text:
What flowering green plant is this?
I got this green plant as a gift many years ago, but I have never seen it flower before. It has a strong, pleasant scent and cool flowers so I'd really would like to know what it is.

The plants sometimes are native to a certain region. Care enough to share yours?

@bonCodigo Sure! I'm in Sweden but I'm quite certain that these are not native here :)

It looks like a "Spider lily" from the Hymenocallis genus.
Here is a picture of Hymenocallis caribaea from wikipedia for comparison:

There are however ~65 species in the genus (according to wikipedia), and I cannot say exactly what species you have.


text:
"Heterozygotic expection" - when heterozygote differs from both homozygotes, but homozygotes are similar
For simple 2-alleles genetic model {a,A} and corresponding quantitative trait Q is typically true that
Q(aa)>=Q(aA)>=Q(AA)
or conversely
Q(AA)>=Q(aA)>=Q(aA).
For example, dominance means that Q(aa) < Q(aA)=Q(AA) , recesivity Q(aa)=Q(aA) < Q(AA) ; in additive models Q(aa) < Q(aA) < Q(AA) etc.
The situation when Q(aA)>Q(aa)~Q(AA) is atypical in biology ("heterozygotic expection ?", "uncooperative alleles ?"). Known example is HBB gene (heterozygotic form gives resistence to malaria but homozygotic mutation form is sickle-cell anaemia). But this is weak example only, because f is evolutionary advantage, not a measurable  phenotypical or biochemical trait.
QUESTION 1: Are there any systematic reviews about this atypical phenomena? (about "heterozygotic expection")
QUESTION 2: Is there a standard scientific term for this phenomena?

You question is a bit unclear, and I think there might be a couple of mistakes in your inequalities. However, I think you are looking for the terms Overdominance (also called Heterozygote advantage) and Heterosis (also Hybrid vigor). Both of these concepts imply that heterozygotes and/or hybrids have a phenotype that lies outside of the range described by the homozygotes (or, for heterosis, either parent or parent population).
Here is a section from "Genetic Dominance: Genotype-Phenotype Relationships" from Nature education - Scitable, which has a bit more information and a couple of references:

In particular, the phenomenon known as overdominance occurs when a heterozygote has a more extreme phenotype than that of either of its parents. Indeed, in a few examples, a trait that shows overdominance sometimes confers a survival advantage in the heterozygote (Parsons & Bodmer, 1961).

You will find more information about overdominance and heterosis in any textbook on evolutionary biology, e.g. Futuyma's Evolution. There are also lots of relevant papers on the subject, and this one might be a nice example and starting point:
Frascaroli et al. 2007. Classical Genetic and Quantitative Trait Loci Analyses of Heterosis in a Maize Hybrid Between Two Elite Inbred Lines. Genetics 176(1): 625-644.

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Insect identification: white spotted beetle

3 pairs of legs, a pair of antenna, wings absent, compound eye, 4-6 centimeter approx. in size.
I found this beetle at my door, in Pune, India.

Whitespotted Sawyer in Assam, india. It killed many plants in my home. I don't know how to deal with this

It is a longhorn beetle (Cerambycidae), most certainly from the subfamily Lamiinae (flat-faced longhorns). The overall apparence with a downward-pointing face, partially divided eyes, robust build and spined pronotum fits well with Lamiinae.
The beetle in you picture is very similar to species in the genus
Batocera, for instance Batocera rufomaculata (also called Mango trunk/stem borer), and the red spots on the elytra fit relatively well. This species is considered a pest on mango plantations in India and Nepal (Hill, 2008 and Insects in Indian Agrosystems), so it's probably not all that uncommon.

(picture from Insects in Indian Agrosystems, from the National Bureau of Agricultural Insect Resources.)
However, there are probably hundreds of species in Lamiinae found in India, and I cannot give you a certain answer.
The striped elytra with raised lines doesn't fit with the species I've seen in Monochamus (suggested in the other answers), so I don't think that is the correct genus.
References:

Hill. 2008. Pests of Crops in Warmer Climates and Their Control

I think it is from  Cerambycidae family,
Batocera parryi -

I don't think this is correct. First, Monochamus scutellatus is a North American species. Second, species in Monochamus usually don't have a striped elytra with raised lines, so I don't think that the genus is correct. It is probably a species from Lamiinae though.

I think that your insect is a White-spotted sawyer. For more information check this: Monochamus scutellatus, commonly known as the white-spotted sawyer or spruce sawyer,is a common wood-boring beetle found throughout North America. Adults are large-bodied and black, with very long antennae; in males, they can be up to twice the body length, but in females they are only slightly longer than body length. Both sexes have a white spot on the base of the wings, and may have white spots covering the wings. Both males and females also have a spine on the side of the prothorax. Most research done on M. scutellatus focuses on their relationship with burned forests and the logging industry,with interest also being shown in their mating behaviours.

I don't think this is correct. First, Monochamus scutellatus is a North American species. Second, Monochamus usually don't have a striped elytra with raised lines, so I don't think that the genus is correct. It is probably a species from Lamiinae though.

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How should species density be calculated for a clumped distribution?
Lets imagine 5 plots of different size are sampled for a target species:
plot#  count  area(m^2)  plot_density
  1      1       5         0.2
  2      3       2         1.5
  3      0      10         0.0
  4      5       1         5.0
  5      2       6         0.33

What is this species' density?  I see two ways to calculate the density that give completely different values.
The first way averages the density at each plot:
$$
\frac{\Sigma(\frac{count_i}{area_i})}{5} = 1.41/m^2
$$
This seems OK but it doesn't do much to control for changing plot sizes.  For example if plot 3 above was 10 times larger the density would still be the same.  In a situation where plot sizes are determined by the environment (say, under natural cover objects) this seems less than ideal.
The second way totals the counts and the search area and divides them:
$$
\frac{\Sigma(count_i)}{\Sigma(area_i)}=0.46/m^2
$$
I prefer the second method because it seems to describe the animals' density more accurately. And I would be happy to use the second method, but my issue is that I am unsure how to calculate a summary statistic for method two since a mean was never calculated.  Method one gives a standard deviation of 2.1. What is the standard deviation for method two??
One possible solution I've come up with involves breaking the larger plots into 1m^2 plots and dividing the number of animals across those smaller plots.  So now I have 24 1m^2 plots with the following "counts":
plot#  count  area(m^2)  plot_density
1-5      0.2       1         0.2
6-7      1.5       1         1.5
8-17     0.0       1         0.0
18       5.0       1         5.0
19-24    0.33      1         0.33

Now, using the first equation above I get:
$$
\frac{\Sigma(\frac{count_i}{area_i})}{24} = 0.73/m^2
$$
With a standard deviation of 1.26.
Is this a reasonable approach?  Is there an established solution to this problem?

To me, there are two issues that are mixed up here (if I understand you correctly). First, do you want to estimate the mean and variance for a statistical population (i.e. to characterize a larger population by independent samples), or do you want to calculate the actual density for a particular area, where you have counted all occurences in that entire area (but maybe divided the area into subareas out of convenience when counting)? This is not clear from your question.
In the second case, your second option of pooling counts and areas is suitable. However, then you have only calculated the actual density in that particular area (ignoring issues of detectability of the organism when counting), and you cannot draw any inferences about a larger statistical population.
If your aim is to draw inferences for a larger statistical population, a start is to calculate the mean and standard deviation (sd) of your sample. In that case, I assume that your samples are chosen randomly and independently from a larger statistical population. Your first option is then the right approach. However, since your samples have different sizes, you might want to attach more weight to larger samples, since they can be assumed to better describe the population average than smaller samples. This is called a weighted mean.
Generally, the weighted arithmetic mean is defined as:
$$\bar{x}_w = \dfrac{\sum_{i=1}^nw_ix_i}{\sum_{i=1}^nw_i}$$
where $w_i$ are the weights for each sample ($x_i$) and $n$ are the number of samples. Using this formula, you will arrive at exactly the same value for the weighted mean as you calculated in your second attempt (0.458), if you use the areas as weights.
The weighted standard deviation is a bit more problematic, in the sense that there doesn't exist one single standard way of calculating this. However, a commonly used formula is:
$$ \sigma_{w_1} = \sqrt{ \frac{ \sum_{i=1}^n w_i (x_i - \bar{x}_w)^2 }{ \frac{(M-1)}{M} \sum_{i=1}^n w_i } },$$
where $M$ are the number of nonzero weights. Other definitions of the weighted standard deviation can be found at Wikipedia: weighted sample variance.
Another version is defined as (called "reliability weights" on the wiki page):
$$ \sigma_{w_2} = \sqrt{ \frac{ \sum_{i=1}^n w_i (x_i - \bar{x}_w)^2 }{  \sum_{i=1}^n w_i - \frac{\sum_{i=1}^n w_i^2}{\sum_{i=1}^n w_i}}},$$
If I haven't made a mistake, these will give the standard deviations 1.15 and 1.22, using your data.
As for the biological interpretation, all calculations of average densities indicate a clumped distribution, since the coefficient of variation (CV) is larger than 1 (CV = sd/mean), but more so if you use a weighted mean. The CV using the arithmetric mean is 1.5, while it is 2.5-2.65 for the weighted mean, which is reasonable since you are giving more weight to the large area sample with a zero count. However, I should also note that you should be cautious about using a weighted mean when you have a strongly clumped distribution, since your run the risk that e.g. a large sample plot land on an area with no occurences, which might bias your density estimate. Generally, when you have a clumped distribution, you need to sample more intensively to get a good estimate of average density, and many small samples is often better than a few large ones.

Great answer, thank you! If anyone else comes along and finds your answer helpful they might also be interested to learn the r package SDMTools has the functions wt.mean() wt.sd() and wt.var(). wt.sd() uses the more common equation that you described above.

