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Does a plant have to have leaves to produce fruit?
Is it possible that a plant can still produce fruit, even though it may not have leaves? Are there any plant species that can produce fruit without leaves?

Welcome to BiologySE! Thanks for your question... you may want to consider editing or adding to it based on the help section "how to ask a good question" - you could definitely improve this question and earn more reputation points.  Check out the help site: http://biology.stackexchange.com/help/how-to-ask

@VanceLAlbaugh Hello and thank you, but I don't know anything else to add to this. The title already says enough right? (I'm not a biologist)

No.
Cactuses
Who hasn't heard of these leafless plants?  But they undoubtedly do produce fruit - which is edible what's more.
So the answer?  No.  Some plants can and do produce fruit without leaves.

I think the cactus spines are technically modified leaves according to wikipedia. I would say the answer "No" should be "No*"!

Cactus spines are defined as modified leaves.  So I guess at this point it comes down to a question of defining leaves.


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Why is trisomy a problem?
I understand that a missing part of genetic information is a problem - the cell does not know how to synthesize a specific protein. But why is it a problem when there's one more copy of a chromosome?
Let's say a trisomy of the 21st chromosome occurs, so the person has Down syndrome. What happens on the molecular level that the person develops the way they develop?

The biggest reason is that excess of chromosomes would disrupt the proportion just like lack of chromosomes do. Over-expression of some genes inteferes with normal cell function.

where have you tried looking for an answer to this question? have you looked in any genetics texts, specifically the concepts of gene dosage, etc?

I tried googling several similar things but I don't think I came across gene dosage. Neither I remember hearing about it at school - that's why I asked the question but now it makes more sense. My bad.

Without going into Down syndrome specifically, let's address the title of your question: Why is trisomy a problem? Or, more specifically, why can it be a problem to have extra copies of genes?
Let's imagine biology to be just a really complicated cake. If you are trying to bake a cake, and you leave out the flour, I think mostly everyone would agree that the outcome product wouldn't be much of a cake at all: that's the condition where you are completely lacking an ingredient, both copies of the same chromosome, a nearly assured fatality.
But let's say you instead include 50% too much flour. What results? You might still get a cake, but it might not taste perfect: maybe a little too bread-like or not sweet enough.
In short: having an extra chromosome means genes on that chromosome are overexpressed. Those gene products could themselves have deleterious effects in excess, or they could affect expression of other genes and cause over- or under-production of those products. Of course it isn't as simple as "+50% expression!" because of regulatory mechanisms ubiquitous in biology, but there is sufficient overexpression to cause some issues.
Really, someone with Down syndrome develops almost completely normally - many other trisomys are fatal in the early stages of development, so we don't become familiar with them. For Down syndrome in particular, you can check out some of the proposed mechanisms on Wikipedia. One suggestion is that some of the cognitive deficits resemble Alzheimer's disease, implying a causative function for amyloid beta in both circumstances. The hypothesis is that amyloid beta accumulates in aging brains, but people with Down syndrome overproduce amyloid beta so they show dementia symptoms much earlier. This comparison is certainly not the only factor in Down syndrome, however.

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Is the central axon of pseudounipolar neurons in dorsal root ganglia typically myelinated
As I understand, sensory nerve cells in the dorsal root ganglion are pseudounipolar neurons, with a sole protrusion from the soma branching into a central axon (or functional axon) and peripheral axon (or functional dendrite). Depending on the kind of nerve fiber, the peripheral axon may be myelinated to various degrees, and even not myelinated at all.
Now in an online lexicon (which is in German, unfortunately: http://flexikon.doccheck.com/de/Pseudounipolare_Nervenzelle), it is asserted, that while the peripheral axons (signalling from the periphery to the dorsal root) are usually myelinated, the central axon (signalling from the dorsal root to the posterior horn of the spinal cord) is usually NOT myelinated. The claim is unsourced. In spite of thorough research on the internet, I have not been able to find any notion whatsoever on the central axon being myelinated or not. So my question:
Is there any evidence that in dorsal root pseudounipolar neurons central axons are typically unmyelinated even when the peripheral axon is? Evidence on human neurons is preferred, but evidence on other species is welcome as well.

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Why would it be unsafe to eat spoiled, but heated, food, but safe to drink spoiled, but chlorine purified water?
To my understanding, spoiled food is not supposed to be consumed even after cooking it, since the heat may eradicate germs, but their toxines may be heat-resistant and thus still active. However, there are some purification tablets which are marketed as making spoiled water potable, apparently containing chlorine or iodine usually. Such tablets seem to be recommended also for water purification by the WHO. In the description of such tablets, their effect on toxines is never mentioned, and I wonder why toxines surviving the eradication of germs seem to be no problem here. Do water borne germs usually not synthesize toxines, or to a much lesser extent than food borne pathogens? Or do such tablets somehow inactivate their toxines?

I've never heard anyone refer to water as spoiled. But water doesn't provide a lot of materials/nutrients from which to produce toxins, I assume. It's difficult to metabolize furiously  in plain water.

Water really doesn't "spoil".  The various purification methods are to kill microorganisms living in the water, which if ingested could reproduce and cause illness.  There are usually not significant amounts of toxins in water.

Thank you both for your comments. I see now that "spoiled" is not the correct term in water. I would have assumed that a body of water (let's say a pond) would still be rich in nutrients, but it seems plausible that nutrient density is low in comparison to items of food, and therefore very low toxin synthesis may occur even in a static body of water.

Water can be more dangerous than you know. Dogs swimming in ponds or lakes with blooms of cyanobacteria have died within minutes. Chlorine or iodine wouldn't affect that water's toxicity. There are plenty of toxins in water, but they tend to harm marine organisms that accumulate them and the animals that eat them.

@EpicBroccoli Yeah, water isn't like...agar or fruit juice.

To some extent you can eat heated spoiled food (the point of cooking really). I recall a concentration camp in France where inmates received sporadically tuberculosis infected dead cows, which they ate following a 24h boiling in water. Water is quite often contaminated but more rarely infected in the sense of supporting active multiplication of pathogens (with notable exceptions in cases of flooding with cholera epidemics for instance). In addition on most of the chlorine tablets it is specified it should only be used on clear water (filtered or not, but no turbid water).

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What does DNA taste like?
I've seen plenty of speculation online, but does anyone know of a scientific study or have a definitive argument?
I'm thinking probably not sweet, because the deoxyribose sugar is bound in the structure of the helix. Salty, due to group I counterions? Bitter due to the alkaline phosphate groups? I'm guessing not sour, because despite the name nucleic acids are in their conjugate base form at physiological pH. I've read some nucleotides can activate the umami/savory taste, would this be significant?
I am aware essentially everything we eat contains DNA, but I'm interested in the taste of DNA itself, pure/isolated if necessary you like.

I'm voting to close this question as off-topic because it is not about biology in the terms of this list.

Where can the list be found so I can review? I feel it is a question about a biological sensation of a significant biomolecule. Is there a SE site that is more applicable?

This is a valid question. It asks for objectively verifiable answers. Tastes are not subjective. Nobody in the entire universe tasets glucose to be bitter. Even if we have deseases that cause deviations in taste, we still can resort to statistics. Most of people would taste the same, because that's statistical mode.

Youtube chemist NileRed chemically extracted DNA from strawberries in this video, he also tastes it if I remember correctly: https://www.youtube.com/watch?v=araeHtN_3Lk
TL;DW: He gets the DNA from the strawberries and says it has a slimy texture as it isn't soluble, and it tastes salty more than anything. Note though that this could be from leftover reactants from the reaction, so take this with a grain of salt.

Haha, take the salty taste with a grain of salt.

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If a woman was fertilized with her own DNA, would it be her clone?
Several questions:

1) Can human DNA fertilize an egg, without having been naturally packaged in a sperm cell?
2) If a female had her ovum fertilized with her own DNA, would the fetus be her clone?
3) If this technology of fertilizing ovum from arbitrary samples of human DNA were effective, would males be unnecessary for reproduction of the human species? (No political implications, just a thought experiment.)

Thank you for your insight!

You might be interested in this.

1)
In principle yes, you could in theory use micro injection to inject haploid DNA into the egg. I don't think this has been used in practice though. However Dolly the sheep was created by exchanging haploid nucleus of a sheep egg with a diploid nucleus from a mammary gland cell.
2)
Not necessarily, DNA is packaged into chromosomes and diploid cells have two copies of the same chromosome (with the exception being the sex chromosomes MALE:XY FEMALE:XX). Remember that gametes are haploid (single copy of each chromosome) and that homologous recombination occurs during gamete formation, therefore the chance of obtaining two identical sets of haploid DNA that also match the females is extremely low, unless all chromosome pairs are completely identical.
3)
In principle yes. I could imagine that DNA extraction from eggs could be used for artificial fertilization and the result of that would be a race of all females.

Thank you especially for clarifying the clone issue (2). Appreciated

No it is not possible. For fertilization only DNA is not required. Sperm is necessary for fertilization because it provides centriole also for cleavage of zygote as ovum does not contain centriole.

Again, see my comment about your answer style.


