, or near other bodies of water. I would guess you have a body of water or swampy/marshy area somewhat nearby where you saw this specimen.
How to distinguish from other (seemingly) similar species?

The Great Blue Heron’s massive size and white in the face separates it from other dark herons such as Little Blue Heron and Tricolored Heron. Sandhill Cranes are more uniformly gray, and adult Sandhills have a vivid red crown. In flight, a Sandhill Crane keeps its neck outstretched and flies with snappy wingbeats, flicking its wings quickly upward. Great Blue Herons fly with their heads pulled back against their shoulders and have smooth, deliberate wingbeats, barely raising their wings above horizontal. Sandhill Cranes are less widespread than Great Blue Herons and are typically seen in flocks. Great Blue Herons travel solo, except if you catch them during migration when you might see up to 10 together. [Source].


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What is this small tree?
I found a dozen of these small trees in a local park that is just an overgrown homestead.  The leaves look something like an elder but the flower clusters surrounded by white, four petaled false flowers are completely unknown to me. What species is this?

Location:  Shenandoah valley in central Virginia, U.S.A.

Sandy soil on inside of a sharp curve of the South River,
just above the flood plain.
This area has been occupied by people, for a couple hundred years,
so this could very well be a cultivated plant.

Please add your location. Most species IDs require knowledge of the general location(e.g., country, region, state, etc.) and preferably info about the surrounding habitat. Thanks.

The location is the Shenandoah valley in central Virginia, U.S.A., sandy soil in side a sharp curve of the South River, just above the flood plain.  This area has been occupied by people, for a couple hundred years, so this could very well be an escaped garden plant.

Brilliant photographs with focusing details.

This is very likely some species of Viburnum.
Viburnum is a genus of about 150–175 species of shrubs in the Adoxaceae family that are primarilly native throughout the temperate Northern Hemisphere.
All species of viburnum (as far as I know) have opposite leaves, as does the specimen in the picture.
Many species of Viburnums bloom in white in the last part of April through early May, and typically you have to pay attention to flower shape and often, more importantly, the leaf shape to differentiate species.
Without location information, an exact species ID is not guaranteed, but your specimen looks very similar to:
Doublefile Viburnum (Viburnum plicatum)

 Source: Dave's Garden

 Source: Missouri Botanical Garden
This species produces two rows of white flower clusters, with both small and large flowers, along the stem.
According to Wikipedia: Viburnum plicatum is a popular ornamental plant, both in its native area and in various temperate regions.
Based on the "double" flower types of your specimen, it's likely V. plicatum f. tomentosum:

Cultivars with wild-type flowerhead structure are sometimes described as a separate botanical form V. plicatum f. tomentosum. They include 'Cascade', 'Lanarth' and 'Rowallane'.2[3] Two cultivars in this group, 'Mariesii'[5] and 'Pink Beauty',[6] have gained the Royal Horticultural Society's Award of Garden Merit.

Habit: A deciduous, multi-stemmed medium-sized shrub that typically reaches 2.5 3 m tall. [Source].
Leaf: ovate, 5-10 cm long, up to 5 cm wide; pointed apex and rounded leaf base; serrated leaf margin; 8 to 12 pairs of veins; pubescent underside; dark green leaf color. [Source].
Flowers: individual flowers form a large (up to 10 cm diameter) flat-topped cyme composed of showy infertile flowers surrounding unshowy fertile flowers. Blooms in May. [Source].

Viburnum is absolutely right. Without location, species will be difficult. And as it is a park, it is probably a cultivar anyway.

@RHA Right. Which is why I picked a common cultivar as the best guess :p. Of course it couldn't be easy and just be one of the ones i know well (rafinesquianum, acerfolium, prunifolium, rufidulum, etc), but for doing a 5 min search without location info, I'd say this is a pretty good guess at species!

It also isn't any European species I know. I am guessing this is an American/Canadian location.


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Elements that make action potential to conduct quicker?
The texts, online materials describe the velocity of conduction of action potential depends on axon's length and cross sectional area e.g. short length and large diameter decreases the resistance. Myelin sheath increases the speed of conductivity as well.

Can someone explain why chemical synapses allow quicker conduction than regular arrangement of sodium fast channels along the axon? Can regular arrangement of Na channels help in propagation of AP (I guess it's referring to the nodes of Ranvier)? What's the difference between fast sodium channel and a 'normal' sodium channel?
The question is: Of the following, which allows action potentials to conduct quicker?
1. Chemical synapses
2. Regular arrangement of sodium fast channels along the axon
3. Small axon diameter
4. Depolarisation suppression through the majority of the axon's length
I picked 2, but the answer is 1. I want to know the reason behind me being wrong and that being correct. 1 doesn't make sense at all to me. Come to think of it, I see that 4 could be the most relevant.

"Can someone explain why chemical synapses allow quicker conduction than regular arrangement of sodium fast channels along the axon?" - This part of your question doesn't make any sense to me. Chemical synapses are for communication between cells. Do you mean nodes of Ranvier and saltatory conduction?

Also what do you mean by "an regularity or irregularity help in propagation of AP"? As far as fast vs "normal" sodium channels...I don't know what you mean there either. Different voltage gated channels can have slightly different speeds, but in general all voltage gated sodium channels are pretty fast. At the level you are learning at there is no reason to distinguish between faster and slower sodium channels, unless you talk about hypotheticals like "what would happen if sodium channels were faster/slower?"

@BryanKrause that's precisely my confusion as well. This was a test paper question not homework. Let me type the question exactly as it is, perhaps you may get a better grasp of the context than I do. Also not a duplicate at all. Because I am really not concern about the myelinated or unmyelinated factor of the axon. It is obvious which is stated in my question. I added the image from wiki (which just happened to be referring to saltatory conduction), I am eager to know the general, main concept of AP conduction on any neuron.

1 is definitely wrong, it is a nonsense answer in this context - your confusion is understandable. None of those answers make much sense to me actually...2 is the closest, but that's not what allows an action potential to conduct "quicker" it's what allows it to conduct "at all."

My only guess as to why (1) is supposed to be correct is that an electrical synapse would make an axon electrotonically longer (this is a bit hand wavy in my mind). But honestly, your Prof did a terrible job writing that question.

Agreed, the question asks about action potentials, strictly speaking, chemical synapses have nothing to do with "conduction" of action potentials, only the transfer of information (initiation/suppression of AP's in the postsynaptic cell). 4. i.e. myelination looks the most likely to me to.

@OliverHouston and the rest here, could you please clarify this a bit?depolarisation suppression through.... I understand the basic concept of how myelinated sheath supports the AP propagation. However I do not get the suppression bit. So for my own learning and knowledge, if you could elaborate or point to a comprehensible resource (to 1st year Bio level) : that would be great.

Basically, the myelin sheath prevents AP's in coated areas, as there's no sodium channels. Therefore action potentials only occur at the nodes of ranvier... Ions diffuse along the axon from one node to the next, depolarising the next node of ranvier enough to trigger an AP, more sodium floods in and diffuses along and so on. It's not well covered, the wikipedia description is OK, but the idea of hopping? I think it's a bit outdated and oversimplified by professors.

@OliverHouston a lot of articles is referring to Depolarisation induced suppression. After this discussion and thanks to you all, as a take away I want to understand depolarisation suppression. Perhaps the jargon is strangling me a little.

@DevonRyan I really wish it was my Prof who wrote it. It is from a national test paper... actually international - sample revision paper. I shall take the rest of the 120 questions with a pinch of salt...

One note about "depolarisation suppression" is that it's not even correct. You don't need depolarisation, you just need current moving (e.g., a chloride shunt) to change the electrotonic structure.

@bonCodigo Eek, good luck with that then!