After finding more time to consider your answer I have minor correction on your answer and a follow-up question.  The weighted mean for the above example is 1.16 not 0.458 like you say. And now consider these three plots: Count: 1, 1, 20; area(m2): 1,1,20.  I would say the density is 1animal/m2 and the three methods in my original post agree.  But the weighted mean is 18.2.  That doesn't seem right. What are your thoughts on this?

If you get a weighted mean of 1.16 you are calculating a mean based on counts, not densities, and the same goes your your new example. It also doesn't make much sense to calculate the average number of occurences (counts) for plots of different sizes, which is what you have done in your example in the comment. If you calculate a mean (weighted or otherwise) based on densities you will get 1animal/m2.

Yep you're exactly right.  Of course you would use the densities when calculating the weighted density. How I didn't see that before is beyond me.  Thanks again.

@AdamC You're welcome. Note that I've added a bit on the biological interpretation, and some issues when using the weighted mean for clumpted distributions.


text:
Understanding intra and extracelullar concentrations (membrane potential)
I have 4 question (not homework)
What happens to the cells membrane potential if:
a) Na+ outside rises by 40mM
b) K+ inside rises by 10mM
c) K+ outside rises by 10mM
d) A- (impermeable ion) inside rises by 100mM
e) Na+ outside decline by 50mM
So my answers are:
a – hyperpolarisering (more negative)
b – Depolarisering (more positive)
c – Hyperpolarisering
d – Depolarisering
e - Depolarisering
I think it like this:
Membrane potential is the DIFFERENCE in electrical potential inside and outside the cell. When we say a cell has a resting potential of -60mV we mean that the cell has 60mV LESS than the extracellular space.
So when I am asked what happens if all of a sudden, the extracellular space increases in mV (first question) then I can say that the difference is now GREATER than 60 mV, it is now in fact 100 mV, as the extracellular space has increased by 40 mV, then plussing the already established 60 mV.
Is this the correct way to think about these problems?

Afaik you can describe the potentials between the two sides of the cell membrane using the Nernst-equation. Yepp wikipedia writes the same here.
Membrane potential is a very important thing, because human cells require stable internal concentrations of Na+, K+, Ca2+, etc... in order to work properly. These concentration can depend on species, for example plants cells work completely different than animal cells, they have higher Na+ than K+ in their cytoplasm. So every human cell has to maintain a membrane potential if they don't want to die. It requires a lot of ATP (energy) to do so... Human cells typically maintain this potential against the blood plasma. Cytoplasm has around 120mM K+ and 15mM Na+, while the blood plasma has about 5mM K+ and 140mM Na+. You can count the membrane potential from these concentrations using the Nernst equation (a short presentation about how). I don't remember the exact mV value, does not matter. So human cells are working hardly on keeping the Na+ outside and K+ inside, and they can possibly die because of membrane potential changes (e.g. when they require too much energy to maintain the internal concentrations and/or osmolarity).
Excitable cells, e.g. nerve cells or muscle cells are very special because they can change their membrane potential rapidly by sending out K+, Ca+ or sending in Na+. This can create small electric discharges, which can be used to send electric signals or contract muscles, etc... Different cells have different discharge diagrams, e.g. axons have something like this:

Figure 1 - axon electric discharge diagram - source

and muscles have something like this:

Figure 2 - muscle electric discharge diagrams - source

Summa summarum it can depend on the cell type what happens, but basicly you can count the new potential using the Nernst equation by the concentration changes you mentioned...

According to answers from the Nernst equation, I seem to have all my answers flipped...What am I misunderstanding about the basics of membrane potential? How is membrane potential explained if not the way I see it?

I mean if I put more POSITIVE ions in my cell, I should get a LESS negative membrane potential?! But it seems to be the other way around??

I put this into a new question as it is boggling me. Feel free to answer it if you like: http://biology.stackexchange.com/questions/23221/problems-understanding-membrane-potential


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How are new people created from the DNA of an aged person. i.e. Why are we young?
The question "why do we age" has been asked numerous times. But why are we young? The cells of the adult human being are an age (time>0), but how can old cells create new cells that are younger than themselves?
I.e, how are young people made from the cells of old people?
I realize that senescence, the act of a cell aging, has to do with the shortening of telomerase over time which puts a limit (the Hayflick limit) on the life of an autosomal cell. So in theory, because cells only make direct copies of themselves but the telomerase shortens with every division, each new daughter pair would be as old as the parent and would continue aging. But how come new people start senescence at time t=0?

Telomeres shorten with every cell division. Telomerase is an enzyme that adds extra copies to the ends of telomeres, extending a cell's lifespan. The assumption that telomeres only ever get shorter is incorrect (though that doesn't invalidate the rest of your question).

Gametes (sperm and ovum), which fuse to form a zygote, arise from germ cells (spermatogonia and oogonia). Germ cells, like stem cells, are maintained carefully i.e the genome is preserved and transposition/recombination events are tightly controlled via different mechanisms.
So these germ cells don't have shortened telomeres. Also, during early embryonic development the future germ cells quickly migrate to an end of embryo and remain there while the rest of the body takes shape.
I'm not sure if it has been demonstrated in an article or not but once I happened to talk to Dr Wakayama (who cloned a mouse frozen for 16 years) and got to know that animals cloned by the process of Somatic Cell Nuclear Transfer have reduced lifespan. (SCNT: the nucleus of a somatic cell is transferred to an ovum and triggered to form zygote).
So, to conclude, if germ cells were not protected from mutations and deleterious recombinations, lifespan would have been reduced with every generation.

I guess it would be good if someone could give a word about epigenetics too! Gametes do not carry the same epigenetics modifications than cells of old people.

That is a good point. It is observed (to an extent) that transfer of somatic nucleus to egg cytoplasm causes epigenetic reprogramming. However, I am sure that the old epigenetic marks are not completely erased.

And I guess it is intuitive that no two cell types have same epigenetic marks.

Oocytes have the special purpose of resetting, reprogramming epigenetics based on many physiological factors of the mother. That epigenetics are reprogrammed by the oocyte accounts for many of the differences between twins.

It could be interesting if a human could use its own germ cells to keep creating "young" cells for itself, and thus never age.


text:
More proteins from diet when common cold and flu?
My coach says that I need to eat 1.2 - 1.5 grams of proteins per kilogram when I have a common cold and flu.
I normally eat one gram of proteins per kilogram, while double it when doing my exercise training.
He explained that the reason why you need to get more good proteins when you are sick is that the body is building antibodies by the adaptive immune system and later for innate immunity.
I think he can be right based only on my own experiences getting better from common cold with low protein diet - it just takes a lot of time, while under high protein diet, you get better faster.
I also think his explanation makes complete sense to me, since antibodies and antigens are proteins.
Why do you need more proteins when you are sick?

Who says antigens must be proteins? Is this true? Many will be peptides of course but surely not all antigens are proteins. Anyway, you don't build antigens, whatever pathogen has infected you does.

no antigens don't have to be proteins, they can be a variety of things like pollen, chemicals, parts of a pathogen, or even endogenous components of cells (such as those which are targeted in autoimmune disease- so technically you can build antigens) and your body produces antibodies against them

Your body needs more energy when you are ill to facilitate the recovery process which includes the production of white blood cells to help fight the infection. This shouldn't be limited to proteins though, carbs are also very important as they are provide high amounts of energy. Basically just making sure you eat a varied and balanced diet is more important when you are ill to make sure your body receives the nutrients it needs to fight infection and heal itself. As it is having to work harder when you are ill it makes sense to eat more high energy foods. Micronutrients are also very important!

Minerals such as selenium and zinc work to keep the immune system strong. These minerals are found in protein rich foods such as beans, nuts, meat, and poultry. — Source

Although if your diet is varied you should be getting plenty of these anyway, without needing to take supplements.

Remember that your coach shouldn't give dietary advice unless he's trained as a dietician. Protein isn't as important as glucose really, that's the thing you burn the most. However you use everything: vitamins to tell the immune cells where to go, proteins to make antibodies, glucose to fuel millions and millions of neutrophils and other cells. Even fat stores may start to move in order to keep your glucose high but not too high. The excess protein is unlikely to do you harm, it'll just get urinated out typically. Minerals can be used by enzymes to make them active that are in charge of destroying bacteria.
So as a rough summary, eat healthily. Exactly how you should eat before getting ill to limit the duration or prevent symptoms in the first place. If you lack the minerals and vitamins during the time you're ill you probably lack them all the time round so don't change what you eat when you're ill, but change what you eat when you're well and then your body will have everything stocked up when you're ill and all you need to eat is glucose and drink plenty of fluids and if possible continue with the healthy stuff.


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Can we use Acetyl Phosphate instead of Acetyl CoA in TCA?
I am thinking Citric Acid cycle and activation of the end parts of Acetyl and alfa-ketoglutarate.
Let's consider only now Acetyl to make things simpler.
I have tried to explain the thing by symmetry - phosphate tetrahedral, while coenzyme A seems to be mostly some V shaped.
However, it does not help.
Can human body use Acetyl Phosphate instead of Acetyl CoA in TCA in some situations?
I know that you can activate acetyl-CoA again by phosphate:
acetyl-CoA + phosphate <-> CoA + acetyl phosphate

Are you asking if acetyl groups can enter the TCA cycle directly from acetyl phosphate? If so, are you asking if citrate synthase can use acetyl phosphate as an alternative substrate or do you envisage the existence of another "citrate synthase".

No, I am not asking if Acetyl group can enter TCA cycle directly. I am asking if Acetyl Phosphate can enter TCA cycle directly. So I am asking if citrate synthase can use acetyl phosphate as an alternative substrate. If no, why?

