text:
Glycosidic bonds
For the glycosidic bond in maltose, why is the glycosidic bond formed between hydroxyl group on C1 in 1 glucose molecule and hydroxyl group on C4 of the other glucose molecule? Why not between, say, hydroxyl group of C2 on one and hydroxyl group of C4 on the other?

In a cyclic molecule of glucose, C1 is the result of the aldehide group linked to C5. This makes C1 a reducing carbon that can share electrons. This is why C1 must always take part in a glycosidic bond.
The other carbon may be C'1, C'2, C'4 etc. That changes the structure and name of the molecule (i.e. two glucoses bound by α 1-4 bond is Maltose and by α 1-6 is Isomaltose)


text:
What is the effect of pesticides on worm growth?
As a new semester begins, we were asked to propose ideas for investigatory projects. Our idea revolves around the effects of pesticides on non-target organisms. Since frequent use of pesticides may potentially affect the health of the soil, we chose the earthworms as our target organism. Our experimental set-up was revolves around studying their growth. Two containers (Container A-Control, Container B-Experimental) would be filled with soil and other things that are essential for worms to live. In container A, normal soil would be used. On container B, we would spray pesticide on the soil and mix them so that it really gets in the soil. After that, we would place the worms (5 each container). The allotted time for data gathering and analysis is 3 weeks. Given this situation, we would observe the behavior of the worm each day for 10 to 14 days (depending on our schedule) and their growth on the last day by measuring their length, weight, and describing their color.
I think that our set-up is logical instead of finding farms that sprayed pesticide for the last 20 or so years which is difficult in our situation. Does anyone have any feedback on the particulars of the experiment based on previous research on the subject?

I'm voting to close this question as off-topic because it is not a question in terms of SE Biology but a request for discussion and opinion. "What do you think?" Is one of the examples of this given in the help on writing questions.

But @David, this is a perfectly valid question on experimental design by a budding biologist. How does the fact that the OP is asking for the opinion of experts detract from the merit of the question? It is my impression that this is what this site is for. This question can be answered with evidence. There may be a range of things that one could suggest but one can cite reasons why an approach is or is not appropriate, or preferred over others. I, for one, would like to reward questions such as this one that show some genuine interest and effort from the part of the OP.

I have suggested some edits to make the question more general. Feel free to modify or rollback if you do not approve my changes.

To @vkehayas (and OP). Please read the Tour and the Help section on Questions to Avoid Asking and you will see why this question is off-topic for this list as it is constituted. 1. It is not a question about biology, as in the three  examples listed under “Ask about...”. 2. It is not a “questions about an actual problem”. 3. It is “primarily opinion-based... likely to generate discussion rather than answers”. 4. It is a “subjective question” having something in common with three of the examples given.

@David, unfortunately I cannot see this question violating any of the criteria. Since we've both voiced our opinion I'd suggest we now leave the community decide on this one.

"Pesticides and earthworms. A review": https://link.springer.com/article/10.1007/s13593-013-0151-z

@vkehayas If you still cannot see why the question is off topic there is no point in further communication with you. I would ask others to read the links I provided.

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sort: votes


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Why do we need to replicate incomplete DNA fragments by PCR from a crime scene?
If the DNA from a crime scene is damaged, why would it be helpful to replicate it by PCR (polymerase  chain reaction)? Even if we get billions of those copies, it is still incomplete, isn't it? How can the PCR make the forensic process easier?

As far as I know (and I know little in this domain), there are statistical to deal with damaged sequences. Typically, different nucleotides have different probabilities of being altered with time and this can be taken into account. However, on a crime scene, there is no reason for DNA to be damaged in any. The main issue is probably a potential problem of contamination.

This process helps with the signal to noise ratio.  In theory, you could use the fingerprinting techniques to dice up the few billion copies of the DNA and carefully measure them.  However, it is far easier to replicate the DNA to increase the number of molecules of DNA available to the process.
Remember, fingerprinting for crime investigations doesn't involve reading the DNA, but merely uniquely identifying it.

does that mean we need about billion of  that same copies to show on the result of gel electrophoresis. so we need to replicate it by PCR

Yeah.  If you think about it, the final step of the process is to stain the DNA fragments after they have been separated by weight.  You need enough material at each position along the gel to make a noticeable stain.  You also need enough of them to be able to use statistics to account for any random variation in your gel.

sorry,could you explain what you mean by "any random variation"? and why the process need to be helped with "signal to noise ratio"

Electrophoresis is dependent on diffusion, which is a rather inexact process.  If a single molecule of your source material finds an easier path than average, it will move further than it should have.  However, if you have billions of said molecules, it is far less likely that all of them will find the easy paths.

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How much heat for how long to Kill RHDV?
Rabbit hemorrhagic disease is caused by the Virus RHDV.  There are two verisions V1 & V2.
It is extremely devastating to both pet and wild rabbits.  With fatality rates reports of 75%+.
It is currently devastating rabbit populations in the US. There are a number of vaccines but non-are approved for use in the US.
I have been reading up about it and found this claim in a few places.

RHDV is also reported to survive exposure to pH 3.0, heat of 50°C (122°F) for an hour Source

.

It survives heat of 122F for one hour. source & source

My question is: How much heat for how long will kill RHDV?

Often, in studies of viral infection, heat-inactivated viral stocks are used as a non-infectious control.  See Matthaei et al. 2014 1 for an explanation of how such a stock was prepared for RHDV:

Heat-inactivated RHDV stock was generated by incubating the virus preparation in 2 ml screw cap tubes for 180 s at 85°C in a water bath to ensure a drop in infectious virus of more than 99.9%

The methods section for that paper cites a study by Duizer et al. 2 on the inactivation of caliciviruses (which include RHDV).  Therein, the authors tested the heat inactivation of canine calicivirus no. 48 (CaCV) and feline calicivirus F9 (FeCV) at 4, 20, 27, 37, 56, 63, 71.3, and 100°C for time periods varying from weeks (4°C) to seconds (71.3 and 100°C):

Times required at different temperatures to achieve a 3 log10 reduction in viable virus titer (TCID50) in DMEM (3 to 4 μg of protein/ml).

Note that, in both studies, viral heat inactivation is carried out in liquid culture, where it is easy to obtain a uniform temperature by mixing.  For heat inactivation of RHDV on food/hay, rate and uniformity of heating will be different.
Citations

Matthaei M, Kerr PJ, Read AJ, et al. Comparative quantitative monitoring of rabbit haemorrhagic disease viruses in rabbit kittens. Virol J. 2014;11:109.
Duizer E, Bijkerk P, Rockx B, De Groot A, Twisk F, Koopmans M. Inactivation of caliciviruses. Appl Environ Microbiol. 2004;70(8):4538-4543.

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Did the eclipse make the leaves fall?
I live in Pittsburgh PA, the eclipse on Monday August 21 was only about 80% coverage here.  It was notably darker, but less dark then an overcast day. The night of August 21, had a low temp of about 70F.  On my daily walk the following day (Aug 22) there was notable amount of fallen leaves from the trees along my daily walk (mostly maple), by this morning (Wednesday Aug 23) the leaf fall has increased such that the grounds crews are out cleaning the leaves.
Did the eclipse make the leaves fall?

I think the photo period has to change for longer than a few hours to cause leaves to drop. I would imagine cold could kill tender growth much faster.

What said by ebrohman is correct. In fact there are two factor that led to leaves falling when fall approaching: photoperiod and the circadian rhythm (24 hours) of the plant.
In the circadian rhythm is possible observe oscillation in proteins expression. Some of the proteins that regulate leaves abscission (aka falling) have an oscillations in their expression and present a pic of the expression in the late afternoon. Moreover to be active this protein need to be on "a dark" condition because the light will lead to proteins degradation.
For exemple
Imagine that in summer there is a long day condition with sunlight present from 7am until 20am (photoperiod) and that the proteins that lead to leaves abscission is expressed by the plant around 6pm (circadian rhythm). Due the presence of the sunlight the proteins will be degrade.
When the hour of sunlight decrease (with fall approaching) the proteins is day by day less degraded and this could led to the plant to prepare itself for the winter, also with the leaves abscission.
If you are interested to know more about the argument I can suggest you an interesting review write by Pin and Nilsson (2012)
Cold
Is possible that a decrease in the temperature lead to a leaves falling. However I think that temperature has to decrease significantly over more day to allow any changes in plants structure.
I hope that my answer could help, if you do not understand something let me know. I will try to explain it in a different way.


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What is the distribution of the major ions across a neuronal membrane for a human neuron?
I have searched for the ion distributions across the membrane of human neurons on the internet but almost all the information refers to the giant axon of the squid. Could anyone give me the ion distribution across the membrane of a human neuron?

Have you tried Guyton-Hall physiology?


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Evolution of leukemia pluripotent short-term cells
I have a problem in understanding the introduction of this paper entitled  "Stability and bifurcation in a model for the dynamics of stem-like cells in leukemia under treatment". As I have no background in biology, it's difficult for me to get the meaning of some terms like:

Short-term cells
Multipotent progenitor cells
Goldie-Coldman Law

On the other hand, the second paragraph is completely confusing to me:

Let $Q$ denote the density of stem-cells population. A percentage $\eta_1$ of these ones are supposed to undergo asymmetric division with one daughter cell identical to the mother cell and the other one committed to differentiation. A percentage $\eta_2$ of the stem-like population differentiate symmetrically and go to the line of mature cells. The rest of them, a percentage $(1- \eta_1 - \eta_2)$ is supposed to self-renew: both cells that result from mitosis are identical to the cell that entred to the cell cycle. The same duration $\tau$ of the cell cycle is supposed for all types of division.

Is there a charitable soul to indicate some web page or youtube video on the subject?

Some background: leukemia is an immune cancer so it comes from the hematopoietic system. Thus, it would be useful to look into Hematopoietic stem cells (HSCs). Note that, in general, the (semantic) hierarchy of stem cells goes: totipotent, pluripotent, and multipotent, in order of less generality (i.e. more differentiated, or more mature as a cell in other words). Maybe reading about stem cells in general would be useful too.

