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What is the biology behind human population dynamics?
A paradox: Human population growth looks a lot like a simple logistic growth pattern. But the simplest interpretation of logistic growth doesn't seem to fit. Is this peculiar to humans, or does it have a biological explanation?

Ecologically, advances in agriculture over the last ~200 years have increased the Earth's carrying capacity for human population, and the human population appears to have grown and started flattening out as we approach the new carrying capacity -- this basically looks like logistic growth (following a change in the carrying-capacity parameter).

The simplest biological interpretation of logistic growth is that birth rates remain constant (driven by constant biological factors), but as the population approaches the carrying capacity, there are not enough resources to go around, so death rates rise to match the birth rate. In human populations, this rise in death rates would presumably manifest itself in the form of widespread famine and resource wars.

But that is not at all what we see in the human population! In fact, we have seen falling death rates due to advances in medicine. For some reason, birth rates have actually fallen to levels roughly commensurate with the death rates (and in most developed countries, the drop in birth rates has actually overcompensated for the drop in death rates, leading to an ageing population). So although the net population dynamics seem relatively simple, the simplest explanation for these dynamics fails spectacularly. This leads to several

Questions:

Is there an underlying biological mechanism linking our approach toward the environment's carrying capacity to a resulting drop in birth rates?

There are compelling sociological explanations -- education and empowerment of women, urbanization, decreased child mortality, access to contraception, etc. all point individuals toward a reproductive strategy of investing more into a smaller number of children. But from a sociological perspective, it appears to be a mere accident that all of these forces are converging at once to save us from a scenario of high birth rates and high death rates. One suspects there might be something more fundamental going on here.

Are there examples of other species which do the same thing -- throttle down their birth rates as they approach the environment's carrying capacity?

Maybe there's an evolutionary advantage to this. A population which generates lots of individuals destined to fight one another or die of hunger before reproducing seems to be wasting a lot of energy, especially if individuals care for their young. An overcrowded, underfed population may be more vulnerable to catastrophic disease (especially in a social species), and reduced individual fitness may actually reduce the total amount of resources the population is able to extract from the environment. If a species relies on cooperation within social groups, then perhaps excess births lead to intragroup competition that undermines group fitness. The basic principle of group fitness -- that sometimes it is more advantageous to help others in one's social group than to act directly for one's own benefit -- may be magnified when populations are stable with little room for growth (just as in a mature marketplace, it may be easiest to cooperate with an established business, whereas in a new sector it may make more sense to grow a new business from the ground up).
So I would look for this phenomenon among species that form cooperative social groups and care for their young -- colony-forming insects and large social mammals spring to mind. From my amateur reading, it sounds like lions might be a non-example, regulating their population by pushing excess or unfit individuals out of the pride to their likely death (or at least, this suggests that the population is not regulated solely via birth rates). But it seems like this could be addressed experimentally: for example, if individuals from a stable population of species $X$ are introduced into a new environment that can easily support a larger population of $X$, then does their birth rate go up?

If the answer to (2) is "yes", then what biological mechanisms are behind this?

Such a mechanism must be interpreted in the context of individuals' reproductive behavior more generally. There will be (a) factors affecting the advantageousness of reproducing, with (b) environmental cues indicative of these factors, (c) factors influencing individuals' actual reproductive behavior, and (d) biological mechanisms by which (b) influences (c).
Among the (a)-type factors we're particularly interested in might be abundance of food, space, disease, social stability,... Candidates for (b) might include crowdedness, air quality, presence of greenery and wildlife, stress levels,... For (c), one might look at libido, fertility, desire for a mate or for children,... For (d), ideally one could get down to the level of things like hormone regulation.

Can we use the answer to (3) to inform an answer to (1)?

Here are a few crazy theories that might be supported.
In urban areas, the smell of other humans and lack of greenery are cues that the population is overcrowded and food is scarce, which via some dedicated hormone-regulation system common to all mammals suppresses the desire to mate or raise offspring (but in the United States, these factors are mitigated slightly by our constant showering and our sparser settlement patterns, leading to a birthrate higher than in much of the developed world.)
The gradual process of political integration and tolerance has led us to identify larger and larger subpopulations of humans as "us", and a sense of being part of a large group with a stable population both upregulates pro-social behavior and somewhat suppresses the desire to have children of one's own.
The elevated stress levels of modern life are a cue that one can ill-afford the investment required to reproduce, suppressing the desire for children.

Wow... this is one long post! I personally don't feel like reading such a long post. You might get more attention if your post is shorten.

Note that if you google your question you'l get tons of information such as this quora post for example.

I think most of the stuff I could find addressed mostly sociological aspects. I tried to organize the question to be skimmable, maybe I'll make a few modficiations to improve this. The stackexchange sites I'm useful have slightly different-looking interfaces.

The edit already make the post much more attractive :) Side note: sociological phenomenon do affect our environment and they are not to be disregarded as irrelevant when talking about human population growth just because a sociologist said it and not a biologist.

Oh good! That's a great point about the sociology -- I'm hoping that the biology of the situation can help to contextualize the sociological situation.

Animals typically have as many broods and babies as they can physically nourish themselves for, given a basic local territory and fair conditions for breeding. So AFAIK, food and weather throttles parents nourishment and broods in a simple biological-economic way. Human hunter gatherers females have an average of 5 babies or something. Todays dynamics are lab/technological biology.

@aliential A relevant fact which I believe I've read is that the adoption of farming actually led to decreased level of health among humans by several metrics, such as lifespan. I believe I've also read that the adoption of farming also led to an increase in family sizes. If this is accurate, it would be a great confirmation that humans can change their reproductive strategy in response to the environment (whether this happens at a species or individual level is unclear). So human history has not been a linear evolution along this axis, which is actually great evidence for adaptability.

Consider that genes doing what you propose would be immediately outcompeted by selfish organisms who try to dominate resources instead, It can only work as group selection which should be a red flag

I think the key point is that humans cannot be modeled as a wild population.

Its actually much simpler than you are making it out to be, carrying capacity is not an issue, humans long since surpassed the planets carrying capacity without advanced technology. The real factor is infant mortality.
consider both K and r strategies
Say you have two sets of parents each starting with the same amount of resources. In r strategy the approach is to invest little in each individual offspring and have a lot of them, K strategy involves investing a lot of resources in each offspring and having only a few. The same amount of resources are consumed by each set of parents. It seems like r should always win, but as long as offspring mortality is low K usually wins. Why because high investment offspring can usually easily outcompete low investment offspring for finding mates as long as they survive.
Who has an easier time finding a mate the man who was half starved as child and has chronic health issues and missing teeth becasue of it or the man who had top of the line nutrition and medical care and is physically fit, with good teeth. these are the extremes but it holds true all long the spectrum, better health, better education, better environment (moving costs a lot of resources), all correlate with more mating success.
For each individual having fewer high investment children is better as long as there is a high likelihood said children will survive. Which has only become true with modern medicine and sanitation. So by each parent doing what is best for their genes and offspring society as a whole has fewer and fewer children, again as long an child mortality is very low.
But for most of human history child mortality was highs so having few offspring did not work, because there was a decent chance all of them would die. Thus having lots of children was the only way to guarantee having any children who live to mate. As child mortality drops the number of offspring who survive skyrockets (thus population also explodes) so mating success becomes a much bigger factor than chance of survival, because the chance of death is so low.  Modern medicine and sanitation has changed the selective pressures on our mating strategies. More K leaning strategy is now evolutionarily favored in humans, so the number of total offspring declines, so the population growth also declines. This is called the demographic transition model.
The correlation is surprisingly tight, as infant mortality drops population growth drops add in things like access to education and it gets even tighter.

I feel obligated to point out the r and K strategy are not binary but ways of describing a spectrum of reproductive approaches.

Thanks, that's very informative! You make the argument that falling infant mortality evolutionarily favors $K$ strategy reproducers. This would explain the correlation between infant mortality  and population growth IF genetic factors largely determine whether an individual human pursues a more r-type versus a more K-type reproductive strategy. If this is really the case, then because the phenotypic swing from r to K has been so dramatic over the last century or so, the genes responsible should stick out like a sore thumb in studies of human genetic change over that timespan.

But absent such compelling evidence, I'm inclined to doubt the hypothesis that genetic factors strongly influence whether an individual human pursues a more r-type or a more K-type reproductive strategy. That's part of why I suspect there may be some more "meta-level" biological mechanism at play. I suspect that humans (and other species) may have various adaptations which enable an individual to toggle between r-type and K-type reproduction based on subtle environmental cues, rather than it simply being a case of individuals with the appropriate genes for the environment outcompeting others

In my hypothesis, I might incorporate your observations by positing that among these "subtle environmental cues", perceptions of infant mortality rates may have very high (or even overwhelming) importance. Of course, I have equally little evidence to support this hypothesis.

@TimCampion very flew behaviors are hard coded in the way you think,  many if not most of instinctually behavior is trigger based, and it is fairly easy for an social organisms to determine child mortality. we know children instinctually keep track of siblings and gender ratios in there community. Plenty of organisms individually  change reproductive strategy depending on environmental triggers.

@TimCampion the biggest problem with carrying capacity is an organism have few ways to assess carrying capacity. more importantly if they were tracking carrying capacity we should see lower population growth in less abundant environments but we don't instead we see it in technological advanced ones, which are the places were carrying capacity is increasing.

I just read about John B. Calhoun's mouse utopia experiments in an interesting history stackexchange post.
The basic result is that when mice are given unlimited resources but constrained by space, their population does initially explode but this leads to a loss of social cohesion and thence to plummeting population levels.
While far from conclusive, this suggests to me that there are indeed some kind of biological fundamentals going on here which control overpopulation by means other than widespread starvation.
I'm sure there's lots more to say!