Enzymes are usually specific to a greater or lesser extent for their substrates. In this case we are looking at citrate synthase which catalyses a condensation reaction in which the acetyl group from acetyl-CoA is added to an oxaloacetate molecule to form citrate. This is the entry point for carbon into the TCA cycle for energy production. The condensation reaction follows an ordered pathway: oxalocatetate binds first and this results in a conformational change which increases the enzyme's affinity for acetyl-CoA by a factor of 20.
Citrate synthase is highly specific for acetyl-CoA as a substrate. The cited reference discusses several aspects of this specificity. The enzyme has a well-defined binding site for CoA, with contacts from both the small and large subunits. This includes the recognition of the adenylyl portion of the molecule.
A relevant quotation from the review:

"Citrate synthase is highly specific towards its substrates. The condensation reaction occurs only with the physiological substrates oxaloacetate and acetyl-CoA."

So, the answer is that citrate synthase cannot use acetyl-phosphate as a substrate because of its specificity for acetyl-CoA.
Wiegand,G and Remington, SJ (1986) Citrate Synthase: Structure, Control, and Mechanism. Ann. Rev. Biophys. 15: 97–117


text:
Properly changing the time scale of a parameter in a growth model
I have a two-population model, where one of the populations is a bacterial culture with its growth described as a logistic growth, with a reported growth rate of $2 \log\hbox{bacteria hour}^{-1}$ and a death rate of $1.5 \log\hbox{bacteria hour}^{-1}$ and a carrying capacity of  $7 \log\hbox{bacteria}$. However, my model studies the interaction between bacteria and fungi in a time scale of days, but if I try to directly rescale these parameters, I get a growth rate of $48 \log\hbox{bacteria day}^{-1}$ and a death rate of $36 \log\hbox{bacteria day}^{-1}$, which is absurd, given the carrying capacity of bacteria.
Is there a standard method for properly rescaling these parameters for bacterial growth, without having to change the model? What alternatives do I have?

These values are not absurd: it's just a different unit, it does not change the reality of th phenomenon.
The fact that your population can grow by a $48$ or $36~\mathrm{log}$ factor in one day, while the carrying capacity is $10^7$ bacteria, only means that the growth happens in less than one day (once the latency phase is over). Many bacterial population can grow in less than one day, it is not shocking.
In my opinion, it is not absurd to use the growth rates in $\mathrm{log}~ \textrm{bacteria} \cdot \textrm{day}^{-1}$. There is not need to rescale values if you just want to convert hours into days.

My issue is that when performing simulations day-by-day the model is doing huge jumps each day, which the carrying capacity is unable to sustain. Would in that case perform jumps hour by hour be better?

It appears to me that a day-by-day study is not in line with the time scale at which bacterial growth occurs. Bacterial growth is generally studied hour-by-hour, or even min-by-min


text:
Which bird is this?
Found this today in my neighborhood, my mom says it's a baby vulture and she has seen many during her childhood (in 1970's) while she lived in a small town around 200kms away from our city. However I want to know of it is really vulture cause there are less than 1000 left in whole state and certainly they don't usually fly around here. Even Monkeys (which are, FYI, common in India in small cities and are not afraid by humans) are mad because of this bird's presence but perhaps too frightened to go near him/her. It'd be nice if you guys can tell me what it is :).

I live in Gujarat, India if it helps.

See a very similar ibis species form Australia here: Bird species ID in the Northern Territory, Australia

@theforestecologist Yeah, ty for the info, good to know that.

It looks a lot like a African sacred ibis (Threskiornis aethiopicus) (wikilink). However, given your location in India, the closely related Black-headed ibis (which some consider to be part of the same species) might be more likely.
The African sacred ibis is native to mainly sub-saharan Africa, but is considered Invasive in some parts of the world (inkl. Europe and parts of Asia). The Black-headed ibis is however a native breeding bird to large parts of Asia (inkl. India), which makes this more likely.

(Black-headed ibis from wikipedia)

Yesss! I was just googling using features and found this bird and then at the same time saw yr answer, I'm quite certain now after your answer that this is it! Thanks a lot

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text:
Resources for similarity between embryos
Is there a scientific paper/reputable image resource out there which I can use that the embryos of different organisms (vertebrata) are similar in their early developmental stages(without falling into the ontogeny recapitulates phylogeny trap) ?
All I am able to find are the haeckel drawings or somethings that suspiciously look like haeckel drawings and after that debacle, I do not want to be using that.


text:
What are the units of Phylogenetic Independent Contrasts (PICs)
PICs are a popular phylogenetic comparative method and I was wondering what units the actual contrasts are in. I want to say they are unitless but I am not entirely sure.

Are you scaling the data?

@Oreotrephes Yes, I'm scaling it by the branch lengths

From what I understand, the answer is; it depends. As you point out in the comment to Remi.b, contrasts are standardized by branch lengths (which are assumed to be proportional to "evolutionary time") before they are analysed (to obtain standardized independent contrasts). However, branch lengths can be come from a number of different sources (divergence times, genetic similarity etc), can be based on different evolutionary models, and can also be transformed (log etc). Therefore, you cannot say what the units of standardized independent contrasts are in general. They would probably not be dimensionless though, since branch lenghts are seldomly (if ever?) expressed in the same units as the raw contrasts. Units such as log(kg)/year or kg/log(year) are more likely. Ultimately, in the usual case, the point of standardizing is to assure that all contrasts receive equal weight in the the analysis, and the creation of suitable branch lengths can be a trial-and-error process, where you e.g. study the relationship between standardized contrasts and the standard deviation of contrasts to see if they have been adequately standardized.
I guess you could describe the process as:

calculate contrasts
calculate standardized contrasts (using branch lengths)
when the contrasts are appropriately standardized, you have obtained phylogenetically independent contrasts.

Here are a couple of relevant quotes from Garland et al., 1992:

...independent contrasts must be adequately standardized so that they will receive equal weighting in subsequent correlation or regression analyses.

also

Second, the statistical adequacy of any proposed branch lengths should be viewed as an empirical issue (cf. Grafen, 1989, 1992; Harvey and Pagel, 1991; Pagel and Harvey, 1992). Third, different transformations -
  and indeed entirely different branch
  lengths, based on different information -
  can be used for different characters. The
  use of different branch lengths for different characters would be analogous to using different transformations for the two variables in an ordinary correlation or regression.

finally

Standardized independent contrasts essentially indicate minimum average "rates" (or, in Bookstein's [1988] terminology, "reduced speeds") of character change occurring along two branches deriving from a
  common ancestor (Garland, 1992). Because
  they are standardized, they do not indicate
  absolute amounts of change. For example,
  a large contrast (absolute difference) between two species at the tips of a phylogeny may yield a small standardized contrast if the branch lengths of that contrast
  are long.

Thanks for your answer. I thought it might be (units of measurement)/(units of time), but that seemed strange to me because those are the same units as rates. Thinking of contrasts as being rates is not intuitive to me, but based on that last paragraph I guess that's what they are. How about that!

Good answer that proved me wrong. +1 I deleted my answer.


text:
Why can one swim longer underwater by blowing out air?
I am a human. I take a deep breath. I swim underwater... After some time, I need to blow out some air. I blow out some air... By doing so, I can swim underwater longer. Blowing out some air gives me more time underwater. Why?
Apparently, dolphins encounter this phenomenon too.

"I am a human" congrats! As for the question, most probably because blowing out air decreases your buoyancy, I've never heard of such a biological response which helps us to swim longer by blowing out air. Dolphins should encounter it too as laws of physics apply on everyone.

Please add a citation regarding your dolphin statement. It would also be nice to see some primary literature where this was tested in a vigorous way, not just your personal experience.

Whales blow out when they surface. Hence the fountain of air/water known as the 'blow'.

@another — Blowing out some air gives me more time underwater.

This is purely a psychological response, and it does not help in decreasing the speed of CO2 level rise. As CO2 level in your blood rises, you instinctively want to breath out the 'bad' air and breath in fresh one. The latter is impossible under water, but the former eases you psychologically a little; you have "started doing something" with your predicament of high CO2 level.
Most freediving courses (as well as my own experience - humble as it is) suggest not to have the last breath substantially larger than your normal one; this comes from people who train to achieve 6-7 minutes dives, so I would assume they meticulously tried various methods.
The key here is not to have a victory over physiology; the key is psychology. Most people fail at diving because they unnecessarily get into a positive feedback loop: they get excited, their brain and muscles become even more active, they produce more CO2, brain receives information about rising CO2 in blood, and it becomes excited even more, produces even more CO2, etc, etc, until a panicked diver surfaces or inhales water. Without such unnecessary excitation, each moderately healthy human would be easily physiologically capable of 3-4 minute dives.
My take is the amount of air you have in your lungs should be primarily the amount that eases your psyche the most and helps to stop needless stress.

The problem is with the high carbon dioxide, not with the low oxygen. Humans don't have oxygen detectors, so we can't respond to that. Humans have carbon dioxide detectors, so we do respond to that.

Very interesting answer! Before apnea diving, taking a last BIIIG breath seems the logical thing to do, in order to have as much oxygen as possible. Why doing otherwise?

Can you please explain "the problem" after taking more air than "the optimum"? Thank you!

I didn't say that taking more air causes a problem. The problem is the instinctive need to breathe. It is triggered to get carbon dioxide OUT (you produce it), not because you need more oxygen IN. The focus is usually on decreasing the carbon dioxide production.

But, in order to avoid having too much CO2, we can blow CO2 out, so the CO2 detectors won't ring too soon?

I try to find the reasons for the 2nd paragraph of your answer: "suggest not to have the last breath substantially larger than your normal one".


text:
Bayes theorem for mutations
MEN 2A is a dominant inherited disease caused by a mutation in the RET proto-oncogene.
The probability of being sick when you have the mutation of the RET proto-oncogene varies with age and is assumed to be 40% at 40 years of age.
With autosomal dominant inherited diseases, this formula can be used, where p indicated penetration and D is the sick allele:
P(II inherits D given that II is healthy) = $\frac{1-p}{2-p}$
The uncle of the son III1 in the tree has the disease so he assumes it comes from I1 or I2. The father of the son II2 is 40 years old with no symptoms.
What are the odds of the father having the mutation?
What are the odds of the son having the mutation knowing the % in the first question?