HSCs have two subtypes: one which can indefinitely renew itself, and one which has a timed lifespan (i.e. it stops being capable of generating new cells of different types after awhile).  It is interesting to note that leukemias have  an analog of these, which is what is being referenced, presumably, in the paper.
See Normal and leukemic hematopoiesis: Are leukemias a stem cell disorder or a reacquisition of stem cell characteristics? for a bit more on this.
Multipotent progenitor cells (MPCs) are also capable of generating new cells, but are capable of less variety than plutipotent stem cells.
They can "choose" to become a more differentiated cell (i.e. choose a lineage).
They also cannot self-replicate (i.e. to divide and create new multipotent progenitors) indefinitely, though they can do it for some number of steps usually.
In other words, an MPC will generate a finite number of cells, whereas a true stem cell can divide indefinitely, given the resources.
The Goldie-Coldman Law (also called hypothesis) can be summarized via:

This hypothesis predicts that the tumor cells develop resistant phenotypic variations towards chemotherapeutic agents. This resistance is independent of the chemotherapeutic agent and dependent on the number of cell divisions that occur after treatment begins. The larger the tumor size or the longer delay in initiating chemotherapy, the more resistant cells. The implication is that a regimen of alternating cycles of two different non–cross-resistant chemotherapy medicines yields a better chance of tumor eradication.
    (From here).

       In other words, it is a model for how cancers become resistant to drugs. See also Improving       Cancer Treatment via Mathematical Modeling: Surmounting the Challenges is Worth the Effort.

Ok, onto the second paragraph. I will be very informal here :)

Let $Q$ denote the density of stem-cells population.

Within a cell population (cancer or otherwise), often there is a small subpopulation of stem cells (the rest of the cells are differentiated cells). So if there are $N$ cells in total, roughly $S=QN$ will be the number of stem cells present.

A percentage $\eta_1$ of these ones are supposed to undergo asymmetric division with one daughter cell identical to the mother cell and the other one committed to differentiation.

Within the population of stem cells (which are a subpopulation of cells), there will be further subcategories with different reproductive behaviours.
Notice there are really only 3 options: a stem cell becomes (a) two stem cells, (b) two differentiated cells, and (c) one stem and one differentiated cell.
This sentence means that roughly $s_1 = \eta_1 S$ cells will divide in the asymmetric pattern given above.

A percentage $\eta_2$ of the stem-like population differentiate symmetrically and go to the line of mature cells.

This means the number of symmetric divider cells is roughly $s_2 = \eta_2 S$ (both outputs will be differentiated.

The rest of them, a percentage $p = 1−\eta_1−\eta_2$ is supposed to self-renew: both cells that result from mitosis are identical to the cell that entered to the cell cycle.

Finally, around $s_3=pS$ cells become stem cells again, i.e. division type (a).

The same duration $\tau$ of the cell cycle is supposed for all types of division.

In order to divide, every cell has to undergo a complex process called the cell cycle. This takes time; in other words, it upper-bounds/limits the rate at which cells can divide. Presumably, different cells take different lengths of times to divide. This assumption above ignores this issue.

Edit (062018): let's take a look at the equation
$$
\tilde{r}(P) = r_1(P)\frac{x_0 - R_0}{x_0^{-p+1}} \;\text{  with  }\;
r_1(P) = \frac{P^m}{P^m + P^m_0}
$$
where $Q$ is the density of the stem cell population, $P$ is the amount of plasmatic drug, $P_0$ is the half-maximum activity concentration, $m$ is the Hill coefficient, $x_0$ is the number of infected cells, $R_0$ is the number of resistant cells, $p$ is the probability of mutation, and $q=-p\in (-1,0]$.
From a high level perspective, we need to account for three effects of treatment:
(1) the building of the cancer's resistance to that treatment,
(2) the increase in drug effect as it gets absorbed and decrease as it is excreted, and
(3) the effect of the drug on the target cells.
First, notice in the differential equations:
\begin{align}
\dot{Q} = f(Q,t) - \tilde{r}(P)Q^{q+1} \\
\dot{D} = -\lambda_0 D + K \\
\dot{P} = -vP + \lambda_0 D
\end{align}
that (2) is being handled in the equations for $D$ and $P$.
Drugs start in some compartment (like the intestines when you swallow a pill) where they are not so useful against leukemia. Here they start with some concentration $K$, and the amount of drug decreases with first-order kinetics, i.e. the first order linear differential equation that shows $D$ decreasing. See an article on pharmacokinetics for more info on this.
Once the drug is absorbed (i.e. contributes to $P$ instead of $D$), it enters the plasma and starts to have an effect on the leukemia cells. (Notice that (2) is being handled here as well, in the $-vP$ term of the differential formula for $P$, which measures how fast your body is destroying the drug.)
Naturally, only the drug concentration $P$ in the blood plasma can affect the cancer cells; hence, the term for $\tilde{r}$ only depends on $P$!
Next, we can see how the model accounts for (3) in the differential equation for $Q$. Again, we have first-order kinetics of $Q$ (by the first-order linear differential relation), modulated by $r$ and $q$. Since $q + 1 > 0$ and $\tilde{r} \geq 0$, we know that as $\tilde{r}$ increases, we are causing $Q$ to decrease faster, i.e. we are hurting the cancer more (good!). Thus we expect that as $P$ (the drug concentration) increases, $\tilde{r}$ should also increase.
Ok, so now for (1). Notice that the equation for $\tilde{r}$ breaks into 2 terms. The second term is $R_T=(x_0- R_0)/x_0^{-p+1}$. This captures the effect of resistance, as the cancer evolves via mutation to gain resistance to the drug. Notice there is no dependence on the drug itself (just as described in the Goldie-Coldman hypothesis). (Note that this may not be realistic, since the drug will induce an (un)natural selection pressure on the cells and encourage the ones that resist the drug to proliferate more easily; however it does simplify the model).
Notice that $R_T$ decreases as $R_0$ increases, meaning that as the number of resistant cells increases, the efficacy of the treatment decreases.
The first term, i.e. $r_1(P)$, describes the effectiveness of the drug as a function of its concentration via the classical Hill equation.
Simplistically speaking, drugs often act via receptor molecules on the surfaces of cells; once all these receptors are saturated, the drug cannot affect the cell anymore! Hence, the effect of a drug "levels off": as its concentration increases, it will bind more and more receptors (and thus have more and more effect, albeit at a diminishing rate), until saturation occurs and adding more drug (i.e. increasing $P$ no longer does anything). You can see this in the equation for $r_1$ since $\lim_{P\rightarrow\infty} r_1(P) = 1$ (though of course $\partial_P r_1 > 0$ still). The $m$ and the $P_0$ simply control this relationship: the Hill coefficient $m$ describes the "cooperative binding" properties of the drug (see the link above for details), i.e. whether binding accelerates further binding or not, while $P_0$ (usually denoted $K_A$, or called the dissociation constant) describes the ligand concentration at which half the target sites are occupied.
Higher $P_0$ means that occupying half the receptor sites requires a higher concentration, which means you need more drug for the same effect, i.e. the efficacy of the drug is poorer; this is why $P_0$ appears on the denominator: as it increases, the effect of the drug on the cells (given by $\tilde{r}$) will decrease.
Essentially, $m$ controls how fast the drug reaches peak efficacy (how steep the curve is), while $P_0$ controls the physical properties of molecular binding (the translation component of the curve).

Thank you for your answer. How do I biologically interpret the formula
$\bar{r}(P)=r_1(P)\frac{x_0-R_0}{x_0^{-p +1}}$ with $r_1(P)=\frac{P^m}{P^m +P_0^m}$.

Dear @Sanaa, I have added to my answer. Hopefully it helps! Incidentally, if you have more questions, I'd prefer if you asked a new question. (It is already tedious for me to scroll up and down to add to this one because it is so long).

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Cockroach brain functional anatomy
In insects like the cockroach the brain is distributed, i.e. some parts lie in the head and some in the abdominal cavity. Which part is responsible for controlling locomotion?

Technically speaking, locomotion is actually not produced by the brain in cockroaches; there are neurological controllers in the legs themselves which produce locomotion even when contact with centralized nervous system is severed.
I include this for reference, because it was not explicitly stated in your question.  However, I believe it was intended to be implied by the phrase "responsible for controlling."  In other words, from my understanding, you're more interested in what section of the brain actually controls those actions in a normal cockroach.
From Central Nervous Control of Cockroach Walking by Charles R. Froutner, you can see even just in the abstract that the movements became spontaneous when the connection with the segmental ganglion was broken, showing that this is very likely where the control is exerted.  (The segmental ganglion, for reference, is a part of the dorsal "brain" you made reference to.)

What is meant by "spontaneous movement"?

@AmitMaurya, from the article referenced: "rhythmic motor patterns, similar to those occurring during normal walking."

Ultimate control has to come from ganglion residing in head,  which receives sensory information from eyes and antennae about obstacles and terrain.

Shouldn't the locomotion after disconnection from segmental ganglion be in random direction?

Just to be clear, the brain is not distributed, it is the thoracic ganglia present in thorax that aid an arthropod for different tasks.
Arthropods have most of their sensory stimuli and motor actions controlled by Midline Brain Neurophils, called Central Complex (CC)
Quoting Journal of Experimental Biology >>

Previous studies have also linked the CC to motor actions. Huber
  showed that stimulation within the CC enhances locomotor activity
  (Huber, 1960). More recently, electrophysiology studies showed that
  the neural activity of some CC units is correlated with, and often
  precedes, changes in stepping frequency.


text:
Does the brain store information and personality traits in different areas?
I'm aware that muscle memory, language etc can remain largely intact after brain injury that impairs other forms of memory, suggesting that different kinds of memory are stored in different places in the brain.
Are your personality traits also stored separate from memory?

If I'm a bigot, I probably came to be that way because of my experiences and what people who are influential in my life have told me. If I forget those experiences and people due to memory loss following brain injury, will I not be a bigot anymore?
I may have certain nuances in my personality because I'm rich - like body language, or that public transport makes me uncomfortable, never having been used to it. If my memory loss is so severe that I don't recall anything about my life so far, will I still have my nuances?

You're talking about several different things, not just information and personality traits.

