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How statistically significant was the "sweaty T-shirt" experiment?
An Overview of the Experiment.
In 1995 there was an experiment that involves young people smelling T-shirts worn by another gender and rating their preference. The researchers found that people preferred shirts belonging to people with a dissimilar Major Histocompatibility Complex (MHC). Another interesting finding was that this preference reversed for the women 'sniffers' that were using oral contraceptives.
Here is a link to the wikipedia entry.
These findings were reiterated by a study in 2005.
My Question.
I'm very ignorant in the subject of pheromones, particularly in humans. For those of us not 'in the know' a result like this seems like magic! I want to get a better grasp on how set in stone pheromone preferences like this are.
Unfortunately I do not have access to these articles at the moment. The actual statistical difference in populations isn't mentioned in the abstracts  (the cynical sceptic alarm bells are ringing!) other than the 2005 one stating that the total sample size was 58, which sounds low given that the total population is split into two.
Generally I'm looking for any supporting or opposing critiques of the study, specifically I want to know more about the statistics of the studies.
My question is:

What statistical validations and scores appear in these studies?

I also am willing to accept answers discussing validation in similar studies. I'm after a number or quantification for how consistent pheromone preferences are.

Proceedings B keeps classic papers like this one behind its paywall twenty years after publication? For shame, Proc B! For shame!
For those looking for a free (but legal) source, JSTOR has the 1995 paper available here (free account-registration required):
http://www.jstor.org/stable/50182?seq=1#page_scan_tab_contents

First, let's consider the original Wedekind et al (1995) study.
Sample sizes seem reasonable, if the effect is not very noisy:

[...] 49 female students (average age: 25.2 years, s.d. = 4.0) and 44 male students (average age: 24.7 years, s.d. = 2.6) [...]

... and the statistical design accounts for individual differences in a fairly robust way:

[...] women were asked to rate the odours of six T-shirts each, three of them worn by men who were dissimilar to the rating woman's MHC (average number of dissimilar HLA-antigens = 5.9, s.d. = 0.26), and three worn by men who were more similar to it (average number of dissimilar HLA-antigens = 2.7, s.d. = 0.74). We tried to present every T-shirt as often to MHC-dissimilar women as to MHC-similar women (average difference of presentations to thc two groups: -0.02, s.d. = 0.73). The presentation was random in every other respect [...]

Rather irritatingly, although the study design involved asking women to rate at least three attributes of the smells (sexiness, pleasantness, and intensity) the study performs a bait-and-switch in its results:

The scores for sexiness are not shown in the figures as they were highly correlated with pleasantness (all scorings: r = 0.85, n =  294; for women who do not take the pill: r = 0.87, n = 186; for women who take the pill : r = 0.83, n = 108, p always << 0.001)

This is a bait-and-switch because even if A correlates with C, and B correlates with C, we do not know that A and B correlate with each other. Of the three measured attributes, 'sexiness' arguably has the most direct bearing on mate-choice. Because analysis for 'sexiness' is not presented, the paper ends up telling us much less than it could have about the relationship between MHC relatedness and mate choice.
The results for 'pleasantness' and 'intensity' look like this:

One further piece of analysis is presented: some number of the female subjects seem to have reported that particular smells reminded them of their partner or ex-partner; or reminded them of family members. Mentioning that a shirt smelled like a partner or ex-partner happened more frequently for MHC-dissimilar shirt smells (~17% vs ~9%; p = 0.038, two-tailed Fisher exact test). Oddly, no written response-collection is described in the methods, so I can only assume that these assessments were ad-hoc.
If this was all of the analysis that had been done on the topic, my assessment would be: this is amongst the many published research findings that are probably false. My main concerns would be that

Not all of the collected data are presented;
The most directly-informative contrast is not shown;
No adjustments for multiple comparisons are made on the statistical tests;
The data that are shown are very noisy, and sample sizes are not huge, raising concerns that the tests are underpowered;
The authors conduct tests based on data-collection which is not detailed in their methods, raising concerns about p-hacking.

And now, the 2005 paper!
Right off the bat, this paper cannot possibly replicate the findings of the Wedekind (1995) paper, because Wedekind et al found significant preferences for dissimilar MHC odours in women not taking the pill, and significant preferences for similar MHC odours in women taking the pill. In this study:

[...] we did not distinguish between, in our statistical analysis, women who were taking oral contraceptives from women who were not.
[...] Nine female participants (31.03% of female subjects) were taking oral contraceptives.

Sample sizes are smaller than Wedekind 1995 in terms of number of participants, but larger in terms of number of contrasts, because this experiment had two different sample types (sweat odour and urine), and had men smelling women as well as women smelling men. Within-individual effects are not modelled, so there is a potential for (e.g.) a small number of generically good-smelling individuals with rare MHC alleles at the population level to bias the analyses - whereas this potential bias was accounted for in Wedekind by performing within-individual correlations. The sample-sizes look like this:

The analysis was a series of Chi-squared tests, for data collected in four different sessions: one with men smelling female urine, one with men smelling female body odour, one with women smelling male urine, and one with women smelling male body odour. All chi-squared tests returned non-significant results with the exception of women smelling male body odour, for which the Chi-squared table looks like this:

So, this study didn't find the same result as the Wedekind study, but then, it couldn't find the same thing as the Wedekind study because of the way the analysis was performed, so that is no surprise. The authors claim that they found a significant effect of MHC relatedness on odour perception, but only in the proportions in the hard-to-interpret 'indifferent' response category. I am inclined to disagree. The authors presumably conducted 16 contrasts (a test of independence and three goodness-of-fit tests in each of four treatment types), and found one instance of p < 0.05. I would argue that the one 'significant' result is best explained as a failure to account for multiple comparisons.
Ending notes
If these two papers were the only things that had been published on MHC-directed mate preferences in humans, I would be far from convinced that the claimed effects were real.
however...
These are far from the only papers on the subject of MHC-driven mate-choice in humans. Wedekind and Füri (1997) conducted an analysis with very similar experimental design to Wedekind et al (1995), but arguably better statistical analysis, and found the same direction of association as Wedekind et al (1995), albeit still with a fairly high noise-to-signal ratio. Subjectively, this goes a reasonable distance towards making me think that the findings of Wedekind et al (1995) were not just a statistical fluke. I'm still not utterly convinced, but certainly more convinced than I would be if Wedekind's final paper on the topic had been the 1995 publication.
MHC-driven mate-choice has also been investigated using facial preferences and mate choice surveys. The combined evidence (across odour preference, facial preference, and mate choice surveys) is reviewed in Havlicek and Roberts (2009).

This is exactly the amount of depth and overview I was after. Thanks for putting up with a relatively vague question. If you do get time to finish your review of the 2005 paper I'd be very interested to hear about it.

@GoodGravy: Answer updated with thoughts on the 2005 paper and a mention of other related analysis. You might be particularly interested in a 2009 review. Enjoy!

The problem with mentioning the other papers that weakly support a link between MHC and mate choice is that it assumes there are no negative studies that were rejected, or never written up. The ease of performing these experiments (in the sort of sloppy, half-assed way that the 1995 paper was done) and the pop-culture attractiveness of the experiment, says to me that it has almost certainly been repeated many times, with negative results that were not published because the experimenters didn't get the results they and publishers wanted.   It's almost certainly not real.

@iayork: I think you are right to have concerns about the file-drawer effect, but I wouldn't dismiss the idea entirely. Of the odour-associated studies, the Havlicek and Roberts (2009) covers five studies with a 'disassortative' result, one with an 'intermediate' result, and three non-significant results. No 'assortative' results. To me, this hints at a weak effect and underpowered studies. I'm unconvinced that 'assortative' findings are unpublishable - the discussions in the 'non-significant' papers say 'regional structure?', which could be spun into 'assortative in this population'.

Keep in mind that the original impetus for these studies -- the idea that MHC is involved in mate choice in mice -- is now mostly disproved; it's linked instead to MUPs.  Admittedly there are some wild species where there's still a possible link, but with a weak theoretical underpinning, terrible experimental design, and a likely huge file-drawer effect, I'm more than skeptical.

@iayork That mouse disproving story sounds interesting. Could you cite something to that effect?

There are multiple papers showing this. The most recent is The Genetic Basis of Kin Recognition in a Cooperatively Breeding Mammal (Curr Biol. 2015 Oct 19;25(20):2631-41. doi: 10.1016/j.cub.2015.08.045); work dates back to at least 2007 (Curr Biol. 2007 Dec 4;17(23):2061-6. Epub 2007 Nov 8.)

@bshane has already provided an excellent answer to the question. However, I just found a recent review published in Molecular Ecology (Winternitz et al., 2016) in which the authors performed a phylogenetically controlled meta-analysis on MHC-dependent patterns of mate selection in humans and non-human primates. They used studies from seven primate species and looked at 30 studies (both observational and experimental) with a total of 58 effect sizes.
Short answer | Conclusion:
Winternitz et al. (2016) conclude that their data suggest a significant preference for mates with higher MHC diversity in humans that seems to be conserved across primates. Diversity here means heterozygosity in MHC loci.

An overview of their major findings:
First, a few words on the methodology. In principle, one needs to disentangle actual differences in the outcome of mating from error/random noise. To do that, they estimated heterogeneity in effect sizes, accounted for study ID and phylogeny effects on heterogeneity, and - for the residual unexplained heterogeneity - constructed meta-regression models with which they identified mediators of the respective effects.  Effect sizes are given as Fisher's normalized correlation coefficients $Z_r$ that is loosely similar to the correlation coefficient $r$ (they refer to ecological literature and claim that $r \approx 0.1 \rightarrow Z_r \approx 0.1$ is a small effect, $r \approx 0.3 \rightarrow Z_r \approx 0.31$ is a medium effect and $r \approx 0.5 \rightarrow Z_r \approx 0.55$ is a large effect). They then used mean posteriors and highest posterior densities (HDP, as 95% confidence intervals) to estimate $Z_r$, i.e. an assessment of how strong the mediators influence the effect. If highest posterior densities do not overlap zero, they consider the finding as a (significant) real effect.
Here is a list of what they found (HDP always in parentheses):

There is a statistically significant preference of MHC-diverse (i.e. a preference for heterozygosity in MHC loci) mates in humans ($Z_r$ = 0.153 (0.020 to 0.283), ten effect sizes). This preference also is a (non-significant) trend in primates (humans and non-humans combined) for preferring MHC-diverse mates ($Z_r$ = 0.128 (-0.064 to 0.373), 17 effect sizes). The preference is stronger in females than in males which is known from several vertebrates.
Across primates there is no significant tendency for favouring mates with MHC-dissimilarity (0.044 (-0.178 to 0.289), 37 effect sizes), even though the direction of effect sizes hints at MHC-dissimilarity rather than MHC-similarity.
For humans, there is larger variation to that point. They found effect sizes that indicate choice of both MHC-dissimilar (see above point, also true for humans) and MHC-similar mates ($Z_r$ = -0.022 (-0.107 to 0.073), 31 effect sizes). The latter may rather be an artifact of assortative mating with respect to ethnicity: effect sizes of MHC-similarity were only significant in ethnically heterogeneous populations, not in homogeneous populations. Further evidence for this comes from the fact that this is only true for observational studies, but not in experimental studies that tend to control for socio-cultural biases.