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How do B and T cells work incorrectly in a person with Systemic Lupus Erythematosus?
Systemic lupus erythematosus is an autoimmune disease in which the body's immune system attacks healthy cells. How exactly do B and T cells attack these cells they mistake for pathogens?

The initial trigger for the disease is unknown and can be different from person to person. However, we do know that there can be environmental or infectious triggers that are further potentiated by genetic and hormonal factors.
The pathology of SLE is associated with the development of "auto-antibodies" or "anti-nuclear antibodies," so saying that B cells and T cells attack healthy cells is not exactly correct - More accurately they produce antibodies against proteins on healthy cells, which form immune complexes, activate complement and induce apoptosis.  To produce auto-antibodies, events occur as follows:

The trigger causes macrophages or antigen-presenting cells (APCs) to display self- or auto-antigens
APCs recruit B cells to start producing antibodies against the antigen
APCs activate T helper cells, which stimulate inflammation and perpetually activate the B cells to produce auto-antibodies

The following immune abnormalities are associated with SLE (particular focus on B cells and T cells)

High levels of circulating B cells
Decreased levels of T suppressor cells, which would otherwise regulate the immune system and auto-antibody production
Abnormal B cell signalling and persistent activation of B cells (IL-6, IL-10)
Prolonged life span of B cells, possibly due to poor immunoregulation (#2)

Reference:
Schur PH, Hahn BH, Pisetsky DS, Ramirez Curtis M. Epidemiology and pathogenesis of systemic lupus erythematosus. Up to date. Topic last updated: Feb 5 2016. Subscription access only.


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What are preparation mistakes that could make red blood cells appear crenate in isotonic solution?
Thank you for your time. I separated red blood cells from a whole blood sample purchased from a blood bank. In isotonic solution, the red cells appear crenate. I would like to know if there is anything wrong with my procedure. I used the following controls:

I purchased two samples which came from two different donors. Both samples are more than 48 hours old.
I used three different solutions to spin the blood including RMPI 1640, saline solution, and phosphate buffered saline. I used multiple solutions because the RMPI is past the expiration date.
I spun one sample at high speed and the other sample at low speed.
The first sample was delivered at room temperature, it was not on ice. The second sample was on ice. I believe the buffers and the blood sample were roughly the same temperature when I spun them.
I mixed the buffer solution with the RBCs by gently rocking the test tubes back and forth.
Thinking that the problem may be when I preparing slides, I cut the tip of the pipette in case pressure was disturbing them.
I used both refrigerator and room temperature isotonic solution when preparing the slides.
I use a spacer in the slides with double sided tape and I seal it with nail polish. I'm not sure if that should matter.

If you have any ideas as to why the RBCs look like burr cells in isotonic solution, I'd greatly appreciate it if you'd share them with me. Thank you!

Oh, the anticoagulant was EDTA.


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What is this plant which looks like "marjoram"?
Place is India.
We are confused about the identity of this indoor plant. My friend is saying plectranthus, possibly barbatus.
I am saying it is marjoram.
Which is correct name for this plant?

It resembles very closely to Marjoram.

This does not look like Marjoram! Marjoram does not have denticulate leaves! Plectranthus sp. has, though. It does not  appear to be P. barbatus either since it has some kind of structures on the leaves that are not visible in your image. Could be another species of the genus ... Please do not consume unless you are sure what it is.

Apparently looks like Coleus aromaticus


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At what temporal scales do forest structures change?
At which time scales do forest stand characteristics (i.e. stand density, species composition, & diameter distributions) change in a temperate European forest which is not managed?
Ideally, I'd like to conclude if a certain quantitative description (based on the variables I've mentioned above) of a forest stand is valid for e.g. 10 years or even 20 years.
A peer-reviewed reference would be ideal.

This question is too broad. What type of temperate forest?

The European Environment Agency recognized dozens of temperate forest types:
 Acidophilous oak and oak‑birch forest types
 Mesophytic deciduous forest types
 Beech forest types
 Mountainous beech forest types
 Broadleaved evergreen forest types
 Floodplain forest types
 Non‑riverine alder, birch or aspen forest types

Community types will experience different patterns and rates of change based on numerous properties including climate, edaphic conditions, stand density, species pools, specific species characteristics, land use history, etc.

See Wright & Fridley (2010)
-Rate at which woody species colonize and dominate old fields decreases significantly with latitude.

Rates of woody succession were highly correlated with both annual temperature...and measures of soil fertility

See Fridley & Wright (2012)

suggest that climate plays a relatively minor role in community dynamics at the onset of secondary succession, and that site edaphic conditions are a stronger determinant of the rate at which ecosystems develop to a woody-dominated state.

See Peet & Christensen (1980)

Examined thinning rates based on initial stand densities -- found rates to be higher in denser stands and later densities became similar regardless of initial density (after 40 years).

Further compounding all of this are issues such as invasive species, shifts in herbivore pressure, plant pathogens/pests, etc.
Also, it's hard to find European forests w/out some type of historical major human influence.

From Parviainen 2005:

Latest estimates show that there are about 0.3 million ha of virgin forest (0.4 % of the total forest area) left in strict forest reserves and other protection areas in the temperate zone of Europe.

So given all of that, it's hard to definitively nail down specifics to answer your question.

Each of these above characteristics/variables/issues will influence both individual growth rates (i.e., tree diameter and height) as well as population and community dynamics.

To answer your question a little more directly:

As shown in the paper linked above (Peet & Christensen 1980), stand density rates vary dramatically based on initial stand densities and succesional stage; high-density stands can see HUGE loss of stems/ha in < 40 years, while low-density sites might see very little change.

Diameter distributions can change drastically, but will likely take multiple decades to shift to the "late-succesisonal reverse j". However, this is strongly dependent on frequency and magnitude of disturbances -- large canopy-clearing disturbances such as major wind events will accelerate this shift in distribution.

Species composition can certainly shift fairly quickly (1 or 2 decades), but typically only in transitional stages of succession or due to major disturbance. Late-stage successional forests (i.e., "mature forests") will typically see very little change in species composition in this time frame, but again so many facotrs will influence that. Because of changing climates, mass introductions of invasive species (both competitors and pathogens), etc., forests appear to be changing more rapidly. [See Israel (2011)].

Overall, forests change continuously, with most processes occurring on the time-scale of decades. However, this depends on scope b/c understory plants can change from year to year, while canopy trees can live for centuries. Noticeable shifts in community composition and biomass are visible on decadal timescales, but only long-term evaluation will demonstrate the effects of past disturbances. The takeaway, then, is that forests chnage on multiple time scales and as a result of many variables; as a rsult, one can never consider a forest as a static community or as a climax type.

However, we have more long-term data sets available and numerous advances in sampling methods that are aiding our ability to understand forest change across time scales. So we are just now beginning to truly understand some of the phenomena on a deeper level.

I'd recommend you start with an overview of the topic:

van der Maarel & Franklin (2013) should provide a number of citations for you to follow:

covers the composition, structure, ecology, dynamics, diversity, biotic interactions and distribution of plant communities, with an emphasis on functional adaptations;
reviews modern developments in vegetation ecology in a historical perspective;
presents a coherent view on vegetation ecology while integrating population ecology, dispersal biology, soil biology,
ecosystem ecology and global change studies;

Citations
 - Fridley, Jason D., and Justin P. Wright. 2012. “Drivers of Secondary Succession Rates across Temperate Latitudes of the Eastern USA: Climate, Soils, and Species Pools.” Oecologia 168 (4): 1069–77. doi:10.1007/s00442-011-2152-4.
 - Israel, Kimberly A. 2011. Vegetation change in Duke Forest, 1977 – 2010. University of North Carolina at Chapel Hill Masters Thesis. 120 pp.
 - Parviainen, J. (2005). Virgin and natural forests in the temperate zone of Europe. Forest Snow and Landscape Research, 79(1-2), 9-18.
 - Peet, Robert K., and Norman L. Christensen. 1980. “Succession: A Population Process.” Vegetatio 43 (1): 131–40.
 - van der Maarel, E. & J. Franklin. 2013. Vegetation Ecology, 2nd Edition. Oxford University Press, New York, New York. Pages 28-70.
 - Wright, Justin P., and Jason D. Fridley. 2010. “Biogeographic Synthesis of Secondary Succession Rates in Eastern North America.” Journal of Biogeography 37 (8): 1584–96. doi:10.1111/j.1365-2699.2010.02298.x.