@anongoodnurse Being a bigot, disliking public transport, body language.. they're all personality traits, surely? Is it the "information" part which is not properly worded or termed? How can I improve the title or description?

The only way I can make sense of your question is if you are asking whether personality traits are innate or not. Is that what you are asking?

@vkehayas No, I'm pretty sure they're acquired. Based on "information". But is that information stored in a different part of the brain than the personality it creates? If so, does its loss change the personality? (Usage of the term "information" depends on further comments from anongoodnurse, who seems to feel it's not really what I'm asking about)

I think your confusion comes from the fact that you take traits and memory to be distinct from each other. The brain processes information and we know that some of the connections between its cells are altered in the process --some call that memory. You are convinced that this is the only way that traits form, through experience at some developmental stage. You are then asking if cells in areas other than those that change during the formation of traits are affected more by the experience of forming a trait. If that were true, they would by definition be included in the areas that are associated with the trait in the first place. Can you see the problem in the logic of the argument?
Many people have followed similarly flawed reasoning, including trained neuroscientists that have been indoctrinated to believe in extreme forms of functional specialization of the brain, a more subtle version of the now debunked theory of phrenology.


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Antibody staining
I am staining tissue sections and I did a mistake, I was supposed to have mixed 3 primary antibodies but I stained only with one of them. After the 1h incubation I washed 10 min with PBS and then I did another hour incubation with the 2 antibodies I forgot to add before. Can that affect my staining? I am afraid I wanted to test different dilution of the first antibody I added alone, and then I added another hour incubation with 2 more antibodies.

Generally for IHC/ICC staining separately with the antibodies is not a problem. Staining with separate primary antibody steps is often done when the antibodies are from incompatible species and so might cross-react with each-other giving non-specific staining.
However, the 10 min wash and 1 hour incubation with the other antibodies may wash off some of first antibody, leaving you with weaker signal than expected. This may affect how "bright" your stain appears after the secondary antibody step.

Is this an ELISA? In that case, I suggest you doing this experiment again because now you are incubating for an extra hour. Incubation time is set at fixed range because increasing it may also increase the background noise of your assay.

Incubation times - sensitivity may be increased with a longer incubation time at room temperature. Be aware that the top of the curve may flatten out and become unusable, limiting the assay range. Additionally, background may increase

Resources:
https://resources.rndsystems.com/pdfs/datasheets/edbapril02.pdf

This is not an ELISA it is immunohistochemistry or immunocytochemistry.


text:
What is functional dissection?
Reading [1] I found the sentence:

Consistently, functional dissection of mouse and human wild-type and mutant RAS isogenic leukemia cells demonstrated induction of methotrexate resistance but also improved the response to vincristine in mutant RAS-expressing lymphoblasts.

I did not find a definition online yet. What is the meaning of functional dissection in this context?
[1]   K. Oshima et al., “Mutational landscape, clonal evolution patterns, and role of RAS mutations in relapsed acute lymphoblastic leukemia,” Proc Natl Acad Sci USA, vol. 113, no. 40, pp. 11306–11311, Oct. 2016.

That means that you dissecting the functions not the elements.

The term 'functional' in this context implies a type of analysis that is able to provide a mechanistic understanding.
The authors first describe their exploratory approach, by which they identified some genes and their mutations that are associated with patient relapse in acute lymphoblastic leukemia. Then they proceed to intervene in the system, by expressing mutated KRAS in mice. When they did that, they observed several hallmarks of relapse in those mice. Hence they can conclude that a mutation of this gene is involved in the mechanism that underlies relapse.
Thus the way these authors use the term 'functional analysis'/'functional dissection' is in contrast to a correlational approach.

The underlying assumption is that by isolating parts of the system and studying their properties and their effects we will be able to understand the physical world. This is a philosophical (metaphysical) thesis called reductionism, which is arguably the prevailing view in the natural sciences.
The first use of the term "functional dissection" I could find is in a 1971 paper on the immunological response of small molecules. Their goal in that paper was to dissociate (or dissect) the effects of small molecules, such as a bovine glucagon, on antibody specificity versus antibody production. They have found that different parts of this molecule were responsible for antigen specificity (all antibodies recognised the N-terminal) and cellular immunity (mostly the C-terminal of the molecule was associated with DNA synthesis).


text:
How much cost would artificial pollination add to common products (fruits etc.)?
I've read about ecosystem services and their possible valuation - statements like "honeybee pollination service in the US is worth 1.6 billion dollars".
Is data available on how this would affect the cost a consumer pays for a given product? For example if the humans must do all pollination of fruits themselves, how would that affect the retail cost of these fruit?

I've made some pretty big edits because I think I understood what you're getting at. However, if I've changed your meaning, let me know and I'll revert back to the original!

The cost would increase; either because pollination services are not provided and the supply is decreased; or because the cost to producers goes up as they must pay for artificial pollination. See the extremely detailed analysis in Winfree et al.
edit
I imagine what you're actually asking for is a $ figure "per apple". This depends on the location, crop, market, etc., but just for a ballpark, if I'm reading the supplementary tables in Allsop et al correctly, the replacement value of insect pollination to apples in the Western Cape of South Africa would represent a 6%-25% increase in production cost (and, if the producers pass that along to the consumers, an equal increase in the cost to consumer).

 Allsopp MH, de Lange WJ, Veldtman R. 2008. Valuing insect pollination services with cost of replacement. PLoS ONE 3: e3128–e3128.
 Winfree, Gross, Kremen. 2011. Valuing pollination services to agriculture. Ecol Econ 71: 9–9. [behind paywall, but posted free here]

I'm unsure about the 6%-25% figure; and would love to see other answers.

Does "replacement value" mean pollination by hand (= no pollination by nature - animals/insects or weather/wing)?

Yes; Allsop et al value several different methods (hence the range 6-25) of human-assisted pollination, considering their costs, the resulting yield, etc.


text:
Under what conditions do dendritic spines form?
I'm looking for resources or any information about the formation of dendritic spines and synaptogenesis, especially in relation to how new connections are formed on a daily basis.
Does the electrotonic signalling along the axons and through the spines cause new connections to be made based on some kind of spatial condition (maybe an electrical or chemical attraction), or is there some larger heuristic here?

Spine formation (spinogenesis) is almost certainly due to chemical, rather than electrical, signalling between neurons. Although there are exceptions (gap junctions, for one), most forms of inter-cellular communication are mediated by chemicals released by one cell and detected by another. You are right that the cues for synaptogenesis are probably localized (the "spatial condition"), but I'm willing to bet the farm that those local cues are chemical in nature.
A recent paper from Kwon and Sabatini (2011) shows that local release of the neurotransmitter glutamate is sufficient to cause a functional spine to form. Glutamate receptors on the dendrite detect the glutamate and a spine forms (within seconds). At least under these conditions, the presynaptic machinery isn't required at all! Of course, in a less reduced preparation, electrical activity in the axon will signal the glutamate release from the presynaptic side. Thus, in this case, spine formation is activity-dependent but is mediated by chemical cues.

Please note that the phenomenon Kwon and Sabatini describe only manifests itself in brain slices from very young animals and not at all in brain slices from adults.

Dendritic spines are thought to grow and recede under LTP and LTD, respectively. See (Bosch and Hayoshi 2011) for a review.
From there, much of the synaptogenesis occurs due to surface molecules present both on the dendrite and the presynaptic axon in the growth cone.  Localization and guidance are achieved through gradients of growth factors in the developing nervous system  See (Kolodkin and Tessier-Lavigne 2011) for a review of all of these mechanics.
How this maps back onto the human CNS and thinking/learning/memorizing is still up for debate, but some of these mechanisms must have been preserved in higher species.

References:
Bosch M, Hayashi Y. (2012) Structural plasticity of dendritic spines. Curr Opin Neurobiol.,22(3):383-8. (Epub 2011 Sep 28).
Kolodkin AL, Tessier-Lavigne M. (2011). Mechanisms and molecules of neuronal wiring: a primer. Cold Spring Harb Perspect Biol., 3(6). [DOI]

Although both classes of phenomena are relevant for synaptic and spine dynamics: 1) LTP and LTD are classically thought to require a pre-existing synapse, 2) what happens in development may be different than what happens in adult life.

I think the insightful comments you've made on my answer and the one above really are worthy of a new answer.  I've been out of the neuroscience game for almost 10 years now, so I definitely defer to your expertise!  Thanks for commenting.

Two classes of factors contributing to spinogenesis have been described in the literature, based on whether they can be considered extrinsic or intrinsic to the dendrite (my classification). Here is a shortlist of evidence in favour of either:
A. Extrinsic:

the presence of extracellular glutamate facilitates spine
formation in tissue from very young mice (Richards et al., 2005;
Kwon and Sabatini, 2011)

new spines preferentially form towards boutons with pre-existing
synaptic contacts (Toni et al., 1999, 2007; Knott et al., 2006; Nägerl et al., 2007)

B. Intrinsic:

new spines tend to form away from pre-existing spines on the
dendrite (Fu et al. 2012)

dendrites with lower spine densities display a higher degree of
spinogenesis (Holtmaat et al. 2005)

A proposed mechanism extrinsic to the dendrite that can lead to spinogenesis is glutamate spill-over. Conceivable mechanisms intrinsic to the dendrite that can control spinogenesis can be the competition for resources (structural proteins, mRNA etc).
Dendrites of pyramidal cells in some areas of the cortex and the hippocampus exhibit a relatively high turn-over of spine formation and elimination (Holtmaat et al. 2005, Attardo et al. 2015), at least as compared to axonal boutons (e.g. de Paola 2006). Whereas some of these new spines stabilize, many disappear soon after their formation. This indicates that, at least in part, their creation is not fully specified by the existence of a pre-synaptic partner, if we assume that the pre-synaptic partner continues to "attract" them (and that's a big if). The relative independence of spinogenesis from presynaptic activity is further corroborated by the fact that most new spines lack a synapse (Knott et al., 2006).
It appears, then, that dendrites over-produce spines in order to sample their environment for potential synaptic partners. The advantage of such a mechanism can be seen when considering the potential wiring diagram changes that neurons can achieve with such relatively cost-less microscopic changes (Stepanyants et al. 2002). It is unclear at the moment at what point between spinogenesis and synapse formation presynaptic activity becomes an influencing factor in the intact adult brain. A theory incorporating the existing information on spinogenesis is forthcoming.