One needs to note that, in general, their reported effect sizes of MHC-related mating preferences in primates are weak (MHC-dissimilarity $Z_r$ = 0.044, MHC-diversity $Z_r$ = 0.153). But nevertheless interestingly, they report a significant effect for choice of mates with heterozygous MHC loci in humans. And - this kind of blew my mind just a little bit - they cite some literature that suggests that heterozygosity in general and of MHC loci in particular is not only reflected in body odour but also in other features like facial morphology.

I have seen many studies on that matter, but I am far from convinced that MHC really effects mate choice. Reasons for this are the following:
 - iayork mentioned it already, the premise for the studies about mice mate choice has been disproved.
 - In population level, almost every one of the studies find no evidence to support MHC based mate choices in general population.
 - Perception studies done in the area have what I consider serious problems in replicating the results. For example, wedekind's both studies feature same smellers and t-shirt wearers, but their answers are not the same as in the first study.
 - The latest perception study cannot replicate wedekinds results and the methods are almost the same.
So we have a hypotese, which has lost its original premise (mice mhc based mate choices), first studies doesnt replicate the results with same individuals, there are only couple of population level studies that suggest disassortative mhc mate choices and the latest study cannot replicate the first two perception studies.
On an individual level, these studies are kind of silly. If the effect is true, how can you discriminate between partners who are dissimilar or similar, if you would score them 5/10 or 4/10. The same applies to the brazilian study: your probability of percepting your partner as indifferent or unpleasant changes based on your HLA-similarity from 50% to 60% in different scenarios. Your overall chance of being 2-3 HLA-similar with this sample is about 10%.
I am just worried about these studies as media picks them up. Some people may come up with anxiety over their partners smell, which is quite silly because with over 50% probability you may be completely dissimilar with your partner regarding HLA, but one still perceives his/her odour as indifferent or unpleasant.
bshane and iayork, do you have any comments of the subject at hand?

can you add any kind of references or external sources to support your claims?

https://www2.psy.uq.edu.au/~uqbziets/Havlicek2009%20MHC%20correlated%20mate%20choice.pdf
Page four one can see population studies. Assortative/ns outnumbers disassortative 4/1
page 5, 6 and 9
https://www.ncbi.nlm.nih.gov/pubmed/26412134 Is the study about rodents.
And the part from the individual level I logically deducted from the results of Santos and Wedekinds work.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2519788/
http://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1000925
The latter of the studies proves that the first one is debunked.
Gipharts study of Dutch families cannot be replicated by Nordlander later.

Under-referenced, primarily opinion-based and probably incorrect post. -1


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Why do squirrels have twitchy bushy tails?
Whenever I see a squirrel in the woods, it is always the big bushy tail flipping around that gets my attention first.  A pray animal with a big bushy flag calling attention to it's self seems to be counter survival, a big flag waving here I am, come eat me.

*Image from Wikisource
Video link, of tail twitching
Why do squirrels have twitchy bushy tails?
Edit to Clarify
Squirrels do not have a high reproduction rate, there are multiple difference between species but most seem to average about half a dozen young per year.. While a pair of rabbits can (though unlikely) create 1300 offspring in a year Wild rabbit and squirrels have similar coloring and predators.  There are of course multiple differences between rabbits and squirrels.  Given the difference in reproduction and a big wavy flag that says come eat me.  It seems that if there is a rabbit and a squirrel sitting on the forest floor eating breakfast, the one waving the flag is most likely to be seen and eaten.

We all know that squirrels love to climb trees. They use their bushy tails to keep their balance and also to keep itself steady as it leaps across treetops. Also, it uses its tail to keep itself warm in summer months It may attract attention towards the animal but the tail serves a totally different purpose.

Clicking on this post I was hopping to see a nice picture of a squirrel...I'm a little disappointed $\ddot \smile$. Also, you probably meant counter adaptive (or simply not adaptive) instead of counter evolutionary.

@Remi.b image and video link provided

Maybe female squirrels just like males with bushy tails? Squirrels are pretty agile and fast. I don't think slightly increased visibility due to a bushy tail is a serious disadvantage. Also, note the coloring of the tail in the picture. In case the squirrel has to hide its tail might even enhance camouflage.

The rabbit eating breakfast has a bright white tail it is waiving when running from predators. And long ears (though not fluffy). I don't really see a lot of difference between the breakfast mates visibility.

Tree jumping.
The obvious answer is that having a balancing ballast is incredibly handy for some of the death defying jumps squirrels perform. The tail is needed for that.
A big bushy tail might be a good counter to predation.
You make the assumption that an inconspicuous tail would be bad for predation. I would challenge that assumption, but I am making an educated guess so feel free to debate this.
Tail flagging in ground squirrels is used to deter predators and communicate vigilance. Perhaps something similar occurs in tree-dwelling squirrels too.
Rabbits have a short white tail which isn't particularly camouflaged. It helps to confuse the predator allowing the rabbit to make sharp turns that the predator cannot anticipate.
In the case of this big bushy "twitchy" tail (which like rabbits, some squirrel tails have white tips, like in your picture), a predator probably cannot see the body and importantly cannot see or is distracted from the footing and pacing of the squirrel. If you've ever seen a dog chase a squirrel, the squirrel is easily able to outmanoeuvre the dog long enough to make it safely to a tree, probably because the dog can't predict the squirrel's trajectory due to the distracting and writhing tail.
Let's say a predator did get its jaws or claws near the squirrel and tried to take a chunk. There is a good chance all the predator will grasp is a bunch of tail fur. The squirrel will probably be sore but will live to tell the tail. (I couldn't resist)

+1, just to have the honor of getting you up to 3k ;-) (and of course for your nice answer)

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Why is an HIV infection considered "incurable"?
My biology teacher told me that if one caught HIV, they cannot be cured because it was near to impossible to be completely virus-free. She said this was because HIV keeps on changing its glycoprotein coat.
Can someone please explain what she meant by "keeps on changing its glycoprotein coat" to me?

I have an exam tomorrow and i am thoroughly confused.

There is a huge difference between "not cured yet" and "incurable." Have you done any research to answer this question yourself?

Seems a bit harsh to down vote a question coming from someone's teacher.  The student can't really be held responsible for using the teacher's bad wording.  At least they're seeking the right answer.

I think this is a valuable, albeit broad, question. @Amory has answered the question well with an appropriate amount of detail.

@MattDMo, if you want to nitpick about not cured yet versus incurable, then I think Amory's point that incurable is a misnomer is valid. You cannot cure a virus. You can cure the infection that they virus causes by neutralizing the virus, but it isn't the virus that is being cured, it is the infection. So the title should really read, Why is an HIV infection incurable? Actually would be is probably better. So Why would an HIV infection be incurable? And the biology teacher is probably just hedging her statement because of The Berlin Patient. Actually I will edit for accuracy.

@AMR I won't speak for MattDMo but I for one am being pedantic in a different way that you are.  I think saying "virus/bacteria can't be cured, infection can" is unnecessarily pedantic; my personal pedanticism is rather "we're just not there yet."  At any rate, I think your edit actually changed the question to much and isn't even quite right - depending on your definition of "virus," there's more to being "cured" than being virus free

@Amory HIV isn't the disease. By virus free I meant that all of the reservoirs in the body were also eradicated. We have only done it with the Berlin Patient... And HAART, technically can be a cure if you do not define a cure as no longer requiring treatment and will no longer be affected by the virus. It turns terminal into chronic, which many are willing to live with.

@AMR That's sort of my point.  You changed "incurable" to "completely virus-free" which aren't necessarily the same thing, nor necessarily what was meant.

@Amory fair enough... It was late and I wasn't thinking in terms of making all remaining proviruses transcriptional inactive, though tat would likely require maintenance treatment, meaning it isn't a cure. This is peer review, if you do not agree with my edit, then submit your edit to mine. With HIV, however, would be inclined to say that cure necessarily entails being virus free. Because even one cell, hat boring a provirus can lead to AIDS if it becomes transcriptionally active.... Unless you can do what happened to the Berlin Patient, and all new immune cells do not have the coreceptor.

The reasons why HIV is "incurable" (a misnomer) are legion:

HIV is a retrovirus, which means it inserts its own genome into the host cell's genome.  You must therefore kill each and every infected cell to rid the body of the virus.
HIV is a lentivirus, which means it has a long incubation period, so it can "lay low" before symptoms are readily detected.
HIV infects CD4+ helper T-cells, macrophages, and dendritic cells, which are responsible for mediating the host immune response.  Thus, it infects specifically the cells we need to fight an infection.
HIV drastically reduces the number of CD4+ T-cells.
HIV has a number of viral proteins that prevent some of the body's antiviral mechanisms
HIV can infect via cell-free (large number of particles, low infection rate) or cell-to-cell (low number of particles, high infection rate) routes.
HIV is wildly variable.  It has a small RNA genome (about 10kb) that mutates very rapidly.  Given the number of viral particles produced each day during infection — well over 1 billion — every single base is mutated every day.

I'm simplifying matters a bit — you should just read the en.Wikipedia article for your own research — but that's a rundown of some of the reasons why.

This is a very neat answer for quite a complex question. Very nice!