I just used the formula above as so for the first question: $$\frac{1-0.4}{2-0.4} = 37.5\%$$
I'm having problems with the second though and I assume to use Bayes formula.
I've tried as so:
$$P(\text{son mut given dad mut}) = \frac{P(\text{Dad mut given son mut}) \cdot P(\text{son mut)}}{P(\text{Dad mut})}$$
I know the probability of the dad having the mutation is 37,5% and the probability of the dad having the mutation given that his son has the mutation is 100%. However I can't seem to know what to put in the probability of the son having the mutation? Any help appreciated, thanks! Sorry for a long question.

We don't know the probability of being sick given that you are homozygous for the mutant allele so we can I guess just consider this to be negligible, so we'll assume that the kid is heterozygote. The allele either come form the dad or the mother with equal probability. the odds are therefore $\frac{0.5}{0.5}=1$. If we were to know that the father (and let's assume the father only) is carrying the mutant allele (let's assume in one copy only), then the probability of the kid to get this allele is 0.5. The odds are $\frac{0.5}{0.5}=1$ again. Did I missunderstand the problem?

I don't understand your calculations and I don't understand why you're trying to use Bayes formula. I don't know the $\frac{1-p}{2-p}$ formula and I don't understand what it is supposed to calculate. It seems to me that you're overthinking a simple problem.
We don't have all the information and need to make a bunch of assumptions but if I understand the question correctly then..
Probability that the father carries the mutant allele
I neglect the probability that a new mutation occurred and that the son is the first carrier of the mutant in the lineage. I assume that we have a probability of 0 of being sick if we don't carry the disease. Because MEN is a pretty bad disease, the autosomal dominant alelle causing the disease is probably kept at pretty low frequency. From wiki, I read that MEN 2A has a frequency of 1/40000. This means that the probability of being homozygous mutant is $\left(\frac{1}{40000}\right)^2 ≈ 10^{-9}$. I think we can safely assume that the sick kid is heterozygous. Given that the kid is heterozygous, the mutant allele comes either from the mother or from the father with equal probability. So the probability it comes from the father is $0.5$ and the odds are $\frac{p}{1-p}=\frac{0.5}{1-0.5}=\frac{0.5}{0.5}=1$
Knowing that the father is heterozygous, what is the probability that a given kids receives this mutant
By the law of segregation, the probability is 0.5 and the odds are 1.


text:
Is human vision sensitive to frequency or wavelength?
In a vacuum, there is a one-to-one correspondence between light frequency ($\nu$) and wavelength ($\lambda$), ie. $\lambda=c/\nu$. But in a refractive medium, $\lambda=v/\nu$, so while the frequency may remain constant, the wavelength may not.
I've seen that in biology, wavelength is mostly used. But, I recall reading that human vision is sensitive to frequency. So, is human vision sensitive to wavelength or frequency?

Huh. It's a question of what wavelengths of light will activate opsin proteins in the retina itself. If you changed the refractive index in the retina photons of the same energy(and therefore, frequency) should activate the same state transitions in proteins.

My guess is therefore frequency instead of wavelength, but if anyone has empirical data I would love to read the methods of that.

I found this answer relevant since he shows that if our eyes detected wavelength a red brick would look green seen from water.

@Aditya P no it wouldn't. It will still appear red because retinal fluid remains the same, so final wavelength reaching retina will still be same

It is not the wavelength or frequency that determines light absorption- it is the energy of the photon that matters. The energy of incident light should match the excitation energy of the chromophore. The medium itself can also affect light absorption by electronically interacting with the chromophore. Frequency is proportional to the energy (given by the relationship $E=h\nu$); while wavelength and velocity change in different media, frequency and energy remain constant.
The chromophore in the opsins (retinal) absorb energy to become active and you can say that they detect the frequency. However, sufficient number of opsins have to become active for the retinal cells to transmit the signal. So the overall light flux is also important. An interesting thing to note is that activation of the opsins hyperpolarizes the photoreceptor cell and reduces its tendency to fire.
Wavelength plays a role in diffraction and therefore diffraction is less in a medium with higher refractive index. Wavelength also determines scattering. So, while the opsins actually detect frequency, the wavelength can slightly affect the overall "vision" because of scattering/diffraction effects.

The energy of a single photon is proportional to its frequency. So if a single photon is detected, its frequency does determine the color.

The more important questions are: Does opsin detect single electron excitation by the photons, or integrate over a period of time and detect the total photon energy? An atom can absorb simultaneously two or multiple photons. I suppose, even if opsin can detect single electron excitation, it can not distinguish between single photon absorption and muti-photon simultaneous absorption. Is that correct? Both cases would imply the eye can not detect the true frequency of individual photons.

@Hans yes of course. Energy is proportional to frequency but I focussed on energy because the transactions (absorption/emission etc) are of the energy. Frequency is a sort of indicator. Regarding opsins: They detect energy of a photon (photon absorption causes a stereoisomeric change) but the retinal cells will respond only if a sufficient number of opsins are active.

Thanks for your answer. You say an opsin is able to detect a single photon. Is it able to absorb two or more photons simultaneously https://en.wikipedia.org/wiki/Two-photon_absorption#Two-photon_emission? Does a retinal cell fire only when the total number of active opsins presumably linked to it or the total energy of the absorbed photons exceeds a threshold? There is difference between the two. Either way, two different compositions of the incoming light can induce the same response from a retinal cell. Is that right? That would limit the resolving power of the retina regarding color.

@Hans as far as I know it is a single photon absorption. The firing of the retinal cells depends on total number of activated opsins but activation of opsins reduces the tendency to fire; there should be a threshold but I am not sure of how the threshold is established, at the moment. Usually different cells in the retina (rods and cones) express different opsins. Some residues in the opsin proteins can affect the absorption frequency of the chromophore (retinal). You can read more about cones/opsins on wikipedia or this linked post.

@Hans I am sorry for the misunderstanding: retinal cells fire less with increased number of activated opsins. I corrected the answer. However, I am not sure if (and how) this is thresholded.

Wavelength-frequency relation is $\lambda=\frac{c}{\nu}$ or $\nu\cdot \lambda=c$ in vacuum. In some refractive media you can substitute $c$ with speed of light at corresponding medium, essentially nothing changes. Speed determines the product of wavelength and frequency, not their ratio, as you suggested. Hence at different speeds frequency and wavelength will both decrease or increase, there is no reason to think that one of them stays constant and the other one changes.
If you still want to make a distinction and describe physical property of light with one of them, frequency $\nu$ would be more relevant as matter/light (photon/electron) interactions work as described by the formula $E=h\cdot \nu$

A short comment: c is always the speed of light, there is no need to "substitute" it, when you have another medium. The speed depends on the medium, so you have to know the specific constant.

Frequency is supposed to remain constant: http://physics.stackexchange.com/questions/59469/why-frequency-doesnt-change-during-refraction

As WYSIWYG wrote, energy is the answer, but to clarify the dependence of energy from momentum... sorry, the dependence of frequency from wavelength, have a look at the animation on this web page: http://www.acs.psu.edu/drussell/Demos/wave-x-t/wave-x-t.html, posted here in what I believe complies with fair use legislation:

It represents a sinusoidal wave, the basic component of any disturbance (as long as you can count on linearity, but that's another matter...).
Frequency tells you how fast the red dot goes up and down. This is what a receptor put in that specific position will sense: a disturbance (here it's the height of a string, in your case the amplitude of the electric field) changing $\nu$ times per second.
Wavelength, on the other hand, tells you how far the maxima and minima of the sinusoid are separated in the medium. In this case, two subsequent crests are separated by $\lambda$ meters. For a given disturbance frequency, this number depends on how fast the wave is allowed to travel in the medium. A slow wave will have a shorter wavelength (because it will travel a smaller distance in space during the time the red dot completes a cycle); conversely, a fast wave will have a longer wavelength.
Note: the speed can depend on the frequency of the disturbance - in that case the medium is said to be 'dispersive' and the relation between frequency and wavelength (or energy and momentum, or - if you are into quantum physics - between energy E and wavenumber k) is called a 'dispersion relation'.
In an isotropic homogeneous medium, the speed is the same in every point and in any direction and you can write
$$\lambda(\nu) = c(\nu) / \nu $$
The frequency is determined by the physical process in the source. It's very hard to change the frequency (i.e. the color, in the visible) of a light wave - you have to resort to nonlinear effects to do that. The wavelength is the result of the interaction with the medium, and changes all the time. But it's customary to express a sort of implied equivalence between frequency and wavelength based on the behavior the light wave would have in vacuum. Hence, when one says 550 nm photon, he is usually implying a photon with en energy corresponding to
$$E = h \ \nu = h \ c_0 /\lambda = 4.226 10^-19 \ J = 2.64 \ eV$$
Where $c_0$ is the speed of light in vacuo.
(Note: the latter value is computed from the one before diving by the charge of the electron).

In the context of human vision, wavelength and frequency are not mutually exclusive, but given by the first equation you pointed out in the question. That is, whenever the range of human vision is given they are not assuming that wavelength and frequency can change independently.

Say you change  the refractive index of the retina. Does the perceived color change?

Also, I think there's a typo in your first equation. I don't have enough points to edit or comment. $v \lambda = c$


text:
Beta oxidation of saturated fats
In my text book there is an example of a 18 carbon long fat and it says that it can run 8 laps of oxidation. I don't understand why it doesn't run 9? 2 are removed each cycle?
Thanks.

I believe your textbook is referring to the fact that you only perform the complete beta oxidation eight times.  Because there's a carboxylic acid at the terminus of a fatty acid chain, the cell takes a slightly different route and reacts it with ATP, which generates a fatty acyl adenylate and pyrophosphate (PPi).  This AMP can subsequently be displaced in an attack by CoASH, at which point the beta oxidation process can proceed in full to begin cleaving off acetyl-CoA.
Here's a visual representation of this activation process, too.


text:
NADH shuttles - Why cytosol?
Why is the malate-aspartate and the glycerol-3-phosphate shuttles located in the cytosol and intermembrane space?
The krebs cycle happens in the matrix so why wouldn't they push electrons from the matrix and into the intermembrane complex for oxidative phosphorylation??