References

Attardo A, Fitzgerald JE, Schnitzer MJ. (2015) Impermanence of
dendritic spines in live adult CA1 hippocampus. Nature,
523(7562), 592-596. https://doi.org/10.1038/nature14467

De Paola, V., Holtmaat, A., Knott, G., Song, S., Wilbrecht, L.,
Caroni, P., & Svoboda, K. (2006). Cell Type-Specific Structural
Plasticity of Axonal Branches and Boutons in the Adult Neocortex.
Neuron, 49(6), 861–875. https://doi.org/10.1016/j.neuron.2006.02.017

Fu, M., Yu, X., Lu, J., & Zuo, Y. (2012). Repetitive motor learning
induces coordinated formation of clustered dendritic spines in vivo.
Nature, 483(7387), 92–95. https://doi.org/10.1038/nature10844

Holtmaat, A. J. G. D., Trachtenberg, J. T., Wilbrecht, L., Shepherd,
G. M., Zhang, X., Knott, G. W., & Svoboda, K. (2005). Transient and
Persistent Dendritic Spines in the Neocortex In Vivo. Neuron,
45(2), 279–291. https://doi.org/10.1016/j.neuron.2005.01.003

Knott, G. W., Holtmaat, A., Wilbrecht, L., Welker, E., & Svoboda, K.
(2006). Spine growth precedes synapse formation in the adult
neocortex in vivo. Nature Neuroscience, 9(9), 1117–1124.
https://doi.org/10.1038/nn1747

Kwon, H.-B., & Sabatini, B. L. (2011). Glutamate induces de novo
growth of functional spines in developing cortex. Nature,
474(7349), 100–104. https://doi.org/10.1038/nature09986

Nägerl, U. V., Köstinger, G., Anderson, J. C., Martin, K. A. C., &
Bonhoeffer, T. (2007). Protracted synaptogenesis after
activity-dependent spinogenesis in hippocampal neurons. The Journal
of Neuroscience, 27(30), 8149–56.
https://doi.org/10.1523/JNEUROSCI.0511-07.2007

Richards, D. A., Mateos, J. M., Hugel, S., de Paola, V., Caroni, P.,
Gahwiler, B. H., & McKinney, R. A. (2005). Glutamate induces the
rapid formation of spine head protrusions in hippocampal slice
cultures. Proceedings of the National Academy of Sciences,
102(17), 6166–6171. https://doi.org/10.1073/pnas.0501881102

Stepanyants, A., Hof, P. R., & Chklovskii, D. B. (2002). Geometry and
structural plasticity of synaptic connectivity. Neuron, 34(2),
275–88. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/11970869

Toni, N., Buchs, P. A., Nikonenko, I., Bron, C. R., & Muller, D.
(1999). LTP promotes formation of multiple spine synapses between a
single axon terminal and a dendrite. Nature, 402(6760), 421–5.
https://doi.org/10.1038/46574

Toni, N., Teng, E. M., Bushong, E. a, Aimone, J. B., Zhao, C.,
Consiglio, A., … Gage, F. H. (2007). Synapse formation on neurons
born in the adult hippocampus. Nature Neuroscience, 10(6),
727–734. https://doi.org/10.1038/nn1908


text:
Super-resolution imaging in vivo
Are there any microscopy modalities or techniques for in vivo imaging at higher resolutions than the diffraction limit?
I was looking at this list: Super resolution microscopy, but they don't talk about in vivo imaging.

Any superresolution techniques relying on stochastic sampling (e.g. PALM, STORM) is extremely difficult to accomplish in vivo, as the tissue would be moving (e.g. due to respiration) and this would hinder a lot the reconstruction of the image.
Apparently it may be possible to do it with STED but I could not find the related paper*, although the same authors recently published some interesting work on living brain slices.
* Note that the images in that article come from this paper, which is not done in vivo.
Thanks to @vkehayas for pointing out that in vivo STED has been done for instance here Nanoscopy in a living mouse brain

I beg to differ on the PALM/STORM point. While I'm a little biased as a co-author of Live-cell dSTORM with SNAP-tag fusion proteins, we had very good experience with live cells and dSTORM. After all, a dSTORM image can be taken in ten seconds, and many biological processes are slower.

@thiton: again, I reiterate that when speaking about in vivo (at least in physiology) one considers a living animal, not a cell culture, which is still considered in vitro (or, for living tissue I ex vivo). I doubt you had many problems of respiration with your cells...

The first paper published with STED in vivo was Nanoscopy in a living mouse brain.. Feel free to incorporate that in your answer if you'd like to.

@vkehayas Thank you! I had not seen that when I wrote the answer, I will add it.

Since the question was asked, the field has seen tremendous growth and even a Nobel prize has been awarded for Super-resolution microscopy. Since other answers have already touched upon how STED, PALM, STORM could help, I would talk about Expansion Microscopy (ExM) and how it has been recently used to image intact zebrafish brain tissue and gastrulating zebrafish embryos [Freifeld et al].
Since the optical resolution is limited by the wavelength of light which gets diffracted if the object being imaged is smaller than the wavelength of light (~300 nm). In order to image small object, what if we could enlarge the object itself to cross the diffraction barrier? This has been done by a team of researchers at MIT who imaged mouse brain tissue in 2015 [Chen et al].

Chen et al. have solved this problem by digesting the mouse brain away after transforming it into a polymer gel but before inducing matrix expansion. But how can one study a brain in which all the neurons are gone? Here, a second idea came into play: For some questions, it would be enough to study a “shadow” of the brain in the polymer matrix. This was realized by first marking molecules of interest in neurons with antibodies. The antibodies then were labeled with fluorescent markers that bind both to the antibodies and the matrix. The brain was then digested away and the matrix expanded. The fluorescent neuronal shadows also expanded and could be studied in “superresolution.” Chen et al. could thus increase specimen size by about a factor of 5 while preserving general morphology, and could visualize cultured neurons and brain slices at 70-nm resolution. This allowed them to observe proteins localized to synapses.

The best part is that conventional confocal microscopes can be used to image these enlarged samples, so the imaging speed is also good.

Freifeld, L., Odstrcil, I., Förster, D., Ramirez, A., Gagnon, J. A., Randlett, O., ... & Martin-Alarcon, D. A. (2017). Expansion microscopy of zebrafish for neuroscience and developmental biology studies. Proceedings of the National Academy of Sciences, 114(50), E10799-E10808.
Chen, F., Tillberg, P. W., & Boyden, E. S. (2015). Expansion microscopy. Science, 347(6221), 543-548.

This question is asking about in vivo imaging but Expansion Microscopy is still performed in fixed samples. If you are claiming that Expansion Microscopy can be performed in vivo you are...stretching the definition of in vivo too much. For an example of true "super-resolution" imaging in vivo see https://www.nature.com/articles/s41598-017-18640-z.pdf.

There have been experiments with Live-cell dSTORM with SNAP-tag fusion proteins in Markus Sauer's lab in Würzburg. If you are using the physiology definition of in-vivo, I'm pretty sure some of my co-workers have measured on live organisms. However, this is work in progress and not fully published; if you are interested, you should ask Markus Sauer directly.
You can use the dSTORM-like techniques (STORM, dSTORM, GSDIM, RPM, etc.) in live cells because the chemical environment in the cell is favourable and the redox system of the cell works for you. The key problem is to get the fluorophores into the cell, but SNAP-tags can help you to do it.
As one of the co-authors, I can tell you that live cell was some pain, but considerably less than getting 3D localization microscopy to work.
PALM is a different story because you generally have longer acquisition times. STED is difficult: If the cell wasn't dead before, the STED beam will ensure it is, either through the intensity or by unbalancing the chemical environment sufficiently. You might have your image before the cell dies, or maybe not.

Yes. A decade ago I've been working on a software for microscope that does what you want.
Here's how the product looks after 12 years of development.
It's optical, however it produces Z map instead if image, and has resolution is order of magnitudes below the diffraction limit:
http://www.amphoralabs.com/production/10404/10708

That does not work in vivo, does it (cell culture does not count as in vivo)?

Wikipedia thinks you're wrong. "In microbiology in vivo is often used to refer to experimentation done in live isolated cells"

well, when speaking about physiology, in vivo means on living animals, isolated cells are considered ex vivo.


text:
What's the best sign language to teach a dolphin?
I know some scientists and trainers used hand signals to communicate with dolphins. The problem is: the dolphins have no hand to express themselves. With chimpanzees, we see how creative they are, not only in creating new words, but also in teaching their offspring without being told to do so (not sure if it was Jane Goodall who told that story in Through a Window).
So, what additional techniques could be used with cetaceans to really communicate with them?

I’m voting to close this question because it is vague and open-ended (encouraging opinions rather than fact-based answers). It also doesn't demonstrate the expected prior research.

In terms of training dolphins, it doesn't matter that they can't replicate a hand signal - just that they can learn to associate that visual stimuli with a behaviour.
For communicating with dolphins, one of the most common modalities is sound, either through playbacks of their own/conspecific sounds, or through synthetic sounds that aren't thought to be in their repertoire. Here is a review from Denise Herzing who has done a lot of this work on a wild dolphin population, with some reference to bird and primate work: https://www.animalbehaviorandcognition.org/uploads/journals/13/04.Nov2016-Herzing_HH(6)-final.pdf

That's a very interesting paper. Thank you!


text:
Are humans an eusocial species?
In the evolution of sociality among animals, different degrees are acknowledged. Some species present overlapping generations, some division of labor, and the minority present reproductive division. Those that present the three traces above are called "eusocial" (e.g. some wasps, some bees, all ants and termites, and an african mole).
Maybe our own species could be eusocial? After all, homosexuality is present in virtually every culture studied by anthropologists. Some say it may bring an advantage to the group via group selection (not having kids of their own, they could study plants, medicine, weapons, and so on). What do you think? Are we an eusocial species?