Nice answer. Your first two points answer the question. A few things you can add. Dendritic cells are the only APCs that can activate naive T-Cells (your cell-to-cell route) but the fact that it is in DCs makes it more insidious. HIV can cause CD4 death in 3 major ways. 1)Apoptosis. integrase causes ds breaks which triggers cell death. 2)Recognition by CD8 cells. 3)Though lysogenic, with enough budding, infected cells will not have enough membrane and they lyse. Also the variability you mention often changes tropism and allows gp120 to have affinity for coreceptors other than CCR5 and CXCL4.

@AMR "Simplifying matters a bit" ;-)

It is good enough to be a reference answer, so I thought might as well make it more complete.

I think the second bullet point suggests a conclusion that may not be readily apparent to a lay reader: a second sentence to the effect of “Thus, there are already a lot of cells to kill even if treatment begins as soon as symptoms appear.” The second-to-last bullet also seems like it needs to state what its significance is: is one or both of these routes unusual or particularly problematic, or is it just that having both in one virus that is notable?

HI virus attaches itself to the CD4 cells making it diffuclt for the body to destory it own cells.
the virus mutates faster and keep changing it shape

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is a musk deer's musk pod in its abdomen, its back, or its bottom/rear end?
I have read/heard different things about where a musk deer stores its perfume
Some links say it stores it in its abdomen just in front of its penis.  Others say the rectum(by which I suppose they mean the backside).
A) https://en.wikipedia.org/wiki/Deer_musk  "Deer musk is a substance with a persistent odor, obtained from a gland of the male musk deer situated in its back/rectal area. The substance has been extensively used as a perfume fixative, incense material, and medicine, since ancient times."
B) https://www.youtube.com/watch?v=r6CZKuSjlhI   7:40  "the fangs, but it's the other end of the deer that attracts more attention - the male's musk gland produces a scent that's irresistible to .. and perfume makers"
C) http://sandwalk.blogspot.co.uk/2009/10/are-you-sexually-attracted-to-male-musk.html   Only the mature male Moschus produces musk. The substance occurs in only one location on the deer's body: on its abdomen, just in front of its penis, is a hairy pouch known as the musk gland. This sac is about the size of a golf ball. It is composed of several layers of skin, with two openings immediately above the animal's urethra.
Quite a few links agree with 'C', that it's in the abdomen near the penis. Are wikipedia and national geographic wrong for putting the musk pod in the backside?

Here's another description of the musk sac. It mentions a musk sac that is "situated between the umbilicus and penis", as well as a caudal gland.

@AndersonGreen  I guess umbilicus is belly button. And since between the umbilicus and penis is the abdomen, it sounds like that's in agreement with  'C'  -  abdomen

does this image help? source

@WhatHiFi i guess maybe the answer is the back underside of a deer has its  penis  and scrotum and still near the back but a little bit further towards the front of the penis, is the stomach.  I will see if I can get to a farm and get a picture of the underside of a deer. will be a bit of a project.


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What program was used to create this visualization of a neighbor-joining tree?
I know there are many programs out there to visualize neighbor-joining trees in phylogenetics. I have a tree in Newick format. Does anyone recognize the features of this image as coming from a particular visualization program? I have tried several that may have produced this but with no success yet.
Note: I have to visually compare a new method's NJ tree with the result shown here, so that is why I really want to know exactly what program was used. This is not a question about software recommendation or opinions. Thanks!

Honestly this looks like something someone put together by hand in illustrator (or a similar program)

Can't you just ask the author?


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Why do some white blood cells have lobed nuclei?
Several types of white blood cells (eg Neutrophils) have lobed nuclei.  Is this for a functional reason?  I have seen people refer to structural differences in the lobes as indicative of problems, but I have not been able to find why the nuclei form into lobes in the first place.  Is this known?

The Neutrophil Nucleus and Its Role in Neutrophilic Function is the most recent review article I could find, but you'll need institutional access. Basically there's still not a lot of consensus and this is an active field of research. A big reason that stands out is the need to migrate through tissues, and  the lobular nucleus may assist there.

Thanks!  I do have an academic affiliation, so I will check out the article.  Thanks for tracking it down!

@Kendall for those without access to the review, could you summarize it as an answer?

I am not sure if this is why their nuclei are the way they are, but this may be one of the coolest functions of the immune cells. Extracellular traps are associated with human and mouse neutrophil and macrophage mediated killing of larval Strongyloides stercoralis Bonne-Année et. al. Basically Neutrophils are capable of using their chromatin to set extracellular traps for large pathogens such as nematodes that are too big to phagocytose. They die as a result , but the are able to "chuck out" their DNA at the worm.


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Do mantises stalk cicadas?
The Chinese Idiom The mantis stalks the cicada, unaware of the oriole behind (螳螂捕蝉，黄雀在后), which the story behind the idiom comes from Shuo Yuan(说苑), refers to those who are attracted by immediate interests without thinking about the possible dangerous results.
In reality, do mantises stalk cicada? Moreover, are cicadas stalked by birds?

Yes, mantises hunt cicadas...

Mantis eating cicada. Source: Dreamstime.
...and yes, orioles hunt cicadas too...

Oriole eating cicada. Source: Bird Ecology Study Group.
.., and what may be more relevant to your idiom: orioles prey on mantises.

Oriole eating mantis. Source: Sustainable Adventure.


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Why do we breath oxygen?
I like this contradiction. But seems like my Biology teacher doesn't.
If oxygen oxidates us, why do we breath it? Why can't we evolve into a new kind of human being that breaths other component of air? Following the need of all species to survive longer.

There is no other air.

@AliceD I think he means another constituent of the atmosphere, IE nitrogen or carbon dioxide.

@jzx - and walk with a fractional distillation column on your back? Now that's evolution

I can answer this question so if anybody wants to close, please first let me answer

Oxygen is the only reactive species in a large enough quantity in the atmosphere with which to catalyze biochemical reactions. Life is a compromise shaped by natural selection and evolution in a particular environment. Without reactive species everything is inert and Life cannot happen.

When life evolved, first came heterotrophs that obtained their organic molecules from their environment. Then came autrotrophs who made their own organic lecyles. The most important autotrophs are photosynthetic organisms. These photosynthetic organisms lived in the water and made glucose from CO2 and H2O. A byproduct of this reaction was O2.
Now, O2 killed off many of the species since it is very reactive. But the remaining species used the O2 for cellular respiration. Before, the cellular respiration was done anaerobically, without oxygen. The way this wroked was that the glucose was oxidated and the electrons from the glucose was used to make ATP, the main source of cellular energy. Once those electrons were used, they were deposited in a highly electronegative element compound, such as Nitrogen containing compounds. When plants produced O2, instead organisms doing anaerobic respiration, since oxygen is an extremely electronegative element, organisms deposited the electrons in the oxygen molecule. This is aerobic respiration. This from of respiration was more efficient and advantageous for land organisms. That is why we use oxygen.
Lungs and breathing is one of the many ways organisms obtain oxygen for delivering to cells to do cellular respiration. Fishes use gills. Most mammals use lungs. Many single celled organisms just obtain their oxygen through diffusion.

Good thing you answered before they bullied me, lol.

lol always forget that part, thanks for reminding


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What are the differences between carnitine forms?
I've heard of L-carnitine, acetyl L-carnitine and L-carnitine L-tartrate. What form(s) occur in meat? What form does the human body manufacture?
Is L-carnitine just a shortened name for L-carnitine L-tartrate?

L-carnitine and L-tartrate are two separate compounds - though a lot of "nutritional supplements" will package them together and seem to refer to them like they are one compound.

Carnitine tartrate is a salt between carnitine (cation) and tartrate (the conjugate base of tartaric acid, anion). So in this case, tartaric acid is not covalently bound to carnitine.
The salt formulation is a little tricky, because carnitine is itself a zwitterion at physiological pH (it has both a positive and negative charge) and so is overall uncharged in pure form. I think the tartrate salt is formed because tartaric acid is more acidic (first pKa = 2.89) than the carboxyl group of carnitine (pKa = 4.09), which leads carnitine to become protonated and therefore +1 charged in a concentrated mixture. The formulation sold by Lonza (which seems to be a major provider) appears to be a ratio of 2 cartinine (68%) to 1 tartrate (32%), which would indicate that tartrate acts as a -2 anion in this mixture (this is a bit surprising as the second pKa of tartaric acid has pKa = 4.40, but maybe I'm missing something).
You can recognize that this is a salt from the naming: the form tartrate indicate a conjugate base of an acid (as in lactate, acetate), and when used in a two-component name like carnitine tartrate (or, sodium acetate) refers to a salt. On the other hand, a carboxylic acid covalently bound to another group is given the suffix -yl, so tartryl carnitine would indicate tartaric acid bound to carnitine, as in fatty acid oxidation.

Carnitine is a molecule that allows transport of carboxylic acids (including fatty acids) across mitochondrial membranes and is involved in fatty acid metabolism. Like many biomolecules it exists as the L-enantiomer in the cells. It can be coupled to any carboxylic acid and in that case is called acyl-carnitine. L-Carnitine L-tartrate is a drug formulation and is a mixture of L-carnitine and L-tartarate (tartarate is not covalently coupled to tartaric acid).

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Genetic mapping problem
A prototrophic Hfr strain of E. coli with the genotype trp+ purB- pyrC+ is conjugated with an F- strain with the genotype trp- purB+ pyrC- . The trp gene is known to enter last. The following numbers of recombinants were isolated:
trp+        purB-    pyrC-       [0]
trp+        purB+    pyrC+       [44]
trp+        purB+    pyrC-      [132]
trp+        purB-    pyrC+      [224]
Draw a genetic map that shows the order in which these genes are arranged and the distances between them.

I started off by making these assumptions:
trp+        purB-    pyrC-       0  (the lowest #, must be double recombinant(DC)
trp+        purB+    pyrC+       [44](must be single recombinant(SC)
trp+        purB+    pyrC-      [132](must be single recombinant(SC)
trp+        purB-    pyrC+      [224](the highest #, must be parental(P)
Now since i know which one is DC and which one is P I can find the middle gene:
trp+        purB-    pyrC+  (224)- P
trp+        purB-    pyrC-  (0)-  DC
The only gene that varies is pyrC thus PyrC is the middle gene.
Consequently, the distance from trp-->PyrC=(DC+SC)/400=(0+44)/400= 0.11 or in map units it becomes 11
similarly, the distance from pyrC->pur B=(0+132)/400=0.33 or 33 m.u.
and here's the part im confused about: I only have 1 parental and i cant make the cross to figure out which is  trp-->PyrC and which is  pyrC->pur B. Even though i'm confident i got the right numbers how do i figure which one is 11 and which one is 33???
ps: I know it's a silly question after solving 99% of the problem it just that im used to do mapping with 2 parentals that i get lost when there is only 1 parental.