Thank you, this is definitely helpful! I know that the question is broad, but I searched in a more specific direction and did not find any literature, hence I tried for a broader approach.

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


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What is this small tissue structure found in kidney?
It's covered with white adipose tissue and it is smooth with reddish brown colour. HE dyed with dimensions 3 cm long and 1 cm wide. I'm guessing that this is a rare thing because I already checked pubmed etc. On the right is a closer picture of the tissue.

Voted to close because this sounds like a homework question - I don't think there would be another reason to ask this question unless you are a student - if you clarify otherwise I would consider retracting my vote. We aren't here to do your homework for you, I'm guessing if this was given as an assignment then part of your lesson was on this structure specifically.

You added that it is rare - what if it is actually very very normal? (where did you get the images from?)

Could you add a pointer?

@SanjuktaGhosh It's the whole structure. The entire pink-tinted area on the top picture. (it's actually quite obvious I just don't want to give the OP the answer if this is homework...)

I can't find anything abnormal. Had a histology course recently so I'm curious if there's something I can't spot. @BryanKrause

@SanjuktaGhosh That's because it's not abnormal.

It's the whole structure and this is not a homework. I saw this on webmicroscope and got really interested. I have been looking kidney histology articles and books and I have hard time figuring out what are these since i'm not studying medicine. Smooth structure made me think it could be multilocular cyst but i'm not sure and the sice of these is huge in kidneys.

Ok...hint: it's a gland. (and it's very normal to have these particular glands on your kidneys..)

@BryanKrause this is interesting. Suprarenal? aldosterone, cortisol etc...

Okey so they must be adrenal glands then. Why did I even think that these would have something to do with diseases...

@KatariinaJ. Bingo. If it makes you feel better, your description at the start was so spot on I assumed it was from a textbook question. If you read about adrenal glands they are often described precisely as being found under adipose tissue on top of the kidneys. The best identifying feature besides the location is the clear separation of tissue type into adrenal cortex and medulla, which are also quite distinct in function.

Thank you for helping me figure out this one with hints. This made me learn a lot. I was assuming way too many things.

@BryanKrause Please post an answer!

@canadianer Done. I like these IDs better than species IDs, those are too hard for me :-P

@BryanKrause Thanks +1. I do too. Wish there were more of them

This is a slice of an adrenal gland:

Source (Creative Commons Attribution-Noncommercial-Share Alike 3.0 License): http://histology.medicine.umich.edu/resources/endocrine-system
These glands sit on top of the kidneys, typically under adipose tissue (which can also be seen in both your image and the image I included here). The most identifying feature of the adrenal gland is its clear separation into two parts: the outer "cortex" and inner "medulla", as labeled on the image.
The two parts have different endocrine functions: the cortex primarily produces steroid hormones, like aldosterone and cortisol, whereas the medulla makes catecholamines epinephrine and norepinephrine (also called adrenaline and noradrenaline). I believe the inset in your image is of the medulla.


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What is a unitary post synaptic potential?
I am reading the paper Cooperative subnetworks of molecularly similar interneurons in mouse neocortex and have encountered the term:
"Unitary (excitatory or inhibitory) post synaptic potential".
I know what is an excitatory (or inhibitory) post synaptic potential.
But what does the unitary refers to?
Thanks!

Unitary EPSPs is the EPSP contributed by a single presynaptic fibre.

Does it mean a single synapse?

No, it means a single presynaptic fibre (which can make several synapses with a postsynaptic fibre).


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How does one confirm the discovery of a new species of plant/animal
Hearing from the National Geographic and the news about the discoveries of new species of plants/animals, I was wondering how can a person confirm when they have actually discovered a new species of plant or animal?
How can they identify with enough certainty that it is not one of the species that has been previously discovered (out of the umpteen varieties of species)? Is there some kind of official/international database of species for plants/animals they typically look up to to confirm it? Also, how is the process of naming of a new species decided and why does it end up being a Latin name?

Basically, you have to examine as much of the relevant 'material' (preserved museum specimens) of the proposed new species and its closest relatives, and compare the diagnostic characters of your proposed new species versus those of its presumed closest relatives to confirm it is actually distinct. For example, with snakes (my field), we use counts of head and body scales, relative distances between features, relative length of tail, hemipene morphology, and even colouration, to determine species.
When combined with genetic evidence of monophyly of the new species and adequate divergence from closest relatives, it becomes a very robust species description.
Finally, names can be accepted or rejected by the ICZN based on existing names for proposed species, though it's a very confusing mess for most groups. I'd recommend checking out their website for more in-depth guidelines

Tried searching a sample  "Galleria mellonella" in ICNZ in the search bar but didn't find anything there

or are there other mayor international organizations that list the Latin names of plants / animals?

these will be relevent https://biology.stackexchange.com/questions/52990/where-can-i-get-a-file-list-of-the-common-and-scientific-names-of-species and https://biology.stackexchange.com/questions/14059/is-there-a-downloadable-list-of-all-species-along-with-their-traditional-classif Tree of Life web project is decent.


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How do we know which Eulerian path corresponds to the DNA sequence?
Bioinformatics textbooks explain one method to reconstruct the whole DNA
sequence from multiple reads. The method builds a graph and finds a Eulerian path in it. The Eulerian path corresponds to a DNA sequence.
However, the graph can contain more than one path. How do we know which path corresponds to the actual sequence?

If the DNA sequence contains repetative elements, and your reads are not long enough to resolve them, you won't know if you have the right path.  Usually you split your results into contiguous regions whose sequence you are confident in.


text:
Can someone please identify this plant?
Photo taken April 27 in Savannah Georgia

Do you know anything about the flowers?

I'm not sure that it has flowers, I think it might just be a leafy shrub. That's why I'm having such a hard time figuring out what it is. :(

It looks a lot like a Muehlenbeckia species to me. More commonly known as the Australian Wire Vine.

@MrG That looks exactly right! Thank you so much!!


text:
What would be the difference if I use the Web server instead of dedicated server for protein modeling and docking?
We know that software tools like I-tasser etc have a web server and a standalone option too. Is there any difference to protein C-scores or efficiency or accuracy if you do it on standalone instead of web server?
What would be the difference if I use the Web server instead of dedicated server for protein modeling and docking?. Available from: https://www.researchgate.net/post/What_would_be_the_difference_if_I_use_the_Web_server_instead_of_dedicated_server_for_protein_modeling_and_docking [accessed Apr 27, 2017].

I don't understand the link to Research Gate. Please explain.

There should be no difference in output.*** The big difference is likely going to be in the size of the analysis you can perform, and how fast the analysis is performed. A lot of web-servers have a job size limit to prevent one person from hogging resources unless you buy greater access. On a public web-server, your job is queued with everyone else's. If the server is in high demand, you may have to wait along time for your analysis to kick off.
***: I said there should be no difference in output and that is true if you set up your server the same as the public webserver with the same parameters used for analysis execution. This could be a good or bad thing depending on what you are trying to accomplish. Some public webservices do not give you access to all parameters, so setting up your own may give you the ability to tune your analysis to a greater degree.