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Neurobiology of tantrums
As mentioned here, tantrums are primarily observed in young children and often involve a loss of self-control, both physical control and the ability to calm after a demand has been met. What changes in neurobiology reduce the propensity for this as children age? (The cause may be partly neurochemical, partly structural.)
I am especially interested in whether the vulnerability to tantrums in the young brain are at least partly due to positive feedbacks. A self-enhancing mechanism for the distress could explain why self-control sometimes suffers. (Positive feedback is also consistent with a colleague's claim, for which I have no source, that the risk of loss of self-control is low if a demand is met quickly.)

source: Stack Exchange

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sort: votes


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Which animals live in trees and make noises like rubber ducks at night?
I was recently at night in a public park in Karlsruhe, Germany. I've heard many (at least 10, probably many more - it's hard to tell) animals in the trees making noises similar to that of a rubber duck which is pressed.
What could that be?

It is most likely a Tawny Owl (Strix aluco), or Waldkauz in German, one of the most common owl species in Central Europe. These owls have many different calls, and you can hear them often here in Karlsruhe at night. Particularly their "kewick" call sounds similar to squeezing a rubber duck. It is usally emitted by female individuals during the mating season, but also males can produce it. Juveniles have a similar call as well. But most of the time - as far as I have noticed - you only hear their more common "hoo-hoo" calls (listen here or here).
Photo of a Tawny Owl:

Image Source:
https://commons.wikimedia.org/wiki/File:Waldkauz-Strix_aluco.jpg

Listening to the kewick call and trying to judge whether it really sounds like a rubber duck * ..... mmhh yeah... Ok, that works! +1

@Remi.b well he said "similar", not "exactly like" :)

It sounded exactly like the "kewick" call! Thank you! I'm positively surprised that somebody could identify that with this little information :-)

@MartinThoma Probably because we live in the same town ;)

@adjan Haha, the world ist small. But we don't know each other, do we?

I have lived close by, but our Waldkäuze didn't sound like rubber ducks, or our rubber ducks don't sound like Waldkäuze. Now I am confused.

@MartinThoma No I don't think so.

Where I live near Vancouver Canada, barred owls can sometimes be heard at night. My older son was convinced that some drunk teenagers were making stupid sounds at night. (Too many noisy drunks lived in the area.) When a bonded pair start caterwauling, they cerainly font sound like owls. Animals can make some very surprising sounds for those not familiar with them!

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What is the name of this whorled-leaf tree in India?
Location: South India
Month: June
Season: Rainy

Branch Distribution:

Leaf of the tree:

The leaves look like those of a Pittosporum

Bucida molineti also called geometry tree

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Is "reaction center" the same as "photosystem"?
I have a diagram which labelled a part of PSI (Photosystem I) as "reaction center". But I have read on several websites that the reaction centers are PSI (the whole complex, not just a part of it) and PSII.
So, which one is correct? And if the reaction center is only a part of these PSI and II complexes, what does it contain? And what does it do?

Reaction centers are specific sites within the photosystems where the adsorbed photon energy is transferred to electrons.

"Photosystem" and "Reaction center" are not synonyms.
According to Lodish (2000):

The absorption of light energy and its conversion into chemical energy occurs in multiprotein complexes, called photosystems, located in the thylakoid membrane. A photosystem has two closely linked components, an antenna containing light-absorbing pigments and a reaction center comprising a complex of proteins and two chlorophyll a molecules. (emphasis mine)

And according to Alberts (2002):

Multiprotein complexes called photosystems catalyze the conversion of the light energy captured in excited chlorophyll molecules to useful forms. A photosystem consists of two closely linked components: an antenna complex, consisting of a large set of pigment molecules that capture light energy and feed it to the reaction center; and a photochemical reaction center, consisting of a complex of proteins and chlorophyll molecules that enable light energy to be converted into chemical energy. (emphasis mine)

Therefore, a photosystem is composed by:

The antenna complex;
The reaction center.

Here is a figure from Alberts (2002):

Figure: The antenna complex is a collector of light energy in the form of excited electrons. The energy of the excited electrons is funneled, through a series of resonance energy transfers, to a special pair of chlorophyll molecules in the photochemical reaction center. The reaction center then produces a high-energy electron that can be passed rapidly to the electron-transport chain in the thylakoid membrane, via a quinone.
Thus, in conclusion, the reaction center is part of the photosystem.
PS: Both quoted texts answer your second question ("And if the reaction center is only a part of these PSI and II complexes, what does it contain? And what does it do?").
Sources:

Lodish, H. (2000). Molecular cell biology. 4th ed. New York: Worth Publ.
Alberts, B. (2002). Molecular biology of the cell. 4th ed. New York: Garland Science.


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Why our arms stop growing if mitosis never stops?
I wonder if there's a balance between cell death a new mitosis .

where have you looked for the answer to this question? do you have any ideas?


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Energy cost of chewing vs production of enzymes
Consider a hypothetical case that you ingest a piece of starch. Which is more costly energetically 1) chewing + reduced amount of enzymes production needed or 2) sole production of all the enzymes for digestion for achieving the same amount of glucose absorption given the digestion time is constant. (There could be different answers for different sizes of starch ingested)

I think an important consideration is the digestion efficiency. Whole food would have to be broken down from the outside-in. By chewing or otherwise mechanically disaggregating the food, the surface area exposure to digest enzymes is increased, which is more beneficial if the endpoint is products liberated over time.


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Is it possible to temporarily paralyze someone through the use of electric signals or focused ultrasound?
I've been reading about how it is possible to send signals to the brain using focused ultrasound or electrical impulses. It is possible to make someone see a certain shape or color by stimulating different areas of the brain. I was wondering whether or not it would be possible to temporarily shut off a person's motor functions by for example, sending signals to the cerebellum or perhaps intercepting them before they can travel down the spinal chord.

With in-depth study and research, it would be possible on 1 person. However, it's unlikely that this type of technology could ever be weaponized.
Nerves and neural networks are particularly known for having unique calibrations per individual. Even if you can decipher every neural communication protocol on a test subject, the signal protocol would be at least slightly different on others, even for crude movement control.
Mind control would be several orders of magnitude harder - each person's brain is different.
Most neurons communicate through neurotransmitters rather than electricity, completely ignoring your control scheme.
Even if none of these barriers existed, people could always block them using "tinfoil hats".

Yes. Those weapons exist, they are called Electroshock weapon, the most famous of which is the taser.
Tasers spill much ink in the media. You have probably already seen their use (and misuse) in videos.

Thank you for answering, but this isn't quite what I meant. I am talking about a non-painful non-invasive procedure that can prevent movement for a desired period of time. For example, this could be used as an alternate method to sedation in a patient that is having violent involuntary convulsions, or whose movements would otherwise need to be suppressed in order to deliver treatment.

I have no sources for this, but I guess the "impact" you need to immobilize a human with this type of method will never be non-painful.


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Why is our voice deeper in the morning?
For most (if not all) people, their voice sounds a lot deeper when they've just woken, compared to how they sound during the day. This effect can easily last for a few hours, like for me today. What are the biological reasons for this? I've heard that it has something to do with relaxation of your muscles during sleep, but I'm not sure how that is supposed to work, and there might be other factors at work.

What is the evidence for this? Are there references to this being a general phenomenon?

@kmm personal experience (n=±20), also, I vaguely remember it being discussed in a pop-science TV show.

Just a guess - higher pitched sounds require more energy than lower pitched sounds (at the same volume). Just after waking up, you are more likely to be tired, so the same effort to speak receives a lower energy input, requiring either the volume or frequency to decrease. For reference, my voice actually switches over to low frequencies when I'm tired as a power-saver feature.

I'm surprised there hasn't been any answer or comments but yes, this is a fairly well known phenomena. It's quite possible that not everyone finds this to be true for them or possible they've never even noticed it. If a person doesn't need to talk for the first 15 minutes to hour, they might not realise their voice is deeper and/or raspier first thing in the morning.
Speech pathologists, voice teachers and professional singers are certainly aware of this. There's been no solid research on why that I know of. After all who's going to fund research into something that's mainly a curiosity with no medical repercussions or profits to be made? Still, there are various thoughts on why this occurs (outside of acid reflux irritating the vocal cords).
During sleep while we're in a horizontal position, a certain amount of fluid collects in our upper body (read from the neck up), so our vocal cords will swell and thicken slightly. It's why our eyes look more puffy first thing when we arise. During the night, we're not using our vocal cords either but while breathing, air is still passing over them. So while the tissues swell a little, their outer membrane dries a little. To counter the drying effect, the body secretes more mucous as a protective coat. This effect is much worse in people who are mouth breathers.
Another possible reason is what voice teachers and singers think happens, too. Vocal cords, being muscles, need to stretch and contract to vary the voice's pitch. Unused through the night, they're nit as limber and can't stretch as well as later. Vocal cords stretch to reach higher pitches. If that idea sounds far-fetched, just remember opera singers and other professional singers need to limber up before performing. They practice hours each day but before a performance, they need their voice to be at its best. Hence they'll practice singing notes up and down the scale.
Supposedly, drinking a cup of lukewarm water first thing in the morning helps, and tea or coffee is supposed to dry out the throat even more. I never drink coffee but, personally, I've found that first hot cup of tea in the morning doesn't just help my voice return to normal but wakes me up.
I've never heard of this effect lasting for a couple of hours though I haven't gone around quizzing people. :) So try either the lukewarm water or a hot drink and see if it makes a difference. You can also try singing or just talking aloud to limber your cords in the morning.
Edited June 14/17
Links (but not scientific studies) where others have noted this phenomena
Why do people's voices sound deeper in the morning? I gave greater credence to the first answer since it comes from an opera singer.
Raspy Voice In The Morning?
And from Music SE Why is my voice lower pitched when I get up in the morning

Can you add references to your answer?

As I said, there's been no real scientific studies done on this (that I know of) but I can include links and will.


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Definition of Cofactor, Coenzyme and Prosthetic Group
This question arises from a student multiple choice question regarding whether certain inorganic ions present in certain enzymes (Cl− in catalyse and Zn2+ in carbonic anhydrase) could be classified as coenzymes or prosthetic groups, and the poster then asked why Cl– was a cofactor for amylase but not a coenzyme.
Expanding this to the general situation, the question becomes:

What is the difference between a cofactor, a coenzyme and prosthetic
group, and where are inorganic ions in this hierarchy?