EDIT:
I actually figured it out, its not a regular genetic mapping problem but the bacterial genetic mapping(in particularly High resolution mapping). Thus, all the steps above are correct and answering my own question the way to figure out which direction it goes is just to compare the parentals given:
trp+ purB- pyrC+

_X_____X____X___
trp- purB+ pyrC-
(NOTE: ignore the trp minus since we solve for it)
doing the crossovers will yield the same results listed above,its just that it's more precise way to know which one is trip --->pyrC and which one is pyrC--->purB
PPS:SMC Bio 22 students doing problem set 1 in the future, you can thank me later.

I actually figured it out, its not a regular genetic mapping problem but the bacterial genetic mapping(in particularly High resolution mapping). Thus, all the steps above are correct and answering my own question the way to figure out which direction it goes is just to compare the parentals given:

I edited the answer and the solution is on the bottom now


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What are the reasons that soap has so different smell and flavour?
Everybody has tried to taste soap in their childhood. One would think that if soap has a tasty smell it would have tasty flavor too. But we know it is not true (in the common cases). But why is there is difference in the senses to our noses and tongues for the same soap?

I am having difficulty understanding your question. Do you mean: "How is it possible for soap to smell tasty, but not be tasty?", or more generally: "why is our instinctive of guess of how a substance will taste, given how it smells, not perfect"?

Exactly, you understand.

I like the taste of soap :) I retracted my close-vote, but I think the question is quite opinion-based.

It is possible for a substance to not smell very much, but to taste very strongly - chili peppers are a great example. They (in my experience) have a rather weak spicy odor, but the taste is much much more intense. In the case of soaps, very small amounts of essential oils are used to give soaps their odors. You may be able to slightly taste them were you to eat some of the soap (definitely NOT recommended!), but the major taste you'd experience is the actual soap - the saponified surfactants that do the cleaning.


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What magnification do I need to see blood cells?
If I want to buy a microscope for my kids to be able to view single celled creatures and blood cells, about what magnification is required?  A Celestron Pentaview digital scope claims up to 600×. Is that going to be sufficient? I somehow get the impression that I'd need 2000× or better, but I'm having trouble verifying any information about magnifications via my good friend Google.

If you know what to look for, 400x is sufficient. Anything higher is usually a marketing claim and not possible with cheap consumer microscopes.

@Chris, That's part of my question actually, as well. If I want to get a good 400× magnified image, then how much higher should the scope be rated for?

I suggest doing a google image search for an idea of what detail you can see at a given magnification.

@canadianer, Oh I've tried that. people are not very clear about magnification at all. sometimes, if you're lucky, they will put the power of the eyepiece, but that is not total magnification.

Resolution is significantly more important than magnification.  You will see more with a good 50X than an inexpensive 500 X.

Depending on how much detail you want to see, 400X (as Chris commented) is definitely sufficient. Remember, the lens(es) under/over the stage are labeled 10X, 20X, 40X, etc., while the eyepiece is generally 10X or perhaps 20X (multiplying the two together gives the final magnification). If your target magnification is 400X, then get a 400X scope - it doesn't need to be rated any higher than the highest magnification you want. 600X sounds nice, it's actually higher than the (non-digital) scopes I routinely use for examining mammalian cell cultures. 400-600X should give a very clear detail of both red and white blood cells.

Quick question. For prepared slides it should be no problem, but if the OP is planning on having their kids prepare their own slides, won't they need Hematoxylin & Eosin stain to really see anything interesting?

@AMR of course, there's a whole bunch of supplies they can/should get to create nice slides, stain various structures, preserve things, etc. That wasn't part of the question, though, so I didn't address it. However, you don't need H&E to see cells - you can see their outlines and occasionally internal structures just with bright phase. I use it to examine growing cells in culture all the time - just take the flask out of the incubator, turn on the microscope light, take a peek, focus, and you're all set.

Same here. I wondered why they would ask what mag they needed to see blood cells, and I thought, Okay, they are going to prick their finger and make a slide, and if they are looking at Google images (or @AliceD addendum) and think that that is what they will see right out of their finger, then they may want to know that they will need to stain the cells to see more than just the outline of the cells. Though I could still look a pond water sample and be fascinated for hours, nothing fancy required. Must have been amazing to have been Leeuwenhoek and not have taken any of this for granted.

As so often in science; it depends. In this case the magnification needed to visualize RBCs depends on the amount of detail you wish to see. Below I have added my 2-cents worth as visual add-on to @MattDMo's answer below:

Blood smear showing red blood cells and two white blood cells at 400x. Source: Microscope Master

Human red blood cells 1000x. Source: Wikipedia

Human white blood cells 2000x. The small dots (red arrow) are Diplococcus gonorrhea bacteria (Neisseria gonorrhoeae), each ~0.5 micrometers in diameter. Some of the neutrophils have phagocytosed bacteria. Source: Waynes World

Red blood cells visualized by scanning electron miscroscopy. Source: Pinterest.
Note: for illustrative and comparative purposes only; electron microscopy is not the most advisable method for home use.

C'mon Mate! They said for their Kids.... Hey mom! Joey is hogging all the SEM time again... Joey, let Sheila have her time to scan for HepB. ;-)

@AMR bwahaha, LOL, I should have pointed out the SEM was added for illustrative purposes only.

BTW the 2kx; do you know if that is degranulation, platelets, or a bad mycoplasma contamination? It is a pretty cool image.

@AMR - It is actually closer to HepB :-) edited. Thanks again for your keen eye.

Helpful.  I was critically reading a "journal" "article" - https://ijvtpr.com/index.php/IJVTPR/article/view/47/123 and noticed that the "40x" images of RBCs seemed way off.  Sadly/amusingly, I noticed other problems with the images, such as a lot of redundancy/near duplication. (And those are just the problems I noticed with the images...)

@WHO'sNoToOldRx4CovidIsMurder ijvtpr seems to be a bogus journal.

Did you not notice the quotation marks I put around journal and article?  SMH.


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Enrichment of slow growing microbes: Large Test Tubes as an alternative?
Well, i would like to enrich bacterial and archaeal ammonia oxidisers from soil samples using Minimal Salt media. They are slow growing microbes. I would like to enrich them with the aim to produce pure cultures.
I have always used conical flasks for enrichment as they provide better aeration, surface area, better distribution of nutrients, etc. However, due to some unavoidable reason, i would like to find an alternative to conical flask. Is it fine to use large test tubes?

I can't think of any reason slant cultures wouldn't work. It's worth a try!

@jzx agar slants in the sense solid media? i would like to use broth (not solid media), may be i can keep the broth in a slant position?

Yes, that was my thought. Obviously not ideal since you'll have to be careful, but if that's all you have on hand it's what I would do.

You want to purify colonies by growing them and streaking? You can use larger test tubes with sufficient air volume (use around 5ml of broth in 20 ml test tube) and proper mixing.

@WYSIWYG, ya, i want to grow them in a selective broth and then get pure culture if possible. Many Literature from NCBI using 50 ml broth (minimal salt media) in a 150 ml Erlenmeyer flask. And since the Ammonia oxidizers grow real slow, the media is replaced (10% dispensed in fresh media) weekly.

@NokImchen can you not provide an enriching medium?


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Why APC's present antigen to T cells?
the macrophages are pretty known well for antigen presenting process and to present the antigens which are bound to pathogens unlike exotoxins (which are free) the pathogen first should be digested and destructed and derive the antigenic portion and present it to T cells then stimulate the B cells to make antibodies. If the macrophages can destruct and digest the pathogen to derive the exact antigenic portion so then whats the need of humoral immunity to be activated because they have already destruct and kill the pathogen if your answer is that the pathogen gets knocked out quickly by antibodies for the second if they invade,so there are millions of other infecting agents every day         invading our body and are omitted by the first line defenses?

To answer your question properly would pretty much require giving an entire semester's course in immunology. As there isn't the time or space to do this here, my suggestion would be for you to read Janeway's Immunobiology This is the 5th edition, and from 2001 is likely very stale, as the current version is the 8th edition, and there have been many advances in immunology in the last decade and a half, but it is a start to your answer and will give you a better grounding.

Let's consider some situations real quick:
(1) A bacterial microbe enters through a fissure in the skin. What does an innate, systemic immune response look like? In short: it's lengthy, uncoordinated and has a lot of potential to damage tissue in the area of infection.
(2) A bacterial microbe enters the blood. The bacterium produces an AB toxin that enters cells and kill them.
(3) The host is infected by a helminth.
In situation 1: Innate immune responses are associated with the secretion of many cytokines and chemokines. Cytokines are associated with the inflammatory response, and chemokines are associated with lymphocyte trafficking. Inflammation and recruitment of lymphocytes, macrophages and the like are good for clearing the infection, but there's a lot of potential to damage the surrounding tissue. Effector cells from the adaptive response incl. humoral immunity don't elicit the same level of damage, and we can illustrate this in mucosal immunity. Since commensal (and some pathogenic) organisms are constantly stimulating mucosal immunity, there are (1) epithelial effector T cells, (2) plasma cells and (3) dendritic cells that make the response to these pathogens fast, efficient and little damage occurs to the tissue involved.
In situation 2: So let's say the pathogen has escaped the immune response, maybe it's encapsulated. There are AB toxins being produced that kill cells endocytosing them. What good will it do for a phagocyte to eat something that ends up killing it? Antibodies are particularly efficient for this extent because they can neutralize toxins they've encountered with the same fast, efficient response as we described above. This is achieved through antigen presentation. The host will then need to find other ways to clear the infection, however.
So: In situation 1 we illustrated that an innate, systemic response isn't always desirable due to tissue damage, and through the presentation to T cells by APCs, a later adaptive immune response mitigates this effect through formation of effector cells. In situation 2, we then illustrated that the first-line defenses can't always respond to the imminent threat for various reasons, which are overcome by the presence of effector cells.
Situation 3: This is the more complex concept. You have different subsets of CD4+ T cells that can be formed in response to the type of interleukin or cytokine that is present when the CD4+ T cells are being activated. This differentiation is driven largely by secretions of activated APCs! The APC performs this critical step based on what kind of receptors the specific types of pathogen are detected by. The differentiated CD4+ T cells, or T-helper cells of class: Th1, Th2, Th17, Treg, etc. each perform different roles which are effective in different situations. For example, you wouldn't see any benefit in throwing Th1 cells at a helminth infection, Th2 is the best effector for this. Treg cells are capable of abrogating autoreactivity, and Th17 cells are needed to assist B cell differentiation in response to antigen detection (which in the case of helminths, the B cell must class switch to IgE and this is stimulated by Th2 cells via IL-4).
Now, in situation 3, we've illustrated that CD4+ T cell intermediates are providing your overall immune response: flexibility, specificity, and checks/balances which are all-at-once critical to healthy functioning. I disregarded MHC-I responses and CD8+ CTL's because this is about APC-driven responses.