Good answer, but it could be made better with some references. This community asks that answers cite reputable sources so as to ensure higher quality (and hopefully accurate) answers across the community. Thanks.


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What is the difference between disruptive, divergent and diversifying selection?
In our lab meeting we were chatting about divergent selection. I was confused at some point because I wasn't sure what was the meaning of this work in comparison to diversifying/disruptive and other types of selection.
Diversifying selection was coined by J. T. Gulick and I haven't found an interesting answer to compare with our contemporary definition of these terms.
The way I understand this is that, divergent selection is broader and include directional selection as well as disruptive selection. Is that correct?

I think you are conflating selection and evolution. Diversifying selection is when the variance of a trait in the population increases and even potentially becomes bimodal. This may lead to divergent evolution, i.e. a speciation event. Whereas directional selection still leads to evolution but not necessarily a the formation of a new species.

What about disruptive selection? It would be the same thing as divergent selection: the formation of a new species? Also, directional selection could also lead to the formation of a new species through anagenesis. In this case, what would be the differences?

I meant diversifying selection not divergent, I've edited my answer as such. Correct directional selection can also lead to speciation through anagenesis. The difference is that when a divergent evolutionary event occurs a new branch is formed (think Darwin's finches). Whereas, with anagenesis the current population changes so much it could longer mate with its "great great grandparents" but because their great great grandparents are longer around we do not consider this to be a branching of the phylogenetic tree.

So, following your answer, both mechanisms (disruptive and directional) could lead to the formation of a new species.
To think of it another way, disruptive selection would be that an intermediate trait has a lower fitness, but divergent selection would actually mean that the bimodal trait distribution is actually moving in opposite directions (i.e. opposing directional selection). Is that what you mean?

Yes that is a pretty good way to think about it.


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MCQ - Independent assortment or Incomplete linkage

Two flies were crossed one wildtype another double mutant sepia(se) and vestigial(vg) yielding 40% wild type 40% se vg, 10% se and 10% vg. The genes show-
a.Complete linkage b.Incomplete linkage c.Independent assortment d. epistasis

My attempt at a solution
Since no. of combination of phenotypes appeared =/= 2 ( there are non-parental traits so) it is not complete linkage.
It is neither epistasis because two genes are controlling two diffrenet phenotypes, not one.
It can be independent assortment or incomplete linkage.
Since the question says double mutant sepia(se) and vestigial(vg) (I am getting the idea that) it is a female and the wildtype individual (with no genotype concerned hint) is a male. The genes are likely on X chromosome.
So..... it is incomplete linkage.
But I'm not sure why not independent assortment.

The word independent in "independent assortment" means that the assortment of the alleles of one gene doesn't depend on the assortment of the alleles of the other gene, which in that case would give you equal percentages for the offspring phenotypes (25% each). Besides that, your assumption regarding the sexes and the chromosome where the genes are found is not correct.

@GerardoFurtado Could you elaborate why it is not correct?

Why would it be?

@GerardoFurtado Nothing much about the wild type flies has been mentioned to determine it's genotype so considering it male would be right- was the thought behind my assumption.

It doesn't really matter on which chromosomes the where concerned genes are located, Now coming to your question.
A> Complete linkage > Complete linkage says that the concerned genes are right next to each other and no crossingover is possible so the expected genotype of the offspring would be 100% parental type. 50% Wild (se+ vg+) and 50% Mutated (se vg)
B> Incomplete linkage > This is the correct answer. According to incomplete linkage, the genes are close but not right next to each other so there is space for crossingover to take place. However, they are still close, close enough to be considered as linked and thus chance of obtaining recombinant offspring would always be less than that of the offspring with parental genotype, parental type always remains over 50% and here the parental type offspring is 80% (40% wild type parental genotype + 40% mutated parental genotype) and 20% recombinant genotype [(10% se & wild type vg+) + (10%vg & wild type se+)]
C> Independent assortment says that there is no linkage and thus no crossingover, this is possible only when the concerned genes are located on different chromosomes but here in the obtained data of offspring it is clear that crossingover did take place and 20% of the offspring is result of the crossingover so this option is not correct
D> Epistasis : In your attempt you mentioned that it is not epistasis because two genes are controlling separate phenotype thus it is not epistasis. your explanation is wrong. Don't get me wrong, the answer is not epistatsis, I am just saying your explanation is wrong, epistasis is the phenomenon where one gene interferes with the expression of another gene, look at the term carefully. I am calling them as genes not alleles. Alleles are different version of the same gene that control the same phenotypic character. In epistasis two different gene that control completely different phenotypic expression are interacting. One gene if expressed prevents the other gene from getting expressed, this not about the dominant alleles where if the dominant allele expresses recessive allele wont express. For example, assume gene A codes for white flower colour and gene B codes for sweet smell. If B gene expresses then A gene wont express. This is epistasis


text:
Was 14,000+ year old DNA "laying around in cave dirt" protected from degradation, or is it just naturally this robust?
In the NYTimes news article No Bones About It: Scientists Recover Ancient DNA From Cave Dirt I've read:

Although DNA sticks to minerals and decayed plants in soil, scientists did not know whether it would ever be possible to fish out gene fragments that were tens of thousands of years old and buried deep among other genetic debris.

I haven't read the original article yet, but I'd like to double check, this is bare DNA molecules, stuck to minerals or other detritus in 14,000 to 550,000 year old compacted dirt? Roughly speaking at least? In layman's terms, just laying around in some caves?
Has something protected the DNA from degradation, or is DNA just more environmentally stable and robust than I thought?
There is also discussion in the Science commentary No bones? No problem: DNA left in cave soils can reveal ancient human occupants.
The NYTimes article goes on to say:

The new study involved searching for ancient DNA in four caves in Eurasia where humans were known to have lived between 14,000 and 550,000 years ago.
Dr. Meyer and his colleagues figured out which DNA in the cave sediment was prehistoric by looking for telltale signs of degradation at the ends of the molecules.

What are the "telltale signs of degradation at the ends" of DNA molecules described in the paper?

need help choosing proper tags...

To be clear they are not finding long DNA strands but short fragments. DNA becomes more robust the shorter it gets. Fragments can last millions of years. The local chemical conditions have a huge influence on how long DNA lasts the oldest being hundreds of millions of years old under ideal conditions.
The ones the archeologists are finding are not even close to enough to rebuild an intact strand but it can be used for matching. Of course contamination is a big problem, anything that dies leaves DNA in the soil. With humans it becomes especially problematic becasue the archaeologists themselves are a major source of contamination.
For an indepth look at contamination protocols, some of which as still questionable, can be found here. Sorry its behind a pay wall.
Likely they are referring to deamination cytosine substitution, which creates mismatched pairs of DNA and occurs more and more as DNA ages.

OK I'll get a hold of the paper soon. When you say millions of years, is that necessarily when found in marrow enclosed in an unbroken bone? Does deamination cytosine substitution refer to the type of process described here: https://en.wikipedia.org/wiki/Deamination#Cytosine ?

"Fragments can last millions of years": citation needed. I'm not saying you're wrong, I just find that surprising (though I am no biochemist so that doesn't mean anything) and would like to read a reference backing it up.

http://www.sciencedirect.com/science/article/pii/0016703794901856  As they mention DNAhas been recovered from amber preserved insects many times. amber vastly retards DNA decay that's why finding a Dinosaur tail preserved amber is so exciting! In the end DNA decay is not like radiometric decay with a largely unaffected rate, local chemical conditions have a huge influence.

@uhoh not necessarily, although depending on the local chemical conditions it may be possible. DNA decay in heavily influenced by local chemistry it's not like nuclear half lives.