On the wikipedia page (https://en.wikipedia.org/wiki/Cofactor_(biochemistry)) a coenzyme is defined as a complex oranic cofactor, so Cl- doesn't count. Another thing that doesn't make it a coenzyme (as far as I know) is that the ion is not directly involved in the catalyzed reaction.

@VonBeche cool! Got it now. Answer that below and i'll tick it as an accepted answer. Thanks!

I have edited the question to make it more general, but retained the specific reference to chloride and amylase as other answers have addressed that.

On the wikipedia page (en.wikipedia.org/wiki/Cofactor_(biochemistry)) a coenzyme is defined as a complex organic cofactor, so Cl⁻ doesn't count. Another thing that disqualifies it as a coenzyme is that the ion is not directly involved in the catalyzed reaction. This amylase contains both a calcium ion, involved in catalysis. The chloride is speculated only to be involved in differentiation between substrates, and is absent in other structures.

Why revive a four-year old question?
Although I do not consider nomenclature of this type terribly important, and the high-scoring answer from @VonBeche is reasonable, I decided to add my own ‘answer’ for several reasons. First this is a highly active question, probably because students are required to make this sort of distinction, second because there have been several recent incorrect answers, and third because none of the answers are supported by an authoritative source (I do not regard Wikipedia as necessarily authoritative). However, perhaps the most important reason is to emphasize that, although there has been a recent attempt to produce a standard nomenclature, in actual practice there is no generally agreed terminology for cofactors.
Authority used in this answer
Biochemical nomenclature arises in a haphazard manner from new research discoveries, and only when the dust has settled, so to speak, do committees try to standardize it. I expected to find something in the International Union of Biochemistry and Molecular Biology Recommendations on Biochemical & Organic Nomenclature but those seem confined to enzyme classification. I have therefore used as a starting point ChEBI — Chemical Entities of Biological Interest. This is a “freely available dictionary of molecular entities focused on ‘small’ chemical compounds” published on the EMBL–EBI website, and is part of the ELIXIR Core Data Resources “a set of European data resources of fundamental importance to the wider life-science community and the long-term preservation of biological data”.
ChEBI Definitions of Cofactor, Coenzyme and Prosthetic Group
URL: https://www.ebi.ac.uk/chebi/searchId.do?chebiId=23357
ChEBI Name: cofactor
ChEBI ID:  CHEBI:23357
Definition: An organic molecule or ion (usually a metal ion) that is required by an enzyme for its activity. It may be attached either loosely (coenzyme) or tightly (prosthetic group).
ChEBI Ontology: cofactor (CHEBI:23357) is a biochemical role (CHEBI:52206)
A number of compounds are listed as having the role of cofactor, including metal ions such as chloride and organic molecules such as NAD (sub-classified as a coenzyme, below) and FAD (subclassified as a prosthetic group, below)

URL: https://www.ebi.ac.uk/chebi/searchId.do?chebiId=CHEBI:23354
ChEBI Name: coenzyme
ChEBI ID: CHEBI:23354
Definition: A low-molecular-weight, non-protein organic compound participating in enzymatic reactions as dissociable acceptor or donor of chemical groups or electrons.
ChEBI Ontology: coenzyme (CHEBI:23354) is a cofactor (CHEBI:23357)
A number of compounds are listed as having the role of coenzyme (ascorbic acid, coenzyme A, NAD etc.) all of which are organic compounds.

URL: https://www.ebi.ac.uk/chebi/searchId.do?chebiId=CHEBI:26348
ChEBI Name:   prosthetic group
ChEBI ID: CHEBI:26348
Definition:   A tightly bound, specific nonpolypeptide unit in a protein determining and involved in its biological activity.
ChEBI Ontology: prosthetic group (CHEBI:26348) is a cofactor (CHEBI:23357)
A number of compounds are listed as having the role of prosthetic groups (e.g. FAD, haem lipoic acid), but none of them are simple metal ions although they are not exclusively organic (e.g. metal-sulphur clusters).
Ontological interpretation and comparison with Wikipedia Entry
The ChEBI entry on ‘Cofactor’ reproduces the opening paragraph of the Wikipedia page on the subject, relevant sections of which I quote below:

A cofactor is a non-protein chemical compound or metallic ion that is
required for an enzyme's activity as a catalyst.
Cofactors can be divided into two types: inorganic ions and complex
organic molecules called coenzymes.
Coenzymes are further divided into two types. The first is called a
“prosthetic group”, which consists of a coenzyme that is tightly or
even covalently, and permanently bound to a protein. The second type
of coenzymes are called “cosubstrates”, and are transiently bound to
the protein. Cosubstrates may be released from a protein at some
point, and then rebind later.

However, the nature of Wikipedia (anyone can edit it) is such that further down the page under the section on Classification, the following appears:

Cofactors can be divided into two major groups: organic cofactors,
such as flavin or haem; and inorganic cofactors, such as the metal
ions Mg2+, Cu+, Mn2+ and iron-sulphur clusters.
Organic cofactors are sometimes further divided into coenzymes and
prosthetic groups.

The section then goes on to say:

[Bryce 1979] noted the confusion in the literature and the essentially
arbitrary distinction made between prosthetic groups and coenzymes
group and proposed…
…cofactors were defined as an additional substance apart from protein
and substrate that is required for enzyme activity and a prosthetic
group as a substance that undergoes its whole catalytic cycle attached
to a single enzyme molecule.
However, the author could not arrive at a single all-encompassing
definition of a “coenzyme” and proposed that this term be dropped from
use in the literature.

Thus, it would seem that there are (at least) four different ways of classifying cofactors. That from ChEBI does not differ greatly from the second Wikipedia scheme (rather than the one it quotes), but the first Wikipedia scheme — distinguishing between coenzymes and prosthetic groups — certainly does.

Bryce’s suggestion to discard the term coenzyme has not been adopted, but his critique of the general nomenclature is a warning against dogmatism in this area. “Fools rush in where angels fear to tread.”

Nice one David, I think this adds considerably to the answers already posted. I second the emphasis on your phrase Biochemical nomenclature arises in a haphazard manner from new research discoveries, and only when the dust has settled, so to speak, do committees try to standardize it. Exam questions and answers are sometimes woeful when it comes to science, especially (i) in fields where strict nomenclature is not a practical way of life, or (ii) in fields where expertise aids in intelligibility of ambiguous terms, or (iii) within frontier research, where clear pictures haven't yet emerged.

Complex enzymes are made up of protein and nonprotein components. The protein part of the enzyme is called Apoenzymes or Apozyme. While the non-protein part of the enzyme is called Cofactor.
Cofactors are two types based on their chemical properties such as…..

Metal cofactors (inorganic compounds)- Metalloenzymes (Metallozymes) and Metal-activated enzymes

Organic cofactors – Coenzymes and Prosthetic groups

Read more here about the major difference between cofactors and Coenzymes.

Please read https://biology.stackexchange.com/help/promotion - I think there is a risk of appearing as a spammer if you are answering already-answered questions with answers that don't add to previous answers and always linking to the same reference site.

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In animals, birds, reptiles and fish, is a male sometimes unnecessary for a female to have/extend a male
Apparently in the human (animal realm) there are females that are female in body but their DNA is (XY) male, apparently 7500 in U.S., but apparently not able to have children ( http://abcnews.go.com/Health/MedicalMysteries/story?id=5465752&page=1)
I understand species like female hammerhead sharks can make clones with no male necessary for their female offspring (clones).  However, can a female make/extend a male, without receiving male fertilization?
If you also happen to know about the insect or plant kingdom please comment there as well.

Rephrasing your question
The question is worded in a funny way. If I am not mistaken your question is

Are there other means of reproduction than cloning that do not require mating with another individual? In particular, I am interested in such mean of reproduction that would allow an individual to create an offspring of another sex.

I will assume this is your question. I don't fully understand the point of the first paragraph though if this is your question.
Answer
Means of reproduction are much more diverse than we tend to think. So diverse that it is sometimes hard to really class each reproduction in non-arbitrary bucket.
Yes that exist! There are several modes of reproduction that may be of interest to you, the main one be selfing. Selfing is when an individual fertilizes itself. Now, by definition, such individuals need to be hermaphrodites, however it is not impossible that there are individuals that look males, others that look females and yet they (typically the females but not only) are able to self every so often.
Just to give a funny example to show how diverse system of reproduction might be. In social ants, the queen can either let the sperm of a male fertilize her eggs and produce a female worker (or a future queen depending on whether the larvae receive royal jelly) or chose to undergo normal meiosis but the gamete from the mother will directly develop into an individual without fertilization and make a male. This is not cloning because 1) only half of the genome is being transmitted and 2) recombination occur.
Related

What DNA does a self-fertile plant's seedling have?
Do males of all sexual species have Y chromosomes?

Hi Remi, thanks for trying to answer my question, sorry for the confusion (I tried to rephrase).  I'm trying to fully understand your ant example.   My question is, can a female produce male offspring with no fertilization by a male?  This would mean she is DNA complete male & female, and does not need the male in the species to procreate males.  Does that exist?

Yes, that's what queen do. If the eggs is fertilize, it becomes a female, if the egg is not fertilize, it becomes a male (males are therefore haploids). This is just one example among many others (although I would not be able to pull out plenty of example out my mind right now).

I don't know what you mean by  DNA complete male & female though. It seems like you think there is male DNA and female DNA. This is mostly wrong. You should have a look at this post, esp. the section Diversity among the species that have sexes of the accepted answer.

Oh, thanks Remi.  What I mean by "DNA complete male & female" is a human man's cells has the DNA makeup to produce, say by cloning, either a boy or girl, but a human woman's cells do not, having XX and not an XY.  Am I seeing things incorrectly?