I wouldn't go so far as to say homosexuality is eusocial - some still become parents by reproduction.   asexuals might be, but if environmental conditions vary, they might reproduce. habitual sexual practice is not non-reproductive behavior I think.  it might be very low chance of reproduction, but reproduction only needs to happen once really.

Well, some wasps and some Paraponera ants sometimes reproduce, even not being the "queen" in the nest. It doesn't mean there is no reproductive division, though. In our species the "reproductive division" (if that's the case) goes together with our high intelligence, that teaches us to have sex just for fun. But my point is that the lack of sexual attraction for the opposite sex may have evolved similarly as eusociality in other species.

it depends on your definition of eusociality - if eusociality does not mean caste reproduction where some castes cannot reproduce, then by all means call it eusocial.  http://en.wikipedia.org/wiki/Eusociality#In_mammals

Thanks for the link. If we are not eusocial, perhaps something in that sense may have triggered the development of homosexuality, that being so widespread in human societies, asks for an evolutionary explanation.

I'm going to hazard turning my comment into an answer....
Even if the answer might be no, you know this is a good thought and there is something there... lets dig a little.
Eusociality in evolutionary biology is by many like Dawkins and Wilson pointing to the evolution of sterile castes of animals, which are very closely related to the breeding caste.  This is how hymenoptera are famed as examples of the importance of kin selection. Worker ants are entirely dependent upon the queen to reproduce the next generation, but they can do so because the queen is close enough to being them so that ants continue to exist as they do.  Not only is this a reasonable way to exist, but kin selection has produced eusocial animals in every
The application of this definition to mammals has been done, but its not a universally agreed upon definition of eusociality.  To a great extent its because the animals can still breed, even if they are inhibited from doing so by a social structure.  Wolf packs and ape troops where the alpha male sires all the offspring are not eusocial - the other males are only deferring mating (sometimes forever) but they are biologically fertile.  This is not eusocial, just social biology.
But to your question, I think the point to be considered is that the dynamic that allows the evolution of eusociality does shape social structures.  Primates are so rational and their brains are so big that their brains allow them to adapt their social matrix such that we can have different roles in our groups depending on the conditions of environment at any given moment, whereas sterility and castes defined by adaptation will change very slowly, we can change our society in just a generation.  Social animals are eusocial in a way, but they are more adaptable by the use of their social reprogrammability.

The question of homosexuality and its role in nepotism is interesting.
According to this wiki article, less than 10% of the population is homosexual. If you consider that homosexuality makes human eusocial because homosexual do not reproduce but help their brothers and sisters to reproduce, then you would have to consider any species where a few percentage of the population produce some kind of altruism to be eusocial. Given that all phenotypic traits theoretically have social impacts, then I would bet that you might call eusocial a lot of species.
It seems wiser to me to limit the definition of eusocial when an important part (maybe 98% minimum) of the population do not reproduce but help others to reproduce. One might also want to consider some other restrictions for a the use of the word "eusocial"
Therefore, using the argument of "reproductive division" I would rather not include Homo sapiens in the list of eusocial species. But it is nothing more than a question of definition. You're free to define your words the way you want and call human eusocial but make sure your interlocutor knows your definitions.
Now, let's say we place the limit to the definition of eusociality at 1%. When more than 1% of the population does not reproduce but help their kin to reproduce, then the species is eusocial. Then, humans would seem to fit in this definition at first sight. But do homosexual in our modern society really help their kin to reproduce? In other words, do siblings of homosexual reproduce more (or have offspring that have a high fitness)? This study investigated the question (as pointed out by @oreotrephes in the comments) and they indeed found some pattern but the difference in reproduction between relatives of homosexual and non-relative of homosexual is is quite weak. But if homosexual don't reproduce and don't help their kin reproducing then, humans is definitely not a eusocial species.
Finally I want to add that individuals from lots of different species have been found to perform homosexual behaviour (see this wiki article). If you want to consider human as eusocial because some homosexuality, then you will have to consider sheeps, labradors and pigeons to be eusocial as well!

Thanks for your comment, Remi.b! I'm using the definition from E.O.Wilson in Sociobiology and other books (The Insect Societies also use the same, if my memory is right). They say nothing about how big is the "sterile caste", only about the 3 traces ocurring together. And if homossexuals change their habits, it doesn't change the reason that behaviour might have evolved in first place - and I think that's the objective within biological reasoning, not to put rules of what we might or not do with ourselves.

Indeed, I have never heard either talking about the number of sterile individuals. But it seems to make sense to me that the whole point of eusociality is that many individuals work for the benefit of one. And therefore, you might see a continuum from some individuals helping some others to many individuals helping one. I guess one would need to define eusociality as an arbitrary threshold along this axis (and some others).

In my last paragraph, I just wanted to say that even if one want to consider that humans were eusocial in the past, he might not be able to say the same for the modern species of human if siblings of homosexual do not have greater fitness than average anymore.

Actually, in social hymenopterans, the queen alone works for the benefit of the worker caste. Because of the genetics of haplodiploidy, when a worker gains a sister, it has a copy of 75% of her DNA. When the queen gains a daughter, it has a copy of only 50% of her DNA. So, no, there's not a "sense" like that "whole point" you mention. Indeed, in different species the logic may vary wildly, according to genetic and/or ecological constraints.

About your last paragraph, I disagree. The cultural time is almost irrelevant close to genetic/evolutionary time. We probably have the same instincts we had 100,000 years ago. Even if homosexuals change their behavior for the next 1000 years (what is highly improbable), this would hardly change the genetics that cause homosexual behaviour. And even if in industrial-western-societies this change happens and is sustained for so long, still there are other societies that would not change alike. That's the reason our cultural behavior are not supposed to define our biological terms. Do you agree?

@Remi.b in regards your last paragraph I think OP is referring to Camperio-Ciani et al 2004 which suggests that female relatives of homosexual men have more offspring than female relatives of heterosexual men.

Nice link, @Oreotrephes! What I mean is: in biology we refer to females as animals that produces big gametes. If a woman has their ovaries removed, would we stop calling her "woman"? Homo sapiens is a biped species, if someone is comatose and cannot walk, would we stop calling him/her "human"? We wouldn't stop being a eusocial species just because of some habit changes in a single century, that's my point, mostly because those changes are usually reversible.

If you call eusocial a species where some individuals help other to reproduce and you find a species where none individuals help others, you cannot call them eusocial because some species cannot reproduce because they evolved in order to help the others. You cannot say that an ant can fly because it evolved ability to fly in its evolutionary history! But anyway, this is just a detail of the last paragraph.

I missed 2 of your comments when post my last comment. Sorry about that. You basically said that culture does not really matter at calling a species eusocial or not, instinct matter at defining species. Well, if you want to. I agree with that but don't think this discussion is biologically relevant. I didn't get your point in your second comment. It seems intuitively coherent that if 0.001 % of the population help a bit their kin to reproduce, then it would be a bit awkward to call this species eusocial. But again, define eusocial the way you want!

You may be right, @Remi.b, but the proportion of homosexuals helping their family is surely much higher than 0.001%.

Yes indeed it is/was probably much higher. probably between 1% and 10%.

I think it depends on the country and the dominant levels of individuality. In the scenario where we evolved, and that still persists in some hunter-gatherer societies, and to a lesser degree in "underdeveloped" countries (i.e. family members count on the support of the others), it's supposed to be much higher.

"some kind of altruism" in your answer is wrong, because the definition of homossexuality is an altruism FROM absence of reproduction. And this is the main point in eusociality.


text:
If ants have an antibiotic gland, how can they spread hospital infections?
Wikipedia describes how antibiotics are produced in ants:

"Metapleural glands ... are responsible for the production of an
  antibiotic fluid that then collects in a reservoir ... also referred
  to as the bulla ... From the bulla, ants can groom the secretion onto
  the surface of their exoskeleton. This helps to prevent the growth of
  bacteria and fungal spores on the ants and inside their nest."

So how are ants often cited as an important problem in hospitals, spreading infections from garbage and through the patients? Shouldn't their natural antibiotics prevent that?

Who says that ants are spreading infection from garbage to patients? Do you have a reference for that?

No, that's just a truism that I heard sometimes.

Truisms are not a very good source of information on this site.

A quick google at "ants hospital infection" shows a lot of scientific papers...

@anongoodnurse A truism is something that is so obviously true that you don't need to justify it. I suspect Rodrigo meant to use some other word.

Let me rephrase your question: if a penicillin pill is rubbed on a MRSA-infested surface, will the pill be safe? Supposing that it is true that ants carry infections and secrete significant amounts of antibiotics (both big ifs), there is no such thing as an universal antibiotic.

Human beings also have many glands which secrete antibiotic fluid, including our tear ducts. Yet humans are certainly an important source of infectious bacteria.

I agree with @tel

I have worked in hospitals (US) most of my life, treating both community-acquired, and more pertinently to this question, nosocomial (hospital acquired) infections, and have read many articles on the subject.
I have never, ever seen ants mentioned anywhere.
People, flies, cockroaches and rats, yes.
Ants, no.
However, ants are vectors in a few foreign studies. The key word in these studies is potential.
As you stated,

From the bulla, ants can groom the secretion onto the surface of their exoskeleton. This helps to prevent the growth of bacteria and fungal spores on the ants and inside their nest.

No antibiotic covers all organisms. Also, the secretions are to protect the ants against infection, not against the carrier state.
Pathogenic bacteria is cultured from ants themselves. The ant can be thought of as similar to a human: humans make antibodies to pathogens but are vectors of many diseases. Ants protect themselves via secretions, but are hosts to potential pathogens.
Part I: Review of Scientific Data Regarding Transmission of Infectious Agents in Healthcare Settings
Hospital hygiene and infection control
Ants associated with pathogenic microorganisms in brazilian
hospitals: attention to a silent vector
Ants in a hospital environment and their potential as mechanical bacterial vectors
Insect/Bacteria Association
and Nosocomial Infection

I agree with that - I have been a lot to hospitals lately and not noticed any ants.