The electrons for shuttling are mainly generated in the cytosol from glycolysis. NADH can easily pass the outer membrane, but must be shuttled over the inner membrane. It is important to consider that the electrons must be fed to oxidative phosphorylation from the matrix of the mitochondrion, and not the intermembrane space.

I believe more NADH is generated during the citric acid cycle rather than the glycolysis? You say that the electrons are mainly generated in glycolysis?
Also is this shuttling mechanism only used for the electrons generated by glycolysis and NOT the ones made in krebs cycle (as they are already situated in the matrix)?


text:
How can toddlers expend seemingly boundless energy when they eat so little?
A toddler's food intake seems very little: only milk and water and some solid food. Therefore, from where does this energy come?

They don't eat little. Consider the volume of milk / food they consume as a ratio of their weight. Quite the contrary they are ravenous machines and their consumption is much higher than an average adult. All cellular energy comes from the hydrolysis of ATP, and the production of ATP comes from the breakdown of glucose. The glucose comes from a sugar found in breast milk, called lactose.

... in grams consumed per baby weight.

Just to add to the answer from @buzrw:
Using data from here and here I have estimated recommended calorie intake per kg for a 2 yr old and for an adult. I've used figures for males and assumed 70 kg for the adult weight which is the "international standard man":

toddler: 120 Cal kg-1
adult: 40 Cal kg-1

So yes, the energy intake of toddlers is higher than that of an adult.


text:
Is the amount of dNTPs rate limiting for very long PCR products?
I'm using the Q5 system and I'm PCRing a product that will have a final length of around 9500 bases. I have noticed that the product is there but very faint. The primer seems to be used up.
So my question is, can the dNTPs be rate limiting in a long reaction? That is, can all the dNTPs be used up in the first PCR cycles and maybe not be available for the later exponential rounds?
It seems you have about 1000 times the amount of dNTPs to the amount of primer (200 µM compared to 0.2 µM). So maybe...or is my basic chemistry off. Any precedence?

IIRC Q5 requires 0.5µM of each primer as mentioned in documentation. In any case, why not just add more dNTP if you suspect it to be the cause?

I am doing that now. But like anything in Biology, I'm sure there are consequences of adding too much.

Add controls in if in doubt

Yes it is possible. dNTPs can also get degraded at high temperatures. Therefore they are added in excess. You can add more and as long as you are not doing real-time PCR don't worry too much about smeary/multiple bands. You can always do a re-PCR.

Adding too much dNTPs can cause problems. They bind magnesium from the reaction buffer, so if you are going to increase the amount of dNTPs drastically, you will have to optimize the reaction again for magnesium.

200uM dNTPs in 50ul reaction mix could produce more than 10ug DNA if all dNTPs were consumed whatever the length of PCR products is. You could detect as low as 5ng DNA fragments by conventional electrophoresis using EtBr. You probably could see a clear band when you load more than 100ng of a DNA fragment. Therefore I am not worried much about the dNTP concentration.
The longer PCR products you amplify, the more difficult it is to amplify. Then you may not get enough efficiency to detect your PCR products. You might want to try lower annealing temp if you do not get any none-specific bands with/without some additives such as DMSO, betain, etc., or use more stronger enzymes. Also touch down PCR may be useful to get specific bands efficiently.
When you increase dNTP concentration, Mg++ effects may be muted because dNTP could chelate Mg++ as Chris mentioned in the comment column.

What do you mean by "stronger enzyme"? Q5 is one of (if not the) best commercially available DNA polymerases.

Oh, I am sorry, I missed that part... Of course, Q5 is one of the strongest. But, it does not mean that other enzymes are not useful. So still, you have a chance to get more PCR fragments by other enzymes such as primestar.


text:
What kind of eye strain causes an visual aurora effect?
When I have done too much reading on the PC sometimes I feel a tickling sensation inside my eyeball. At first I didn't even notice the tickle, however my eye would start to see blurred in one area, and a growing halo of yellow blue orange stars grows outwards from one place in my visual field. the shape is not very round, it growns like a mycelium shape, where the border is very bright with stars and lights.
So the effect resembles a mushroom growth ebbing slowly outwards from a point over the space of 30-45 minutes, where my vision in one eye becomes overcome with a blurring effect and a flashing colored araura, and an annoying tickling/electrical effect inside the eyeball. it can be more or less pronounced, and sometimes I can barely read anything up to 1 hour afterwards, and after 2 hours it has returned to normal.
I have 9.5/10 visual acuity, and this started occuring every few months since I was 33.
I can't find what I am experiencing, all the eye disorders and symptoms seem to describe different issues than what i have.
What can it be?

That's called a scintillating scotoma, and it should be present in both eyes (cover one eye when it's happening and see if it isn't the same in the other.) Look it up. It's a kind of a migraine. It's not serious (honest), but you should let your doctor know you're having them. I have them too. I think they're fascinating.

Thanks that's a very good answer, if you write it as the answer i'll mark it as true.

We're not supposed to answer medical questions. :(

I'll have to check if it is unilateral and if my irises are the same size afterwards. I found a page which sais that some versions can be caused in the retina: https://www.reviewofoptometry.com/article/visual-aura--and-scotomas-what-do-they-indicate there's masses of pictures of scintillating scotoma on the image search too. thanks again.

most ocular migraines can't be medicated and they are more "trippy" than than noxious. It's also a neuroscience and optical quesiton. anyways, the answer helped a lot with knowledge.

They are trippy to me as well. They are treatable if serious enough. I can't read without great difficulty when I get one. Luckily, it never happened to me at work!


text:
Is it the theory of the 5 senses obsolete?
An enigmatic topic in traditional science was labelled as the mystery of the 5 senses, and how to best group senses by type.
Is that theory now meaningless?
Do Scientists still agree that that there are 5 types of sense, and no salient new 6th sense which can't be classed with the others?
There was widely accepted merit for that summary classification, because it was the best logical process to approach a complex subject.
The theory questioned the controversial logic of these groups: Soundwaves, Photons, Chemical scent of the air, chemical scent of taste and touch which represents any nerves found in the rest of the body.

This is a question and answer site about specific biological facts and concepts. If your question is whether there is a sense other than the five you fail even to mention, please give some reference to sources in support of it as a basis of discussion of the evidence for or against it. Your question is wrapped up in references to teaching, relevance, monikers, enigmatic topics, clades and the like, but their seems little of substance inside.

A knowledgable man commented:...[ "We have only 5 senses, a 6th sense has been controversial" - This is meaningless. There are well over 5 senses. The 5 senses thing is a biology myth taught to children. – ]... Sorry, I have some wrong words due to not being English. The question is: whether the 5 sense theory is today inaccurate?

I don't think there is any non-trivial biological content in this question, and there is no "mystery." I don't know what knowledgeable man you are referring to but it is trivial to list more than 5 senses - the idea of there being 5 senses goes back to Aristotelian views of the world. This question really just seems like an opinion-based question of whether it makes sense to teach about 5 particular senses.

Your comment is in conflict with David's so apparently there is a question to be resolved. If your own view has a factual basis, you can briefly quote the scientific terms for those facts via an answer post?

No, because your question isn't about biology - it isn't good to answer bad questions here. If you want to ask "are there more than 5 senses" then ask that. And I don't think my comment differs much from David's in this occasion, as rare as agreement between us can sometimes be ;)

Regarding your English, my criticism was that you were using empty flowery language of the type one might expect from undergraduate philosophy students. Just get to the point if you have a question and state it clearly and simply, providing sources for any contentious point of view you wish information on. But make sure you are talking about science, not metaphysics.

It depends who's counting and according to what criteria.
Some neuroscientists argue that smell and taste are one sense because altering one produces substantial changes in the other.
Conversely, if you break down the senses to receptors, you get at least 5 different for taste and 1000 or more for smell.

Apparently one should not trust psychologists to count receptors. That 1,000 figure for olfactory receptors probably comes from adding both genes and pseudogenes. Counting only the former gives around only around 400: https://www.ncbi.nlm.nih.gov/pubmed/23585039


text:
What percentage of genome do slugs and scallops have in common?
We can know genetic distance of thousands of species. The OTT tree of life gives genetic distance for nearly all species. Is there a resource to compare the genomes of any sequenced animals to know the percentage of DNA they have in common? I wanted to know for slugs and scallops.

The question is actually not that easy. Many parts of the genome will fail to align and many aligned part will differ in length. So the question "What percentage of the genome species A and species B have in common?" is actually quite undefined.


text:
How do drugs tests check so many substances?
There are about 170 drugs banned for sports and many other drugs that can be used in crimes.
How can blood tests practically detect so many different substances? Do they divide the sample into 170 different micro samples? How are sports and criminal blood tests arranged to be comprehensive?

There are a lot of different methods to test samples for drugs. The most common for a "screening" test, like one might encounter before being hired for a job, are based on immunoassays. These use antibodies to detect certain substances in the sample. These are good for testing for a few drugs or categories of drugs (like THC, benzodiazepines, opiates, amphetamines, etc.), however they can't test for a large number of drugs at once, and often won't tell you the specific drug (e.g. it'll say "positive for benzodiazepines", not "positive for alprazolam"). If someone tests positive on one of these screening tests, then the samples can be re-submitted for further testing to clarify what is causing the positive result.
Drug testing for elite athletes is a whole different story. The World Anti-Doping Agency has established protocols for the Athlete Biological Passport, which uses standard methods to test samples and record various biological parameters over time, to ensure that athletes aren't manipulating their bodies artificially.
The exact details of how this is done is pretty complex, but they don't need to divide samples into a bunch of separate samples and test each one for a single drug. These standardized kits are able to be run on one urine sample (divided in two) and a couple of tubes of blood, the same size you'd get drawn at a doctor (just 3-5 mL each).
One way they test for many different substances using a single tube is through gas-chromatography mass-spectoscopy (GC-MS), which is a combined method to separate apart substances in the blood and identify them by their molecular weight. By comparing athlete's blood and urine samples to known patterns produced by banned substances, they're able to test for many different compounds using a single sample.


text:
Identify this larvae that lives on a musrhoom?
I was in the forest near the Rhone river in France and I uncovered some mildewy wood bracket fughi (Ganoderma) on a fallen willow tree. It was a scene from a sci-fi film. some arthropod larvae of 2-3cm had built cocoons within a web, and the cocoons were empty and the larvae were wondering around on the mushroom.