Have you looked at the post I pointed to in the comment and in the post? Your issue is to think that all species are GSD while they're not. On top of that, your issue is to fail to recognize that in some GSD cases sexes are differentiated by copy number variants (CNV) (e.g. C. elegans) and therefore a single parent could just increase or decrease such number of variants.

Thanks I just read it.  So with social ants, if the male is involved in reproduction the offspring is always female, and if he is not involved, then the offspring is always male?

Yes, in most ant species at least.

Does Caenorhabitis elegans fit your description?

There are two C. elegans sexes: a self-fertilizing hermaphrodite (XX) and a male (XO). Males arise infrequently (0.1%) by spontaneous non-disjunction in the hermaphrodite germ line and at higher frequency (up to 50%) through mating. Self-fertilization of the hermaphrodite allows for homozygous worms to generate genetically identical progeny, and male mating facilitates the isolation and maintenance of mutant strains as well as moving mutations between strains.

Thanks for contributing.  I'm confused about this -- read the link you gave: how does the female create an XO if she only has XX?  Apparently, "Nondisjunction is the failure of homologous chromosomes or sister chromatids to separate properly during cell division. There are three forms of nondisjunction: failure of a pair of homologous chromosomes to separate in meiosis I, failure of sister chromatids to separate during meiosis II, and failure of sister chromatids to separate during mitosis"

Comment cut me off.  Anyway, how does she, XX, make an XO without him (XO)?

@Ray O is not a chromosome. O means absence of a chromosome. Hermaphrodites have two X chromosomes while males have one.


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Dissolving cell pellet after sonication
I was doing a protein prep and I made a mistake. After sonicating my cells, I was supposed to centrifuge and collect the supernatant (my protein is soluble and comes in the supernatant). I however, forgot to centrifuge and loaded the entire solution after sonication (debris and all) onto a Ni-NTA column.
Is there any way to dissolve the cell debris so that I may be able to recover the NTA beads?

Follow the instructions that came with your column for cleaning. The resin will probably be fine, but you'll need to thoroughly clean the column. My GE columns recommend washes of:

20% EtOH
30% Isopropanol
1M NaOH
1M NaCL
SDS in 0.1M Acetic Acid
Stripping buffer (EDTA)

Wash between each with several column volumes of distilled water. You may not need to do all of them. Then just recharge your column with a 100 mM Ni solution (or metal of choice)

You could try to resuspend everything and carefully decant, this would get rid of most of the cell material, as the beads will sediment much faster. Then wash the column with a ridiculous amount of acid or base.
But you should just discard everything and take new beads, they're not that expensive (maybe 10-20$/ml resin).

You might also try washing with guanidinium.


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Can a virus be transmitted from a sweating person out to another person?
In the sport of Jiu-Jitsu, close contact with many partners is common. Many times these partners are sweating profusely (Yuk), which in turn drips on the other person sometimes into the eyes, nose, and yes mouth. I am just wondering if viruses can enter in this way.

Sweat per se, at the source, is not likely to be contaminated with bacteria or viruses. However, that's a moot point, because as soon as it's produced it's on contact with the sweaty person's skin, which is invariably coated with bacteria and potentially with viruses. Sweat can therefore act as a medium for transferring infectious agents between two hosts.
Examples of this are described in Contact transmission of vaccinia virus from smallpox vaccinees in the United States, 2003–2011:

Among adult male cases, the most frequently reported activities associated with vaccinia transfers were wrestling, grappling or sparring (n = 18) [12,18–20]; household interactions (e.g., sharing towels, clothing) (n = 6); unspecified “contact” (n = 4); and football or basketball (n = 3).

(Vaccinia virus is the vaccine for smallpox. As such it's far less dangerous than smallpox itself, but as an ancient vaccine it's also much more dangerous than the vast majority of modern vaccines, and exposure to large concentrations of the virus in an uncontrolled setting is potentially risky.)

In short, yes. Virus particles, or bacteria on one persons skin can end up being in the sweat that is transferred from one person to another. They can also be transferred by direct physical contact though, so the sweat isn't the only source of transfer.
I will caveat that a healthy person shouldn't need to worry about the amount of harmful bacteria in sweat as the numbers will be so low that their immune system can take care of it fine.


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Why do bacteria eat enamel?
What causes tooth decay bacteria or acids?
I've been told that it is a combination of both but why would bacteria eat enamel?  There are much easier supplies of protein for bacteria to munch through (such as gums) and many of the elements within enamel are not needed for bacteria to respire. Is bacteria eating enamel a myth and if not why do they do it?

While I can't find any specific sources regarding bacteria eating enamel, I highly doubt this is what's happening in our mouths. I doubt this because your point is likely true - minerals in enamel provide no added benefit to the bacteria. I would ask a dentist about this to be sure though.
However, what is certainly true is that the acid produced by the bacteria in dental plaque is what causes tooth decay and gum disease. More specifically, S. mutans is the primary culprit behind dental plaque. Most notably is that S. mutans is an anaerobic organism and because it doesn't require oxygen to respirate, the pathway results in lactic acid as a by-product. This lactic acid is what makes enamel prone to demineralization and if untreated, can irritate your gums, causing gingivitis. It's also worth noting that not all bacteria will do this - not even all anaerobic bacteria that release lactic acid will do this. S. mutans is likely one of the few bacterial species that can survive in your mouth because of it's ability to withstand low pH environments in your mouth and form biofilms - able to nicely stick onto teeth.
S. mutans has no need to munch through enamel or gums. Much of what it breaks down for respiration can be easily obtained from the food and drinks that are left behind after a meal - mostly sugars such as sucrose.

Bacteria feed upon food particle left between n around the teeth and feed upon them. They also produce metabolic acid which corrodes tooth enamel.

Hi. Could you elaborate your entry and add references, like links to credible open sources? See help page for more information on how to write a good answer. I would also suggest to use standard English words to ensure readability. Here's a link to [edit].

The bacteria actually aren't eating the enamel, they eat the food attached to the enamel and excrete acids that wear down the enamel.
Over the decades there have been various experimental treatments for chronic tooth decay where S. mutans gets gene-edited for alcohol fermentation instead of lactic acid fermentation.


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References concerning the relative population sizes of predator and prey
In an ecosystem, say there are two species in a predator-prey relationship. What is the most typical ratio of these species' population densities? For instance, it could be that for every fox, there are ten rabbits. Actually, the precise ratios are somewhat irrelevant; mostly I would like to know if we can say that the number of prey is generally larger than the number of predators.
I would like references to articles, textbooks, etc. that contain information about such ratios.
Note that this is aimed at the number of species within a single ecosystem. However, if this information is hard to quantify (perhaps because it is hard to define where an ecosystem ends), global populations could be used as an estimate.
Forgive me if this is ill-defined or trivial, I'm a physicist by training.
Thanks.

A way to reword your question is Typically, how many individuals are there at each trophic level?. Keywords, you should be looking for are "food chain", "trophic level", "trophic dynamic", "cascade effect" and "trophic pyramid".

@Remi.b Ah, that makes sense, thanks! Do I even need a reference to say that there are more individuals at lower levels? Isn't it necessarily so, considering that not all the energy (some is lost) from one level can be transferred to the level above it?

@Remi.b Hmm, but then what if the ecosystem is not very clearly trophically stacked/separated (so it is more appropriately called a food web)?

No ecosystems are. But I would have thought your question as necessarily implying this simplified categorization. The model you present is an even more extreme simplification of the reality of food webs after all. Don't get me wrong, I think the question is of interest (I up voted it). You don't need reference or anything for your post to be valid. I was just trying to offer you some vocabulary that may help you (or other users) to look for such estimates.

@Remi.b Sorry, I should have been more clear: I didn't mean that I needed the reference in order to ask my question, here on the site, but rather for the thesis I'm writing (I'm working with population dynamics), where I claim that prey are usually more abundant in number than the species preying on them. After your comment it seemed self-evident that this was the case, so I was wondering whether a reference was even needed in my thesis.

It is kinda obvious that higher trophic levels have fewer individuals than lower trophic levels but the actual ratio is not obvious of course. It is always good to cite though, esp. for a thesis where there is likely no upper bound on the number of citations.

@Remi.b Right, I agree. If you have any suggestions for useful articles, please do let me know. I will try searching a bit using the key words you suggested. Thanks again!

For your curiosity, the post What prevents predator overpopulation? is loosely related.

You are indeed correct that the prey of predators are usually more common than their predators, especially if you focus on "true" predation (i.e. remove parasitism and parasitoidism). As a rule of thumb, the energy conversion between trophic stages is 10% (first proposed in Lindeman, 1942), which sets one sort of bound on the density relationship between predators and prey. The relationship is extremely variable though, which is easily understood if you consider the density relationships of hares and foxes vs. whales and krill.
For a general reference, Hatton et al (2015, "The predator-prey power law: Biomass scaling across terrestrial and aquatic biomes") might work, even though it is mainly framed in terms of biomass. However, the paper clearly states that biomass and density usually go hand in hand. The main result of the paper is that the biomass relationships between predators and prey collapse to very regular power laws (exponent 3/4) across ecosystems.
As mentioned above, and depending on who you ask, parasitism and parasitoidism are sometimes seen as types of predation. There, the density relationships between "predator" (parasitoid) and "prey" can be very different, especially at certain points in time or at certain lifestages. For instance, in insects it is not uncommon for one "prey" (host) to give rise to a large number of newly hatched "predators". This means that the number of parasitoids can probably outnumber the number of hosts, at least at smaller spatial scales, at some time periods (e.g. late summer, before the parasitoid is hit by high winter mortality).

"The main result of the paper is that the biomass relationships between predators and prey collapse to very regular power laws (exponent 3/4) across ecosystems." This.

Thank you for the answer! Another example of predator outnumbering the prey would be phages vs. bacteria.

@Lovsovs Definitely! If you go small and use a liberal definition of predator this is indeed common.

mostly I would like to know if we can say that the number of prey is
  generally larger than the number of predators.