Ants can and do carry loads that are several times their own weight. I grew up in an area with a lot of ants, and a common scene was a long trail of ants acting as a food supply line. Once a morsel is located, they create a long feremone trail to that morsel. A large clump of ants is always working to break the food into smaller pieces, and several ants are usually on their way back to the colony carrying large crumbs. Often these crumbs are the first thing you notice, rather than the actual ants, because they are often so much larger than the ants themselves.
In a hospital, most of the food that ants would scavenge would have fallen from the plate of a human being. Many of those human beings would be carriers of disease. I would expect that the trail that these ants walk is littered with plenty of crumbs-of-crumbs that fall off of their load along the way. If these were large enough for us to see, they would get the attention of the ants and they would carry them back to their colony. But a particle of the microscopic crumb dust they do leave behind might carry several specimens of the germ that sickened some messy patient, even if the ant that dropped it was relatively sterile.

Other than the fact that ants carry bacteria on their food particles, there could also be alternative reasons that they can spread infections.
Just like antibiotics derived from bacteria and fungi have caused resistant pathogen strains to evolve (MRSA for example), it could also be the case that the bacteria naturally living around the ants have evolved some degree of resistance to the antibiotics, perhaps by effluxing sufficient amounts of them by overexpressing pump proteins to the levels that the antibiotics are only mildly bacteriostatic instead of bacteriocidal. These bacteria can then fall off the ants while in the hospital and lead to disease.
It is reasonable to assume that this could evolve, since the ants frequently communicate socially with one another, and any resistant bacteria or fungi can then quickly colonise a previously empty niche, thus creating significant evolutionary pressure for this.


text:
How does the human spine move during healthy deep breathing?
When I googled, I found a lot of questionable sources from various nonscientific sources about human breathing.
Is there any science about what the human spine does during healthy deep breathing? Which parts move forward or backward during inhalation and exhalation?

There is nothing like "healthy breathing" (or unhealthy to name the contrary). Breathing is a necessity life.

@Chris Many adults spend their entire lives without ever experiencing the benefits of deep "diaphragmatic" breathing. Beyond increasing the risk of under-oxygenation, shallow breathing puts unnecessary strain on muscles, resulting in chronic problems. Proper breathing can help with stress, anxiety, insomnia, and other conditions.

@vkehayas That sounds like junk science to me. The benefits of breathing exercises for health have very little to do with the healthiness of particular breathing patterns or oxygenation. Respiration is under homeostatic control and you breathe as much as you need for your current oxygen usage.

Please forgive me, but I find this a very strange question. Why would one's back movements be the focus of a question about breathing? The back is the structure around which breathing occurs, i.e. the ribcage is attached to the back as are some muscles involved in breathing. The back mostly doesn't do anything. That's why normal breathing isn't hampered at all by immobilizing the back (e.g. leaning back hard against a wall.) "Healthy deep breathing" is a myth, unless you're at high risk for pneumonia (e.g. post-operatively).

What is certain is that your breathing patterns --both inhalation and exhalation-- depend on your emotional state. If you have been conditioned on a certain emotional state, e.g. PTSD, you will breathe differently when triggered. Changing the breathing cycle can change your emotional state as the two go together. Most trained singers, actors, dancers, and athletes --people who do something with their bodies-- will attest that they must master their breathing control to do their work. I agree, though, that the question of the spine's movement during breathing does not appear interesting to me.

@vkehayas - I wasn't aware that there was any breathing pattern not involving inhalation and exhalation. I'll say that focusing on your breathing can influence physical and emotional states, but not that the two necessarily go together, e.g. hyperventilation does not usually trigger anxiety, sudden breath holding does not result in pain, etc., whereas the inverse is usually the case.


text:
Can one dendrite pass through another?
While tracing dendrites on EyeWire I encountered the following situation. They belong to an Orientation Selective Ganglion Cell.

It's the first dendrite I've noticed with such a clear 'hole' in it, though which another dendrite passes.

Is it possible for one dendrite to pass through another? Perhaps I shouldn't have 'connected' the top part with the bottom part?

I can't think of any reason that would explicitly prohibit a dendrite from travelling through a space created by another dendrite's branching pattern. In non-EM images of dendritic branching patterns I don't think I have ever observed dendritic loops, but of course, that has nothing to do with whether or not they occur. Nonetheless, I think there are more likely explanations for what you are seeing in these particular images.
As shown, the upper and lower parts of the "dendrite" in the first image do not look like a continuous structure. I would guess that you are looking at a synapse or some other contact between two different processes in the first image. The 3-4'o'clock connection in the loop suggests this interpretation. Can you see vesicles in the images around those connections?
The other dendrite that shows up in your second image might be a glial cell or some other cell's dendrite that participates in the synapse. Alternatively, the other dendrite may just be a chance passing of two dendrites that don't interact functionally.
Of course, it could be that you and the computer have just completely misunderstood the data. My understanding of the Eyewire interface is that the computer guides a lot of the identification and doesn't easily allow you to see the surrounding areas so you can't track structures all the way to their sources. In such a situation, it seems probable that you would end up with ambiguous instances like this that you would have a hard time resolving without more information/expertise. But maybe Seung or one his colleagues can come weigh in on that?

"I don't think I have ever observed dendritic loops" ... On the images it did look like a loop, but I've noticed big staining gaps before. "do not look like a continuous structure" I don't know how the 3d model algorithm handles additions, and how much you can rely on it visually, although it does look like the structure is rounded prior to touching, which could indicate it's just a staining gap.

"doesn't easily allow you to see the surrounding areas so you can't track structures all the way to their sources", ... correct. It's mainly just tracing neurons for now, but they are planning to work on other possible tasks as well. I agree that in many cases I am uncertain about what to do, ... hence this question, and your help being greatly appreciated. I'm still very curious to see how the project will evolve.


text:
Book recommendation for studying biology for neuroscience
I will be starting a double degree in neuroscience and mathematics very soon, and I realised that an understanding of human biology can really help me out, and so I'm looking for an introductory level biology textbook that also covers things in great detail. I have no background in biology whatsoever.
Also, am I supposed to learn about the biology of plants for example before diving into human biology or can I just get started with human biology straightway.
By the way, I'm not looking for a biology textbook that has a mathematical approach, just the traditional approach can suffice.

Book recommendations are off topic for the biology stack exchange

Will you be an undergraduate student?

@BryanKrause yes

Presumably with those majors you will take a general biology course your first year, and subsequent courses in genetics, cell biology, and physiology most likely your second year. Each will come with an a textbook no doubt.

Yeah well, from my experience with mathematics for example, the textbooks recommended in the course outline were not really great, they were very surfaced level and focused more on application rather than theory and rigour. The textbooks I found most useful were actually recommended to me by the maths overflow community. So I'd naturally assume that it'll be the same case for neuroscience, hence the reason I posted this question, plus I'd also like to start studying these subjects early, even though i'll be introduced to the fundamentals once I commence my degree. @BryanKrause

It is not clear to me whether you are looking for a general biology (as you've indicated in your question body) or neuroscience (as you've indicated in your previous comment) textbook. The two most popular neuroscience textbooks are arguably Kandel's "Principles of Neural Science" and Squire's "Fundamental Neuroscience". Both devote a few introductory chapters discussing topics that could be described as general biology.

I agree with @vkehayas, you could add Purves to the list as well. I just don't think there is going to be a good answer for what you are looking for though: a introductory textbook that covers things in great detail is kind of an oxymoron, and it's going to be entirely a matter of opinion to resolve the conflict between the two. There is far more to understand in biology than there is in the foundations of mathematics.

Ok, Fine. I'll join. Kandel is excellent. I took his class back in the day. If you had one nueroscience textbook, I would definitely recommend that over Purves. Sorry @BryanKrause . You'll want Albert's MBoC as well.

I never said Purves > Kandel just adding it to the list :) @DanHall I haven't personally used Kandel ever but have certainly heard good things.


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Help on reconciling seemingly contradictory evidence about fetal experience
Fetal awareness and especially fetal pain are controversial, political issues. However, I do not wish to get into politics and want to merely stick to the scientific evidence. I have found statements about fetuses in the womb that seem to contradict each other, yet there has been no reference to the opponents in either side.
Some believe that fetuses do not have awareness in the womb and cannot feel pain. Here is an argument along those lines, claiming that fetuses cannot feel pain, even when their nervous systems and brain are developed, because the chemical environment within the womb suppresses awareness and experience that shapes the brain only happens outside the womb.
However, some other evidence seems to claim that fetuses can have experience. Twins can interact with each other in the womb as early as 14 weeks of gestation, as stated here. It is possible to learn in the womb, and newborns, even after they are born, can retain this knowledge, as stated here.
I'm not sure what to think. Are some of these statements, such as the idea fetuses are not aware, just incorrect? Or can interaction and learning occur without awareness somehow? (I know pain is distinct from awareness, interaction, and learning. What seemed particularly strange was the idea that fetuses have no conscious experience whatsoever, especially as no one making that claim, as far as I know, even mentioned the evidence about interaction and learning at all).

FYI, your third link gives a 404 response.

@vkehayas It doesn't for me, so I'm not sure what happened to you. Sorry.

I know close to nothing about the subject of self-awareness in fetuses.
But learning —and certainly interaction— can occur without anything close to human "awareness", as evident by the fact that systems without a brain (and even without neurons) can learn. Any system that can process and store information is capable of learning. Does your definition of awareness include anything more than this? Conversely, organisms with a very simple brain can display aversive behaviour.
For an example of memory without neurons, see the Wikipedia article on immunological memory.
For examples of aversive behaviour without a proper brain see Zhang, Lu, and Bargmann 2005 and Babin et al. 2014

References
Zhang, Y., Lu, H., & Bargmann, C. I. (2005). Pathogenic bacteria induce aversive olfactory learning in Caenorhabditis elegans. Nature, 438(7065), 179–184.
Babin, A., Kolly, S., Schneider, F., Dolivo, V., Zini, M., & Kawecki, T. J. (2014). Fruit flies learn to avoid odours associated with virulent infection. Biology Letters, 10(3), 20140048–20140048.

Um, don't fruit flies and C. elegans have an actual brain? Yes, I know it would be a very small brain, but it still counts as a brain, as far as I know. Anyway, stuff such as invertebrate awareness is controversial as well, to say the least, but I don't believe there has been 100% proof that they aren't conscious, and some scientists believe it exists.