Neat! Please update with location and approximate size of larvae and fungi. Thanks!

Thanks, added that info, Rhone Alps, France, 2-3cm. perhaps I have to take one captive in controlled conditions and see.


text:
What are the differences in the two possible methods to calculate the Hardy-Weinberg Equation?
I am more than flabbergasted by calculations of Hardy-Weinberg equilibria. The formula's theory assumes a binomal distribution of allele frequencies in a population, and hence allows the comparison of observed phenotype frequencies to an ideal model distribution.
$$
p^2 + 2pq + q^2 = 1
$$
with
$p^2$ = Frequency of homozygous phenotype PP
$2pq$ = Frequency of heterozygous phenotype PQ
$q^2$ = Frequency of homozygous phenotype QQ
There are two different methods of working with the HW equation that I have come across, and they do not seem to be compatible; used on the same data sets they yield wildly different results. I feel like I'm not seeing the forest for the trees, to be honest.
Is either of these methods (technically) wrong? How do I decide which one to use for each data set (i.e. is it valid to use method #1 on 3-allele-data sets)? Or do I just use whatever method is easiest? Doesn't this lead to discrepancies in the results? This seems like a big thing, especially when comparing real-world observation data to assumed HW distributions.
Example data set (EST/California) and results of HW calculations. I'm using observed phenotype in the place of the original data's observed genotype.
Phenotype     n  |   HW1   HW2p   HW2q
PP           37  |  33.9   37.1   28.8
PQ           20  |  25.0   23.0   28.2
QQ            7  |   4.5    3.8    7.0

Calculation method #1
As suggested by above-linked data set source and Beebee/Rowe's Introduction to Molecular Ecology, alleles are simply added up to get values for p and q respectively:
Phenotype    n  |   P    Q
PP          37  |  74    0   (37 * PP = 74 P)
PQ          20  |  20   20   (20 * PQ = 20 P + 20 Q)
QQ          7   |   0   14   ( 7 * QQ = 14 Q)
Sums        64  |  94   34

From this we can directly infer p/q: $p = 94/(94+34) =0.73$ and $q = 34/(94+34) = 0.27$; with the condition $p + q = 1$ remaining true.
Using these values for p and q in the HW equation yields:
$$
p^2 + 2pq + q^2 = 1
\\
(0.73)^2 + 2(0.73)(0.27) + (0.27)^2 = 1
$$
And a population-wide phenotype distribution of
Phenotype      n
PP         33.92    p^2 * 64
PQ         24.96    2pq * 64
QQ          4.48    q^2 * 64

Calculation method #2
The second method of utilising the HW equation is a lot more direct, and just about every text book I could find uses this method to solve 3+ allele problems (as, for example, blood types); Wikipedia commends its usefulness in calculating heterozygote frequencies of genetic diseases in large populations.
In this calculation frequencies are directly inferred as per the definition of the HW equation. This means $p^2$ is equal to the frequency of the phenotype PP (see above).
$$
p^2 = \frac{37}{64} \\
p = {\sqrt 0.578} \\
p \approx 0.76
$$
$$
q = 1 - p = 0.24
$$
Leading to a HW distribution of
$$
(0.76)^2 + 2(0.76)(0.24) + (0.24)^2 = 1
$$
With a new ideal phenotype distribution:
Phenotype      n
PP          37.1    p^2 * 64
PQ          23.0    2pq * 64
QQ           3.8    q^2 * 64

Inverting the calculation by starting with $q^2 = 7/64$ leads to even more diverging results:
Phenotype      n
PP          28.8    p^2 * 64
PQ          28.2    2pq * 64
QQ           7.0    q^2 * 64

Using both $p^2$ and $q^2$ inevitably violates the condition $(p+q)^2 = 1$.

Welcome to SE Biology, which is a question and answer site about biology. You have obviously put a lot of effort into this, but at present I don't see any question. This is, admittedly not my field, but if there is no question posed in the title, begining or end of your post, it is difficult to know what you wish to know. Are you asking which of two types of calculation is correct? If so, please edit your post to make that clear at the outset, otherwise it risks being ruled "off-topic" on the basis of "unclear what you are asking".

Hi David, I thought his post was clear. Perhaps the title needs to "rogatized," but the questions are in the end of the main post before the computational addenda: "Is either of these methods wrong? Do I have to decide which one to use for each data set? Can I even use method #1 on 3-allele-data sets?"

Hej David, hej vipatron!
You're right that my questions are not as clearly defined as I thought they would be. I would like to know where the differences between those two (three) equation stem, and if either is more valid/accurate than the other model

G'Ra. Please use the @ so I know you have responded to my comment. Only the poster gets automatic notification. You need to edit your question. A comment response is insufficient. @vipatron — A question needs a sentence with a question mark.

And then there's Gene driving which destroys all of your calculations :-/

You are throwing numbers into an equation without understanding it.
If you know the numbers for pp, pq and qq, you don't use HWE to recalculate them.  So your last statement in Calculation 1 is nonsense.  What you've done there is calculated the proportions for a population in HWE where the p=0.73, but you were already given the actual distribution in the population, so pretending like your theoretical calculation trumps the given data is nonsense.
Calculation 2 only works perfectly if your population is exactly in HWE.  Yours is a little off, that's why it won't give you quite the same p and q's as calculating it properly, by actually counting up the p alleles in the homozygotes and heterozygotes.

Okay, so the Hardy-Weinberg Equilibrium is just that: an equilbrium.

In physics, a system (some object) is at equilibrium when no net energy crosses its boundary with the surroundings.

no energy change means no change in motion (the state of the object) due to outside influence on the system.

In chemistry, a system (the beaker/reaction container/cytosol) is at equilibrium when no change in the concentration of the chemical species inside of it occurs over time

no chemical makeup change means the (molecular) state of the atoms in the system is free of energetic influence from the outside world.

In the H-W Equilibrium, a system (the gene pool) is at rest when no change in the frequency(concentration) of its alleles occurs over time.

no change in the frequency of alleles means that there is no outside influence on the state of the gene pool.

Just like in basic physics, we have to define our system. If our system is the gene pool, then even the behaviors of the organisms in whose cells those alleles are found are outside of the system. The system is only the alleles aka gene pool.
The most important part about understanding the H-W Equilibrium is that it only applies when those conditions of the gene pool being free from outside influence hold. In fact, in the link you gave, the introduction has it in the second sentence (don't feel bad, I missed it the first few times, too—too focused on applying the algebra to understand what it was really saying):

The model has five basic assumptions:
1) the population is large (i.e., there is no genetic drift)
2) there is no gene flow between populations, from migration or transfer of gametes
3) mutations are negligible
4) individuals are mating randomly
5) natural selection is not operating on the population.

Let's break them down/group them:

2: Obvious in terms of equilibrium == system is in isolation from surroundings
4 & 5: Selection pressure (4: sexual selection, or 5: natural selection) is not pushing on the system.
1 & 3: Random effects are not pushing on the system (1 = statistical sampling error that can push small populations, and 3 = mutation that pushes the system like adding a new chemical species to a system at rest.)

With that solid grounding in the theory, let's move on to your questions about the algebra. Remember, the equilibrium only applies when the gene pool is not being pushed around by external factors. Which means that the physical copies of alleles (gametes) should pair randomly with the possible gametes at every mating. If those assumptions didn't hold true, then the math of the equilibrium wouldn't hold up. If you run the numbers on a system at equilbrium, barring small amounts of sampling error (reducible with a bigger n), the H-W Model's predictions will be accurate. All the methods will yield similar results.
However, if the predicted values don't match the actual with one method, you can assume that other methods will also yield inaccurate predictions, and that the two different calculation methods' predictions will vary widely from each other, largely because of the assumptions you are making (Method 2: 1 = p+q), or aren't making (Method 2).

Hello vipatron!
Thank you for your clarifications. I am aware of the limitations of the HW model, but have to be honest with myself in admitting I've never given them this much thought.
But if I'm understanding this right, both modes should -- in an ideal HW population -- yield the same results, but will inevitably lead to skewed distributions as long as "real" (i.e. "non-ideal") populations are observed? Considering that measuring real deviations from the HW model ideal is most I've seen HW used for, doesn't having two options lead to two significantly different results?

I’m not a pure biologist. So, I don’t think I can answer your question except with a supposition backed by experience. Let’s say you were testing a hypothesis: you need to make some estimate of the values for p & q, and then be able to quantify the degree of deviation. Using the “exact method” of allelic frequency count, you can get a single estimate of allelic frequency and then create a null hypothesis about what the gene pool would look like if it were in equilibrium. But, I would prefer to see someone’s real work and explain why they did that rather than talk into the wind.

Oh, and you are understanding my answer.

@vipatron Under the listed assumptions, HW equilibrium is reached in a single generation. The term "equilibrium" is hence a little funny and there is not much over time dynamic that would lead to equilibrium. The expression HW rule is also common and it avoids the term "equilibrium".


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In the Selfish Gene, the chapter about ESS, how do the doves spread their genes?
In his explanation of the Evolutionary Stable Strategy, in the Selfish Gene, Richard Dawkins repeats a couple of times, that a population of hawk-type males would make the ground for a dove-type individual to spreat his genes, because the dove always retreats against a hawk and if an average hawk loses every second match, than he'll be worse off than the dove that always retreats and stays unhurt.
My question is - how dose a male, that does not win a single contest for a mate and therefore doesn't get to mate at all, spreat his genes?
Does the ESS imply that there are ways to breed bypassing the contest?