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Why was the intramuscular route selected for palivizumab administration to infants, instead of the subcutaneous route?
The majority of monoclonal antibodies administered by an extravascular route to adults are administered subcutaneously.  Does anyone know or have hypotheses about the reasoning behind why palivizumab and motavizumab were designed for intramuscular administration?  A key point may be related to the fact that they are administered to infants as young as one week old, rather than adults.
FDA documents are at this link:  https://www.accessdata.fda.gov/drugsatfda_docs/bla/2003/103770Orig1s5033.pdf


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Breathing faster to lose (more) weight?
I understand that when the human body loses weight, the vast majority of that weight is lost as $CO_2$ (and a small bit is lost as water). I expect the predominant way $CO_2$ exits the body is through exhaling.
So, let's take a human with no influx of carbon (they are not eating); I expect such a person is slowly losing weight, a near infinitesimal amount with each breath (correct me if I'm wrong).
If the person breathes faster (more breaths per minute), that causes an increase in the rate at which $CO_2$ is expelled, correct (more mass per minute)? Is this rate expected to decrease, i.e., as one breathes faster, less $CO_2$ is contained in each subsequent breath? Or, does perhaps the body mobilize and oxidize carbon fuels (carbohydrates first and eventually lipids) to generate $CO_2$ in an attempt to restore homeostatic equilibrium?
Could breathing quickly and heavily possibly cause an increase in the $CO_2$ content of exhaled breaths? That is, would voluntary hyperventilation cause an increase in heart rate (and thus increase in carbon catabolism)? How much $CO_2$ is in a typical exhalation during exercise?
I realize that without exercise, the amount of $CO_2$ being lost during normal breathing is nearly negligible. But perhaps laying down and breathing quickly could cause a measurable increase in the net rate at which mass leaves the body. What do you think?
Thank you for your time.

Well, if you lay down and do situps & pushups, you will breathe faster and probably lose weight.  (Unless you eat more to compensate for the calories burned.)  Likewise if you stand up and walk faster, or run.  But just breathing faster without some sort of exercise will most likely just cause you to hyperventilate and pass out.

I remember reading somewhere that if you breathe faster that your body will adjust. Now I'm talking about breathing a little faster bit by bit... not going straight to a panic attack.

The rate of CO2 production is normally set by the rate of metabolism and breathing rate is determined by the level of CO2 in the blood.  What you are suggesting is known as hyperventilation. Because blood CO2 plays an important role in maintaining the pH of the blood, hyperventilation can lead to a dangerous increase in blood pH, referred to as respiratory alkalosis.
Apparently one response to respiratory alkalosis is an increase in metabolic rate as the body tries to compensate for the increased rate of loss of CO2. However, respiratory alkalosis is dangerous so I don't think hyperventilation is a viable strategy for losing weight.

There are two organs which govern pH: the lung and the kidney.  If one is having some problem the other steps in to correct it.  The body does not like pH to drift far from 7.4.
CO2 gas is blown off or retained by the lungs.  More CO2 = more acidic.  CO2 is in equilibrium with bicarbonate HCO3-.  The kidney handles that.  More HCO3- = more alkalinity.
Chronic respiratory acidosis is pretty common - people have bad lungs and they cannot get rid of CO2.  If you have acute respiratory acidosis (like a heroin overdose, and you are not breathing enough) it is hard for the kidney to move quick enough to help.  But for the chronic form you see the kidney holding on to a lot of HCO3- and not letting it go in the urine, to keep the pH up.
Chronic respiratory alkalosis is unusual but the kidney would do the same thing in reverse: dump bicarbonate to let the pH come down.
So in the short term you can screw up your pH and get rid of a trivial amount of calories but in the long term net CO2 loss will be the same.
A better way to exhale calories as CO2 is to produce more CO2.  Your respiratory rate will automatically increase to get rid of it and keep pH normal.  A good way to produce more CO2 is to oxidize fat and glucose molecules to produce ATP for your muscles.

Disclaimer: Not a doctor, a biologist, or a scientist.
This TEDx talk by Ruben Meerman explains the process of the mass loss via CO2 via exhaling.
The mathematics of weight loss | Ruben Meerman | TEDxQUT (edited version)
His explanation to increasing CO2 by-product of oxidizing fat was to increase O2 intake by raising your heart rate. This raises your respiration rate.
So increasing your O2 intake is one way. What about increasing your body's oxygen level as measured by an oximeter? And during exercise, does the oxygen level go down? How about during sleep? Would using an oxygen mask during exercise, or during sleep, increase your oxygen levels?


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why do overweight individuals sweat more than ordinary people?
A common phenomenon that I have noticed while traveling in buses is that overweight individuals seem to sweat a lot more than people with ordinary weight. Is this a coincidence or is there some science behind this?

This study found that only 2.3% of the variation in whole body sweat loss was explained by body fat. However, body size had greater effect. Could you update your question to include a link to reputable evidence that overweight individuals do sweat more?

@Michael_A The study is about exercise and is not ceteris paribus with the study of obesity on sweat.

The question is based on an anecdotal observation of obese people sweating a lot on buses.  So no the study is not an equal comparison, the study is superior; they specifically isolate the effects of body fat on sweating. It is specific to exercise but what would be equal evidence, does the study need to involve buses?

Well there are some overall, simplified answers, but every individual is ..well.. individual.
First there is the ratio of volume to area. As interaction between two mediums normally is depended on their common/shared surface. If we state, that an overweight person A has more volume than a skinny person B of same height, A also has a larger surface as B, but not in the same scale the volume is increased.
The easiest way to describe is with spheres, let's assume bellies are kind of spherical ;-) . A sphere with diameter 2r=1d (hint: one dimension) has a surface of π4r²=πd² (hint: 2dimensions; 2nd power 2²=4; d²=(2r)²=4r²) and a volume of $$\pi\frac{4}{3}r^3=\pi\frac{8}{6}r^3=\pi\frac{1}{6}d^3$$ (hint: 3dimensions; 3rd power 2³=8).
So, if we manipulate r it's manipulated to the 2nd power for surface and to the 3rd power for volume.
So, if we double the radius, we have 4 times the surface, but 8 times the volume.
Humans are biochemical machines, we take an energyform we can exploit to fuel our processes keeping us alive. These processes also produce heat, which is kind of a nice sideeffect allowing us to operate in cold climate. But in hot climate we need to get rid of the heat.
As I stated before, interaction is surface based. Person A has a lot more heat producing volume than B, but the surface isn't that much bigger, so A's surface has a higher urgency to interact with the medium around than B's surface (so more sweat for example). Also more tissue produces more heat. But again disclaimer: different tissues have different activities.
Furthermore fatty tissue has an insulating effect, which reduce interaction even more. Other way round the heatloss of an overweight person isn't as dramatic as for a skinny person in sudden cold.
But these are simplified answers, there's much more to it. Like bloodpressure, thyroid, biological activity. Which can be influenced by so many more things.

Great answer! It would be great to get more about primary and secondary factors of sweating.

It would be great to get sources here.


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How does one determine the sex ratio of a ZZ and ZW cross?
In Campbell's Biology Chapter 14-15, Mendelian Genetics & The Chromosomal Basis of Inheritance, question 12 reads:
12) In birds, sex is determined by a ZW chromosome scheme. Males are ZZ and females are ZW. A recessive lethal allele that causes death of the embryo is sometimes present on the Z chromosome in pigeons. What would be the sex ratio in the offspring of a cross between a male that is heterozygous for the lethal allele and a normal female?
A) 2:1 male to female
B) 1:2 male to female
C) 1:1 male to female
D) 4:3 male to female
E) 3:1 male to female
The correct answer is A. In my Punnett square, there were two male and two female so shouldn't the answer be C?

Let $Z$ be the chromosome carrying the non-lethal dominant allele, and $Z_l$ the chromosome carrying the lethal recessive allele.
The Punnett square goes:

$Z_lW$ is not viable, so there are two possible male genotypes ($ZZ$ and $ZZ_l$) and only one possible female ($ZW$). So the correct answer is A. indeed.


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Is it possible to cut a 10cm (4 inches) basil stem and regrow its roots for replanting?
I have a basil plant that got really distressed by repotting it and all the leaves from the lower parts of the stem fell off and the stem itself turned brown. RN its trying to escape its new pot as best as it can.

I'd like to reign it in and cut the tops of the 4 main branches it has from where the green starts, regrow the roots in a jar of water and then plant it back. I know that this is how one can multiply a basil plant, by cutting under each node but I just want to keep the branches whole. The thing is, I don't know if the stems would survive the process as it may be hard to pull enough water for the whole length of it.
So question is, would the basil survive if I do this?


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After digesting food, where does the energy go before being stored by the body?
I'm trying to piece together a simplified model on how the energy flows in the human body.
From what I understand:

We store enough ATP for around 2 seconds of maximum exertion
We store enough kreatinine for around 8 seconds of heavy exertion
Blood glucose amounts to around 60kcal worth, enough for 30 seconds of intense activity
Our glycogen stores are what we mostly run off in the day to day, the amount seems to be anywhere between 1-3x of the daily resting metabolic requirement, depending on fitness, so 1500 - 4500kcal worth for most people.
Fat is where excess goes but it takes time to build, looking at various studies it seems that the most extreme fat creation/destruction that our bodies are capable of is around 1000kcal worth per day or ~0.29kg/day

Based on this, I'm treating glycogen as our main "battery". Fat is for long term storage and everything else is a chain for increasingly more intense and shorter exertions.
Now to top off our glycogen stores, I see two typical ways - either digest food or burn fat. Leaving fat out for the moment, there seems to be a discrepancy between how quickly we can digest some foods like refined carbs and how fast our bodies can possibly restore our glycogen stores.
It seems that we can absorb some carbs like pure glucose for example almost immediately whereas glycogen stores take at least 20h to restore, even if you're a super fit athlete.
That leaves me with the question - where does this energy go meanwhile?
Of course, I imagine that just eating 1000kcal worth of pure glucose will probably result in a diabetic coma but it doesn't have to be this extreme. Even just eating 1000kcal worth of white bread seems to overwhelm our bodies ability to store it all in glycogen by the time we are done digesting it.
So again, where does this energy go in the meanwhile?

I love that you've presented what looks like research in your question, so +1. :) But where, may I ask, did you get this information?