Furthermore, I was actually talking about the point when the nervous system and brain do develop in fetuses. The argument I mentioned was not about whether those things had developed (they have by that time), but whether the chemical environment in the womb suppressed consciousness. The studies you mentioned don't seem to be relevant anyway, come to think of it.

@Inflationary_Bubble You asked if learning is possible without awareness. If you accept that the immune system does not have awareness, then I demonstrated one way learning is possible without human-like awareness. If you are willing to consider that the immune system and C. elegans have some rudimentary form of awareness, the only consistent thesis is panpsychism.

@Inflationary_Bubble Then it becomes a matter of identifying the degree of awareness which is an empirical question that is not really possible to answer with current methods, although it is reasonable to assume that the maturity of the fetal nervous system could be a relevant parameter. But please note that in that case the apparent contradiction also dissolves, as awareness is no longer a binary feature. The definition issue of whether you call it a brain or a collection of ganglia in the case of C. elegans is inconsequential for the answer.

@Inflationary_Bubble The fundamental problem in the apparent contradiction is then that you consider awareness as a binary feature (you either have it or you don't). However there exists no clear line dividing aware from non-aware systems. In my opinion, it is more productive to think in terms of information processing and storing.

@vkehayas - I think that your answer would benefit by including the points raised in the comments above.

@LinuxBlanket Agreed, will try to do if I find the time. Feel free to do so yourself if you'd like.


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Using proportion or a diversity index when dealing with just two strains
I'm looking at diversity maintenance in an experimental system consisting of just two strains. I have count data. I can calculate their proportions and I can use that data in my statistical models, or I can calculate Shannon or Simpson diversity, and use that data.
My question is: When dealing with just two strains, is it really necessary to use a calculated diversity index, or will proportions do just fine?
The benefit of using proportions is that it's a more accessible metric - not requiring any (albeit fairly basic) knowledge of diversity indices and how they alter the data.
Having calculated Shannon, Simpson, and proportions, and run all three through my models, it makes no difference which I use - the data are quite emphatic. My slightly educated instinct is, in this case, to use the most simple metric, but I'm looking for some opinions on the case.

Extended upon the suggested statistic
The proportion $p$ is definitely not a good measure of diversity. A proportion of 0 or 1 both indicates no species diversity as only one species exist. If one species, never reach a frequency of 0.5 in your data it might be reasonable though. Otherwise, something like $p(1-p)$ could be a statistic of interest.
If you're willing to use $2p(1-p)$ (instead of the above $p(1-p)$) as index of diversity, then you could make the point that it can be easily extended to $S$ species with $1-\sum_{s=1}^S p_s^2$, where $p_s$ is the frequency of the species $s$ by analogy to the genetic diversity within populations (see Nei 1973).
Note that these statistic will be sensitive to the sample size. For example, if you sampled only one individual, then this individual can only belong to one species and your measure of diversity can only be zero. You might want to compute an unbiased estimator for this statistic.
Your goal is to reduce the reader's cognitive load
Your goal is to use a statistic that will communicate easily. If your readers are going to be very much used to Simpson's or Shannon's indices, then even a mathematically simpler index might end up leading to an extra cognitive load onto the reader.
IMO, it will be hard to give a more definite answer without knowing 1) who are going to be your readers (which journal are you aiming to publish in) and 2) what are the exact data manipulation and interpretation you are aiming to do based on your results. For example, if it makes the comparisons among graphs easier by using a simpler statistic over a more complicated once, then choosing the simpler statistic is a good idea.
Good statistical analysis
In any case, it is essential that you to try out (and you did) different measures of species diversity and make sure that your conclusion is robust to these different measures and explain in your methods that the chosen statistic won't matter. That will make your point and your choice of statistic much stronger.


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What is the real meaning of the statement "*ontogeny recapitulates phylogeny*"?
I tried searching in this site but couldn't find an appropriate answer to the title question: what is the real meaning of the statement "ontogeny recapitulates phylogeny"?

What kind of appropriate answer are you looking for? A simple google of "ontogeny recapitulates phylogeny" reveals lots of quite good answers.

Actually, the statement "ontogeny recapitulates phylogeny" has been largely discredited in modern biology.  The stages of embryonic development were thought by Ernst Haeckel to resemble ancestral species in evolution.  That is, early embryos appeared to have tails and gills and resembled fish, later embryos resembled quadrupeds, and so on.
However, embryos do NOT actually resemble adults of ANY species.  More accurately, one could say that early embryos of different species resemble early embryos of other species, and later stages differ more and more as specialized traits of different species become more obvious.  On the early extreme, one fertilized ovum shows very little difference in gross appearance from any other fertilized ovum, and the blastula of different species look very much alike, but as different organs and limbs become better developed, those of different species begin to look more and more different.
This actually only describes SOME of the changes that occur in embryonic development.  Other changes are not so simple.  One very good book that discusses the strengths and weaknesses in this area is the book "Ontogeny and Phylogeny" by Stephen Jay Gould.

As an embryo develops, it passes though stages with characteristics of some of the more primitive forms in its evolutionary lineage. An example is the pharyngula stage of the human embryo, which bears branchial grooves in gill pouches. in fish, these develop into gills.

As far as I know, this is exactly what the phrase means. Why is it down-voted?


text:
Can living cells be imaged with electron microscopy?
According to this article from October 2009, http://news.mit.edu/2009/electron-microscope

"Electron microscopes are the most powerful type of microscope,
  capable of distinguishing even individual atoms. However, these
  microscopes cannot be used to image living cells because the electrons
  destroy the samples."
"Now, MIT assistant professor Mehmet Fatih Yanik and his student,
  William Putnam, propose a new scheme that can overcome this limitation
  by using a quantum mechanical measurement technique that allows
  electrons to sense objects remotely. Damage would be avoided because
  the electrons would never actually hit the imaged objects."

Is it possible yet to image living cells with an electron microscope? If not, has there been any advance in this direction?

As far as I can see, this remains only a proposal, though it isn't quite my field, so it's possible someone has presented results at a conference somewhere.
Taking a look at the citations of the original paper [Noninvasive electron microscopy with interaction-free quantum measurements, Putnam and Yanik
Phys. Rev. A 80, 040902(R)], there don't seem to be any experimental implementations: https://scholar.google.com/scholar?cites=17617747827527972037
From the news story you linked: "[Yanik] expects the work will launch experimental efforts that could lead to a prototype within the next five years." A good reminder about making time estimates!

what is your field/occupation? Just curious to know if it's the answer of a microbiologist , a physicist or what

I'm a physicist who works in biology, so if this became big, I'd probably have heard about it. (But I'm not an imaging specialist or an EM person - that's my caveat!)

if this idea would actually work someday, do you think it would be able to image cells only superficially, or could it get inside and below the surface of the cell?  Does a traditional electron miscrocope only scan objects superficially?

Not sure! I think it is possible to scan some depth (100s of nm?) with traditional EM, depending on energy, but less than the size of a typical eukaryotic cell. Because of this, there are methods for "slicing" cells to look at the interior, or milling away parts of the surface. Obviously this is pretty destructive, too!

According to this http://www.mpq.mpg.de/4867802/13_02_21, they were about to start "testing the theory" in 2013  with a budget of 4 million and the work was going to last 3 years and a half.. they dont say in which date they were going to start

@Pablo In my opinion, if something like this became feasible to the point that researchers of biology (rather than EM physics) were able to use the technique, it would very quickly become known to just about everyone in biology because it would be such an important step. These groups got a grant to try it out because it would be a big deal and because they came up with a plausible mathematical approach - from the recent citations linked by AJK it seems like they are still working on the physics, and still far from the biology.

well, if you ever get news on this dont forget to update the topic.. I thought something like this was close to happen when I started reading news about scientists being able to read people's thoughts and words they were thinking, but aparently for doing that they only needed to know the cells and neurons superficially, knowing which neurons became activated during a speech, or measuring electrical activity and blood oxygen levels

@Pablo The thought reading experiments are very different from this, completely unrelated, and a bit overstated. They are based on fMRI or EEG and are dependant on a substantial training sequence to teach a model about patterns of brain activity observed in a single subject in a limited number of situations.

According to this "but living cells and tissues and whole, soft-bodied organisms require chemical fixation to preserve and stabilize their structure." https://en.wikipedia.org/wiki/Scanning_electron_microscope . Does it mean it's possible?

While it may not be possible yet to image live cells with EM, it is possible to image live animals. For one example, Ishigaki et al. (2012) imaged live ticks (Haemaphysalis flava) with scanning electron microscopy. They could even see the ticks moving their legs inside the microscope for about 1 min after they went in the chamber. The ticks were still alive after they were removed from the vacuum inside the microscope. Half of those exposed to the vacuum and the electron beam died within the next two days, but the rest remained alive for at least two more weeks. Apparently, ticks that were only put inside the vacuum all survived just fine. It was only when they were blasted with the high-energy electron beam that their chances of dying increased.

Live ticks in SEM
Notice that the scale bars in panels B-F should be in $\mu m$, not $mm$

This is not the first study to succeed in imaging live organisms with electron microscopy; that was Pease et al. in 1966. It appears that in some insects the ionizing beam induces the polymerization of "extracellular substances" into a thin (~5 $\mu$m) membrane that acts as a protective "nano-suit" (Takaku et al. 2013). Takaku et al. (2013) could induce the formation of a similarly protective thin membrane by using polysorbate 20, a broadly used surfactant. Artificially inducing the formation of similar "nano-suits" may be a more promising way to image live cells with electron microscopy rather than relying on quantum mechanical measurements. Takaku et al. (2013) even go as far as to speculate that the natural formation of similar "nano-suits" may have acted as a protective shield for prokaryotic extremophiles that could have invaded the earth during early evolution (panspermia hypothesis).