If this is actually your real question, the answer is straightforward: the most widely-used classification of trophic strategies that I'm aware of (Lafferty & Kuris 2002; full reference below) includes the requirement that a predator attacks (first dichotomy) and kills (second dichotomy) multiple victims in its lifetime. So your statement is necessarily true; if each predator kills more than one prey, prey must (generally) outnumber predators.
Be aware that this ignores micropredators, parasitoids, parasites etc, though.
Reference: Lafferty, K.D., and A.M. Kuris. 2002. Trophic strategies, animal diversity and body size.  TREE 17(11): 507-513.


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What is the standard electrode potential of human blood?
Healthy humans have a pH of around 7.4 (slightly basic.) But if you hooked up the blood as a battery how much electric voltage would one generate, what is the standard electrode potential?
This seems to me like it should be important for stuff such as transporting ions across the cell membrane.
If I think about it this question basically comes down to if things like iron tend to dissolve $\ce{Fe -> Fe^{2+} + 2e^-}$ (SEP of 0.44)  or precipitate $\ce{Fe^{2+} + 2e^-->Fe}$ in human blood.
Because of important chemicals like haemoglobin I think the SEP should be around 0.44 but differs depending upon whether cells are absorbing oxygen from it or recharging it with oxygen. Maybe this would even vary depending on whether heavy exercise is happening.

Not related to the question: the blood pH of 7.4 is not basic: that's the neutral pH. The neutral pH varies according several factors: 7.0 is the neutral pH of pure water, and even so at a given temperature only (25 C). At 0 C, for instance, the pH of pure water is higher than that 7.4 for the blood. Thus, have in mind that a blood with pH of 7.3 is acidic, not basic.

@GerardoFurtado Right.  $K_{eq} = e^{\frac{-\delta G}{RT}}$ so the neutral equilibrium and resultingly pH varies with temperature. I just never connected that to acid stuff.

Sorry, I'm just a bit confused.  I thought the electrode potential depended on the oxidation and reduction potentials of the two dissimilar metals, not on the electrolytic medium.  Am I missing something?

@anonymous2 In a Galvanic cell one electrode will dissolve and another electrode will gain a coating. If an electrode is stuck in the human body the electrode would start to gain some kind of coating or start to dissolve. In response, the body would start to deal with the excess of new ions or deal with the loss of ions and maintain homeostasis for a bit until the person starts getting sick.

@StevenStewart-Gallus ah, gotcha.  Thanks for the clarification. :)

I don't think @anonymous2 is confused, I think the question makes no sense. You can't just stick an electrode in the blood, the electrode has to be made of something. Your explanation skirts around that problem: "In a Galvanic cell one electrode will dissolve and another electrode will gain a coating" - what's the electrode that is dissolving and what's the electrode that is gaining a coating?

I see that you edited your question, but you still keept a clearly wrong information (the blood being slightly basic). I can't understand why.


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Is there a measurable variance in neuronal transmission speed and fidelity?
My understanding of how neurons transmit signals is pretty basic - dendrites receive signals (both excitatory and inhibitory), transmitting them to the cell body where, if a sufficient depolarization builds up, the axon fires an action potential, sending the signal along. This entire process is carried out by various ion channels, especially voltage gated ones. My question is this - do we know how sensitive the speed and reliability of the process are to genetic variations that control how these ion channels are built? Is it robust enough to permit small variations, or is any change catastrophic? If it permits small variations, do we know how variable the human population is for features like signal fidelity (low rate for failing to fire when the neuron should, and low rate for firing in the absence of stimulus) and transmission speed?
Considering the difficulty of studying humans, is this sort of information known for mice, rats, primates, or etc?

Action potentials are pretty robust in most circumstances, but minor tweaks at various stages of the process, whether conduction, neurotransmitter release, or post-synaptic responses, sometimes affecting only certain populations of cells, are thought to be behind many neurological disorders and conditions, including schizophrenia, autism, epilepsy, multiple sclerosis, and some peripheral neuropathies. Of cousre many of these conditions have both environmental and genetic influences, so it is often difficult to attach a specific genetic cause.

There is a certain amount of variation in the genes that regulate ion channel/receptor structure, much of which has little/no affect on neuronal function. But as @BryanKrause says, many are known that do cause neuronal disorders. A very interesting question, but I don't know the genetics well enough to provide a decent answer.

@OliverHouston What I was trying to get at, although maybe not too clearly, is that a lot of the variation in those genes does not deterministically cause disorders, but that variation may predispose certain individuals to those disorders. For Sean: it isn't directly related to your question, but on the issue of robustness you could read some papers on multiple sclerosis. MS is a demyelinating disorder, which eventually impairs conductivity, but it actually takes quite a bit of demyelination before the symptoms are noticeable.

@BryanKrause My main interest is less in disorders and more in variations and trade-offs in how these things affect performance. For instance, I could imagine that tuning the depolarization needed to trigger down could lead to faster nerve conduction, but also less reliable signalling. Another way to imagine it is the extent to which a plurality of strategies in the trade-off spaces manifest themselves.

Got it - based on your SE background I see you are mostly a physics/math person. I would highly recommend the "NEURON" simulation which is freely available and documented in various places. There are pre-existing models that you could tweak to test some of your hypotheses. For example, if you are talking about conduction, rather than action potential initiation, you will find that one of the important factors in both threshold and reliability is voltage-gated sodium channel concentration. However, more Na+-VGCs will mean both a lower threshold and more reliable signalling.

Also note that in biology if you ask about variability: "do we know how sensitive the speed and reliability of the process are to genetic variations" - the answer is almost always going to depend somewhat on the phenotype. If a variation doesn't cause any disorder, there is no selective pressure to prevent that type of variation, so over generations that variation will tend to increase on average. The presence of some low-efficacy genetic causes for some of the disorders I mentioned is good evidence that there is some variability in the population, though.


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What do we mean by distribution of species?
What is meant by distribution of species in the following context?

density-independent factors tend to limit the distribution of individuals and therefore of species.

I formatted your question, to improve readability.

From the limited context of the quote, it is referring to this definition of distribution (via Merriam-Webster):

a :  the position, arrangement, or frequency of occurrence (as of the members of a group) over an area or throughout a space or unit of time
b biology :  the natural geographic range of an organism

Or, if that isn't simple enough, it just means where the members of the species are located. In different contexts it may be simply the range, i.e., the space where any individuals of that species are located, or it might actually refer to the density as well.

Welcome to Biology.SE!

Species distribution is the manner in which a biological taxon is spatially arranged.

In the specific sentence you suggest, it seems that the term species range would have eventually be a little bit more appropriate though. The species range is the delimitation over space where individuals are found. The species range is just the maximum value in every possible direction of your species distribution.
Note however, that we often don't care too much about such semantic details (the sentence sounds correct to me).
Next time, please specify where you get the citation from 1) because context often matter and 2) because it is a copy right issue to not cite your source.

Same as above in simple terms
The term species distribution (and species range) describe the geographical locations of individual of the population (of a species). We are talking about a single species here. The term distribution takes the same definition than it does in statistics if you are used to it.
Imagine you have a population of oak trees. You can position every single individual tree over space Consider the drawing
Each individual is represented by a circle. The blue line represents a river.

Description of the species distribution: There are no individuals south east of the river. There is a clutch of high density at the north west of the study area.
Description of the species range is given by the red circle

The difference between species range and species distribution does not matter much for your purpose. The point is that you understand those terms are concepts describing the geographical locations of individual of the population (or the species if you prefer)

Hi can you please explain what that definition means using simple words ? My english is not good enough to understand that. By "species range" do you mean the amount of biodiversity within a particular species ? Or what ?

@Maxwhite Does that help?


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Are bacteria incapable of producing cytokines such as interleukins?
As far as I understand, bacteria cannot produce cytokines such as interleukins. However, I have not read an explanation as to why they cannot. Perhaps it has to do with an evolutionary limitation. Yet, if this is the case, why would bacteria be incapable of acquiring new functions such as cytokine production during their evolution, especially intracellular bacteria which reside within immune cells. If bacteria have not been able to acquire this function, then maybe it has to do with a biological constraint (size of the proteins, amino acid composition, machinery or bioenergetic capacity). If anyone knows the exact reason or has a knowledgeable explanation I would really like to read it. Thanks.

For what reason should they produce interleukins? To attract immune cells?

@Chris IL-10, for example, is immunosuppressive. It should not be surprising that pathogens can produce immunomodulating molecules, including cytokine homologs. I'll post an answer later.

Agree with Chris above - what functions would cytokines play when produced by a bacterium? I'm not familiar with whether or not bacteria make cytokines (of why they would)... maybe there could be some sort of theoretical role for making 'decoy' cytokines as a way to throw off the endogenous immune system. Just a random though that I have no data to support...

It seems especially pertinent to point out from the start that many cytokines are anti-inflammatory/immunosuppressive. The immune system has evolved to remove pathogens from the body, and normally these cytokines act to deactivate the immune response once an infection has been cleared. It should not be surprising that pathogens have co-evolved defences to the immune system, including interference with cytokine networks and even production of anti-inflammatory cytokine homologs, ostensibly to subvert the immune response. Below are but a few examples of this.

Viruses
Kotenko SV, SAccani S, Izotova LS, Mirochnitchenko OV, Pestka S. 2000. Human cytomegalovirus harbors its own unique IL-10 homolog (cmvIL-10). Proc Natl Acad Sci USA 97(4):1695-1700.

Many viruses exploit the strategy of using homologs of cellular cytokines or cytokine receptors to shield virus-infected cells from immune defenses and enhance virus survival in the host. The presence of virus-encoded homologs of cellular proteins may be an indicator of the importance of these cellular components in immune mechanisms for combating this virus in vivo. A number of herpes viruses harbor homologs of IL-10. Epstein–Barr virus (EBV)-encoded IL-10 (ebvIL-10), the first viral homolog of IL-10 identified, shares many but not all of the biological activities of cellular IL-10 and may play an important role in the host-virus interaction. In addition to EBV, another virus, the Orf poxvirus (OV), which can infect humans, has its own IL-10 homolog, ovIL-10.
...
IL-10 has several immunosuppressive activities that would be favorable for CMV, such as down-regulation of MHC class I and II expression, inhibition of production of inflammatory cytokines, and interference with antigen presentation. Murine CMV infection induces transient early expression of IL-10, which plays an essential role in MHC class II down-regulation. EBV infection causes expression not only of ebvIL-10, but also of human IL-10. We demonstrated here that human CMV encodes its own functional IL-10 homolog, which is expressed by CMV-infected cells. Thus, it seems likely that herpes viruses acquire many advantages by using IL-10-specific biological activities either of virus-encoded or host IL-10s.