@anongoodnurse I didn't keep a list of sources but its what I noted down after reading a bunch of related articles and conclusions of studies. The numbers aren't nearly exact but I just need a general idea of how it works to create an approximation for a game. I did continue looking into this meanwhile and found a few errors - for one, blood glucose is never really supposed to be used up and is there just to shuttle the calories around and second, only the glycogen in the liver is available to the whole body (~400kcal worth) but it seems that's enough for a day or so as muscles have their own.

Thanks, that makes sense. The numbers are just way, way off. Serum glucose levels are kept between ~70 and ~110 mg/dl between meals. Above that, we're making glycogen, below, we use it. It's a constant balance. All of it, though, is homeostatic in mechanism. (2 seconds of max exertion? What's kreatinine? Do you mean creatine? 8 seconds?) It seems we'd all be dead after 10 seconds of hard exertion. If it's for a game, use any numbers you want.

Your focus is on glycogen and athletics. Can you clarify whether you are concerned specifically with skeletal muscle glycogen by editing your question. At the same time, after reading my answer, please reconsider your use of the word energy.

@anongoodnurse Yeah, it seems that blood normally has just 4g of glucose in it in total and yeah, I do mean creatinine. The 2 and 8 seconds I fished out of some research done on weight lifters, apparently they hit similar "wall"s as marathon runners do after exhausting a particular store of energy and were unable to perform on the same level until recovery, all though these "wall"'s are easier to miss as it takes just 10 seconds to rebuild the ATP stores and around a minute for creatinine.

@David Its not just about athletics, though it does make up a large portion of the  expenditure if you're a sword wielding game character. My goal with the model is to meaningfully limit the amount of exertion one is capable of, as well as introducing fluctuations in a persons muscle, fat and other tissues. I want my knights to be able to get fat as well as have them starve over a long campaign and the consequences that come with it. I use the word energy because by my impression, anything converted to sugar by digestion ends up as usable energy at some point regardless of the path taken.

Creatinine is a waste byproduct, and has no role in energy. I'm sorry, but your claims just don't fit with reality. Molecular Biology and Physiology don't live in these tiny compartments you've put them in.

@anongoodnurse I mean phosphocreatine

It is hard to be sure what the poster is asking exactly, but my best effort is the following:

It takes 24 hours to replenish muscle (?) glycogen after carbohydrate
intake, therefore the “energy” from the digestion of the latter must
exist in some form in the intervening period. What and where?

There are several problems with this question which need to be clarified so that it can be recast in a form suitable for answering.

There is a failure to distinguish between energy and
molecules.

Certain molecules have the potential to release biologically utilizable energy when subject to particular chemical transformations, or have the potential to be converted into compounds capable of such transformations and which can be stored in the body. This distinction must be made in a scientific discussion of the topic.

It is not clear whether the question relates to muscle or liver
glycogen. From the reference to the (atypical) human beings termed
athletes, I assume that skeletal muscle glycogen is intended.

This is important, because the functions (and regulation) of liver and muscle glycogen are quite different.

The question seems to assume that muscle glycogen is major end-product of ingested carbohydrate in mammals.
The question seems to assume that mammalian metabolism prioritizes
the replenishment of muscle glycogen over other metabolic fates for ingested carbohydrate.

Neither of these assumptions are true. The skeletal muscle has a limited capacity for glycogen storage. Despite the plethora of irrelevant and undocumented figures in the question, this is not mentioned.
Likewise, the question does not consider whether there is any difference in replenishment of glycogen in the normal recovery after muscle exercise compared with that combined with a large intake of carbohydrate. This is relevant to the second point. The mammalian liver is the organ most involved in distributing glucose and fats to the body, and as far as glucose is concerned its first priority is the brain and nervous tissue, not skeletal muscle. The way the liver and its target tissues handle glucose depends on the hormones of feeding and starvation — insulin and glucagon, the latter of which does not affect skeletal muscle.

Finally, the actual question seems to have been obscured by scientifically meaningless assertions such as “I'm treating glycogen as our main "battery"”, and recitation of figures that are largely irrelevant to the actual question — when you unearth it.

Rephrasing the original question, removing the use of the term energy and its implicit, but erroneous, assumptions, actually gives us two questions.

What, quantitatively, is the metabolic fate of glucose following a high-carbohydrate meal in an average (e.g.) Western adult male.
Why does it take 24 hr to replenish muscle glycogen?

The quantitative answer to the first question can, I imagine, be found in the literature, although more thoroughly in laboratory animals. There must be radioactive tracer studies on rats exhausted in treadmills. In general depending on the physiological state of the organism and the tissue it can be oxidized via glycolysis and the tricarboxylic acid cycle, generating the ATP currently required for various anabolic reactions, converted to glycogen, fat or creatine (depending on the tissue) or its metabolites used in synthetic processes. I presume an excess can even be excreted in the urine.
If it really takes 24 hr to replenish muscle glycogen, I assume that is because the integrated regulation of cellular metabolism does not treat it as a priority. It may be that, even in the fed state, the combination of blood glucose and insulin concentration only drives a slow replenishment. It would be interesting to know the actual rate of replenishment.

I think the question was perhaps not asked with the specificity or precision that a biochemist would expect, but I think it's a reasonable question if you interpret it more from an exercise physiology standpoint. In that case, what OP describes as "energy" might ultimately come down to "(potential for) ATP". My interpretation is that they are not asking so much about "what happens" in terms of biochemical pathways of digestion but rather in resolving what they have found as some inconsistencies with the estimates they have learned about for different reservoirs of "potential ATP".

+1 one for the expanded answer, but one word of caution on the comment: "questions are written in English which has a scientific vocabulary of precise terms which may be understood unequivocally" : this website attracts interdisciplinary audience (of which I am). Most physicists would feel more at ease with the usage of the word "energy" in the OP than in your answer. This said, again, I am of the opinion that your answer is also very good for a non-biologist reader and that's the real point.


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Is it possible to train allergic resistance by exposing yourself to allergens?
My hypothesis is that one can decrease the allergic reactions over time by continuously exposing yourself to slowly increasing doses of allergens.
Is there any scientific evidence pointing this right or wrong?

This is exactly the point of allergy shots. The continuous exposure to an allergen causes tolerization. Maybe instead of me writing a bunch of stuff up check out this simple Wikipedia article:
http://en.wikipedia.org/wiki/Immune_tolerance

Then if you have specific questions you can ask them here.
Hope that helps.

Can you add a few-word summary?

Yeah I can do that.

The phenomenon called oral tolerance is quite a common way to reduce allergic reactions. Basically patients have to eat a lot of the antigen with their daily diet under the supervision of doctors, so in time allergic reactions can be alleviated. The idea behind this is that our immune system is much more tolerant to things that get in our digestive system (in most cases). Here is a good article on oral tolerance from Nature.
Citation: Pabst, O; Mowat, A M - Oral tolerance to food protein Mucosal Immunology 2012 https://doi.org/10.1038/mi.2012.4


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How does the body "know" how to metabolize foreign substances
As a freshman biochemistry major, I find myself befuddled by our body's ability to perform complex chemical reactions to break down foreign substances. I can see how we would evolve explicit pathways to deal with substances we would find often in our environment of evolutionary adaptedness, but we also process things we would never have encountered before. How does the human (or any organism's) body do that without explicit programming?

Can you comment a little further? Do you mean in the context of immunology, i.e. processing foreign pathogens? Or do you mean processing small molecules, i.e. drugs?

@jwillis0720, I think he means processing small molecules such as drugs that the body might metabolise in the liver.

@jwillis0720 The term for such substances is Xenobiotics.

you are right. had to refresh my memory :)

One strategy for xenobiotic metabolism seems to be making a lot of similar enzymes with different substrate specifities. Lets take the cytochrome p450s as an example. These are a class of enzymes with 57 genes identified for humans, and I don't know how many alternative splicing products are made from those genes. As a class, they are responsible for about 75% of drug metabolism and are predominantly found in the liver. They work by using a heme group with a carbon monoxide to add oxygens to xenobiotics. Here is a diagram of the mechanism:

It's been too long since my drug metabolism class to go into more detail on these enzymes, but there are other classes of enzyme that fit this multiple enzyme strategy such as the 2 monoamine oxidases, 5 flavin containing mono-oxygenases, and 4 epoxide hydrolases. So the body doesn't really know how to break down xenobiotics, but has a wide array of enzymes with broad and overlapping substrate specificities that work on whatever they happen to bind to, whether it's an endogenous hormone or pharmaceutical compound or toxin.


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Will "circus peanuts" biodegrade, and how?
I have a compost barrel, and it is currently staffed by black soldier fly larvae. They eat pretty much anything, which is very satisfying to observe. I put a handful of the candy known as "circus peanuts" in there, and they haven't touched them so far. As you can see following the link, the ingredients are:

sugar, corn syrup, gelatin, pectin, soy protein, food coloring, and artificial flavor

I assume these things are biodegradable, being "food", but if my star decomposers won't eat them, then what will? What can I expect to happen to these items in the compost heap?
As a follow-up question, was this a bad idea? Should I take them out and throw them away, so they can rot in a landfill instead?

The lack of moisture in them is probably the main difficulty. You might try crushing one so that moisture from the rest of the compost can enter it.

Time answered this question. I didn't do anything to the candies, but moisture eventually worked its way in. After a week or so, they were showing definite signs of breaking down. After two weeks, I couldn't see a trace of them!