I don't know enough about the model to really give an answer, but I guess that if a dove keeps trying he might eventually come across a mate who isn't being protected by a hawk. The dove's strategy isn't winning fights, but in finding opportunities where there won't be a fight.

Game theory
Your question is not as specific to biology as you may think. The hawk-dove game is a type of game in game theory, a field of mathematics. Game theory is used in biology, in economics, in psychology and many other disciplines.
The hawk-dove game is often called the chicken game. If a game is defined as a chicken game, then it has an equilibrium different from 0 or 1. Otherwise, it may not.
You need to fully specify the scenario of interest to figure our what type of game we're dealing with to know what type of game we're dealing with and what are the possible equilibriums.
For more information, have a look at the mathematical field of game theory.
You specific scenario
The scenario as written in your post is not fully discribed. In your question, you define the doves such as they have a fitness (or a payoff in game theory terms) of 0, whatever is the state of the population. For such case, of course, a frequency of doves of 1 cannot be an ESS. However, under such case, you are not dealing with a hawk-dove game. I suspect you misunderstood the game as defined by Dawkins (it is also possible that Dawkins did not fully define the game he's talking about).
In short...
In short, I can't say much else than just "read more about game theory". However, you might want to cite exactly Dawkins so that we can understand exactly how he describes the specific game at play and comment on the expected outcome.

A male that does not mate will not spread his genes. Females might, if they have the option to reproduce asexually. However, this is probably not the answer you are after though. What you need to do is to look at the assumptions behind the game theory model being used.
For instance, some of the assumptions in a basic ESS-analysis are usually:

that the population size is infinite.
that the game payoffs are fitness modifiers and do not determine absolute levels of fitness.

Point 1 means that the game payoffs refer to the average payoff of individuals in each type of encounter. Point 2 means that there is always a baseline level of fitness, so all strategies are able to reproduce. Sometimes, assumption 2 is reformulated in terms of asexual populations, which means that all individuals will be able to reproduce (so the hawk-dove game will strictly not the modelling access to mates).
Therefore, doves (which never escalate a contest) will be able to "spread their genes" (win the contest) 50% of the times when there is a dove-dove contest (here is a description of what appears to be the normal version of the hawk-dove game). A single dove that enters a population will also be able to reproduce, even though it will never win contests (based on assumption 2). Again, remember that the game payoffs are fitness modifiers and does not determine the absolute level of fitness.
This means that individuals that play the dove strategy will still be able to spread their genes to later generations, but this doesn't preclude that certain dove individuals never get the chance to reproduce. This also means that there isn't any need for "ways to breed bypassing the contest", since one of the assumptions is that all strategies can reproduce, and in this case all strategies also have a payout option where they sometimes win the contest (which is the case for the hawk-dove game).

You are adding assumptions that are not there.
You assume not winning equals not mating, it doesn't, if a dove meets a female by herself they mate. The example of elephant seals he uses shows this, some males fight others wait for unattended females.

Oh, didn't notice that..


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Is this answer about the limiting factor correct?

The graph shows the result of adding both phosphorus and nitrogen to different algae populations. I have a hard time figuring out why the correct answer is C, I thought that  groups 4 and 5 would have nitrogen as a limiting factor because adding it increases their growth. Help me please.

Welcome to Biology.SE. Please avoid posting text as images. Images are not searcheable and the format can be unpleasant. While it is easy to read in your case, nobody needs to know that you have 48% of battery left! Also, it may give a feeling that you're not putting much effort in the posting a nice question and this is probably why you got a down vote (the down vote was not from me). Also, "Help me please" makes it feel like your begging for help which is never really welcome on SE sites. You might want to edit all that.

I agree with you, and think that there is a mistake in the "Correct answer". The interpretation in the "Explanation" seems to be correct though ("Algae at locations 4 and 5 exhibited growth in response to fertilization with nitrogen."), so I think that there is a typo/mistake in the "correct answer". The answer should be D.
Normally within ecology (and especially in reference to nutrients, such as  nitrogen and phosphorus), limiting factor refers to the substance/nutrient that is in short supply within a particular environment, and is therefore limiting the potential growth of organisms. For examples, see any ecological textbook or Blumenthal et al (2001) (as an article example, picked at random). The concept of limiting factors is related to Liebig's_law, which states that growth of organisms is determined by the scarcest resource, and not the total level of resources.
When performing a couple of searches now, I see some instances though where the term limiting factor is used on the opposite way, in reference to toxic substances. One example of this is Imadi et al (2016), where monomeric aluminum reduces root growth due to aluminum toxicity. This is not the most common use of the term though.

You might want to mention Liebig's Law of the Minimum here (https://en.wikipedia.org/wiki/Liebig%27s_law_of_the_minimum).

@arboviral Good call - now added.


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Is this a roach or a beetle?

I'm pretty sure it's a beetle due to the lines on it's back/rear but I'm not positive and if I'm wrong I need to take action quickly. Thanks in advance :)

Welcome to Biology.SE! Have you tried searching for similar images or compared your insect with pictures of cockroaches? It is expected that you will demonstrate that you have done some research on your own before asking questions here — for example try: https://bugguide.net/.  For information on how to use this site, please check out the tour: biology.stackexchange.com/tour and then the help pages on how to ask questions on this site: biology.stackexchange.com/help/how-to-ask. Thanks!

Please add where and when the creature was found. This is expected for species-id questions.

@tyersome The OPs insect is not an Anobiidae, as your comment suggests. For one, the pronotum and head angle is completely off.

@fileunderwater: Great I learned something!

This is a click beetle (Elateridae), so not a cockroach. This is most easily seen by the long pointed corners/angles at the posterior part of the pronotum, which is part of the “click” mechanism they use to flip themselves when they land of their back, or to startle predators.


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Wolbachia - cytoplasmic incompatibility
I read that cytoplasmic incompatibility in Wolbachia occurs when wolbachia-infected male insects mate with wolbachia-free female insects and produce non-viable offspring. By contrast, wolbachia-infected female hosts produce successful offspring irrespective of the infection status of their mate.
I was wondering - what are the long-term effects of this on the size/structure of a insect population? How will this be different from a non-infected population?


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How are lysosome membranes protected from the attack of hydrolases?
Lysosomes are a bit like the suicidal bags of cells. They help to clean cells, have an acidic pH and contain a large number of hydrolyzing enzymes.
But why don't these hydrolyzing enzymes attack and destroy lysosomes' membranes?

Early histochemical work indicated that the internal surface of the lysosomal membrane has a glycocalyx - a layer of polysaccharide, presumed to have a protective role.

Neiss, W. F. (1984) A coat of glycoconjugates on the inner surface of the lysosomal membrane in the rat kidney. Histochemistry 80, 603–608

Subsequently it was found that major membrane proteins of the lysosomal membrane are protected from proteolysis by glycosylation:

Kundra, R. and Kornfeld, S. (1999) Asparagine-linked oligosaccharides protect Lamp-1 and Lamp-2 from intracellular proteolysis. J. Biol. Chem. 274, 31039–31046

See this paper for a more recent study of another lysosomal membrane protein:

Schieweck O. et al. (2009) NCU-G1 is a highly glycosylated integral membrane protein of the lysosome. Biochem. J. 422: 83-90

NCU-G1 is the mouse orthologue of the human C1orf85 protein. The NCU-G1 gene encodes a 404 amino acid protein. This is a Type 1 transmembrane protein - i.e. the N terminal domain is directed to the extracytoplasmic surface of the membrane. In vivo the protein is detected in 70 kDa and 80 kDa forms. The discrepancy between the polypeptide size and the molecular mass is shown to be due to extensive glycosylation. The protein sequence includes 9 potential glycosylation sites.


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Do bacteria with capsular antigen always have a capsule?
Assume some bacteria have capsular antigen.
Do these bacteria always have a capsule?
I think not, I think the antigen only makes it possible.

This is a general question.

I personally see no problem with most of Masi's questions and I like this one.

Are you asking if the bacteria always will have a capsule or only if they will always be capable of producing a capsule?

@jarlemag Good questions! I mean the latter question. I think answer to your first question is no. I think the capsule is degraded in some phase eventually.

In short: It can depend on your definition of encapsulation.
According to the Oxford Dictionary of Biochemistry, a capsular antigen is defined as

any of the antigens, usually polysaccharide in nature, that are
  carried on the surface of bacterial capsules. The term K antigen is
  used for those that mask somatic (O) antigens.

In general, capsule polysaccharides have complex structures and are produced by a the action of several enzymes, with the genes necessary for production of the capsule typically making up a gene cluster in the genome (see for example Chen et al.: http://www.biomedcentral.com/1471-2180/10/274). On the face of it, it would seem somewhat unlikely that a bacterium would produce a known capsular polysaccharide antigen without retaining the ability to produce a capsule, as the selective advantage of the capsule then would be lost.
In actuality, the answer might depend on how you define "have capsular antigen" and "capsule". Historically, several methods have been used for demonstrating encapsulation. Methods based on staining microscopy or colony morphology observations tend to identify fewer strains as encapsulaed than does serotyping (reaction of serum with antigen). With this in mind, strains that can be shown to be encapsulated without serotyping are sometimes referred to as "highly encapsulated" to distinguish them from strains that test positive for encapsulation through serotyping only.
For discussions of capsule detection methods as applied to Staphylococcus aureus, see Sutra et al. (http://jcm.asm.org/content/28/3/447.full.pdf) and O'riordan and Lee (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC321462/).  O'riordan and Lee writes

Isolates belonging to the remaning serotypes produce nonmucoid
  colonies on solid medium, and their colony morphology is
  indistinguishable from that of strains lacking a capsule. Some
  investigators have referred to nonmucoid, encapsulated S. aureus
  isolates as microencapsulated to distinguish them from the atypical
  mucoid strains.