References

 - Ishigaki Y, Nakamura Y, Oikawa Y, Yano Y, Kuwabata S, Nakagawa H, et
   al. (2012). Observation of Live Ticks (Haemaphysalis flava) by
   Scanning Electron Microscopy under High Vacuum Pressure. PLoS ONE
7(3): e32676. http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0032676
 - Pease, R.F.W., Hayes, T.L., Camp, A.S. and Amer, N.M., (1966). Electron microscopy of living insects. Science, 154(3753):
   1185-1186. http://science.sciencemag.org/content/154/3753/1185
 - Takaku Y., Suzuki H., Ohta I., IshiiD., Muranaka Y., Shimomura M., and HariyamaT. (2013). A thin polymer membrane, nano-suit, enhancing
   survival across the continuum between air and high vacuum
   PNAS 110 (19): 7631-7635. 10.1073/pnas.1221341110

I'd love to see how well waterbears survived.

@Daniel Given that tardigrades are able to survive orbiting in space, as you are probably aware of since you brought them up, I am confident that they can do at least as well inside the EM column.

Indeed. Anyone got a spare electron microscope and some tardigrades? And why on Earth hasn't this experiment been done already? Quick! Let's publish!


text:
Sodium potassium balance in a cell
In a resting cell at steady state, is sodium influx or potassium efflux higher according to the concentration gradients and permeability, and given that the sodium potassium ATPase is active?

If potassium ions were alone inside and outside of the cell, they would be tended to diffuse along out of the cell due to high gradient inside. Because of potassium ions have positive charge, potassium lose would cause negativity inside. Within a few seconds, potential loss would rise enough to be able to stop potassium exit out of the cell. Because against decreasing concentration gradient, there would be reverse direction electrical gradient increase so these forces have to be balanced somewhere. For a large mammal nerve cell , needed potential gradient is about-94 millivolts.
We can assume similar concepts for sodium ions also. This time direction will be outer to inner side of cell. And this makes a positive potential (about +61 millivolts) due to gaining positive ions .
When we calculate total diffusion potential for only one ion, Nernst equation is used. For ions more than one we have to use Goldman equation, which is more complicated , instead.
Goldman equation consists of three factors:

Electrical charge for each ions.
Permeability for each ions.
Concentrations inside and outside of the cell for each ions.

Major factor on this resting potential is membrane permeability. For potassium ions, membrane permeability is about 100 times more than sodium ions. Because potassium leakage channels makes potassium leakage more easier than sodium. When we put this factor on Golman equation, we find resting potential about-86 millivoltes which is closer to potassium diffusion potential.
(source:Wikipedia)
(source:KhanAcademy)


text:
Where can I find a picture of the inflorescence of Epipremnum aureum (golden pothos)?
Epipremnum aureum (golden pothos) is a very popular house plant - attractive and almost impossible to kill.
Also, it is a flowering plant with flowers produced in a spathe up to 23 cm (9 in) long, according to Wikipedia.
I have been trying to find further documentation of these flowers, in particular a picture, without success. Can anyone help?
(Google image search produces some stock photos that claim to show E. aureum flowers but I am skeptical about these.)

Figure 4d on page 6 of (Hung, 2016) shows a flower the authors managed to induce in E. aureum (This is one of the papers that mgkrebbs cited in his answer).

Hung, 2016 - Chiu-Yueh Hung, Jie Qiu, et al., "Gibberellin deficiency is responsible for shy-flowering nature of Epipremnum aureum", Scientific Reports 27 June 2016, DOI: 10.1038/srep28598 Creative Commons Attribution 4.0

You may find it quite hard to find an image of the flower of Epipremnum aureum as it is almost always described as "shy flowering".  Here "shy" seems to be an understatement, as the first recorded flowering was reported in 1962, and the latest report of flowering I found mentioned was from 1964 (Boyce, 2004).  Chiu-Yueh Hung et al say "Since 1962 there is no report of E. aureum flowering both in wild as well as in cultivation" (Hung, 2016).
Even though the name Epipremnum aureum was assigned in 1964, one still encounters it under several other names, including binomial names using the genus names of Pothos, Scindapsus, and Rhaphidophora.  Perhaps most problematically, one finds some use of Epipremnum pinnatum for it, as for some time it was considered a cultivar of that species based on the form of the flower. Consult Boyce for a good overview.
Boyce, 2004 - P. Boyce, "A review of Epipremnum (Araceae) in cultivation", Aroideana 27:205 (2004) [PDF].
Hung, 2016 - Chiu-Yueh Hung, Jie Qiu, et al., "Gibberellin deficiency is responsible for shy-flowering nature of Epipremnum aureum", Scientific Reports 27 June 2016, DOI: 10.1038/srep28598, [PDF].


text:
Is mating between human and non-human primates theoretically possible?
I wonder if it is theoretically achievable to produce living offspring between a human and a non-human primate. Great apes have 24 pairs of chromosomes compared to our 23, however, it is known that a mule is made from a donkey (62 chromosomes) and a horse (64  chromosomes).
Are there other reasons why this human/non-human primate hybrid can't survive?

I don't know if it is theoretically possible (I guess yes), but there have been actual experimental attempts to do so, that all failed.
https://en.wikipedia.org/wiki/Humanzee


text:
Why have certain plants evolved to contain psychoactive compounds?
Plants such as marijuana (Cannabis) and kratom (Mitragena speciosa) contain compounds that affect the human brain. Why have these plants evolved to incorporate substances like THC and mitragynine into their leaves/flowers?

The evolutionary history of different plants expressing psychoactive compounds can vary, and in many cases it's difficult if not impossible to pinpoint a particular origin. However, we can make some general observations:
Homology across wide ranges of species
Despite the differences between, say, a human versus a locust, animals share a lot of their physiology. Mammals and insects tend to use different neurotransmitters for different purposes, for example, but the actual neurotransmitters and their receptors are often homologous. A plant could therefore develop a compound that acts as a neurotoxin in certain insects, but also has some psychoactive effects in a human. Nicotine is an example of a psychoactive compound that has insecticidal effects: not only does nicotine protect a tobacco plant, but humans have even used nicotine as an insecticide. Plants could of course also develop toxins to protect them from other mammals, and those would be even more likely to have effects in humans.
There is even homology across kingdoms, such that plants could make compounds to prevent growth of competing plants, act as antibiotics/antifungals, etc, and all have a possibility to act on some homologous proteins that humans have.
Artificial selection
Once humans are aware of a plant's psychoactive or other medicinal properties, that plant can be cultivated and selected for desirable properties. In the case of a compound like THC, there is good evidence that this has occurred recently. In the case of plants that produce opiate compounds, many have been cultivated by humans for thousands of years, so they are a lot more prevalent than they would be if humans had not chosen to do so.
Selection bias
Maybe I should have opened with this one, because I think it's very very important to be aware of. I'm not talking about selection in evolutionary terms here, but in terms of cognitive biases. Selection bias happens when you focus on certain outcomes and not others. There are innumerable compounds produced by plants that can potentially have some biological activity in humans: thousands and thousands. Some do have psychoactive effects, others have effects on other body systems, and many have little effect at all besides dietary contributions. You notice all of the plants that do produce something "interesting" but ignore those that are benign or simply toxic.

WRT the last point, the function any particular compound performs in a plant might well have nothing at all to do with its psychoactive properties.

Indeed, that was the point I was trying to make with my first point, maybe it was unclear.


text:
Speed of molecules in human cells?
What is the average speed of molecules in human cells?
Are there molecules moving much faster than others? What is it due to?

Speed? Are we talking about rate of diffusion, directional movement by energy expenditure or something else, please clarify.

And what kind of molecule?


text:
What animal is this (snake/slug/worm)?
I found this guy in my driveway this morning. I live in Northern Florida, near Jacksonville.
I initially thought that it was a baby snake (note the black on brown lengthwise stripes), but it moves very slowly and methodically, like a slug, perhaps. Never saw a slug so long and skinny.
He's about 3.5 inches (90mm) long, and can hold his head up high to look around, raising up almost a third of his total body length.
Maybe some kind of worm?
The "hammerhead" style head is what is making me scratch mine.

Look up (Google Images) "hammerhead worm". You'll see your pretty little guy.

They are also likely to be invasive to North America, so feel free to squash if you prefer. .

Or catch it and see if it will eat an earthworm.


text:
Since the matter in the brain is recycled every few days how does consciousnesses work?
Since parts of the brain are recycled every few days does that mean that materialistic theories of consciousness don't work?

How does any other body part work, when the actual matter is generally recycled over shorter or longer periods?  FTM, how does your car keep running when you have to keep filling the gas tank, replacing tires, batteries, & other parts?  If you kept it long enough that you eventually had to replace every single part, wouldn't it still be a running car?

Notice that the link you provide concerns development, where plenty of things change. You have added a tag for proteins but do not really discuss the implication of protein turnover given the prominent role that modern neuroscience gives to translation-dependent synaptic plasticity. @jamesqf The question is not how can the brain work given the turnover, but if we can for example claim that a person is the same over time. Or put differently, how much of this turnover is critical for "consciousness". If none of it is, then "consciousness" cannot reside in matter, or so the argument goes.

@vkehayas: The turnover/consciousness argument is, at least to me, so obviously false ("not even wrong" comes to mind :-) that it's actually hard to think of how to refute it.  But consider a computer as an analogy.  With RAID storage, you can replace one of the hard drives (often hot-swapping while the computer is running), and all the data will remain unchanged.  Over time, you could replace all the disks.  With a largish cluster, you can swap out CPU nodes while programs are running, and (if properly designed) they'll continue working just fine.  (Continued...)

... The programs (and presumably consciousness - not that I'm claiming to know what that is) are PROCESSES that aren't tied to specific bits of matter. You can replace the underlying hardware, whether it's silicon chips or proteins, and the process continues unaffected.

That was an interesting read, and I saw nothing to support your statement that "brain parts die every few days".
Neural plasticity demands that some synapses degrade as new ones are formed. But there are (an estimated) 100+ trillion synapses (some put it an order of magnitude higher) so, really, a few here and there means little. It's when there is wholesale loss that problems arise.
A strong argument for a materialist theory of consciousness is that as neurons involved with memory die, so does memory. This is evident in the transition that occurs in early childhood allowing for the formation of long term memory as well as the degradation of short-term memory and other brain functions in people with, say, Alzheimers.
Hippocampal Neurogenesis Regulates Forgetting During Adulthood and Infancy Science 9 May 2014