I did my best to provide something robust without going into deep detail, if anyone has a problem with the content let me know!

In nature and biology, the question of 'why something happens' is difficult to answer. Because, biological processes are 'not designed' to address a deficiency or fulfill be a need of the organism. On the contrary, biochemical processes undergo changes (induced or otherwise) leading to a number of new related processes which may confer advantages in altered environments. Therefore, to accomplish a task, every organism may use multiple pathways.
Eliminating a foreign molecule or an agent, is generally accomplished by a co-operative action of innate and adaptive mechanisms of immune system. Although innate mechanisms often can control propagation of some foreign agents, adaptive immunity and subsequent memory mechanisms of B and T cells are fast acting in subsequent exposures of many agents.

I'm not really sure this directly answers the question.  It gets to the issue of asking "why", I suppose, but that might be better phrased as a comment.


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My hand was stabbed with a pencil tip 10 years ago - why is the graphite still visible?
I, and multiple people that I know, have permanent marks (up to 30 years) from a graphite pencil puncturing the skin. The palm of my hand still shows a very clear mark where my hand was punctured by a pencil 10 years ago in school.
Why/how does the graphite remain in the skin indefinitely?

Perhaps your question has the same answer as this one: http://biology.stackexchange.com/questions/36712/why-do-tattoos-persist-if-body-cells-are-regularly-renewed

I had the same thing happen to my leg. I think it eventually went away, but it was definitely many years.
I am going to go with the Tattoo answer. The way tattoos work is that Macrophages in the skin phagocytose the heavy metals in the inks. Because the heavy metals do not interact with Toll-like receptors, or any of the other pathogen receptors that macrophages have on their cell surface, they do not induce a transcriptional signal into the nucleus of the macrophage to induce it to chemotax out of the dermal tissue and into the lymphatic system, so they just sit there. The YouTube channel Smarter Every Day actually has two interesting videos on tattoos Tattooing Close Up and How Laser Tattoo Removal Works.
Macrophages are long lived, so unless they receive transcriptional signals to get them to move out of the tissue they are in, they will just sit there, and if they happened to have engulfed the heavy metals in tattoo ink, or the graphite from a pencil jab, then they sit there with a vesicle filled with that compound. As graphite is pure carbon, I wouldn't worry that much about it, but it is also not not in a form that the body can use, so it will persist. If eventually the macrophages are induced to move, they will likely take their contents with them, which is why tattoos fade over time.
It also is likely that the graphite was taken up by several macrophages in the region, in particles large enough that they cannot be cleared and remain visible, but not so large that the macrophages could not phagocytose them.


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Chance of child inheriting at least one copy of an allele - heterozygote mother, unknown father
Our genetics professor has posted up working for previous examination answers, but I am not convinced that his answer is correct. My answer is close but may just be due to co-incidence.
Question: There is a dominant "risk" allele with a frequency of 5%; what is the chance that a woman with one copy of this allele, and her husband will have a child with at least one copy of the allele.
Heterozygote frequency: 0.095
Non-risk allele homozygote frequency: 0.9025
Risk allele homozygote frequencyy: 0.0025
Professor's answer:  0.50 (woman's chance of passing allele) + 0.095/2 (heterozygote frequency in population divided by chance of passing allele) = 0.5475
My answer:  There are three possible situations, that the husband is homozygous recessive, homozygous dominant and heterozygous. The probability that any child will have the allele in each situation is 50%, 75% and 100% respectively.
Hence my answer = (50% x 0.9025) + (75% x 0.095) + (100% x 0.0025) = 0.525

What is a risk genotype in a autosomal dominant disease - just the probability of being diseased?

To me, it is unclear whether the "disease" allele is dominant or recessive. Your statements "Homozygous recessive frequency: 0.9025" and "risk genotype (autosomal dominant)" could be impying that the disease is dominant, while the professor's answer is indicating that it's recessive. The answer also depends on whether you know the disease/carrier status of the father, and you and your professor are treating this information differently. [cnd...]

[cnd:] You could argue that the disease status of the father will be known (irrespectively of being recessive or dominant). Your professor's answer is based on that information while you are treating the fathers status as completly unknown.

I think the professor may have forgotten to also add the probability that the father is homozygous for the risk allele

It seems that what you are trying to do is calculate the probability of the child having at least one copy of the "risk allele" which I will denote as "A" (and it's counterpart "a").
First of all you know that the mother is Aa, and the child will get one allele at random. The probability that the mother passes on the A allele is then 0.5.
The tricky bit is the seemingly unknown genotype of the father. However, you do know genotype frequencies, which are the probability for the fathers three possible genotypes.

If the father is AA then it is certain the child will get the risk allele, and the probability of the father being AA is 0.0025.
If the father is heterozygous then there is a probability of 0.5 he will pass on the A allele, and the probability of the father being Aa is 0.095.
If the father is aa there is a probability if 0 that he will pass on the A allele.

Combined these give the probability that the father carries at least one A and will pass it to his child.
$$(1 \times 0.0025) + (0.5 \times 0.095) + (0 \times 0.9025) = 0.05$$
The probability of the child getting at least one A is then the probability of getting it from the mother plus the probability of getting it from the father.
$$0.5 + 0.05 = 0.55$$

I wrote out every possibility, and I agree with yours.
Mom passes good allele  50.00%
Dad is homo wt  90.25%
Odds of 0 bad alleles   45.13%
Mom passes good allele  50.00%
Dad is het  9.50%
Dad passes bad allele   50.00%
Odds of 1 bad allele    2.375000%
Mom passes good allele  50.00%
Dat is het  9.50%
Dad passes good allele  50.00%
Odds of 0 bad allele    2.375000%
Mom passes good allele  50.00%
Dad is diseased 0.25%
Odds of 1 bad allele    0.12500%
Mom passes bad allele   50.00%
Dad is homo wt  90.25%
Odds of 1 bad alleles   45.13%
Mom passes bad allele   50.00%
Dat is het  9.50%
Dad passes bad allele   50.00%
Odds of 2 bad alleles   2.375000%
Mom passes bad allele   50.00%
Dat is het  9.50%
Dad passes good allele  50.00%
Odds of 1 bad allele    2.375000%
Mom passes bad allele   50.00%
Dad is diseased 0.25%
Odds of 2 bad alleles   0.12500%
Odds of 0 bad alleles   47.50%
Odds of 1 bad allele    50.00%
Odds of 2 bad alleles   2.50%


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Living intermediate species?
Hypothetical question regarding three animals 'species' {A, B, C}.
Are there any examples in nature where {A and B} cannot regularly produce viable offspring, however {A and C} and {B and C} can regularly produce viable offspring.
I imagine that such a situation could arise if {A, B, C} have a common ancestor, but {A and B} are sufficiently different from each other, but not from C.

The hybridization situation you describe could be found in ring species, and is partially related to this concept.
For instance, the three species A, B and C could have partially overlapping distributions, such as:

In such a situation (assuming that the relative distributions have been stable over evolutionary time), A and C might be able to produce offspring, as well as B and C, while A and B might not produce viable offspring if they would meet.
Here is a picture from the wikipedia page for a similar situation, showing interbreeding between seven gull species in the genus Larus:

However, I also know that the ring species concept has been challanged, mainly by the fact that there are very few good empirical examples of ring species. See for instance the nice blog post "There are no ring species" by Jerry Coyne, which may also include a couple of examples of species groups that are relevant to your question.
Also, the hybridization patterns that you describe can be caused by other processes, for instance specific reproductive barriers between groups of species (molecular or behavioural). My answer is therefore merely mentioning one possible explanation for the hybridization patterns you ask for, but there are many other processes to consider.

I don't know what the molecular mechanism behind this phenomenon is but one possibility is presence of a set of lethal mutations that can be compensated in certain crosses.

I don't know either, and it will depend on particular species pairs. My last point is mainly that there exists other examples of the type of hybridization patterns that the OP describes, that doesn't involve ring species. There are probably examples of sympatric species where A+C and B+C can produce viable offspring, but not A+B, depending on specific features of their reproductive barriers.

Re Jerry Coyne's blog post -- What is it about Darwinian Theory that engenders so many dead-end conjectures and false pedagogical stories?

@user23715 Maybe that a naive version of evolution is higher fitness + selection -> perfect adaptation, which easily can lead to pattern-based apparent adaptation (or other "outcome" assumed to be the result of evolution) -> inference assuming selective forces

Maybe it's the underlying theory though and not just a naive understanding of it? See the recent "news" about Great Ape Evolution (Pliobates cataloniae). --- If the underlying theory is sound wouldn't it be driving field and lab work that supports itself instead of "turning it on it's head" as happens so often? --- The Standard Model in particle physics is known to be incomplete yet has truly underpinned the associated research. --- NDE and biology? Meh, not so much.

@user23715 Are you saying that the modern account of evolution has often been turned on its head? If so, when? What about the finding of Pliobates cataloniae do you find problematic (I've only seen a couple of headlines so far)?

The Mods will probably move this to chat but, in a nutshell: What is it about NDE that produces ideas like Ring Species or a proposed "tree" for the evolution of the Great Apes, and yet when field work is done in support of the idea, instead of reinforcing it, the theoretical concept gets "turned on its head"? --- Contrast this with Plate Tectonics, a theory that fruitfully guides field work in geology --- Or the aforementioned Standard Model in physics. These latter two have proven themselves time and again. NDE not so much. There is seemingly nothing about NDE that drives fruitful research.