Parasites
Ouaissi A. 2007. Regulatory Cells and Immunosuppressive Cytokines: Parasite-Derived Factors Induce Immune Polarization. J Biomed Biotechnol 2007(4):94971.

Another intriguing aspect in the parasite relationship is the fact that parasites could release factors that mimic host cytokines. For instance, (1) hydatid ﬂuid fractions mimicked IL-1, IL-2, and IL-6; (2) an IFN-γ homolog that binds to the IFN-γ receptor and induced change in lymphoid cells has been identiﬁed in an intestinal nematode; (3) two homologs of the human macrophage migration inhibitory factor (MIF) have been characterized in the human parasitic nematode Brugia malayi and termed Bm-MIF-1 and Bm-MIF-2, both having functional properties similar to the MIF human counterpart; (4) Toxoplasma gondii releases cyclophilin-18 (C-18) that signals through the chemokine receptor CCR5 leading to the IL-12 synthesis by dendritic cells and a strong protective response; (5) the tapeworm Hymenolepis diminuta has been shown to express an IL-12-like peptide, one of the suggested hypothesis being that the peptide could act as a competitive antagonist for the IL-12 receptor, thus contributing to the general immunosuppression.

Bacteria
I have not found such explicit examples of bacteria producing cytokine homologs. However, their ability to produce immune modulating, paracrine signalling proteins, which is essentially the definition of a cytokine, is well known. The following reviews are quite extensive and provides numerous examples:
Wilson M, Seymour R, Henderson B. 1998. Bacterial Perturbation of Cytokine Networks. Infect Immun 66(6):2401-2409.

In recent years it has become apparent that bacteria produce many molecules which have profound effects on the capacity of leukocytes and tissue cells to produce selected cytokine networks. Thus attention will have to switch from the current view of the host cell as the only controlling factor in cytokine biology, once the bacterium has stimulated this cell, to one in which the bacterium, by modifying its exported or structural molecules or by direct interaction with the cell, can directly modify cytokine networks.

Henderson B, Poole S, Wilson M. 1996. Microbial/host interactions in health and disease: who controls the cytokine network? Immunopharmacology 35(1):1-21.

Recent cytokine transgenic knockouts demonstrate that the normal benign response to commensal gut microflora becomes a lethal inflammatory state in the absence of the cytokines interleukin 2 or interleukin 10... We propose that the ability of the multicellular organism to live harmoniously with its commensal microflora must depend on mutual signalling involving eukaryotic cytokines and prokaryotic cytokine-like molecules. Such interactive signalling sets up non-inflammatory cytokine networks in tissues which form the background on which responses to infectious microorganisms must be built and related... It is now clear that bacteria contain and produce a large number of diverse molecules which can selectively induce the synthesis of both pro-inflammatory and immunomodulatory/anti-inflammatory cytokines.

Finally, the mechanisms by which bacteria can co-evolve such cytokine-like molecules is discussed in this review:
Stebbins CE, Galan JE. 2001. Structural mimicry in bacterial virulence. Nature 412(6848):701-705.

Recent studies have begun to reveal that many bacterial pathogens mimic the function of host proteins to manipulate host physiology and cellular functions for the microbe's benefit. This is in contrast with the strategies used by some pathogens that involve microbial products with activities lacking clear counterparts in eukaryotic cells. Here we consider recent structural work that provides unique insights into the mechanisms of host mimicry by bacterial virulence factors. In some cases, these factors are homologues of host proteins that have been incorporated into the genome of the pathogen and subverted for its benefit. In others, convergent evolution has produced new effectors that have no obvious relationship to host factors. However, although hidden at the sequence level, the determination of the crystal structures of several bacterial factors and bacterial–host protein complexes has revealed the presence of mimicry at the molecular level.

Bacteria don't produce cytokines naturally (while some might be 'useful' for immune suppression, bacteria can't use human genes/DNA, which has introns, and the chance to randomly come up with a gene that makes the correct protein would be astronomically low).
However, bacteria CAN produce cytokines, if they are engineered to so: here is a company that sells various cytokines, many of which they produce in E. coli. To make this work the company had to remove all introns from the cytokine producing genes and add a bacterial promoter to the gene.
The only thing, which is needed for some human molecules to work (e.g. antibodies), that bacteria can not produce (at least with current technology), are glycosylations of proteins. I checked it quickly and it doesn't look like cytokines are glycosylated (at least in principal, there are very likely some exceptions).


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Name of this plant
I contact you all with great pain because my cute little plant is slowly deterioriating. I need you help. Do any of you know the name of this plant and/or the caring specifications for it? If it helps, it stays in South America.
Thanks you all.

Do you think it is native in South Africa or do you think it could be ornemental? If it is ornemental, you will have better chance of getting an answer on Gardening.SE.

That's a crassulacean native to Madagascar, called Bryophyllum daigremontianum.
It has a synonym, Kalanchoe daigremontiana (funily enough, bot Portuguese and Spanish Wikipedia pages — since you are in South America — use this synonym).
Its common names are "Mother of thousands". "Mother of millions", "Mexican hat plant" and "Devil's backbone".

Regarding how to care your succulent, unfortunately this is off topic at Bio SE (but have a look at my comment below).

PS: regarding you poor plant, here is an advice from a guy that normally kills his succulents: you're probably adding too much water.


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Did I understand the definition of "gross primary production" correctly?
According to wikipedia

Gross primary production (GPP) is the amount of chemical energy as biomass that primary producers create in a given amount of time.

So if a plant creates 6g of biomass in 1 second for example, then the amount of chemical energy stored in the 6g increase in weight is the GPP?

Yes, you more or less got it!
If you have only 3 primary producers (say 3 plants) in a given ecosystem.

Plant A produces 2g of organic carbon per second
Plant B produces 5g of organic carbon per second
Plant C produces 1g of organic carbon per second

, then the GPP is 8g per second.
This produced organic carbon can be in the form of leaves, root or whatever tissue these plants are growing.
Note: the numbers chosen are irealistic both in terms of production per second and in terms of number of plants in an ecosystem.

gC (grams of carbon assimilated) m-2 (m squared) year-1", what is meant by "grams of carbon assimilated" ?

The whole point of primary producers is to fix carbon. That is to take inorganic carbon (such as $CO_2$) and make it organic (such as $C_6H_{12}O_6$ aka glucose). This is why we are typically particularly interested in carbon and not so much in water.
For more info, you should have a look at an intro course to respiration and calvin cycle.
Note that if you remove water from an organism you are roughly speaking left with 75% of carbon, 10% of Nitrogen and the rest made of different elements.

alright thanks,,, and when we say that the GPP is measured in "gC (grams of carbon assimilated) m-2 (m squared) year-1", what is meant by "grams of carbon assimilated" ? i quoted this from my book and i dont know what they mean by that.

Okay so if a plant makes for example 100g of organic product in one second then the mass of carbon in this 100g is the GPP in gC per second , right ?

wait what did you edit yesterday ? i cant see the difference. Can you please answer my last comment ?

Yes, you were right. Note however, that when you read a paper you want to make sure that they really measure the mass of carbon and not just the dry mass or the energy freed from combustion as many authors may use proxies.


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What is the name of this thorny plant?
Location: South India
Month: June
Tree:

Leaf:

Its Flower:

EDIT:
For avoid confusion about ID this species, I even added its flower now.

Your tree appears to be from the Genus Dichrostachys.
It has several species, quiet a number of them have been reported only in Madagascar.
There are two species found in India, D. santapaui and D. cinerea.

How have I reached this plant?

The leaves of your plant are bipinnately compound. They gave me the impression of Mimosa pudica.
Of course it is not one. Mimosa pudica become creepers with time
and have short and thin prickly thorns.
Resemblance of an unknown organism with a known one can indicate shared derived character(s) (Synapomorphy), meaning they can be related.
Google's algorithm is often able to trace this relation. Look at the keywords I had used. If it doesn't one needs to experiment with the keyworks, note the word Fabaceae, it is the family to which Mimosa belongs.
Wikipedia  often is just the right place to start one's research.
The description of Dichrostachys cinerea is what I checked next, after having ascertained that is found in India.

Dichrostachys cinerea is a tree characterized by bark on young branches, dark grey-brown fissures on older branches and stems and smooth on the spines.
They typically grow up to 7 metres (23 ft) in height and have strong alternate thorns, generally up to 8 cm (3.1 in) long.
  Flowers of the Dichrostachys cinerea are characteristically in bicoloured cylindrical spikes that resemble Chinese lanterns and are 6–8 cm long and fragrant.
The species tends to grow in rainforest zones.In India, it can occur in dry deciduous forest.

Every thing fits well upto Genus Dichrostachys.

Dichrostachys is an Old World genus of legumes in the Fabaceae family.
Their Acacia-like leaves are bi-pinnately compound.
Unlike Acacia their thorns are hardened branchlets rather than modified stipules. They are native from Africa to Australasia...

The next thing I exhaustively checked were the species under this
    genus. I checked their
    locations,
    out of all two species have only been reported in India; D.
    santapaui and D. cinerea.
The reason behind this unusual format is to show you  how to fish. I will leave the rest of the hard work of digging up the species to you .

Few interesting facts about this genus:

Its name is derived from the Greek words dis (two), chroos (colour) and stachys (grain ear or spike), which in combination suggests their bi-colored inflorescences.