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Why are there seven entries for Pimpinella dioica in the Catalogue of Life?
And six for Haliclona digitata, and five for Ichneumon varius. A couple of the duplicate entries are synonyms for other species, which is understandable, but most are the "accepted name". Shouldn't there just be one Pimpinella dioica? By my count there are 3068 species with two or more "accepted name" entries in the 2014 database. Where do these duplicate entries originate? Do they serve a purpose or are they errors?
Probably a question for catalogueoflife.org forums, but they don't seem to have any discussion area, so seeing if anyone here can answer.

While any large database may have errors that can lead to multiple entries (sensu har-wradim's answer), I think most of the multiple entries detail the taxonomic history associated with that species. Your link to the sponge Haliclona digitata provides a clear example. First, dismiss the H. digitata (Schmidt, 1862) entry. As clearly stated, it is a synonym for a different species of sponge, Tedania anhelans.
The remaining entries are all links to various homonyms of H. digitata. Skimming through the World Porifera Database entries (via the "Online resource" links), provides the necessary information. Lendenfeld's use of Chalinorhaphis is the original description. It is the senior homonym, meaning the specific epithet (digitata) has precedence over junior names. The junior names include Adocia digitata (Baer) and Gellius digitatus (Koltun). It was probably Tanita & Hoshino that transfered digitata to the genus Haliclona but I cannot verify this without seeing the article.
The taxonomic history can also be tracked for Ichneumon varius, but the linked databases don't hvae as much detail as the Porifera database for H. digitata. Still, it suggests that the description by Pontoppidan in 1763 is the senior homonym, and the subsequent uses by Cuvier, Gmelin and Muller are junior homonyms.
This is also what I think har-wradim is alluding to for Pimpinella dioica. Unfortunately, the Umbellifer database seems to have little detail in this regard.
The Catalogue of Life provides a convenient mechanims to begin a thorough search for the taxonomic history of a species.

This is because Catalogue of life is a database created and maintained via consulting other, taxonomically narrower databases. This leads to propagation of the original inaccuracies and introduction of new ones during the process of data transfer.
In the case of Pimpinella dioica, for example, the information was imported from the World Umbellifer Database. If you search there for "Pimpinella dioica" you get a list of names, only one of which is explicitly labeled as synonym (by Linné, the same one as in CoL). CoL interpreted this situation as if others were accepted as valid, BUT this was not the case: all other records are marked as "provisional" and most of them actually contain information about probable synonymy in "Comments".
Moreover, in the description of World Umbellifer Database the one can learn, that the database guarantees accuracy principally for generic names only.


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Why do humans seem so much more prone to disease than animals?
It seems like when we observe animals in the wild, the occurrence of noticeable disease in adult individuals is much lower than in humans. Why?
There are a number of reasons that this could happen, but I want to know which reasons contribute the most, or what other reasons I haven't thought of could be involved. So, here's my list of theories:
1) Animals that are prone to disease usually die when very young, while humans in developed countries are given vaccinations/medical attention and have a much greater chance to live to adulthood and advanced age. However, even taking this into consideration, it seems like human populations in third-world countries with little or no access to medicine are much, much more riddled with disease than animal populations appear to be. (Or do they only look that way because that's what we see the most of in the news?)
2) The animals that we see in documentaries are generally purposely selected for viewing as being healthy individuals or a mostly healthy group. This doesn't account for YouTube's many amateur safari videos and pictures, however, where it still seems like animals die much more from territorial disputes or preying than of disease. Safari-goers aren't likely to sit around filming diseased animals, but it still seems like animals 'in the background' and in herds appear to generally be very healthy when it'd be pretty easy to notice a somehow diseased or disabled person in an equivalently large group on the sidewalk.
3) Most humans don't know what common wildlife diseases look or sound like, and at a distance they all appear healthy to us even if there is a roughly equivalent percentage of disease among adult animals as among adult humans.
3a) Animals are much better at concealing the symptoms of their common diseases than the average human, as a defense mechanism from predators. (I know that cats are particularly good at not showing that they're in pain, but I'm not sure how many other animals behave this way.)
4) While most modern humans go out of their way to do every possible thing they can to make sure an infant survives, animal parents purposely kill, abandon or even eat young that they can sense are diseased or disabled in some way. I saw an example of this on a youtube video where a lion cub was gored by a cape buffalo and its back legs were paralyzed. After numerous failed attempts to nudge the cub into standing or walking properly, the mother purposely killed the cub with a suffocating bite and ate it. (Did/do humans practice this to any significant extent? I once read about a culture, can't remember which, that didn't consider an infant viable enough to even name until it was at least 3 months old. I also read that either the ancient Greeks or the Romans would bathe a newborn in wine, and if it survived, it was deemed strong enough to deserve a chance at life. I don't know how true either of these claims are, though. But that's kind of a different question, so consider it optional 'bonus points' to answer.)
5) Diseased and disabled animals are killed off by predators or rivals quickly enough that the populations we see are filled with healthy animals just because the infirm are constantly weeded out. This doesn't address animals that have few/no natural predators or rivals, such as in the case of areas that have so many deer with no natural predators that human hunters must cull them to keep them from reproducing out of control. Are these populations more prone to adulthood diseases than populations that have natural predators?
6) At about seven billion, humans are easily the most populous species that is the size of humans. Other animals with larger populations are much smaller than humans. Compared to other animals of our size or larger, we are intensely overcrowded, leading to lots of people coming in contact with lots of other people all the time, frequently on an international scale as thousands of planes and ships travel around the world on a daily basis. This only covers contagious diseases, though. Even the most isolated hermit could die from a genetic condition that he had since before he was born.
7) Stress. Animals live what we would consider to be a very high-stress life, but they experience their stress in short, intense bursts. Humans, even (especially!) those who live in first-world countries with lots of information to learn and lots of things to do, often get to the point where they can't figure out where the 'off' switch for their stress is. Stress is a silent, gradual killer, and it's possible that minor genetic conditions that may have otherwise been fairly benign or unnoticed turn ugly as a person ages through a life where stress is constant.
8) Diet. It's no secret that there's a lot of heart disease and other diet-related issues in the modern world, but I don't know if that covers ancient humans, and there seems to have been plenty of disease to go around in the olden days even when people ate purely natural foods.
I can't think of any other theories at the moment. One way I thought of to possibly help answer this question was to take into consideration domestic animals - how many diseases do veterinarians have to treat compared to how many diseases human doctors have to treat? This line of thought is rather tainted by the fact that domestic animals are often given vaccinations of their own, though, but it doesn't seem like they receive nearly as many as humans do.
This is my first time asking a question on stackexchange, so I hope I've given you plenty of meat to chew on with this post. I look forward to the replies!

This is a totally legitimate question I myself have wondered about many times; I would have very much liked to see it answered in more detail.  Even if most animals (silently) suffer more than, say, my neighbours, this is far from a fair comparison, which would need to hold at least some factors equal by assuming the human is in a laissez-faire, sink-or-swim environment as opposed to being ridiculously cared for and which the current answer does not do.  The question as I see it still stands.

How in the world is this opinion-based?

I'd have closed it for a number of reasons.  The top being overly broad.  @KevinKrumwiede the question itself is an opinion.  There's no mention of research linked showing that animals are less prone to disease than humans. The entire question, though the ample theories are interesting, is based on an opinion.

@Nathan The idea that animals are more prone to disease is not an opinion.  It is either right or wrong.  (Or more precisely, likely to be right or wrong, as with all empirical knowledge.)  The question could certainly be improved by adding references for its premise, but the lack thereof does not make it an opinion.  That's simply not what an opinion is.

Many examples of animals which have more difficulty maintaining their population size than humans exist. This is partially why some species go extinct. The Tasmanian Devil is at high risk for extinction from a genetic predisposition for cancer onset by infection. Your premise that humans are unhealthy is not sound. Humans are long lived, genetically diverse animals which reproduce exceptionally. We are among the most successful species.

What do you mean by "the most successful"?

Biological success is an encapsulation of various quantifiable elements like: genetic diversity, lifespan, reproductive efficiency, and more. I used the word "success" to refer these items as a whole.

I thought that the population bottleneck from the Toba eruption made humans have fairly low diversity and that humans were very inefficient at reproduction, both due to their lengthy developmental periods and their relatively low birth rates from birth control. I predict that some sort of widespread invasive tree is the most successful based off of the criteria you gave.

You should investigate then, ask another biology stack question about comparing mammalian genetic diversity and what it means.

This answer seems to suggest that humans are actually less prone to disease than other animals, and that our diverse genetic pool is the reason why. Let's see some references, this is more or less stated as fact without much to back it up.


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Would humans eventually evolve to fight off fatal diseases if we didn't treat/vaccinate for them?
I am definitely pro vaccination, and the question is a bit morbid because people would die, but assuming that we didn't treat or vaccinate people for fatal diseases such as Ebola or the black death, would the surviving people pass along a trait that eventually would lead to near immunity for that disease?
Are there any examples of diseases that humans "contract" but they are immune to? Or any examples of immunity through human evolution?
What about in animals? Are there diseases that have been naturally eradicated?

Sure.
When the Europeans settled the Americas, 90%+ of the native American inhabitants were wiped out due to diseases like smallpox that the Europeans clearly had developed resistance to. Clearly, the surviving native americans had resistance, and the Europeans had gone through some similar event previously in history.
The bubonic plague that was the cause behind the black death wiped out large percentages of populations, but selected for survivors with resistance:
Black Death Left a Mark on Human Genome
Caveats:

Often evolving to fight off disease involves mass death, like with >90% of the native american population dying.
There is always the chance that a future pandemic can come that human biology fails to simply evolve a resistance for and gets wiped out.
The Earth is changing rather quickly. The past is not a guarantee for the future.

There is no resistance against small pox. The disease disappeared with vaccinations, not before. This is slightly different for the pest of the middle ages, but still there is not widespread resistance against the pest. Can you please add some references for your small pox claim?