@user23715 Exactly what are you referring to with "NDE" (not familiar with the acronym)?

Neo-Darwinian Evolution.

@user23715 If you truly believe that "There is seemingly nothing about NDE that drives fruitful research." you must be either ignorant about what is going on in evolutionary research or ideologically blinded. I don't think we will get further in this comment-field discussion though.

"Ring Species" was an idea birthed by NDE thinking. "Ring Species" do not exist... or maybe one example exists. What's wrong with NDE that it promotes thinking like this? --- Compare with the fruitfulness of the Standard Model in physics or Plate Tectonics in Geology. It just seems odd to me that the fundamental theory in Biology doesn't actually produce anything worthwhile. Advances in Population Genetics, Molecular Biology, etc. have all taken huge leaps irrespective of any potential underlying link to NDE. --- Name any recent (50 yrs +-) advance in Biology needs NDE to be understood.

The term that describes this phenomenon is 'clinal speciation', and the easiest examples to point to are all 'ring species'.
Wikipedia mentions four ring species examples. Three are avian examples (Larus gulls, Song Sparrows, and Greenish Warblers), and one is a plant example (Euphorbia tithymaloides).
The classification of the Larus gull complex as a ring species is contested. Liebers et al (2004) argue that the isolation-by-distance model, with genetic contact at all near points of the species' range, is not well-supported by genetic analyses for this species, and that the species' genetic structure is better explained by a series of 'splitting' events associated with long-distance colonisation followed by genetic isolation of the new colony.


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Do the effect of inbreeding depression disappear after the first generation of outbreeding?
An animal that is the result of generations of inbreeding tends to have lower fitness. (More diseases etc.) This is usually explained by harmful but recessive mutations that exist in all populations, but in inbred animals end up occuring on both copies of a gene in a chromosome-pair.
If the problem of inbreeding is that the two sets of genes in the chromosome pairs are too alike, does that imply that the offspring of an inbred animal will revert to "normal" fitness as long as the inbred parent was mated with an unrelated animal? Seeing as the inbred parent can only transmit one copy.
Or is the situation more subtle?

This depends on if you are talking about animals in the wild, such as isolated populations, or humans, or whether you mean research animals. Inbreeding tends to breed homozygosity, so as you said, if you have a recessive disease causing allele within a bloodline, then even if only one of the founders was a heterozygous carrier, then inbreeding can give rise to afflicted homozygotes. However, for lab strains, it is actually desirable to use completely inbred lines where all animals are as near to 100% identical (from a DNA sequence perspective) as you can get. This makes genetic mutational analysis far easier (possible).
It also depends on the alleles in question. Not every mutation is purely dominant or purely recessive. You can have situations, such as with some tumor suppressor genes, that diversifying the population by outbreeding to someone with a functional tumor suppressor, will still cause the offspring to have only a single working allele, and therefore an increased probability that they can sustain a random mutation that will knock the working gene out. You can also have cases where having one functional copy of the gene isn't enough, so the offspring are haploinsufficient. You need two doses of both working copies of an allele to display the non-afflicted phenotype, though the afflicted heterozygote has a better time of it that the afflicted homozygote, who has none of the working allele.
You also have X-Linked conditions. If the maternal lineage is inbred, then all of the males will be afflicted and females will be carriers.
Another possibility is that the outside breeder is a carrier of the mutant allele so the offspring remain homozygous or the outside breeder has an allele of the gene that comes with its own defect. They may not be afflicted, as they could be heterozygous for a working copy, but their offspring with the inbred line could be heterozygous afflicted because neither of the alleles they inherit are functional, it is just that they are not functional in different ways.
Sexual reproductions main advantage is that it is supposed to increase diversity in the population and increase survivability of the species. When you have isolated populations or inbreeding by choice, then this can circumvents the benefits. Not all inbreeding, as seen with laboratory strains and selective breeding of domesticated animals, is deleterious. It is just that the breeder needs to be careful of the choices made and cognizant of how the genetics can work. Animals displaying a diseased phenotype should not be allowed to produce offspring, and you need to evaluate the siblings of that animal as well as the parents to insure that you do not have problems in that lineage.


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An alternate cure for AIDS?
Is is possible to cure AIDS patients by using white blood cells of blood cancer, by fooling HIV to attack a false target?
Is it possible to wrap HIV in a physical boundary, such that it has no interaction out side the wrapper, so the functionality of the cell will not be affected by HIV?. Since all cells in out body are replaced within three years, after 3 years, the HIV affected victim will have fresh HIV free cells.

So you're trying to cure pest with cholera? Leukemia also causes problems with the immune system (since mainly only one clone is maintained) so this wouldn't be a good idea.

why not give a try in a worst case?

Because HIV can be controlled for quite a while with the actual medication. And who will be the person conducting these experiments? This is unethical.

The reason AIDS develops is that your normal run of the mill immune cells are plenty potent enough to kill off all of your Helper T-Cells that are infected with HIV, so now you want to let loose killers that are not necessarily specific to cells infected with HIV that will lay waste to everything else?

What would you choose when your treating physician gives you the option: leukemia or antiviral treatment? HIV is not lethal anymore these days, at the least life expectancy can be substantially prolonged. Admittedly, treatment is life long and not a cure, but you'll live.
Leukemia on the other hand, is life threatening and needs immediate treatment. Treatments for leukemia are primarily chemotherapy, and perhaps radiation therapy, biological therapy, targeted therapy, and stem cell transplant, all of which are by no means guaranteed to be curative.
But interestingly: a Berlin leukemia patient with HIV was actually cured after receiving chemotherapy and having received HIV-resistant stem cells to repopulate his white blood cells (Source: Medicine Net). The donor carried the relatively rare mutation called CCR5delta32. People with this mutation lack functional CCR5, the protein that HIV most often uses to enter cells.
Why is this not a standard treatment? The Berlin patient serves as a good example, because the patient suffered intestinal and neurological symptoms due to the chemotherapy. And besides being dangerous in itself, chemo is truly a grueling experience to go through. And in fact, this patient was the only instance in which this approach was followed (Source: Medicine Net).

Then why not try the vice versa: treating Leukemia with HIV?

@JohnyRoyan - All cancerous cells need to be killed off. AIDs infects many, but not all.

At least we can have a try, no ?

@JohnyRoyan - trying new treatments needs careful risk-benefit analysis as well as ethical consideration. Given the grave dangers associated with leukemia, and minimal chance of success, both will not have a positive outcome I'm afraid.

is it possible to wrap HIV in a physical boundary,  such that it has no interaction out side wrapper, so the functionality  of the cell will not be affected by HIV. Since all cells in out body are replaced within three years, after 3 years, the HIV affected victim will have fresh HIV free cells?

No. See this answer to 'How fast do different organs turn over cells?' and this answer to 'Why is an HIV infection considered “incurable”?'.

I wouldn't say it's not lethal. Just because people can survive a decade or more with treatment does not mean it will not kill them.

@forest, thanks, I have toned down that statement.


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What is biological intuition?
Whenever I read or learn about prediction tools or aligners or motif detectors, I also hear that they are lacking in something called biological intuition. But I haven't been able to find a solid definition of what that is. Can someone please explain?

This is how I understand it: Bioinformatics tools are amazing at answering questions. The more specific the question each individual module of a tool can answer, the better their quality.
However, what they cannot do is ask the right question. You can find motifs with scores attached to the hit, but you cannot predict the relevance of that find. Is it a motif for a transcription factor binding site that inhibits a promoter for a downstream gene thereby suppressing activity, or does it bind a different factor enhancing a gene further downstream?
These questions need knowledge of the domain and of the genomic context, and this knowledge base is constantly evolving. Tools are getting intelligent, but they cannot have this intuition because they are still designed my human beings and we are always ahead thanks to experience.


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Ways to identify that proteins are regulating different genes experimentally
As part of my study I have been given this hypothesis:

HIF 1a and HIF 2a regulate different genes in multiple myeloma

What ways do we have to identify that these proteins are regulating different genes in multiple myeloma? I recall in lectures something being mentioned about using antibodies to isolate the regulatory elements, but can't find any specifics.
Any help is seriously appreciated!

Chromatin immunoprecipitation (ChIP) or ChIP-Seq are the first methods that pop into my mind. Essentially, DNA is cross-linked to bound proteins (transcription factors, histones, etc.) by various methods, then broken into pieces by either sonication or digestion with micrococcal nuclease. An immunoprecipitation is then performed by adding antibodies targeting your protein of interest (HIF-1α and HIF-2α in this case), allowing them to bind to their targets, enriching them using bead-conjugated Protein G (or Protein A), then reversing the cross-linking. The enriched DNA can then either be subjected to PCR for known genes (ChIP), or it can be sequenced and aligned with a reference genome to determine all bound sequences (ChIP-Seq).


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Help Identifying Tree
I live in the upper southeastern region of Arizona in U.S. There's a type of tree growing in my back yard that I can't seem to identify. Its growing in an arrangement very similar to an ocotillo plant.  It has single spiny stems coming up out of the ground.  They don't branch out but have large sharp spines with leafs growing out of them.  It doesn't look anything at all like any of the native desert plants in the area.  There's mesquite and sage and various types of cactus.
At the moment the stems are about five feet tall.  I took clippings about two feet in length and photographed them.  It seems I'm only able to post two links so I've chosen the clearest images that I have.  I'm very curious as to what this is and any help would be greatly appreciated.

Have you ever seen flowers or berries? although I am not familiar with the flora over there I would suggest it could be a Pyracantha (Rosaceae)

I have seen that up in the mountains in this area but only above a certain elevation and mostly among oak trees.  This plant's spines have claws like a rose bush.  My sister said it appeared about four years ago and she tries to uproot it every spring but it keeps growing back.  As far as she can tell she's never seen it bloom any flowers or produce berries.  She thought it was a type of mesquite known in the area as "cats claw" but it's leaves do not look like any kind of mesquite leaf I've ever seen.  It has a lush green appearance that contrasts it from the other desert plants in the area.

Can you take a picture of the whole tree and a picture up-close of the leaf?

Also, you mention also seeing this in a montane oak forest. Could you comment on the elevation, the aspect (side of the mountain), species of oak, possible presence of conifers, how dense the understory is, or anything else notable about the habitat you've seen it in?