Dichrostachys cinerea, known as Sicklebush, Bell mimosa, Chinese lantern tree or Kalahari Christmas tree (South Africa).
D. cinerea is used in Ayurveda.

Great answer! You know what they say Give a man a fish, he'll eat for a day; teach a man how to fish, he'll eat for a lifetime. By explaining how to find the name of a species on our own, you have taught me and the OP how to identify on our own. Brilliant job I say!

Maybe it's
Prosopis juliflora:

It's popularily known in South India as சீமை கருவேல (translitered as:Seemai karuvelam). It's an invasive weed introduced in 1880.
It belongs to the Fabaceae family of plants. It flowers quickly after leaves form:

I hope this helps.

I added flowers also now.


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how do microtubules polymerize?
given that micro tubules are involved in so many processes in cells, it seems that such a complex "highway" would require some advanced underlying mechanism to orchestrate its assembly in a direction needed for the cell, such as towards a kinetochore. multiple search results on google and textbooks simply just state polymerization as is without explaining how these events happen. so how are microtubules polymerized and how is this polymerization oriented directionally ?

Microtubules are made up by $\alpha$- and $\beta$-tubulin units, the wiki page for this will link you to a short section on microtubule dynamics, which is the basis of how the growth & shrinking of microtubules is controlled:
Microtubules grow (by addition of $\alpha\beta$-units) and shrink (by dissociation of these units) primarily at the '+ end', which is the one in the cell periphery not at the centriole. Actually both of these reactions (growing/polymerisation and shrinking/de-polymerisation) usually happen at the same time but with different speeds. These speeds depend on whether GDP or GTP is bound by the $\beta$-tubulin at the + end, the (relative) concentration of GTP-bound free monomers and other structural proteins. Except for the GTP/GDP bound state in the mircotubule all of these factors can be controlled (or altered) by the cell through various mechanisms (some are listed on the 2nd wiki page I linked; I may add some specific ones if I have more time).

the wiki page you listed mentions MAPs and plus end tracking proteins, if a cell needed to, for example, send a mircotubule to attach to a kinetochore or orient its Golgi bodies to a specific side of a cell (like how a t cell orients its own golgi bodies before releasing its effector molecules ), would the directionality of this polymerization use a concentration gradient ? or perhaps a series of signal proteins in a cascade?       edit: just trying to get a good conceptual framework of cystoskeleton protein interactions


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Nutrition mineral intake method
I always wonder if rather than getting minerals from food, can I directly eat them and will they have same effect as in food,
e.g. can I eat iron filings for iron, magnesium and drink hard water for calcium?
Is there any difference between having minerals through food or directly eating metals?

Please avoid using texting language for Qs & As on the main site, I have edited to fix grammar.

To absorb essential elements, body must get them in form of stable ions.
So for calcium and magnesium, our body absorbs them from the hard water in the same way it obtains from other sources and uses them identically.
For iron, we cannot obtain iron from iron fillings because iron reacts with water and other chemicals in our body which can produce harmful effects.
For further information on absorbtion of calcium from hard water visit http://goaskalice.columbia.edu/answered-questions/calcium-hard-water


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Why is my white hair turning black/dark brown?
The only change I have made is I started taking a multivitamin daily (centrum silver, men over 50) about a month ago....Now I see black hairs in my beard and on my head.  I was prematurely gray (started at age 20) and have been completely gray/white for the last 20 or so years. Just curious...


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Why shouldn't dogs eat chocolate?
I was wondering why dogs shouldn't eat chocolate. Can't dogs just excrete the indigestible component in their droppings?
It's common knowledge that dogs shouldn't eat chocolate. What I don't know is why chocolate would kill them, from a specifically biological perspective.

Welcome to Bio.SE! I upvoted this question because it generated an interesting answer to me. Generally, for future posts do consider doing a bit more research and explaining what you discovered before posting. This community isn't a "homework service".

Please note that chocolate is toxic also to humans, the difference is that we can tolerate much higher doses. There are also some positive effects of cocoa ingestion so I am not asking anyone to stop eating cocoa-based products. Just adding some context.

Dogs can eat chocolate just like you can eat nightshade: once. Maybe update the question to say "shouldn't"?

@zzzzBov can have (at least) two meaning - being physically capable of and being permitted to do something. E.g. "you cannot drive more then 50 mph in this zone".

@MaciejPiechotka, sure, and "literally" means "figuratively" as well but that doesn't mean one needs to use ambiguous phrasing when better options are available.

@MaciejPiechotka What's your point? My (hypothetical) dog can eat chocolate in both senses of the word. He is physically capable and is allowed to do so (because I'm a (hypothetical) bad owner and I don't care); but he still shouldn't do it.

"Why shouldn't humans eat cyanide? Can't humans just excrete the indigestible component in their droppings?"

@imallett If you don't know why cyanide is poisonous or even that cyanide is poisonous, but do have a basic grasp of the organism's functioning, that's really not such a stupid question. I suppose you're trying to make the point that ingesting a toxin is generally a bad idea, but that doesn't really answer questions centered around why something is a toxin, which this question appears to be. Lots of interested dog owners will be able to tell you that chocolate contains cocoa which contains theobromine which is bad for dogs, but not specifically why theobromine is bad for dogs.

I'm voting to close this question as off-topic because it is trivial. This site is for biological academics, researchers and students, not for people wanting nutritional advice for their pets. Try a vet.

The reason is simple: Chocolate contains cocoa which contains Theobromine. The darker the chocolate is (meaning the more cocoa it contains) the more theobromine it contains. This is a bitter alkaloid which is toxic to dogs (and also cats), but can be tolerated by humans.
The reason for this is the much slower metabolization of theobromine in the animals (there are reports for poisonings of dogs, cats, birds, rabbits and even bear cubs) so that the toxic effect can happen. Depending on the size of the dog, something between 50 and 400g of milk chocolate can be fatal. As mentioned by @anongoodnurse the cocoa content in milk chocolate is the lowest and much higher the darker the chocolate gets.
The poisoning comes from the Theobromine itself, which has different mechanisms of action:
First it is an unselective antagonist of the adenosine receptor, which is a subclass of G-protein coupled receptors on the cell surface which usually bind adenosine as a ligand. This influences cellular signalling.
Then it is a competitive nonselective phosphodiesterase inhibitor, which prevents the breakdown of cyclic AMP in the cell. cAMP is an important second messenger in the cell playing an important role in the mediation of signals from the outside of the cells via receptors to a reaction of a cell to changing conditions. The levels of cAMP are tightly controlled and the half-life of the molecule is generally short. Elevated levels lead to an activation of the protein kinase A , an inhibition TNF-alpha and leukotriene synthesis and reduces inflammation and innate immunity. For references see here.
The LD50 for theobromine is very different among species (table from here), with LD50 as the lethal dose killing 50% of the individuals and TDlo the lowest published toxic dose:

The LD50 also differs between different breeds of dogs, so there are online calculators available to make an estimation, if there is a problem or not. You can find them for example here and here. The selective toxicity makes it even an interesting poison for pest control of coyotes, see reference 4 for some details.
References:

Chocolate - Veterinary Manual
Chocolate intoxication
The Poisonous Chemistry of Chocolate
Evaluation of cocoa- and coffee-derived methylxanthines as toxicants
for the control of pest coyotes.

Very interesting, thanks! I always assumed that dogs couldn't/shouldn't eat chocolate because of their lactose intolerance, similarly to why you might regret giving your cat milk if it hasn't been drinking milk its whole life.

Milk chocolate is rarely a cause of poisoning in dogs because it's the lowest in cocoa powder.

From these articles, I gather that you can, however, give your dog white chocolate because it contains barely any theobromine. Or is that a gross misunderstanding of the article?

@Nzall I think anongoodnurse's answer addresses quite well what you ask about.

@NickT, mostly the Thebromine itself, https://toxnet.nlm.nih.gov/cgi-bin/sis/search/a?dbs+hsdb:@term+@DOCNO+7332 Human have fairly high tollerance to many toxins, some argue it is part of the same resistance to mailliard compounds we evolved after we started cooking our food.

@anongoodnurse It's a bit complicated. Yes, milk chocolate has relatively little cocoa (and thus theobromine), but it is also the sweetest - and dogs like sweet things (unlike most cats, for example, which is why cats aren't in much of a danger of theobromine poisoning despite their lower tolerance and body mass). Dark chocolate would be far more dangerous if the dog actually ate it.

@Luaan - Understood. Chocolate is actually more toxic to cats, but because they don't like sweet things, they are less often poisoned. A dog will usually - usually - not have access to enough milk chocolate to kill it, unless the owner's child is selling candy bars! The point is, milk chocolate is the least harmful of the true chocolates.

I may or may not have been calculating my chocolate LD50 for my bodyweight when I saw that table.  You know, just to be safe!

@CortAmmon Taking the numbers from the other answer, when you weigh around 80kg (just for easier calculation) you would have to eat about 100 ounces (or about 3kg) of cocoa powder or about 1600 ounces (about 45kg) (if my rough calculation is right here) of milk chocolate. Theobromine would most likely one of your smaller problems...

So humans can literally die from eating too much chocolate!? A casual search suggests dark chocolate contains about 10% theobromine, so eating 0.7Kg (1.5 lb) of chocolate will kill the average (70kg) person. That means the name given to the popular death by chocolate recipe maybe wasn't given in jest.

@Bohemian is average person able to consume ~4000 kcal in one go? I wouldn't be surprised if it killed someone even without theobromine.

@Bohemian - the wikipedia article the table comes from suggests that the quantity of theobromine is much lower than 10%: the highest proportion suggested for dark chocolate is 1.4%, or about 0.2% for typical "refined" chocolates.  So the figure is much closer to 7Kg, which seems a lot more reasonable.

@MichaelKjörling actually, not, their answer does not address that point.. It doesn't mention WHITE chocolate, as in the one made using a different end product of the cocoa bean processing. I'm not talking about milk chocolate or any other of the chocolate types they mention.