Why else did small pox cause such a higher incidence of death among native indians? A quick google doesn't answer that question, but I just presumed it was enhanced resistance, and I can't think of any other reasons. Europeans didn't have complete immunity of course, but simply more resistance.

Do you have a source that it was only small pox? There are a number of other diseases (including flu, measles and so on) which got transferred there.


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Is it possible to dock multiple ligands with the target?
Is it possible to dock multiple ligands with a target? If so, what is the suitable software used for? -- Is it possible to fix specific docking region for the target (or) automatic?

Huameng Li and Chenglong Li have done multiple ligand docking in two (AFAIK) of their works:

Multiple ligand simultaneous docking: Orchestrated dancing of ligands in binding sites of protein
Drug Design Targeting Protein–Protein Interactions (PPIs) Using Multiple Ligand Simultaneous Docking (MLSD).....

The method is called Multiple Ligand Simultaneous Docking (MLSD). I am not at all an expert in this field and you should read the first paper for details on how they implemented this. This algorithm was implemented on AutoDock.

I thank and appreciate [WYSIWYG] for your wonderful answer. I have referred the both articles before, but there is no proper protocol for applying the problem in the AutoDock.

Perhaps you can see this paper. They talk about implementing automated docking and this is referred by Li and Li.


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What is this arachnid?
I came across a photo on Wikipedia depicting an Oreocereus celsianus with what looks to me like some kind of harvestman on it. The photo was taken at the San Francisco Botanical Garden.  Can anyone identify the arachnid in the photo?  (See link below for full-size image.)

Source: https://commons.wikimedia.org/wiki/File:Oreocereus_celsianus_1.jpg

It sure looks like the harvestmen I saw growing up in northwest Missouri, but I never knew their exact names.

nice photograph......it looks like harvestmen...but what is that thing it sits on ?

The latin name for this animal is Leiobunum rotundum and Nelima fuscifrons, order Opiliones.
examples:
link

Wrong continent.

@augurar. This animal is spread elsewhere, the back pattern is identical, the description is identical. I did not find any argument against this match, actually.

Several other Leiobunum species also have this pattern, see e.g. some of the photos on http://www.bio.sdsu.edu/pub/spiders/OPIL/.  But I think you have found the correct genus.  It probably would not be possible to identify the exact species without examining some microscopic characteristics.


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Why is Pilobolus phototropic?
Pilobolus is a fungal genus whose fruiting bodies consist of a stalk ending in a spore mass that is launched via turgor pressure to disperse the spores.  The fruiting bodies grow towards light, which ultimately influences the direction in which the spores are launched.
It seems that gravity-directed growth would be sufficient to ensure an upward trajectory, so I'm wondering what the value is of phototropism.  Has this been studied at all?

Most of the "why" questions have no scientific answers. Reasonable questions I can imagine in this context would be: "how does it work?" (pathways involved), "how did it evolve?" (evolutionary history of individual components of the system and of the system as a whole) and "what kind of biological role does it play?" (if we knock out some key components of the phototropic system: would it break/diminish spore dispersion?).

@har-wradim I'm most interested in the third question - i.e. what adaptive benefit does the phototropism confer?

My thoughts - pilobolus is only 1 cm tall. Its spores need to be ingested by an animal to complete its life cycle. Suppose some detritus like a dead leaf landed on or near it. If it only responded to gravity, the spore mass would be ejected into the leaf and back onto the dung on which it grew, and will not likely be eaten until the dung is thoroughly decomposed and the area re-grown with vegetation for host animal to feed upon (herbivores give a wide berth to feces when feeding). By growing toward the light, the spore mass misses the dead leaf and travels over a meter away, onto vegetation th


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Can anyone identify this bug?
Spotted in Czech Republic. Our office was hit with cockroach infestation, so I'm afraid if I haven't carried one home.

Looks quite like a cockroach. Did you damage it somehow?

From my experiments with cockroaches as a kid (and crickets, mouses. frogs, ants, gecko's) this cilinder definately reminds me of their egg sac.
(English is not my primary language, forgive any mistakes)

It is German cockroach (Blattella germanica) with two dark parallel streaks on it's pronotum.
The one in your picture is a lady laying her ootheca.

It is a pest.
Here's it in different stages of life cycle.
Things you might like to know:

Blattella germanica occurs widely in human buildings, but is particularly associated with restaurants, food processing facilities, hotels, and institutional establishments such as nursing homes.
German cockroaches are omnivorous scavengers. They are attracted particularly to meats, starches, sugars, and fatty foods. Where a shortage of foodstuffs exists, they may eat household items such as soap, glue, and toothpaste.
The German cockroach reproduces faster than any other residential cockroach, growing from egg to reproductive adult in approximately 50 – 60 days.

Source: Wikipedia and different pest service websites.

Finally found it!


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Log-tranformation and GWAS
Before doing any GWAS (genome-wide association study) it is necessary to check for the normality of the phenotypic distribution. If the phenotype is normally distributed only once it is log-transformed, what phenotypic data do I have to use while doing the GWAS? The non-transformed one or the log-transformed?

How is the significance computed? If the computation assumes that the response variable is normally distributed (which is likely the case), then you need it to be normally distributed (hence log-transformed in your case).

Related https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3869493/

Yes, use the log-transformed phenotype. if you want to use a normally distributed error term, and this will only occur if the phenotype is log-transformed, then you must log-transform the phenotype.
The phenotype should be distributed in the same manner as the error term in your regression model of the GWAS.
$pheno = \beta_1 X_D + \beta_2 X_A +\epsilon$
$\epsilon = \mathcal{N}(x | \mu,\sigma)$
Following the central limit theorem, most of phenotypes are normally distributed.  However, there are cases where a Bernoulli distribution is correct, and a logistic style regression should be used.


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Why don't the apples seeds from grafted trees produce the same kind of apples?
As Wikipedia says:

Grafting is a horticultural technique whereby tissues from one plant are inserted into those of another so that the two sets of vascular tissues may join together.
In most cases, one plant is selected for its roots and this is called the stock or rootstock. The other plant is selected for its stems, leaves, flowers, or fruits and is called the scion or cion. The scion contains the desired genes to be duplicated in future production by the stock/scion plant.

So why I don't get the apple-tree of the scion kind if I plant the seeds from an apple which has grown on such a tree? I would expect that the genes in the apple seeds must be the same. However if I plant the seeds, I have to graft the new seedling again.

The reason most apples are produced from grafted trees is that apples don't breed true.
In a large number of crops, you have "lines" of crops. Basically, if you breed two plants of the same cultivar together, their offspring are similar enough to both parents that it performs like the parents. The reason for this is that these crop lines have been interbreed with each other for long enough that the population is self consistent, and the important alleles are present in frequencies that mean all progeny are likely to inherit them.
However, the types of apples which are sold commercially are not from these sorts of cultivar lines. Instead, they've been obtained from "sports". That is, the chance production of either a particular hybrid gene set, or sometimes from random mutations that happened on an adult tree of another apple variety. For example, the Granny Smith occurred from a chance seedling which was discovered by Maria Ann Smith.
These apples don't necessarily have "consistent" alleles. For example, it may be heterozygous for certain genes. If you have Aa alleles at one gene, if you self-pollinate the plant, you're going to get a mix of AA, Aa and aa genes in the offspring, the last of these isn't going to be the same phenotype as the parent. Now recognize that this is happening at multiple genes across the entire genome, so there are many chances to get non-parent-like allele combinations. Add to this the issue of co-dominance, where the heterozygote has a different phenotype than either homozygote (that is, BB isn't like Bb), and the chances that an offspring has a gene with a non-parent like allele combination is pretty high.
There's a further complication that some apple varieties like Honeycrisp are self-sterile. Even if Honeycrisp could theoretically breed true, there's no way for it to fertilize itself, meaning that all fertilization events are hybridizations.
Now you can certainly grow apple trees from seed. The planted seed will grow up into an apple tree, but the chances are that the combination of alleles it received by random chance from its parents will not result in an genotype that produces any commecial apple phenotype. Instead, you're likely to get regression to the mean, meaning the apple tree will be like the ancestor of apples - a crab apple, or at least crab apple-like. - But there's a small chance that it will have commercial apple-like properties, which may or may not be like the parent. This is how new apple varieties are formed, after all.
The only way to guarantee that the genotype of an apple tree is close to the parent plant is to propagate it by cloning, and the easiest and cheapest way to clone trees (at least apple trees) is by grafting.
(As a final note, remember that the seeds get their genome from the flowers and the cells which produced the flowers. The genotype of the rootstock - grafted or not grafted - has no bearing on what genes are present in the seeds. You'd have the same issue with apples breeding true even if the parent tree was on its own rootstock.)

According to such sources as North Dakota State University Ag Department (https://www.ag.ndsu.edu/hort/info/fruit/graft.htm) one primary reason for continued grafting is unaltered reproduction. Apparently some fruit stocks (scions, in grafting terminology) will produce true fruit, but the seeds within the fruit will not be genetically identical to the original fruit. This makes sense in the idea that fruit reproduction is sexual in nature and requires separate genetic stock from another plant in the form of pollen.
The original fruit would be true to form, but the seeds within it could be adulterated with foreign genes.
Another factor (that comes from more personal than referenced sources) is that often hybridized plants are not able, either intentionally or inadvertently, to reproduce from their own seed. This requires purchase of new material every year for planting or new scions for additional grafting.