@theforestecologist  I removed the plant in Oct.  This pic is nearest to how it looked but not as dense or as high.
The elevation where I spotted a cluster of the red orange berries similar to the Pyracantha was above 2,600 ft.  The azfirescape website is a close description to the area.  I can’t say where exactly I saw it only that I know I have seen a red cluster of berries like it  before.
link
link

It looks like this could be Lotebush, Ziziphus obtusifolia. The thorny branchlets and blue-green color (at least, as it appears in the photos) suggest Ziziphus to me, although you could compare it with the photos or description here. If it is in the buckthorn family, it does seem to key out to Ziziphus using the Christie et al. key.
If you wanted to be sure, you could follow up with the ASU herbarium (see citation).

Christie, K., M. Currie, L.S. Davis, M.-E. Hill, S. Neal and T. Ayers (2006). Vascular Plants of Arizona: Rhamnaceae. Canotia 2(1): 23-46. Open access

The leaves aren't a perfect match for any of the photos I've seen, but the description does note that the leaves are quite variable, especially in young shoots.


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The biggest underground living animal
It's easy to find information about the biggest animals at land / at sea / in the air. But what was the biggest underground-living animal that ever existed?

No animals that were forced to live underground (e.g. pit ponies)
The animal should live at least 95% of its life under the earth (e.g. foxes)

There are two possible answers:

By length
By mass

My first guess was a mole

Okay, maybe not 95% of the time, but as you put ever existed, I would throw the cave bear's hat into the ring. https://en.wikipedia.org/wiki/Cave_bear.

cave bear are not primarily cave dwelling, their fossils are found there, just like "cavemen"

Graboids!   .........But seriously are you just looking at terrestrial burrowers, if not moray eels might be a contender.

Microchaetus rappi
Microchaetus rappi, the African giant earthworm, is a large earthworm in the Microchaetidae family, the largest of the segmented worms (commonly called earthworms). It averages about 1.36 m (4.5 ft) in length, but can reach a length of as much as 6.7 m (22 ft) and can weigh over 1.5 kg (3.3 lb).(https://en.wikipedia.org/wiki/Microchaetus_rappi)
Giant Gippsland earthworm
These giant earthworms average 1 metre (3.3 ft) long and 2 centimetres (0.79 in) in diameter and can reach 3 metres (9.8 ft) in length; however, their body is able to expand and contract making them appear much larger. On average they weigh about 200 grams (0.44 lb). They have a dark purple head and a blue-grey body, and about 300 to 400 body segments.(https://en.wikipedia.org/wiki/Giant_Gippsland_earthworm)

I think you got the record! +1 It'll be hard to find any bigger without going with the kind of far-fetch example I gave.

Key Words:
To aid in your search, you might want to try searching the term "Fossorial."

Fossorial animals are animals that are adapted to digging and life underground.

Though note: Lessa et al (2008) use fossorial to describe species that spend a substantial fraction of their lives outside their burrows, while they use subterranean to describe species that perform most activities underground.

You might also want to examine a list of troglobites.

Troglobites are animals that live entirely in the dark parts of caves.

Big Species
I think large specimens of @JayCkat's suggested species (Microchaetus rappi) will be tough to "beat", with large specimens reaching 6.7 m and 1.5 kg.
However, here's a list of other species anyways:
Some extant large species of fossorial animals:

Cape dune mole-rat (Bathyergus suillus): 27-35 cm (up to 39cm including tail); 570-1350 g

Supposedly, some blesmols can reach a weight of 1800 g.

Russian Desman (Desmana moschata): 18-21 cm (up to 41 cm including the tail); 400-520 g
Giant Armadillo (Priodontes maximus): up to 1.5 m; up to 50 kg

It spends all day in underground burrows though it hunts above ground at night.

Olm (Proteus anguinus): up to 40 cm long.

 Cape dune mole-rat

 Giant Armadillo

The only info I could find via a quick search for prehistoric fossorial animals:

A series of 240 million year old underground tunnels/chambers suggest some burrowing species lived there. [Source: Seeker].

"You should imagine the tracemaker as a stout, short-bodied, four-legged animal with a short tail and short neck...The trunk was about 20-25 centimeters (8-10 inches) in length.

Bonus:
How about the deepest living animal?

That award goes to the "Devil Worm" (Halicephalobus mephisto), a nematode that has been found living at 3.6 km below the surface!! ...(tied w/ Plectus aquatilis).

Though at 0.5 mm, it's definitely not winning the largest trophy :p.

 Citations:
- Lessa, E. P., Vassallo, A. I., Verzi, D. H., & Mora, M. S. (2008). Evolution of morphological adaptations for digging in living and extinct ctenomyid and octodontid rodents. Biological Journal of the Linnean Society, 95(2), 267-283.

@TheWho oops, you already listed the Russian Desman. you'd think I would have noticed the 2 year old post! :p.

I don't know if there is a bigger animal, but the biggest mole is the Russian desman with 400-520g and a length of
18-21 cm (35-41cm including the tail)

Can badgers qualify? They shelter underground and get a significant proportion of their food underground as well, I don't know if they stay there 95% of the time though. Wikipedia gives them as going up to 17kg and 90cm in length.
I thought a snake might get the record for length but there don't seem to be many burrowing snakes and they seem to be small. Given the sizes of other non-mammalian tetrapods and how few of them are burrowers whichever the largest underground animal is may well be a mammal.

Why probably a tetrapod?

@Rodrigo Because I didn't think worms got as long JayCkat revealed! Land invertebrates are by and large much smaller than land vertebrates, with even the biggest land invertebrates being only as large as rather small land vertebrates, so I assumed they weren't in the running.

If you accept far-fetched argument, I've got an individual that weight more than a ton! But let's start with a simple example of a large troglodyte.
Blind cave eel
The blind cave eel (Ophisternon candidum) is a troglodite. It is a pure white fish growing to 40 cm, with an eel-like body, no eyes, and a thin rayless membrane around the tip of the tail. I could not find its weight but it probably does not weight much! Just like many troglodite species, its distribution range is very restricted. It only occurs in a single location in Western Australia.

Fungus
Well a fungus is not an animal (but is closely related), so it does not answer your question but I still wanted to mention it. There's an individual fungus that covers 965 hectares. See this popular article.
Ant supercolonial individual
The individual ant is of course not that big but it is not uncommon to consider a colony as a superorganism. You might want to have a look at major transitions in evolution: revisited for a discussion about the concept of individual for social species. Note also that most ant casts spend most of their time underground in the nest.
From wikipedia

Until 2000, the largest known ant supercolony was on the Ishikari coast of Hokkaidō, Japan. The colony was estimated to contain 306 million worker ants and one million queen ants living in 45,000 nests interconnected by underground passages over an area of 2.7 km2 (670 acres). In 2000, an enormous supercolony of Argentine ants was found in Southern Europe (report published in 2002). Of 33 ant populations tested along the 6,004-kilometre (3,731 mi) stretch along the Mediterranean and Atlantic coasts in Southern Europe, 30 belonged to one supercolony with estimated millions of nests and billions of workers, interspersed with three populations of another supercolony. The researchers claim that this case of unicoloniality cannot be explained by loss of their genetic diversity due to the genetic bottleneck of the imported ants.[citation needed] In 2009, it was demonstrated that the largest Japanese, Californian and European Argentine ant supercolonies were in fact part of a single global "megacolony".

Considering a weight of 3.5 mg per individual, a colony of 306 millions ant weight more than a ton (1071 kg exactly) and of course this excludes their constructed habitat which could arguably be considered as part of the individual.

"most ants spend their time underground in the nest" Do you mean they spend most of their time underground, but 95%?

@Rodrigo Depending on the cast, some ants spend a fair amount of time outside the colony. I don't know exactly what fraction of the time of foragers are spent outside and I would suspect it would varies from species to species. So I used a safe phrasing. I edited "most ants" to "most ant casts"


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What is a common body composition in mammals?
The Physiology Of The Racing Greyhound states that most species have about a 40% muscle mass to body mass ratio. Understanding Body Composition puts "optimal fitness" in humans at 16-25% body fat for women and 12-18% in men. These add up to pretty much anywhere from 50% to 65%, leaving 35-50% as more or less unaccounted for. In looking, I have been unable to readily locate any further breakdown, let alone any source that provides a full breakdown. At least Wikipedia is lacking in specifics in this regard.
In adult, healthy mammals, what is a common body mass breakdown into muscle tissue, fat, bone, and internal organs, by percentage of total body mass?
I am particularly interested in wild carnivores, but almost any mammalian species will do in a pinch. Specific examples and citations are appreciated.

If this question is a better fit on some other site, please feel free to migrate.

Think about the variety of body compositions in different mammals, even within a single species, heck across the life span of an individual; a bear coming out of hibernation will have a dramatically different composition compared to a bear going into hibernation.

@KevinCarolan That's why I wrote "adult, healthy mammals" and did my best to allow for answers discussing only specific species. However, if you feel that the answer is "there is no data available", then even though it pretty obviously isn't what I was hoping for when I wrote the question, that could certainly still be a valid answer to the question. (However, I still suspect that the figures quoted at the linked pages must come from somewhere.)


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Zygote Implantation and Pregnancy Detection
In a normal pregnancy, the embryo (blastocyst) implants between 8-9 days after ovulation.  My understanding is that it is able to implant because the fertilized embryo produces a hormone that triggers the uterus to prepare for implantation.

At what point after this implantation can the first signs of pregnancy hormone be detected in the blood stream? (Hospital Birth Detection)
At what point after this implantation does the uterus prevent further embryo implantation


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What signals a ribosome to stop production when the cell is out of available amino acids?
In the production of a protein molecule, there have to be a ready supply of free-floating amino acids. When a given codon for adjoining, say, serine comes up, how are the serine molecules found out of a soup of 20 different types of amino acids?
For example,
Meleagris gallopavo (turkey) small muscular protein
NCBI Reference Sequence: XP_010724014.1  88aa GI: 733873411

 1 mskqpashvk aiqaninipm gafrpgaghp hkrkevtpee veesvpatee ekdkkhlpga
61 iklpgpavnl seiqniksel kfvpkaeq

has 9 alanines, 1 aspartate, 11 glutamates, 2 phenylalanines, 5 glycines, 4 histidines, 6 isoleucines, 11 lysines, 4 leucines, 2 methionines, 4 asparagines, 10 prolines, 4 glutamines, 2 arginines, 5 serines, 2 threonines, 6 valines, 0 tryptophans, 0 cysteines, 0 tyrosines.
So the cell would deplete glutamates much faster than aspartates and obviously infinitely faster than tryptophans. So, as the concentration of glutamates drops drastically with the production of each new turkey muscle polypeptide strand, getting diluted by the nonreactants tryptophan, cysteine, tyrosine, wouldn't the reaction rate get exponentially slow?
And when the last available glutamate residue gets attached, and if it happens before the polypeptide is complete, yet it needs one more glutamate to complete the chain, what signals the ribosome to "stop looking for more glutamates"?