OK this is great - Thank you for adding Amino acid racemization in amber-entombed insects... This will make great reading!


text:
Generate mesh surface from protein structure
What tools are most widely used for generating a mesh surface of a protein from an x-ray crystallographic structure (from the PDB)? Pros and cons would be appreciated.
I'd prefer the output to be a watertight triangle mesh of the protein surface.
Also, I'd like the tool to be scriptable (i.e. no need to open a GUI).
So far, I've been playing with MSMS and EDTSurf. But I was wondering what was standard in research, as well as if there was anything in the standard bioinformatics libraries.

Do you want to visualize the protein surface or the electron density map? (PyMOL can do both.)

PyMOL and Chimera can do that, and both can be script-driven. The PyMOL wiki is full of examples, and probably already has some how-to that would get you started. Chimera also has a complete documentation.


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Do mutations in one bacterial strain have the same effect in other strains within the same species?
I would assume so, since they are the same species after all. I am asking this because I am doing a bioinformatics project for school and I cannot find any protein mutations for the specific bacterial strains that my department has managed to isolate. The proteins I have identified as stress proteins are within their genomes, but there is no known mutations I have found while perusing the literature. Mutations for these proteins are present in other strains though. Any help would be greatly appreciated.

Different strains of the same species have differents genotypes (ie different alleles and therefore express different proteins).So if your protein A in strain 1 has some effect, it could have the same effect in strain 2, but not necessarily.
Indeed lets imagine that protein A interact with protein B in strain 1 to produce an effect. If protein B is absent in strain 2, or different, protein A will have no effect. My point is if you have a mutation in one strain, the same mutation would not necessarily have the same effect (although it is very likely) in an another strain beacause both strain don't express the same proteome.

Hi welcome to Bio.SE! We ask that answers be well supported and/or cited in order to improve the quality of our answers in this community. Please provide support/references for your answer.

Hi. Sorry, I did not know that. I'm afraid I have no english reference to cite. It is just basic population genetics : in a population the individuals are not clones but show genetic diversity.

If you provide sources, it will probably be reasonably simply to find English translations, so don't worry about that :)


text:
Streamside plant identification - Oregon
This is in the western cascades forest in Oregon. Leaves are at the ends of branches only, lives mostly in slightly muddy areas next to streams. Produces small black berries.

Posts (especially species ID posts) should have all photos copied directly into the post and not linked to if possible (i.e., as long as copyright issues allow). This way, we avoid the issue of having an ID question with non-working photo links in the future. Please copy the pics from your "More photos" link directly into your post. Thanks!

Yeah, I tried to do that, but it didn't work because they're too large. Is there a way I could get around that?

I'm not sure what you mean by too large? You mean that they're >2mb when you try to upload directly from your computer? If thats the case, you have to either crop/lower quality or post them somewhere else 1st (which, typically lowers their quality). I simply copied them from your other site and put them here.

Wow nice way composing the post, showing necessary details.

It's a plant in the family Ribes, which includes currants.
If it stinks when you crush the leaves, it is probably Stink Currant, or Ribes bracteosum, a plant found in the Pacific Northwest.

Leaves are large, like maple leaves, sparsely hairy to smooth, with 5 to 7 lobes, stinky when crushed.  Flowers are numerous on mostly erect clusters; with white petals and brownish-purple to greenish-white calyces.  Berries are blue-black with a whitish bloom.

The leaf and berry are a good match. There are ~150 species, so it's a bit difficult.
It could also be Ribes acerifolium, or Maple-Leaved Currant.

Shrub with spreading branches but no bristles. Leaves maple-like, 1–3 in. across, with 5–7 rounded, finely toothed lobes. Hanging stem of 8–12 greenish flowers, each less than 1/3 in. across with tiny red petals and stamen filaments broad at base. Berry black, coated with bluish powder. Grows from mid elevations to treeline in Cascade and Olympic mountains.

I could not find a photograph that was not copyrighted. The flower color was pinkish to brownish.
It's not a perfect identification, but it's closer than 'in the ballpark'. If you google "Ribes western Cascades", you'll see what I mean. :)

Thanks, that gives me what I need. I looked through a fairly comprehensive identification guide of Pacific Northwest wildflowers (had a whole lot more than any book I've seen), and every native flower I've seen was in it except for this one for some reason.

@Tzacol - Because Murphy's Law... or it's not been identified yet. It does say brownish-purple though, so I woiuldn't rely too heavily on the color of the flower. :)


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Can a regulator genes be more highly expressed when it has more places to bind?
I am doing some research on small cell lung cancer and, from what I have found, many tumors show high levels of ASCL1, which is a regulator for neuroendocrine cell differentiation. However, no papers propose a mechanism for the higher levels of ASCL1. Instead, many of them refer to ASCL1 target genes with "amplified" enhancers and propose that ASCL1 may bind more frequently to these enhancer regions.
In general, if there are more places for the regulator to bind on an enhancer, is it possible that this is sufficient for the regulator to be more highly expressed?


text:
What is this plant & it looks like USA tree " Carya ovata"?
I saw this tree in India. It was so fascinating because its leaf looks like Carya ovata, which only grows in the USA & Canada according to Wikipedia:

Carya ovata, the shagbark hickory, is a common hickory in the Eastern United States and southeast Canada.

Is it really Carya ovata or something else?

This looks nothing like Carya ovata.

Also, please add close-ups of the leaves, (supposed leaflets) and trunk if possible for a better chance at a correct ID

Are the branches opposite or alternate?


text:
Was Raymond Gosling supervised by Rosalind Franklin?
The story of how the structure of DNA was deduced is fairly complicated and controversial, but most parties agree that a key pieces of data was "Photo 51", an X-ray diffraction image of DNA taken by Raymond Gosling in May 1952 (or possibly other similar images taken at the time as part of the same study).
Ray Gosling, who took the photo, was a doctoral student at the time. The Wikipedia page for the photo indicates that he was supervised by Rosalind Franklin, at least for a while:

James Watson was shown the photo by Maurice Wilkins without Rosalind
Franklin's approval or knowledge (although by this time Gosling had
returned to the supervision of Wilkins).

One controversy in the story is that the photo was shown to Watson and Crick without Franklin's knowledge or permission, which should have been sought first as she was his supervisor.
However, this article discussing a 2015 play about the issue (called Photo 51) includes an explanation by Professor Tony North, who was also supervised by Wilkins and shared equipment with Wilkins and Franklin, that:

Wilkins had to know what Gosling was doing, as he rather than Franklin
was his PhD supervisor. Franklin was ineligible for the role because
she did not have a formal university position, but a personal research
fellowship, Professor North said.
“The result is that Maurice had every right to know what Raymond had
been doing and what results he had achieved, so that he had a right to
see photo 51 without seeking Rosalind’s permission,” he said.

A quote from a primary source seems more credible. I also know from experience that other lab members often play a substantial role in training or supervising doctoral students without necessarily having a formal role in their supervision (i.e. being registered as a supervisor).
Was Rosalind Franklin, at any point, formally supervising Raymond Gosling's doctorate?

I'm voting to close this question because it would be more appropriate on the History of Science & Math Stack Exchange site.

@tomd yes, my mistake - I thought it was an Oxbridge thing. Now removed.

Well, according to this editorial in Nature:

Next week marks the 60th anniversary of the publication of the famous Watson and Crick paper — and that of two other papers on DNA that appeared in the same issue. Neither was so high profile, but each was essential to the structure’s discovery. Both were written by scientists at King’s College London: one by Maurice Wilkins and his colleagues Alec Stokes and Herbert Wilson, and the other by Gosling and his PhD supervisor, Rosalind Franklin. (emphasis mine)

There is also a podcast, an interview with Gosling himself (at the age of 86)! The full podcast can be found here: http://www.nature.com/nature/podcast/index-pastcast-2013-04-18.html
Source: Nature 496, 270 (18 April 2013) doi:10.1038/496270a


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What is preliminary work in a biological investigation?
Here is an example of preliminary work that confuses me (from an A level Biology exam question). Please help me by providing an explanation of preliminary work in the generic sense, then use the example below.