Grafting is not always the answer.
My persimmon grafting was successful, but the produced fruit is the fruits of the stock (from seedling), not the scion, when I used the own seeds from the scion; while the same scion is grafted onto a wild persimmon stock, it produces desired fruits of scion.
Let's say: A is grafted persimmon imported from Asia
           B is stock grown from the seed of fruit of A
When A (scion out of A) is grafted onto B, the fruit is different from A.
But, when A is grafted on wild American persimmon, the fruit is the same as A.


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Does CPH4 exists?
What is the purpose of CPH-4? Is it well represented in the movie Lucy?

there is an enzyme called CPH4 synthase (http://en.wikipedia.org/wiki/6-carboxytetrahydropterin_synthase) but not sure what it does.

Luc Besson admits (more or less) that the name is made up (http://uproxx.com/gammasquad/2014/07/scarlett-johansson-lucy-clips-luc-besson-addresses-the-haters/) although he claims the molecule is real. Who knows what it is.

This question appears to be off-topic because it is solely based on a science fiction movie. This is more suitable in Skeptics-SE

http://skeptics.stackexchange.com/questions/22785/is-cph4-from-lucy-real/22820#22820


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How can I measure bee and wasp population?
Bees and wasps in our garden disappeared suddenly last year - I asked a question about it at Why our bees might have suddenly disappeared. This year, I see that some bumblebees are active now. I'd like to measure the population of bees and wasps in the garden over the year, and see if the numbers change when the nearby fields are sprayed.
I note the question How best to count bees entering and leaving a hive to measure hive activity? but I don't have a hive to count. Our bees come from far away, and I'm interested in multiple species from multiple nests, and wasps too. So I'd need to count the number visiting the garden. But, can I count reliably? It will vary with weather, and the number on any one plant will vary greatly depending on plant flowering dates.
Is there any established protocol for counting bees and wasps in the wild to look for population changes over time?
I can't spend too much time on this - I might manage an hour every week. Or, I could set up camera recording, if someone knows some really clever software to do the counting. But I still can't imagine how to overcome the variation.
Thanks!

 Short Answer
No. You cannot appropriately examine population dynamics using the approach you've described.
You can, however, examine how foraging frequencies vary/correlate with field spraying (though this might take more effort than you're looking for).
 Long Answer
You're not going to be able to properly quantify population levels from casual observance.

Because you would be unable to effectively identify individuals, you would be unable to know if you're seeing different individuals or repeats of previous individuals.
The data are also biased toward those species or individuals that use the habitat features in your particular garden and are biased against those that do not (Parsons & Szewczak, 2009).
Further, you would have no way to identify which hives/nests that individuals are coming from (without watching them leave the nest directly), so you would not know which populations are represented at any given sighting.

Unfortunately, although the question you link to (How best to count bees entering and leaving a hive to measure hive activity?) would allow you to better examine/compare separate populations, those methods likewise suffer from the same shortcomings listed above.

What you can figure out:
Your causal observance can at best be used to quantify foraging frequency in your garden.

In other words, you would just be able to count how many bees visit your garden at any given time and compare those values at different discrete time points. You could compare this to a number of environmental variables to look for trends.

In your case, your approach would look something like the following:

You could count the number of sightings (or landings or feedings) in various random locations throughout your garden.

Each of these locations should be randomly selected, and you would preferably collect numerous random samples from each of various "habitats" (i.e., different locations, different flowers, etc.).
You must return to the same locations each time and spend the same amount of time at each location each sampling period.

You can do simple statistics on these different samples across all sampling periods to examine foraging frequency trends across time.
If you directly measure a number environmental variables (e.g., temp., precipitation, humidity, cloudiness, etc.) you'll be able to rule out variance in your data due to these factors.

Proper background research would be required to determine which variables might be important to measure.

Finally, you could do regression/ANOVA analyses to examine any correlation between nearby field spraying on your foraging activity.

However, there are a ton of variables that could affect the trends you see, so final analyses will likely be weak at best.

Measuring those aforementioned environmental variables will help with this, as will increasing your sampling rate. See Power Analysis

Power analysis is an important aspect of experimental design. It allows us to determine the sample size required to detect an effect of a given size with a given degree of confidence. Conversely, it allows us to determine the probability of detecting an effect of a given size with a given level of confidence, under sample size constraints. If the probability is unacceptably low, we would be wise to alter or abandon the experiment.

Note: Work by J.E. Eckert (1933) showed that (honey)bees can travel multiple miles from their hive/nest, so unless those fields are mutliple miles away, any pesticides could very well impact the populations visiting your garden.

Another Option:
You could perform Trap Counts to try to approach quantifying populations rather than just quantifying foraging behavior.

This method is used frequently for other insects. However, I found very few reputable sources examining bees/wasps.

One example: Danka & Gary (1987) estimated foraging populations effectively, but they did so by collecting data at the hive entrance.

Though there is an inherent issue with trap studies as well:

As Petrovskii et al (2012) point out:

Traps are effective at providing relative counts that enable comparisons but are poor at delivering information on the absolute population size.

However, Petrovskii et al (2012) show that a ‘mean-field’ diffusion model is capable of revealing the generic relationship between trap catches and population density.

Their paper is freely available here.

Citations

Danka, R. G., & Gary, N. E. (1987). Estimating foraging populations of honey bees (Hymenoptera: Apidae) from individual colonies. Journal of economic entomology  80(2): 544-547.
Eckert, J. E. (1933). The flight range of the honeybee. Journal of Agricultural Research 47:257-285.
Parsons, Stuart and Joseph M. Szewczak (2009). Detecting, Recording, and Analyzing the Vocalizations of Bats In: Ecological and Behavioral Methods for the Study of Bats. Thomas H. Kunz and Stuart Parsons, ed. The Johns Hopkins University Press, Maryland, 2nd ed., pp. 91-111.
Petrovskii, Sergei, Daniel Bearup, Danish Ali Ahmed, Rod Blackshaw (2012). Estimating insect population density from trap counts. Ecological Complexity 10: 69-82. http://dx.doi.org/10.1016/j.ecocom.2011.10.002.

Wow! I need to do some reading! Thanks for all this, let me get back to you.


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What is the mechanism responsible for the periodicity of hiccups?
Hiccups (singultus) are caused by involuntary spasm of the intercostal muscles and diaphragm, producing a sudden inspiration with associated glottic closure. It seems the neurobiology of the reflex has been relatively well worked out (nicely summarized in this review):

Afferent limb: the vagus, phrenic, and cervical sympathetic chain
Central mediators: the hypothalamus, medullary reticular formation, and brainstem respiratory centers
Efferent limb:  primarily mediated by the phrenic nerve but also including the intercostals, and secondarily the recurrent laryngeal nerve to cause glottic closure

To my knowledge, hiccups are always cyclical, with a period of between 1 and 30 seconds. According to the afore cited article, this interval is relatively constant it a given individual. The cycling stops after some time; efferent vagal tone can suppress it, or it stops spontaneously. My question is:

What is the mechanism responsible for this periodicity?

Something must be triggering that afferent limb every 1 - 30s, but I can’t think of a normal physiologic process that triggers the firing of one or more nerves with such periodicity and then stops abruptly.

Check out Van Der Pol (chaotic) oscillator. It can be used to model heart rhythms. If a stimulus is applied to the oscillator, it will return to the curved envelope discussed in the article.
However, if "pushed just right", the oscillator's current state will be pushed towards the very center of the loop, and it will stop oscillating. This is the mechanism by which a sudden blow to the chest can stop the heart.
Reading up on hiccups, their "almost regular" interval sounds similar to a chaotic oscillator. The abrupt stop may represent pushing the oscillator towards the middle of the limit cycle, from which it cannot recover, effectively stopping hiccups


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What is the difference between influenza A and B viruses that causes their distinct seasonal patterns?
I recently learned from an answer at health.SE* that influenza B tends to occur later in the season compared to influenza A. According to the graph in that answer, during this year’s flu season the peak for influenza B was mid-March, compared to late December for influenza A. I’m wondering why this is. What are the virological factors that account for this difference?

*Now public!

Regrettably, I don't believe we know - we don't actually know why influenza is a seasonal disease in the first place. There are a number of possible theories, discussed in this review, but none of them are compelling enough to be a definitive causal explanation
In terms of the difference between Influenza A and B, B mutates at a much lower rate, which may explain the slower rate of dramatic antigenic shifts, but that isn't enough to disrupt the seasonal cycle by a few months at most.


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are sperms considered living
recently i got into a debate with this question on hinduism.se ,
as the link given above shows, are sperms considered as living or non-living
as far as my knowledge is concerned, sperms undergo locomotion, senescence, more over the best thing to say they are living is they contain genome, i.e. haploid sets of chromosomes
so in short are sperms living or non-living

Given that there is no definition of life that even comes close to being commonly accepted, any question that asks "Is X considered alive?" has a high chance to generate highly opinionated answers and is thus unfit for the SE format.

The question of what is living is nothing but a matter of definition. We can only tell you what are the standard definitions of what is a living thing but no absolute truth exist behind these definitions. Therefore, I am afraid that all discussions here will bring anything new to your ethic or religion related discussion.
I want to argue that the @user137's answer is very misleading for two reasons. First, he based his discussion exclusively on the "reproduction ability" definition of life. Second because his definition of reproduction might be misleading as well.
Reproduction is not only cell division obviously. Following this same definition one would not consider a human to be a living things but only to be a collection of living (and non-living) things. It is important to understand that a spermatozoid is just one phase of a life-cycle. This phase yield to the next phase. That's it. It seems weird to say that a kid is not alive just because he cannot reproduce. It seems weird to say that a grandmother is not alive because it cannot reproduce. You can say however that a kid is a living thing that cannot reproduce and at another moment of its life cycle it will be able to reproduce (assuming it will survive to this age). One should not think of spermatozoids as something totally detached from the human phase as we know it. These things just form a cycle and it seems to me miseleading to say that a part of this cycle is not alive. Saying such thing would yield someone to think that two living things create non-living things that by fusion will become alive. That seems weird. But again, it is nothing but a matter of definition. I cannot say that user137 is wrong, I cannot only say that his definition seem neither useful, intuitive nor common among biologists.
You may want to have a look to life-cycle and to understand what are the haplontic and diplontic phases with a bunch of wikipedia readings.
Other concepts such as the ability to synthesize its own components, having a boundary between interior and exterior and ability to response to environmental stimulis are often used in order to define what is a living thing and what is not.