Under normal conditions, it will not run out. Glutamate can be synthesized by the cell, so as long as there is a nitrogen and a carbon source, you can make it. Also the cell is degrading proteins all the time and those amino acids get recycled by the cell.

When cells run out of amino acids, more and more of their tRNAs remain uncharged. This elevated ratio of uncharged/charged tRNAs trigger complex signalling pathways that control amino acid biosynthesis, general reduction of translation, halting ribosome biosynthesis, autophagy (includes ribophagy - digestion of ribosomes) to recycle cells' components, etc. This can be clubbed into general amino acid control (GAAC) and involves the super important regulatory kinase protein called as Target of Rapamycin (TOR) and other transcription factors. The regulation of amino acids level is one of the most basic and important features of cellular metabolism and can be found conserved from yeast to humans. In addition to GAAC, there can be pathways for some specific amino acids as well.
There is not shortage of scientific literature. To start with you can read following article:
http://www.cell.com/trends/cell-biology/abstract/S0962-8924(14)00036-1
http://jcb.rupress.org/content/206/2/173.full

For the most part, there is no signal to a ribosome to "stop looking for more glutamates".  If there is a shortage of a needed amino acid that prevents a ribosome from continuing elongation of a polypeptide, the ribosome simply waits for the needed tRNA-amino acid complex to become available.
The main effect of a lack of amino acids for protein synthesis is to cause inhibition of new initiations of translation of mRNAs into proteins.  This form of translational regulation occurs when a protein called GCN2 senses the lack of an essential amino acid, which causes it to disable the initiation factor needed for a ribosome to start translating a new mRNA strand.

And what about the No-Go decay mechanism?


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What is the name of this flower?

This is from Bangladesh though I am not sure it's native here

Seems Plumeria , of Apocynaceae. Tree?  Add image of leaves. Give better description

Google image search gave me answer as "Plumeria"

I never knew that was possible with Google Images. +1 :D

Google has lot of such very less known functions :P

Not all plants could be so easily identified with google image (till). Maybe this flower's simple shape and color made that easier.

Also known as FrangiPani in Africa. Has lovely sweet scent, I have a white and pink tree in my garden, they are about 8 ft tall. Doesn't like frost

White Frangipani: Plumeria Spp. In Bengali: কাঠ গোলাপ (pronounced Kath Golap). Straight translation is wood rose or pink and they do have rose color.


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Plant species ID, Bangladesh

This plant is quite common in vegetations near swamp areas in Bangladesh. I have included multiple picture hope that compensate for the bad quality.

Any chance you could give a close-up of the flower?

Probably Salvia genus: https://en.wikipedia.org/wiki/Salvia but that's just a guess, I never learned botany.

These pictures are terrible. The best I can tell is that the plant has inconsistently perfoliate leaves. this might help with the ID

I'm from West Bengal and don't know this plant. Since this plant is common to your locality, please upload photos of far better quality. You could take help of any friends's camera if your camera is troublesome, and could take photograph under bright sunlight, that will shorten the exposure time, so less haze. Please provide enlarged image of the inflorescence and flowers. You could give image of interior/ dissection of flower.

maybe this plant grow well in salty condition like Sundarban mangroves.


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What are the branches of system ecology?
What are the branches of system ecology that scientists research in nowadays? Or what can system ecology can applied to, or be used?
I have read its Wikipedia page, but sadly it doesn't answer my question. The most relevant section of it is the "Closely related fields", but again, it doesn't answer my question directly.
From what I understand, system ecology is a sub-field of theoretical ecology. It uses thermodynamic in physics to explain a biological system, with the help of network thinking and some technique of visualization. I have presented this in detail what I understand on my website.

Related: How is the Energy Systems Language used in ecology?

The new keyword yields more results, but they still aren't satisfied me. Thanks for your compliment, may I see your site?

What are the branches of system ecology that scientists research in nowadays? Or what can system ecology can applied to, or be used?

This field is often referred to as systems ecology or ecosystem ecology. It is the study of ecosystems. Thermodynamic principles are often used to construct food/system webs (networks) to understand cause and effect within the system. But I think systems ecology can be considered beyond just a numerical approach to include social (human) dynamics.
A great primer for systems ecology is that by Howard T. Odum:
Odum, Howard T. "Systems Ecology; an introduction." (1983).

I have presented this in detail what I understand on my website.

After reading the post on your website I have some recommendations for complex systems science groups/hubs in which you can look for potential mentors/collaborators/ideas:

International Institute for Applied Systems Analysis (IIASA; Austria)
Santa Fe Insitute (US)
National Socio-Environmental Synthesis Center (SESYNC; US)

so if the question is "what are the branches of system ecology?", then the answer is "food web with application of thermodynamic is the only branch"? Is that correct?

I don't know how to answer how many branches there are, since Systems Ecology comprises theories from all over the place. There are groups which focus on ecological interactions only, and those that attempt to incorporate social-ecological interactions.

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


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Was the Okazaki fragment experiment ever replicated?
Prof said that the experiment "proving" the existence of Okazaki fragments was never replicated.
Is this true? I tried looking on Google Scholar and I cannot find any experiments talking specifically about the existence of such fragments. Wikipedia also doesn't list any other researchers "finding" Okazaki fragments.

You mean replicated in another lab?

Yes that's what I mean

Are you sure your professor wasn't talking about the STAP cell retraction The first author on that paper was Obokata.

It seems that many people have done experiments based on the results of Okazaki fragments and published positive data. This means they suggest existence of Okazaki fragments directly or indirectly. When you say an experiment is never replicated, you have to mentioned what actually they did. Because we never know if the articles mentioning Okazaki fragments show the exactly same experiment or take other experimental approach. http://www.ncbi.nlm.nih.gov/pubmed/?term=Okazaki+fragment%5Btitle%5D

Formation of Okazaki fragments in polyoma DNA synthesis caused by misincorporation of uracil - Brynoff, et.al. Cell; Volume 13, Issue 3, p573–580, March 1978 one of many, but you only need one to disprove your professor.
You do not always need to replicate the exact same assays in order to validate a model. Replicate means reproduce the same experimental results in which to draw the same conclusion. Another person need not reproduce your work exactly, so long as your results were the results of experiments that you were able to reproduce on your own. Standards for Replication in Science

In addition to the wealth of work done on Okazaki fragments, it's important to note that the original work in the 1960s showed how both lagging and leading strands of DNA can be replicated despite the 5' to 3' direction of DNA polymerase. Work starting with the identification of Okazaki fragments underlies much of what has been learned since about replication forks. That might be the best "replication" of all: forming the basis for decades of continued research.


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Which organelle synthesizes glycogen phosphorylase and why?
I know that glycogen phosphorylase is not synthesized in the rough endoplasmic reticulum of liver cells, unlike many other proteins such as insulin receptor, lysosomal enzyme and serum albumin. I would like to know the organelle where glycogen phosphorylase is made and why it is made there.

Protein translation occurs via ribosomes bound to strands of messenger RNA in the cytoplasm; these structures are called polysomes but don't have a membrane surrounding them so you might not want to call them organelles. Polysomes making proteins destined for secretion, for the plasma membrane, or for some organelles (like your examples) are directed to the endoplasmic reticulum via a signal peptide typically near the beginning of the translated sequence. The combination of polysomes and endoplasmic reticulum is what is called rough endoplasmic reticulum. See this Wikipedia page for a more complete explanation of how particular proteins are targeted to their correct locations.


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Why doesn't telomerase activity cause DNA to get longer each time a cell undergoes DNA replication?
Telomerase extends the ends of the lagging strands in order for all of DNA to be be copied. Doesn't this also mean that DNA gets progressively longer each time it undergoes replication? Why is this not the case?

I will assume that you are referring to humans, though much of the research to elucidate telomerase function was performed in yeast.
The first reason is that only a small subset of somatic cells express telomerase. Most somatic cells are terminally differentiated and mitotically inactive, so they are not called upon to replicate their DNA and divide. And when they do, their telomeres get shorter due to the 3' end replication problem.
The end replication problem arises due to the biochemical limitations of DNA Polymerase. Pol requires a primer, 5' to 3', in order to bind to the template strand and begin to catalyze the elongation reaction. So when DNA Polymerase gets to the 3' end of the template strand, it is unable to catalyze the reaction because it doesn't have a free 3' hydroxyl. When the end RNA primer that was used to catalyze the Okazaki fragment just before the 3' end is removed, there is no place left on the template strand to prime, so there is no 3' hydroxyl to begin the elongation reaction and you are left with a 3' overhang of single-stranded DNA.
On the 5' end of the Template Strand, even though the polymerase is able to catalyze the reaction all the way to the end, the end of the chromosome is processed and nucleotides are removed to make a single-stranded 3' overhang on this end. The overhangs are necessary to do strand invasion to form the T-Loops of the telomeres. So every time a chromosome in a cell that has inactive telomerase replicates, it gets shorter.
For the cell types that have telomerase actively express, such as lymphocytes, partially-differentiated stem cells, and the precursor cells to sperm, there is a negative feedback loop based on the length of the telomeres, which in turn regulates the activity of telomerase. Telomerase maintains the ends of the chromosomes, especially in these mitotically active cells, but it will only elongate them to a certain point.

It has long been known that telomere length is regulated by a negative feedback loop (reviewed in Smogorzewska and de Lange, 2004). Long telomeres contain more negative regulators that limit further telomere elongation by telomerase. Because of this, the enzyme preferentially acts on the shortest telomeres in the cell (Hemann et al., 2001; Zhu et al., 1998).
  - Loayza, et. al.; Cell; Volume 117, Issue 3 30 April 2004