Thus, if both "have capsular antigen" and "have a capsule" is defined by a positive serotyping result for a capsular antigen, then all strains with a capsular antigen as detected by serotyping have a capsule per definition. If on the other hand you define encapsulation based on ink staining microscopy or colony morphology, there are definitely strains that produce K-antigens and don't qualify as "encapsulated".
Note that while bacterial capsules consist mostly of polysaccharides, capsule proteins make up a second class of capsule antigens. One example is the Caf1 capsule antigen protein produced by Yersinia pestis: http://en.wikipedia.org/wiki/Caf1_capsule_antigen

Thought I'd mention that there's also a K-antigen in E. coli, K30, which is present both in the bacterial capsule and as a low molecular weight-form lipopolysaccharide (LPS) on the cell surface, but as far as I can tell the second form is only present when there is also a capsule.


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Which hormones/factors affect Calcium absorption in the small intestine and its regulation?
I think the question is very broad and cannot find precise mechanisms.
I am not sure about the precise mechanisms of the regulation.
I think they are at least Vitamin D, diffusion and specific calcium channels: calbindins.
More specifically, calbindin-D9K and the basolateral calcium pump transport calcium from cell interior to extracellular space.
The calcium gradient should also be free, -2-6 mmol/l, in the lumen to allow diffusional calcium absorption from the interstitial space.
Similarly, free calcium concentration in the extracellular fluid of the lamina propria.
I think that the most important mechanism for this absorption is the electrochemical gradient of sodium across the epithelial cell boundary of the lumen, similarly as for carbohydrates.
To keep the extracellular space free from calcium, the NA/K-ATPase i.e. sodium pump has to work.
I did not find any hormones that affect the intestinal calcium absorption.
Which factors affect calcium absorption and its regulation?

Parathyroid hormone increases intestinal calcium absorption by increasing production of vitamin D, which in turn uses calbindin. It also enhances calcium reabsorption from the kidney and the release of calcium from bone.

Is there any other hormones or factors that affect the calcium absorption in the small intestine?

The only other hormone involved in calcium homeostasis that I know of is calcitonin and that not only plays a minor role but doesn't have intestinal involvement. If there are any other they would be very minor.

As @AndroidPenguin said Vit D3, calcitonin and parathyroid hormone are main hormone regulators. You can check this review. It talks about Sex hormones having indirect roles.


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Species diversity in cheese and yoghurt?
There have been studies on the number of species on humans and in various other environments. I was wondering how many species including: viruses, bacteria, yeasts, and fungi inhabit ordinary farm yoghurt, supermarket yoghurt, and cheeses like parmesan, edam, and blue.
I can find some studies, but not an actual count of species diversity in living dairy products.

Does the work you found include that by Rachel Dutton (http://www.theduttonlab.com/publications-1/2017/6/14/publications)?  It would be helpful if you could summarize what you have already found.

Nice find, I didn't see that. http://www.asmscience.org/content/book/10.1128/9781555818593.chap12 sais that there are relatively few species in cheeses. And this study suggests that there are 5-7 main bacteria in the ecosystems, although I didnt find a specific reference on the total diversity. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4222527/figure/F3/

Great — I hope you'll post an answer your own question once you feel like you've digested the available literature!

We did some work on mozzarella cheese: https://www.ncbi.nlm.nih.gov/pubmed/30621867.
However, we only studied bacteria. The group of Danilo Ercolini is leading a lot of work in metagenomics of several kinds of cheese (I mostly took inspiration from their work). You can look there for some reference.


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Why does smoking change the human voice?
What happens to the biology of the voicebox of smokers?
Women's voices can change to croaky men's voices, and vaper's voices develop "white noise" content, like a TV set to static, compared to their original voice which is closer to an oboe reed. I am curious why the white noise content and What happens to the voicebox and what happens to the sound of humans that smoke?

Smoke is hotter than air and passes through your vocal cords (before getting to your lungs), irritating them.
Irritation produces inflammation and inflammation produces mucus and general edema that could affect the biomechanics of your vocal cords, especially if you're a seasoned smoker.
The edema of the vocal cords is called Reinke's edema, which is classified as a benign polyp and will definetely make your voice more low-pitched.
I just saw that you added vaping in your question.
Since vape contains irritating chemicals too, I think its effects wouldn't be much better than smoke..obviously it depends on how often you smoke/vape.
Also, check this article:

Significant research has been conducted about the effect of cigarette smoking on the larynx and vocal cords. Several studies also suggest that exposure to electronic nicotine delivery systems can cause cellular hyperplasia (growth of cells) and metaplasia (change in cells) in mucosal lining in rats. It is theorized and likely that the same would occur in human tissue. Another experiment assessed the toxicity of vegetable glycerin, which is known to be harmless in liquid form. Its effects change in aerosol form. The experiment concluded that the substance led to squamous metaplasia of the epiglottis epithelium. Other research shows that nicotine in cigarettes is likely to lead to cancer, including in the mouth and larynx.
If the delicate lining of the vocal cords are exposed to hot, vaporized chemicals, the tissues are likely to undergo change and lose their ability to behave normally. This may produce hoarseness, loss of vocal range, voice fatigue, or vocal injury.

and finally:

These diseases and their effects on the voice can deeply affect singers and other people who use their voice for  a living. The only option to avoid these is to abstain from vaping completely.


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Why do sloths come down from the trees to defecate?
I'm under the impression that most sloths exhibit this behavior, but why? They are slow moving and so have no way of escaping from predators when on the ground. Not to mention the energy they expire to break from their normally sedentary lifestyle.
They may only have to defecate and urinate once a week, but it strikes me as an unnecessary risk.  Why not let gravity do all the hard work?

From Wikipedia:

Sloths go to the ground to urinate and defecate about once a week, digging a hole and covering it afterwards. They go to the same spot each time and are vulnerable to predation while doing so. The reason for this risky behaviour is unknown, although some believe that it is to avoid making noise while defecating from up high that would attract predators. Consistent with this, they reportedly relieve themselves from their branches during storms in the rainy season. Another possible explanation is that the middens provide the sloths with one of their few methods of finding one another for breeding purposes, since their sense of smell is far more acute than their eyesight or hearing. It has also been pointed out that individual sloths tend to spend the bulk of their time feeding on a single "modal" tree; by burying their excreta near the trunk of that tree, they may help nourish it. [Source]


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Why is the mosquito a definitive host in malaria?
I thought that the definition of a definitive host was that the parasite had to sexually reproduce in that particular host.
I've been told that mosquitoes are the definitive host for the plasmodium parasite, but I thought that the fertilization (and thus the sexual reproduction) takes place in the human?

Plasmodium falciparum (the main causative agent of malaria) and other Plasmodium species have a very complex life cycle, with stages in the female host Anopheles mosquito, in the human liver, and in the human circulatory system, where it primarily resides in the erythrocytes (red blood cells, or RBCs):

During a blood meal, a malaria-infected mosquito injects sporozoites in its saliva into the human host (1). Sporozoites travel through the circulatory system and first infect hepatocytes (liver cells) (2, stage A) and mature into schizonts (3), which rupture and release merozoites (4). After this initial replication in the liver (exo-erythrocytic schizogony (A), which can last a minimum of 5.5 days), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony (stage B)). Merozoites leave the liver and enter the circulatory system where they infect red blood cells (5). The ring stage trophozoites mature into schizonts, which rupture releasing more merozoites, which continue the cycle of infection of RBCs (6). Some immature trophozoites, in the so-called "ring stage," differentiate into sexual erythrocytic stages (gametocytes) (7). Blood stage parasites are responsible for the clinical manifestations of the disease.
It is important to note here (in answer to your question) that while the male and female gametocytes are formed at this stage in the human (the equivalent of meiosis), sexual reproduction does not occur until the micro and macrogametocytes are taken up by a mosquito.
The male (microgametocytes) and female (macrogametocytes) gametocytes are ingested by a female Anopheles mosquito during a blood meal (8) - only female mosquitoes (of pretty much any species) drink blood. The parasites' multiplication in the mosquito is known as the sporogonic cycle (stage C). While in the mosquito's stomach, the microgametes penetrate the macrogametes generating zygotes (9). The zygotes in turn become motile and elongated (ookinetes) (10) which invade the midgut wall of the mosquito where they develop into oocysts (11). The oocysts grow, rupture, and release sporozoites (12), which make their way to the mosquito's salivary glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle (1).
Sources

The Centers for Disease Control and Prevention: Malaria
Wikipedia: Plasmodium falciparum biology

The answer contains a lot of information, some incorrect, and does not answer the question.
The mosquito is the definite host of plasmodium, despite the humanocentric way this parasite is always looked at.
What happens in the human is the generation of the gammonts (named gametocytes). In the mosquito, these develop into the gametes (microgametes and macrogamete) and sexual reproduction takes place. In the then formed zygote, meiosis occurs, but is not immediately followed by cytokinesis.
As Plasmodium is haploid, the occurrence of meiosis relative to the formation of gametes is shifted in time, but this does not effect the definition of when sexual reproduction takes place (anyway both occurs within the mosquito).
Mirko Singer

Please add some references to your answer.


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What term describes insects that must eat protein to reproduce?
I know there is a specific term for insects that need to consume protein to produce viable eggs, as well as a term for those insects that don't need to consume protein to produce viable eggs.

I assume you are referring to species that needs to eat as adults before they can reproduce. Or are you only interested in species that specifically has to eat protein before they can reproduce (as adults or in general?)?

@fileunderwater I'm referring to a term that describes insect adults that must eat protein before they can reproduce.

The term I was looking for was anautogeny, or an anautogenous insect. I had slightly confused the definition, with the actual definition being; 'a gravid female insect that requires a blood meal before oviposition'.

Well, if you are satisfied with your own answer to the question, you might want to accept it. :)