The toxic ingredient in chocolate is in the mythylxanine class, a substance called theobromine. It is much like theophylline; overdoses of theophylline used to be very common before the advent of inhalers for the treatment of asthma. (Chocolate also has some caffeine in it, which may exacerbate the effects of theobromine.) As @Chris stated, it is only slowly metabolized in dogs.
Generally, toxicity depends on the size, age, the breed of the dog, any medical problems the dog may already have, as well as what type of chocolate was consumed. The larger the dog (given no other predisposing factors), the more theobromine they can handle, and older dogs tend to have more problems than younger ones.
Here is the dose of theobromine that can cause dangerous symptoms, and death:
20 mg/kg (or 20 mg/2.2 pounds, or about 10 mg/pound) may cause agitation, hyperactivity and gastrointestinal signs such as drooling, vomiting, and diarrhea.
At >40 mg/kg, cardiac signs can be seen, and include a racing heart rate, high blood pressure, or even heart arrhythmias.
At >60 mg/kg, neurologic signs can be seen, including tremors, twitching, and even seizures.
Fatalities have been seen at around 200 mg/kg (~ 100 mg/lb), or when complications occur.
Here are the approximate amounts of theobromine per ounce of chocolate:
Cocoa powder: up to 800 mg/oz
Baker’s chocolate (unsweetened): up to 450 mg/oz
Dark chocolate: 150 mg/oz
Milk chocolate: 50 mg/oz
So, theoretically a 40 pound dog (medium-sized dog? My Border Collies each weigh 42 pounds, and are considered medium-sized) will not die if it eats a Giant Hershey's Symphony Bar (a very yummy 6.8 oz / 204g) because that's less than 10 mg/pound. I've never put this to the test, however, and would not recommend it.
Info at https://vcahospitals.com/know-your-pet/chocolate-poisoning-in-dogs

Would you be willing to specify theobromine content in some other, more internationally useful, unit as well? Say, mg/g or mg/kg, or mg/litre, or whatever is convenient.

I have answered the toxicity part in mg/kg, which is an international unit of measurement. There are 28.5 grams per ounce in milk chocolate, slightly more in baker's chocolate and cocoa powder. I have no idea why.

@MichaelKjörling there is a Firefox extension that will convert stuff on the fly. It can be set to show conversions on a menu, or annotate inline, or various other options.  Never fret communicating with your Americqn friends again!  Esp. useful for cooking sites and such where traditional measurements reign supreme.

In this case, I think his list is perfect with the mismatched units!  We have figures for toxicity in mg already, and chocolate candy is sold and sized in oz.  So this allows ready values to be found, looking up and converting in one step.

@JDługosz "chocolate candy is sold and sized in oz" In some countries, perhaps, but not where I'm at. I looked all over the wrapper for a candy bar I had at home, and nowhere does it say oz anything. And of course, I think anongoodnurse's comments that the number of grams per oz differs based on the product being measured is proof enough that such information helps international readers!

I had a chocolate loving dog. She was 12 lbs. The vet said she could have it, provided she wasn't given too much. So his rule of thumb was not to feed her more than I would allow the average 2 year old in 24 hours. Which is two pips ( or two pieces from Hershey's bar). She lived to 16 yo. So yes, chocolate is a hazard to dogs, but like all things done in moderation it should be fine. Check with your vet.

Chocolate contains substances known as methylxanthines (specifically caffeine and theobromine), which dogs are far more sensitive to than people. Different types of chocolate contain varying amounts of methylxanthines. In general, though, the darker and more bitter the chocolate the greater the danger....For instance, 8 ounces (a ½ pound) of milk chocolate may sicken a 50-pound dog, whereas a dog of the same size can be poisoned by as little as 1 ounce of Baker's chocolate!

Chocolate Toxicity Meter for Dogs

Could you support your answer with any credible online reference? Almost all the time answers on Bio Stack Exchange are supported with reference(s) so that the readers can verify the claim put forward by the answerer. And accordingly upvote or downvote. One can also comment on (others') posts just to share and not to answer, but it will require them 50 reputation points which one has to earn by writing Qs and As (which are eventually upvoted as a sign of appreciation {I think}).

Obviously, depending on the dosage you can feed dogs some chocolate without outright killing them. They might have some digestion problems, vomit, or look just fine even though cocoa is toxic for them. But why on Earth would you do that? What are the benefits?

@Tytoalba: To be fair, it could be hard to find sources which show that it is not toxic, even if it were harmless. It would be like trying to find a source which plausibly states that strawberries are not toxic for humans.

@okolnost - Do you like grilled meats, say, a steak? Do you know how many co-carcinogens grilling a steak deposits on the surface of your steak? Sure, you might not get cancer right away, but why risk it at all? What are the benefits? Well, it's exactly the same thing with dogs and chocolate.

Yeah it could be hard. But isn't it done all the time while researching questions which are just not popular and don't show up on simple web results. It is a commonplace for Speceis-ID questions actually. @Michael

OP - I edited your answer to provide support and a source. If the edit is undesirable, please feel free to roll back. :)

@anongoodnurse Similar principle, quite different magnitudes. Also, human deciding for himself about costs and benefits seems to me as different from poisoning a dog on purpose. Are you actually supporting this or is this more of an intellectual exercise (not a bad one, in fact).

@okolnost - It depends on how you look at it. I want my dogs to be happy, so they get treats and all kinds of exercise/interactions. A little milk chocolate on occasion doesn't hurt them any more than running after tennis balls. A little bit of milk chocolate on occasion won't harm the vast majority of dogs. But there are those purists that won't indulge a dog, but will indulge themselves in grilled meats, alcohol, etc.

@anongoodnurse Understood. I would probably try to find a different and healthier treat for my dog (if I had one), as I do with my treats. But I can see your point and I when I think about it I would probably let you take care of my dog (again, if I had one). :-)

@okolnost - Lol at your last comment! Thanks! :D


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Help me identify this caterpillar looking insect
Can someone please help me identify this caterpillar looking insect from the Caribbean?
Thanks.

Hi, if you specify the island, the habitat in which it was found and the dimensions of the caterpillars it helps the ID.

They look like the caterpillars of Alope sphinx (Erinnyis alope)

There is a webpage on a dedicated website here:
https://www.butterfliesandmoths.org/species/Erinnyis-alope
Among the pictures in the linked website you can find one with the green and brown morphs/stages of the caterpillars.


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Measuring the Rate of Photosynthesis
Update: I have just received a grant to pursue this research.  However, I must still perform the preliminary experiment described below before dipping into my very limited funds.  Thank you for any ideas.
What are some accurate methods to measure the rate of photosynthesis that can be performed without access to a professional laboratory?
I am a citizen scientist who is designing a experiment to measure the rate of photosynthesis under different conditions.  Although this idea stems from my interests as an amateur horticulturist, it has grown to into something of real scientific potential.  However, I must conduct this experiment on a low budget without access to a professional laboratory.
Furthermore, I should note that it is almost impossible to quantify photosynthesis by measuring gas emissions in this scenario. The only way to keep the plants in a stable environment with equipment that I can afford is in an open, climate controlled room, (as opposed to a closed testing chamber that could trap gasses).
Any ideas on how to measure the rate of photosynthesis would be greatly appreciated.

One of the simplest measures of photosynthesis is just measuring how much your plants grow (i.e., weigh them). Of course this technique is imperfect because of other influences on growth, the amount of time you have to wait to get a measurable change, and ideally you would want to use the dry mass of your plants to avoid water content differences, but you have opted to exclude the methods that get around those problems.

Thank you for the suggestion.  In fact, when running a similar experiment a few years ago, I quantified my results by taking the mass of each plant.  You raise a good point about taking the dry mass though, a factor which I neglected to consider.  However, I am trying to gather as accurate a data set as possible in order to show definitive correlation between photosynthesis and my variable (if any exists).  That would give me some hope of taking this experiment to a university laboratory for further testing.

Depending on your plant you might be able to mass only a part of the plant, like harvesting one of each of a leaf pair several days apart. You would compare the ratio of the second leaf to the first, in different plants that are your control/test groups. Whether that is feasible would of course depend on the growth pattern of your plant. Also if your hypothesis doesn't depend on a certain plant, you could use a fast-growing model species. Arabidopsis is a favorite in biology labs.

My hypothesis does not depend on a particular plant.  Thank you for the suggestion of Arabidopsis.  Although I will do further research on that species, do you have any other suggestions for fast-growing plants that could be grown indoors from seed with a relatively small footprint (like growing in Jiffy Pot starter trays)?

If you dry the plant and use dry weight, that's how they measure photosynthesis, because all the carbon found in the plant is a balance of respiration at night and over-compensating photosynthesis in the day.
http://ibbiology.wikifoundry.com/page/Explain+how+the+rate+of+photosynthesis+can+be+measured

Thank you for the link.  It raises some interesting points that I will take into account.  Overall, I believe that dry mass will be the most effective method for quantifying growth.  However, I am always open to new suggestions as I design this experiment.


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Why does the clavicle ossify intramembraneously?
The clavicle is the only long bone which ossifies as a membrane bone. I studied this process, but I can't find the reason why it features intramembraneous ossification?


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What does a typical, perfectly healthy vaccinium corymbosum (highbush blueberry) leaf look like?
What does a typical, perfectly healthy vaccinium corymbosum (highbush blueberry) leaf look like?

Colour (darkness of green, redness)
Waxiness
Veins

I'm guessing that soil ph, nutrients, and other factors play a part. Vacciniums seem to have very specific needs, and as far as I know, assessing the leaves is one of the best ways to determine plant health.

Vaccinium species are ericaceous plants (acid soil loving) so they will not do well in alkaline soils, and/or being watered with hard water. In fact they have a narrow optimum pH range 4.8 - 5.2 (Source http://www.westernfarmpress.com/management/blueberry-iron-chlorosis-has-multiple-causes)
The pH of the soil will effect the plants ability to access the minerals in needs from the soil, and mineral deficiencies will indeed show themselves in the leaves first.
Here is a photo of a healthy Highbush Blueberry leaves