Your best chance of actually reaching an answer for yourself (*) to this is by parallel.
Do you consider independetly-living single-celled organisms alive? This includes bacteria, amoeba, bacteria, some parasites such as plasmodium (the malaria germ), and more.
Sperms are not quite independently-living single-celled organisms. They have many things in common with the ones mentioned above: they move, metabolise, communicate and sense, and most importantly they can cease to do all those things, i.e. they do what we commonly call, "die".
The main difference is, they don't reproduce themselves, they are the reproduction vessel for a larger organism.
There is absolutely no objective way to decide whether that difference is sufficient to decide that all those single-celled creatures are alive and sperms aren't, it's a question of definition. You might even decide that you don't consider bacteria or anything that exists commonly as single cells "alive", and thus this whole approach is pointless. In any case, it's not a biological question and thus should be discussed somewhere else.
(*) For yourself because there is no false or correct answer as long as nobody can get more than two people to agree on a definition of life.

Damn.. this is getting into a huge debate.
There are different levels of life. What we mean by living when we say living is generally an Organism.
This is highly debatable. If you say viruses are nonliving because they need a host then almost every hetertroph is nonliving because they need the support of autotrophs.
An organ is living as long as it remains inside the body; similarly a cell in a multicellular organism can be considered alive only if it remains associated with the multicellular whole.
So is a single man alive?? Well he can eat, carry out metabolism, form a habitat but he cannot reproduce. Man as an organism is alive as he can sustain cell division and metabolism within himself but in that restricted zone human population is dying. He is living because he has the potential to reproduce. It is same as a lone enzyme- it can carry out its metabolism but will one day degrade unless it is re-formed.
Sperm on the other hand is just a vehicle- it doesn't have the potential to sustain itself; its sole aim is to deliver the potential to the egg so that life can be created.
To conclude- the question of what is "life" is purely philosophical. A more scientific question would be - "What is a stable, self-sustaining and dynamic biological system"

exactly, this was what I had in mind when we had that debate with OP. A sperm is nothing more than a cell which very predefined function. It's not able to live a life of it's own.

Sperm, in my opinion can't truly be considered "alive"...but they are living. Bear with me before you skip my answer.
A cell can be considered a "living" thing since It has RNA/DNA, it imbibes nutrition, it grows and is destroyed, we cannot say however that it is alive. It has a specific set of instructions coded into the RNA which it follows till its death (which is also protein,and hence RNA, mediated). Alive is a term reserved for organisms and not single haploid somatic cells. On the other hand...sperms have spiral mitochondria hence they contain RNA.
In short..yes..they can be considered living

i think you too follow hinduism so what views do you have in regards to my question on hinduism.se, let us continue on hinduism.se

Sperm are unquestionably alive, according to all or most sensible definitions of life (They move around, they have goals, they eat things, they die). They are not, however, a human or animal life.
Vineet Menon has a shaky grasp of species definitions, and I'd like to correct some misunderstandings. Chromosome number is not that useful in distinguishing different species. There are a large number of genetic disorders that alter your chromosomal count without making you not a human being. (Klinefelter, Turner, Edward, Down, etc.) It's also worth noting that all mosses are haploid except during the sporophyte stage of their life cycle, when they're diploid. I doubt Vineet Menon intends to categorically declare mosses 'not alive'.
Your blood is alive, and your feces is also thriving with bacteria. Some yogurt is alive, most cheese is alive. All fermented beverages are alive, or were once. Bread dough is alive. The argument you linked to is debating whether or not they are alive enough to qualify as a macroscopic living thing for ethical purposes, which is an entirely different question. A chicken definitely qualifies, single-celled algae like spirulina, mushrooms, and yeast do not. Eggs, fertilized or not, seem to be somewhere in the middle. It is a continuous spectrum with people and cats and chickens and things at one end, and viruses and tuberculosis and dirt at the other. Eggs and sperm and mushrooms I would put somewhere in the middle.
So whether the answer to the question 'Are gametes alive?' is unquestionably yes;
The answer to the question of whether or not that makes them 'a life' is up to you.

I don't think that because something has life in it, it can be considered alive. Would you consider a rock alive if it was covered in bacteria? Similarly, you cannot consider yoghurt, cheese, etc as alive.

The rock is just a big pile of silica(probably). The lichen on the rock is definitely alive. As a composite object, I'd go with 'sure, that rock is alive'. (some) Yogurt is definitely alive. I wouldn't give it civil rights, but there's a big difference between rocks and yogurt. There's also a big difference between yogurt and a cat, though, so I see your point of view. The phrase of the day is 'it's a spectrum'. The important part here(for me) is there is such a thing as 'dead yogurt'. If it can be killed, surely it is alive?

So a dead human is actually alive because there are bacteria in it? Your answer seems more philosophical than biological.

The human is dead. The body is alive, sort of. The gut is definitely still alive.

One requirement most biologists have to consider something living is the ability to reproduce. This is why viruses are generally not considered alive. They contain proteins and DNA or RNA, but require infecting a host cell and hijacking its replication machinery to reproduce itself.
Fully differentiated sperm cells cannot divide and therefore can't reproduce. Their only role is delivering DNA cargo to an oocyte and creating an embryo. An individual sperm cell is just as alive as an individual neuron or muscle cell. These require nutrients and energy, carry out metabolism, perform functions, contain DNA, but a plate of neurons won't grow into a human.

By this definition anyone who is infertile is non-living, which seems absurd to me!

@AlanBoyd I believe user137 was referring to groups, rather than individuals. People in general can reproduce on their own.

there are sterile individuals too in the living populations which cannot reproduce by any means, so are'nt they alive?

@J.Musser is correct. The definition applies to groups. The average human is fertile and can reproduce, and is considered alive. Infertile humans are still humans and still alive. But no individual human cell can just grow into another human. The cells are parts of the organism, not organisms in themselves.

@user137 so you mean life comes non-living stuffs??

@agharehanabbas It's a problematic definition, but it seems to be well accepted. Wikipedia has more detail at http://en.wikipedia.org/wiki/Definition_of_life#Definitions But this definition of life always bugged me because it should be possible to build a machine that takes materials and energy from its environment, and builds a copy of itself. It would fit all parts of that definition, but would it be a living organism or just a fancy computer?

@J.Musser thanks, I hadn't previously thought of this distinction. However it still creates some problems. Imagine a species going to extinction, with two males and one female left. There are three living organisms in this species. Then the female dies: the males are no longer living organisms. As far as I can see the only counter to this is to say that the 'group'  has to be large to meet the definition of living, but this is even more problematical.

@AlanBoyd That isn't correct. There need to be both male and female humans in a population, therefore two males do not equal a proper population, they are alive, but disabled.

@AlanBoyd It is like spaying a cat, then calling it dead, because it cannot reproduce. That isn't it's natural state, just like two male humans isn't a natural state for the global human population.

Based on this definition a lot of cells in the human body, which are not dividing, would be called dead.

Using this definition, flawed as it is, to declare sperm unalive is... problematic? They are, on a fundamental level, the only cells to 'reproduce' on a population scale in the male body. Declaring humans alive because of their reproductive potential but sperm unalive is crazy.

@Chris The individual cells are alive, as together they form a living organism. Now, a single-celled organism that cannot reproduce I wouldn't define as living. It always helps me to have something concrete, and you have to draw the line somewhere.

But in the same logic sperm cells are living (you can treat them in a way that they are not able to fulfill their function) as a part of a bigger organism.


text:
What is the minimum functional biological light sensor?
As a follow up to this question regarding the evolution of the eye, it was suggested that primitive eyes only needed to evolve a light sensor and could perhaps use the existing biochemical cascade infrastructure.
What is the minimum of this biological light sensor? Please provide a detailed biochemical description of how many proteins are involved and their interactions which can be "hooked up" to the existing biochemical cascade infrastructure. (to the best of our knowledge)

What do you mean by minimum?

minimum would be molecule of retinol, i suppose. 11-cis-retinal will switch to trans isoform when exposed to light. Some enzymes sense that and launch signal transduction which gives rise to vision

The minimum biological light sensor is just an existing signaling molecule that, by chance, also has some change in its activity due to light.  There are several ways this could happen.
One extremely simple example would be based on a G-protein coupled receptor (GPCR).  GPCRs are a family of related signal transduction proteins (the largest family) that sit on the surface of a cell's membrane.   Each one is sensitive to a molecule or small group of related molecules.  When exposed to the molecule it is sensitive to, the GPCR sets of a series of chemical cascades that trigger some activity in the cell.  For example, it can serve as a signal for the cell to move towards the place where the chemical was detected, or move away.
Now, imagine that, just by chance, the molecule the GPCR is sensitive to has some sensitivity to light, in that when exposed to light the molecule either has a larger or smaller chance (even slightly) of binding to the GPCR.  This is not improbable, a ton of biological molecules have this characteristic, in fact many have substantial responses to light even though they are not involved in light-sensing pathways.  A good example is called "photoisomerization", where the same molecule can have more than one shape, and switches between two shapes when exposed to light.
This would be a biological light sensor.  Not necessarily a very sensitive one, but once you have such a basic light sensor, natural selection would take over and lead to stronger and stronger effects.
In fact, this is pretty much how our eyes work today.  It uses a GPCR whose target is a molecule that changes its shape when exposed to light, which makes it no longer able to bind to the receptor, shutting of the signaling cascade.  What is more, this molecule is not only used in sensing light, it is a precursor to a molecule needed for gene transcription and signaling.
In fact, you can splice light-sensitive GPCRs from bacteria (which are different than those in animals) into non-light-sensitive animal cells, and those molecules will automatically integrate with existing GPCR signaling cascades, rendering the cell light sensitive.

interesting. i wonder how you would explain the emergence of say the pit viper's infrared camera which started off in a full blown animal (according to wikipedia it evolved independently in boas,pythons, and vipers). maybe i will post that as a new question.