A company is in the process of developing a new stain-removing washing liquid.
  They want to include a protease enzyme to digest the proteins that are responsible for some stains on clothes. Plan an investigation to discover the optimum concentration of protease to use in this new stain-removing washing liquid.'

Here are the answers suggested as the preliminary work:

see if proposed method will work / will provide
  measurable results
to check for suitable conditions for digestion
  e.g. temperature, pH
select timescale (for measuring stain digestion)
idea of selecting a range of protease concentrations
check if the type of {protein / stain} is affected
select suitable dependent variable for measuring {digestion / removal / eq} of the {stain / protein/ eq }

Now, in my process of understanding what preliminary work is, I want to
question is there any other preliminary work that could be done on this investigation? Seems like there is a lot more to prepare for such an investigation. For example, at first sight, I suggested that secondary research needs to be carried out in order to identify the mean amount of stain and its distribution around that mean. Then that will be the suitable substrate concentration to be used. I also mentioned researching the type of proteases that the company wanted to use, alongside carrying out the preparation of the range of concentrations of enzymes that need to be used.


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Does the pyloric sphincter contract after ingesting only liquid?
At university, I was told by one of my fellow students that the reason why eating before going on an alcohol laden night out was a good idea, was because the pyloric sphincter contracted once food was in your stomach, and only let it into your lower intestines gradually. Their theory was that if you then drank alcohol, it would also sit in your stomach (with your food) and would only be let into your intestines gradually as the food was allowed through, thus slowing your rate of inebriation. Drinking on an empty stomach would conversely not cause the pyloric sphincter to contract, thus allowing the alcohol to enter your intestines at a much faster pace. However, I've been trying to find some online sources to corroborate / disprove this, and I'm having problems finding any information on it at all.
So my question is: does the pyloric sphincter stay relaxed if only liquid is consumed on an empty stomach?

The answer from CATARANTHUS looks good, but if you want to see another source of information try here.

NO IT DOESNT CONTRACT AFTER INGESTING LIQUID
1)The pyloric sphincter always remain  tonically contracted even in an empty stomach.However this tone of the pyloric sphincter is insufficient to prevent the passage of liquids to the duodenum.Thus almost all the liquid intaken in an empty stomach passes immediately to the small intestine.
2)Filling of the stomach triggers an enteric reflex that increases the tonical contraction of the pyloric sphincter.When fluids are taken then,their rate of passage to the duodenum is considerably reduced.(Although little is slowly absorbed into blood from the stomach).
REFERENCE:TEXTBOOK OF MEDICAL PHYSIOLOGY(GUYTON AND HALL)
3)As the small intestine is the seat of absorption,delaying passage to it delays large amount of alcohol absorption into blood.This not only delays its effect in the body but also fascilitates the persons capability to intake more alcohol.(This varies considerably in different persons but the central physiology is this)
REFERENCE:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1705129/


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Webtool to design guide RNA (gRNA) for use with CRISPR-AsCpf1?
My goals are to use a free webtool to:

Identify guide RNAs (direct-repeat sequence followed by the targeting sequence) appropriate for use with AsCpf1 in order to target a specific segment of genomic DNA.
Estimate efficiency and specificity of using the guide RNAs identified by the tool.

Unfortunately, when I tried to do this using the CRISPOR tool, the "Job Status" never advanced past the "Waiting" stage, even after 10 minutes. Attached is a screenshot to show what I see.
Specifically, I used the following settings in my query:
I named my sequence:
Mm Acaca block2 from BLAT alignment
In "Step 1" I submitted this sequence:
aactaaatct ccagcatctc catccccttc ttaggtttat ttattttatg ggtatgagtg
tatgtccgtg caccacatgt gtgcctggtg tctaccaagg taagtagagg tatacaaacc
cttggaattg aattatccac catgccgtca ggtgctggga gcaaattcag gtcctctttt
agagcagcaa gtatttccag ccacttagtc acctctgcag ccccttattt tcacagtctt
gagacaagaa tctcactctt tagcccatat tggcctggaa ctttaggcag tcctgccgga
gtttcagact gctgggatga caggcctgac ccattacgtc cactaaggat ggtttccttt
cctgtgagct agcagcatgt agactccaca aggctcctgg ggaagtgttg ttatagtatg
ttatagtata gttgcgaaag gaaggttttc agaagatatg ggtattacga agaaattcta
tgtaaagttt cttttggatt ctctgtttgt atAGATCCAG CATGTCTGGC TTGCACCTAG
TAAAACAAGG TCGAGACAGA AAGAAAATAG ACTCACAACG AGATTTCACT GTGGCTTCTC
CAGCAGAATT TGTTACTCGT TTTGGGGGAA ATAAAGTAAT TGAGAAGgta agttaaactt
actaaactat ttcgcttgaa gtatgtgaga tttcatgcct agatttgttg tttctgttca
aaaggatatt taggttttta gggactttgc ctttttatgc agggctatcc tttctgtctc
cctagcatgt tactaataca taatctcact gtgtacctgt gtttttacat

In "Step 2" I selected:
Mus musculus- Mouse- UCSC Dec. 2011 (GRCm38/mm10)...

In "Step 3" I selected:
TTTN-23bp - Cpf1 Acidaminococcus / Lachnospiracea

My questions are as follows:

Should I do anything differently to use the CRISPOR tool for my goals?
Are there other free webtools available for me to achieve the goals I outlined above?

UPDATE: I emailed the folks at CRISPOR, and they informed me the site had been down, but they have since restarted it. Hopefully, their restart is sufficient, but I will leave my question up with the hopes that others can point me to more webtools.

Crispr tech. is very cool. Was wondering if you wouldn't mind explaining a little bit a bout the technology and your process described above?

Most online tools will only help you to design gRNAs for Cas9 because it is the one that is most commonly used. I found an online suite called RGEN tools that also has an option for AsCpf1.
However, if you don't find it satisfactory then my suggestion is that you either design your gRNA manually or write your own script (which won't be that complex).

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


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Material(s) That Tissue Can Grow Into And/Or Not Be Rejected?
I once watched a special on Dr. Roger Leir, a doctor made famous for removing supposed ET implants. Whether they were as such or not isn't important for this question. What is important is that he documented the removal of several devices that were at least partially made of material that tissue would somewhat grow into so that the body wouldn't reject it.
The question is: what, if any, such materials exist? Of course what the body won't reject and what it will grow into are two different things. I'm interested in both. It would also be helpful to know where people tend to discuss this and what companies are working on it. This is a question of biology and material science.
When I think of materials that won't be rejected, the only thing that comes to mind are materials made out of tissues themselves (like cat guts). Of course, we have things like pacemakers and all manner of implants but I don't know to what degree the body accepts them. Keep in mind that devices wouldn't have to be made entirely of such materials, just the outer shells of them.

You might be interested in the emerging science of tissue engineering, including "growing" organs on a scaffold, either artificial or biological in origin. Simpler transplants have already been successful.


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Which variables are controlled in the mammalian womb to ensure a healthy environment?
Recently, researchers have had some success with artificial wombs. Which aspects of the womb are difficult to replicate through technology?