The pit organ is just a more sensitive version of the standard heat-sensitive cell.  It doesn't require anything new at all.

my point is that it's not just a cell. it's a whole system see http://en.wikipedia.org/wiki/Infrared_sensing_in_snakes

Yes, it is a system, but it is not a new system, it is a modification of the normal temperature-sensing system.

ok and how about the platypus bill or the elephantnose fish's probe etc.

I am not familiar enough with those to say.

Yes, I am familiar with the pit organs. This is getting very off-topic, though.

Let us continue this discussion in chat.


text:
Are we more/less resistant to infectious diseases during an allergic reaction?
To my understanding, an allergic response is a non-adaptive response of the immune system to some molecule. The molecule in question is therefore "thought by the immune system" to be infectious although it is not. An allergic response is triggered by immunoglobulin of type E ($IG_E$) and causes an immune reaction.
I'd expect immune responses to not be instataneous, that is I would expect that it takes some time in order for the immune system to achieve some reaction peak. In consequences, I have been wondering whether someone that is under an allergic reaction is more resistant to early development of infectious disease because the immune system is already "switched on" prior to the infection. On the other hand, I would have thought that the body resistance to anything is lowered during an allergic reaction 1) because the allergy diminishes "general health" and 2) because allergic response may kill body cells.
Are we more/less resistant to infectious diseases during an allergic reaction?

An allergic reaction is caused by by IgE antibodies - which are part of the adaptive immune system. When you are allergic, the reaction happens very fast after the exposure to the antigen.

There are a number of issues with your question, and the short answer is no.
Immunity to pathogens is conferred by antibodies, but not usually of the IgE group. Pathogens usually stimulate IgM -> IgG; IgAs are present in mucosal surfaces.
There are multiple kinds of "allergic responses", and each carries its own risks.

Type I reactions (ie, immediate hypersensitivity reactions) involve immunoglobulin E (IgE)–mediated release of histamine and other mediators from mast cells and basophils.
Type II reactions (ie, cytotoxic hypersensitivity reactions) involve immunoglobulin G or immunoglobulin M antibodies bound to cell surface antigens, with subsequent complement fixation.
Type III reactions (ie, immune-complex reactions) involve circulating antigen-antibody immune complexes that deposit in postcapillary venules, with subsequent complement fixation.
Type IV reactions (ie, delayed hypersensitivity reactions, cell-mediated immunity) are mediated by T cells rather than by antibodies.

Limiting ourselves to allergic responses mediated by IgE, we have anaphylaxis, allergic asthma, urticaria, angioedema, allergic rhinitis, some types of drug reactions, and atopic dermatitis. These reactions can result in something as mild as urticaria or as life-threatening as anaphylaxis. None of these conditions carries an increased or decreased general immunological response to pathogens.
If allergy affected immunocompetency, one would expect to see, for example, an increased incidence of fungal infections in allergic individuals, but this is not the case. Allergy does not result in an immunocompromised condition, nor does it result in a primed response (an idea popular in the 90's). They are mediated by different pathways.
Effector mechanisms in allergic reactions
The production of IgE
Allergy, Parasites, and the Hygiene Hypothesis
Immunocompetence and allergy

I also had this doubt once; is it not possible that there is a general hyperactivity irrespective of the antigen involved (Something like excess interleukin signaling. I don't know if there is a condition like that).

@WYSIWYG - There are 37? ILs now which do different things. If you're referring to autoimmune disorders, then yes, it's a "hyperimmune" IL- mediated response of a certain kind (or, better, kinds). That's a huge can of worms (or maybe chicken-and-eggs). Some kinds of autoimmune disorders carry an increased risk of infections, but this is usually due to tissue damage, not decreased responsiveness to pathogens. Maybe I'm not understanding the deeper issues here (more likely they're too complex for me). But I don't see much in the literature about protective effects with autoimmune disease.

Isn't allergic rhinitis compromising the mucociliary escalator?

@abukaj - allergic rhinitis affects the nasopharynx, not the trachea, so, no.

@anongoodnurse I am sorry but I see no connection with trachea... One of causes of common cold is a malfunction of the escalator in nasopharynx due to a sudden change of temperature. Why then rhinitis has no similar effect? Or am I extrapolating meaning of the mucociliary escalator?

@abukaj - There are no cilia in the URT until the tracheal level. If you believe there is an "elevator" in the nasopharynx, I'd love to know why. I think you may be extrapolating the "mucociliary elevator"'s functions to where they do not exist. The cilia in the trachea down are vital to protection against pathogens.

@anongoodnurse I have read somewhere (googling for connection between weather and common cold), but as I googled to check whether I am extrapolating I have found: http://carrsconsulting.com/thepig/disorders/defence/mucociliaryescalator.htm  (From the nose to the end of the bronchi (inside the lung), the surface is lined with a series of barrier cells. [...] These barrier or epithelial cells also have small “hairs” or cilia on them) and https://www.colorado.edu/Outreach/BSI/k12activities/interactive/actidhpamucociliary.html (The mucociliary escalator covers most of [...] nose.)

@abukaj - The very first sentence in your first link explains that cilia start at the tracheal level. I am happy to discuss/teach people who are sincere in their desire to learn and who are open to learning. Misrepresentation of the contents on one's own links means you either do not understand or you just want to prove a point. I will consider this discussion now closed.

Let us continue this discussion in chat.

This is a very good question which is an active research topic!
I can just say that we do not know the correct answer to it but we have some evidences that some allergies are connected with autoimmune diseases.
You called this

1) the allergy diminishes "general health" and 2) because allergic response may kill body cells.

I would say that there can be a mechanism between allergies and autoimmune diseases.

IgE Mediated allergy to wheat in a child with celiac disease. There has been later found other cases on this but not published in PubMed.
The link between coeliac disease and IgE-mediated allergy is not very clear.
Pharmacological intervention with Montelukast (a leukotriene-antagonist) can possibly in all sorts of ways. However, research is going on about this because the mechanism is unknown.

I picked celiac disease here because it is been connected to many other autoimmune diseases and is the most undiagnosed disease.
I consider Montelukast because its mechanism in IgE and because of its latest research findings with childhood asthma (about 2001), see this search in PubMed, and in successful treatment of opportunistic diseases in HIV/AIDS, see this publication.


text:
Effects of selection on effective population size
Background
The effective population size ($N_e$) is a central concept of evolutionary biology and is influenced by several parameters. For example: sex ratio bias affects $N_e$ $\left(N_e = \frac{4N_mN_f}{N_m+N_f}\right)$ and varying population size over time influences $N_e$ $\left(N_e = \frac{n}{\sum_{i=1}^n\frac{1}{N_i}}\right)$. There is a post on how overlapping generations influences population size.
Question
Selection also influences the effective population size. Intuitively, I'd expect that the higher is the fitness variance, the lower is the effective population size as fewer individuals contribute to the next generation. Am I right? How (what is the mathematical formulation) does fitness variance influences the effective population size?

From Conner and Hartl's A primer of ecological genetics:

"Any variance in reproductive success among individuals greater than
  random expectations, a commonplace concurrence in natural populations,
  reduces effective population size."

So yes, selection does reduce the effective population size and for the reason you suggest - it removes some individuals from the mating pool/ reduces their contribution to the next generation. Mathematically it can be derived as
$N_e \approx \frac{ 8N_a}{V_m + V_f + 4 }$
where $V_m$ and $V_f$ are sex-specific variances of offspring production (males are often more variable in reproductive success than females).
They give an example of selection affecting $N_e$, in a population of deer 33 males had four times the variance ($V_m$ = 41.9) in reproductive success of 35 females where variance was $V_f$ = 9.1. Thus effective population size was
$N_e \approx \frac{ 8 * (33 + 35)}{41.9 + 9.1 + 4 } = 9.9$
The notation $N_a$ is the actual number of individuals in the population. This can be seen in the calculation of effective population size when the number of males and females are not equal
$N_e = \frac{4 N_m N_f}{N_m + N_f} = \frac{4 N_m N_f}{N_a}$
An example is a population of 80 males and 80 females compared to a population of 70 males and 90 females. Both populations have equal sizes but effective population size is reduced by unequal sex ratios
$N_e = \frac{4 * 80 * 80}{160} = 160 \neq \frac{4 * 70 * 90}{160} = 157.5$

+1 Nice! $N_a$ is just the population size I guess. What does the $a$ in index stands for?

I'll take a look tomorrow, just got home, can't remember why it's $N_a$ as opposed to anything else. @remi.b

edits done @Remi.b

Wow, usually when people say that they "I'll have a look at that tomorrow", it means that they won't never give any more attention to the post. But you actually came back and answered my question in the comments! Thank you

@Remi.b I'm guilty of that a lot, I think I still owe you an answer on evolution of the G-matrix!!!

Note that this is just the effect of non-heritable variance in fitness. Heritable variance can have much larger effects.