It seems you are referring to this recent advance:
http://www.sciencemag.org/news/2017/04/fluid-filled-biobag-allows-premature-lambs-develop-outside-womb
https://www.nature.com/articles/ncomms15112
Involving putting premature lambs (delivered via caesarean) in bags of nutritive fluid and connecting the umbilical cord to an apparatus to oxygenate the blood.
Your question asks which variables are controlled in a mammalian womb, which I think is a misleading way to look at what a womb does and thus what the difficulties are with reproducing it. Namely, it makes it sound like the womb is a container whose purpose is to keep environmental variables (temperature, pressure, etc) at a good value for the development of a fetus. The problem is the womb doesn't just contain the fetus, it feeds it via the placenta. And the placenta is a structure built by fetus during embryogenesis, that connects to the lining of the uterus and enmeshes itself with it so that there is a huge surface of contact between the blood vessels of the mother and the blood vessels of the placenta, so oxygen and nutrients can pass through the mother's blood vessels to the placenta's and from there to the fetus via the umbilical cord. This allows the fetus to get all the nutrients and oxygen it needs to develop.
The "Biobag" these researchers created for these lambs is designed for fetuses who are advanced enough in their development that the main problem they have with surviving outside the womb is that their lungs are immature; the main purpose of this contraption is to allow oxygenation via their umbilical cord while keeping their lungs filled with fluid. And it also seems like they're being fed via that fluid, which suggests they're mature enough to get nutrition via their digestive system.
The paper gives quite a few details of the challenges involved in even that comparatively low level of uterine service. Infection, setting up the cannulas and oxygenating system so that the blood flow is just right and doesn't overtax the fetal heart, making sure there is no clotting, haemorrhage or brain damage...
I imagine the main challenge of making an actual artificial womb that's usable from implantation on would be emulating implantation itself, with artificial endometrial lining that a placenta could naturally develop in and intermingle its blood vessels with and somehow accurately reproducing the flow of blood that's necessary to feed the placenta. If we assume an artificial womb for a fetus that already has an umbilical cord, so we basically need to emulate the placenta's job not the uterus', but can be used earlier than Partrige et al's Biobag, then I imagine all the concerns they had about cannula size and getting the blood flow just right would be a million times harder with tinier, less-mature umbilical cords and fetuses. Not to mention if they need to put nutrients in the blood and not just oxygen.


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Is this a variety of banana slug (Ariolimax columbianus)? (California)
These very dark (dark grey to black) banana slugs are an anomaly. I live on the north coast of California and see many slugs every day. These particular slugs I find only on the west-facing headlands at the ocean. There is no cover from the sun since there are no plants taller than about a foot. Also these particular slugs are never longer than 2-1/2" to 3". Are they a sub species, a variety, or something else? Thanks for taking the time to answer.

Banana slugs are comprised of three species:

Ariolimax californicus
Ariolimax columbianus
Ariolimax dolichophallus

Ariolimax columbianus, or the Pacific banana slug is known to have black spots, sometimes so large as to cover their entire body (Source). This is certainly the genus of the slug you've shared.
At times, you could be seeing a Black slug which is well-established in Washington and Oregon. I only include this information as I have noticed this species occasionally in Southern British Columbia and wondered if it was the same species as the Banana slug. It isn't. The picture you've attached is not a Black slug (note the pronounced frills on the back of the Black slug specimen)


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How does the cell cycle affect stem cell fate?
I keep reading about the stages of the cell cycle affecting stem cell fate, however I do not understand how. After all, any cell will have to pass through the whole of the cell cycle, and go through every state.

If you are referring to cells that are differentiated in adults:
Some somatic cells in multi-cellular organisms are post-mitotic, that is, the cells cannot divide, or said in other words, they don't enter in S phase. This cells are said to be in G0 phase, because they keep synthesizing proteins but the won't replicate their DNA.
Another thing we could say about cell cycle having something to do with cell division, is that in G1 and G2 (and , of course in G0) different cell types, produce different proteins. ie: a skeletal muscle cell, produces lots of proteins associated with the contraction, but neurons not so much.
If you are referring to the first cell divisions in a multi-cellular organism's development, then:
in cleavage, the cells are dividing synchronously, and they avoid some cell cycle stages, like g1 or g2 (in cleavage, the cells are just dividing and replicating their DNA; the protein synthesis happens with mRNA inherited from the mother). In this stage, there is no cell growth at all. After some cell divisions, they have to start synthesize mRNA  and, because of that, they start to divide asynchronously. Eventually the cells (for this and also for many other reasons) get differentiated.
I hope this answer is useful :)


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What could cause sudden deafness and deliriousness on a boat adrift?
I'm reading a completely nonfiction book  called In the Heart of the Sea, and in it, the characters are lost at sea without food and they are starving. They cast lots to see which crew member will be eaten, and it lands on one of them. He asks for the night to resign himself to his fate, and the other members accept. However, by midnight, he'd become deaf and by morning he was delirious. Why would this happen? It wasn't starvation-induced because they'd used up the very last of their rations that night in a large meal. So why did the threat of death induce deafness and deliriousness?
Edit: And it was 100% true: not only was the book nonfiction, there are accounts from the surviving crew members of the event.

Maybe because the author wanted it to? I think it will be difficult/impossible to get a biological explanation for every event in a work of fiction, and psychosomatic reactions aren't all that well understood (and can be a matter of some debate).

@BryanKrause: No- it was completely nonfiction, but even speculation would help.

Ah I see - could be psychosomatic, could also be that he ingested seawater, maybe trying to kill himself so his crewmates wouldn't have to do so: dehydration could cause both of those symptoms. Could also be that the emotional stresses interacted with dehydration he was already experiencing, or the anxiety caused nausea/vomiting/diarrhea. It's also possible the accounts from the surviving crewmembers were not entirely accurate.

Also depending on what food they were eating and their metabolic state, that large meal could have contributed as well. I edited the title to something more appropriate in case others think this can be saved, but I still think it's too speculative a question to be on-topic for biology.SE.

sounds more like dehydration, eating will only exacerbate that especially a protein heavy meal. digesting protein uses more water than digesting anything else. a sudden switch from carbohydrate rich biscuits to solid proteins would require much more water, so if they are rationing water someone with marginal dehydration could be pushed over the edge unless they take more water rations as well.

He probably had hypernatremia: salt toxicity from drinking seawater.  That definitely can cause delirium.  It was harder to nail down that hypernatremia could cause deafness specifically but I found that for pigs.
http://www.merckvetmanual.com/toxicology/salt-toxicity/overview-of-salt-toxicity

Affected pigs may be blind, deaf, and oblivious to their surroundings;
  they will not eat, drink, or respond to external stimuli.

It would be easy to think a person was deaf if he were altered / delirious / encephalopathic.  His brain does not process what he hears and so he is oblivious - like these pigs.


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Is there a cellular physiological response to desiccation in animals?
There has been much research on the molecular effects of high levels of temperature for animals, specifically regarding heat shock proteins, protein denaturing and energy investment into stress tolerance.
I understand generally, the effects of desiccation with respect to the importance of moisture, specifically for aquatic animals (eg. oxygen uptake), but I can't seem to find much information on cellular-level responses to desiccation stress.
Are there are well established effects of desiccation on a cellular level or if there is a physiological response in the cell (eg. production of hsp)?

Try a search on Google Scholar for "cellular response to desiccation" - you might also try "cellular response to dehydration" or to "hyperosmotic stress."

I have searched Google Scholar extensively and found most research is on plants and algae. There is a bit on Drosophila , it seems sometimes desiccation results in hsp production but I've been reading up on but I'm pretty much stuck here.

What about my suggestions to look at dehydration or hyperosmolarity? I'm not exactly sure what's out there because I am more familiar with organism-level reactions to water stress rather than cellular adaptations but with 70,000 some results (although I agree, it looks like a lot of work on plants, which is why I was suggesting those other search terms) I'd expect you to find something in there.

Your over thinking it, search "Osmoregulation animal cells" here is two results. http://www.annualreviews.org/doi/abs/10.1146/annurev.ph.43.030181.002425?journalCode=physiol And  https://www.ncbi.nlm.nih.gov/books/NBK21739/

@BryanKrause "Hyperosmotic stress" has been effective as has "cellular response to desiccation". I think I was over-thinking it John.

What's protocol now, should I delete the OP


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How does an isotonic environment affect fish?
Fish receive oxygen needed from water that passes through their gills. If fish were isotonic to their watery environment, what problems would this pose to them?

This sounds like it might be a homework question. We try not to answer homework questions here (we use the term broadly to include any sort of coursework, as well as under researched questions where supporting information is very easily accessible), because figuring out those answers independently is an important part of the learning process. However, if you can show how you are thinking about the question and what work you have already done, then we can help out.

dependson the fish and what kind of environment they are adapted to. Some fish woun't notice others will die within minutes.

Some fish are isotonic to their environment (I read that in some book and they had examples but Google is failing me. Here is a paper instead talking about fish doing well in an isotonic environment). It isn't an issue for getting oxygen; I assume you think that because you think fish get oxygen via osmotic pressure, but "isotonic" (and "hypotonic" and "hypertonic") refer to the transfer of water via osmosis. A fish that's isotonic with its environment doesn't need to take special measures to avoid its cells swelling or shrinking as water floods in or out of them; it doesn't say anything about which specific solutes are in that water to make it isotonic.
As far as oxygen goes, oxygen is constantly being consumed by the fish's tissues so the diffusion is always going to go in the right direction (unless the water doesn't contain enough oxygen in the first place, in which case fish won't survive). In addition I imagine fish blood contains many molecules that preferentially bind to oxygen in ways that make this process even more efficient.


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What kind of insect is this found in North America in April?
I noticed this small insect that probably measured 5 mm in length on my coat lapel. Not sure whether or not it had been inside or landed outside on my coat. Photos were taken in Nashville, Tennessee, USA in April. It was alone and I have never seen an insect like this one before. Just trying to figure out whether this bug is harmless or something that could be a problem. . Here is another photo taken of the same insect.

It is a ladybug larva.  They eat aphids.  I have handled many and never been bitten.
https://test.whatsthatbug.com/2010/10/25/ladybird-beetle-larva-ladybug/


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Do trap door spiders have 10 legs?
I was reading this National Geographic article, 50 New Spiders Discovered In Australia when I became confused by the two trapdoor spider species photographed. I looked up trapdoor spiders and looking at pictures, they all seem to me to have five pairs of legs. I know spiders have eight legs; can someone tell me what am I missing here?
Ctenizidae:

Euoplus:

Cork lid:

(OK, so I found out that the things next to the mandibles are pedipalps. How are they different from legs on these beasts?)

Antennae, mandibles, maxillae, chelicerae, pedipalpi and legs are all appendages of arthropod metamers. However, they have different functions and embryological/evolutionary origins.Regarding your specific question, palpi don't have the metatarsus, i.e., they have one segment less than the legs. Besides that, they are functionally used to manipulate objects (you can clearly see that in the big palpi scorpions have), mating (sperm transfer) etc, but not walking.

Oh, by the way, spiders don't have mandibles, as you said in your last paragraph.

All spiders have eight legs. The two on front are called Palps

The definition of a leg from Merriam-Webster is

"One of the rather generalized segmental appendages of an arthropod used in walking and crawling"

As Gerardo Furtado has already stated, the front pair of appendages are called palpi and are not used for walking, but for mating and manipulating objects. By this definition, palpi are not legs and therefore trap door spiders have 8 legs, not 10. More information on the rather large pali found on trap door spiders can be found in P.D. Hillyard's The Private Life of Spiders.

Image from Biodiversityexplorer.org.


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Heritability in population genetics
What is the difference between narrow sense heritability and broad sense heritability?
Does heritability in the broad sense refer to the degree of genetic determination?
Heritability in the narrow sense refers to additive effect of alleles , what does it actually mean?

The answer to this question should give you everything you need.

Heritability in the narrow sense
Heritability in the narrow sense $h_N$ is the genetic variance $V_G$ over the overall phenotypic variance $V_P$
$$h_N = \frac{V_G}{V_P}$$
More information at Why is a heritability coefficient not an index of how “genetic” something is?.
Heritability in the broad sense
The heritability in the broad sense $h_B$ is the additive genetic variance $V_A$ over the overall phenotypic variance $V_P$
$$h_B = \frac{V_A}{V_P}$$
Decomposing of the genetic variance
Adding together the additive genetic variance $V_A$, the dominance genetic variance $V_D$ (and the epistatic genetic variance $V_I$) sums up to the overall genetic variance $V_G$. Here I will ignore the epistatic genetic variance
$$V_G = V_A + V_D$$
, where
$$V_D = x^2(1-x)^2(2\cdot M_{12} - M_{11} - M_{22})^2$$
$$V_A = 2x(1-x)(xM_{11}+(1-2x)M_{12} - (1-x)M_{22})^2$$
, where $M_{00}$, $M_{01}$ and $M_{11}$ are the measurements of the phenotypic trait in genotypes 00, 01 and 11 respectively.
Highly related

Why is a heritability coefficient not an index of how “genetic” something is?
Additive genetic variance with nn alleles
Additive genetic variance with nn loci


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Apple-seed-sized black bug, not very leggy - (Canada)
Can anyone identify this bug:

I'm in Toronto (Canada), 9th floor of a highrise building.  Most of the apartment is wall-to-wall carpeting, though the kitchen, entrance, and washroom are tiled.

We're going to need a better picture.

Darn.  I killed it and flushed it.  :(

Can you describe it? How does it move? Where's the head in this picture? Maybe even label the picture you have.

Sorry, I can't.  I'm at the age where progessive lenses are needed.  I was actually relying on the photograph to be able to see the details better.  At least it doesn't look like a bed bug, but I am curious what it is.


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Does anyone know what this living creature is?
There are two different things I am trying to identify. I live in Lexington, Kentucky. The first one I started seeing was a small white larvae looking worm thing. They would very in size but never bigger than a few centimeters long and very thin.  I started seeing these around my house about two months ago.  I had not seen them before.  It seemed like they showed up all of a sudden.  They were in the floor and on the furniture.  I never would see them move. When I would try and pick them up or investigate, at the slightest touch they would turn to liquid almost like water, clear.  Just disappear.  The other form I am seeing is a bit bigger I don't know if they are both the same species just in various stages or if they are 2 separate species.  The second ones I seen were almost an off white with rings vertically around its body. With hair all over them.  Some were hairier than others and they were not all the exact same color.  It seemed to me that they used their hair as a weapon or defense not sure how that was intended.  They started showing up on my hanging cloths in my closet as well.  Shortly after we started noticing small holes in our cloths.  I call them creatures since I am not sure what they are.  They then started burrowing into us. I never seen the darker one with hair burrow but for sure the small white larvae looking one.  But only me.  Not my kids or husband.  The doctors can't tell me what they are.  The darker one in the picture came out of my leg.  When I got it out it was still alive.  They seem to prefer my nose and sinus's.  I spent hundred on exterminator and have not seen anymore.  The pest control company said they had never seen them before.  The one picture of the white larva is one that I had to download.  I accidently lost all of my pictures on a phone before they were downloaded to my computer.  That picture is identical to what I have found.  I may have more pictures.  I will go thru all of them in the morning and try to add some here.
Hairy:

White in colour:

Welcome to Biology.SE! Could you please edit your post and give the location of where you took the pictures?

Do you have better pictures? Give the size? Is there a reason one of the pictures is 5 years old?

I have lost some of my pictures due to a phone issue.  I will go thru all pictures I have in the morning and get some more added.  I had to download that picture, but it is identical to the ones in my house.