text:
How do I effectively visualize data showing change in a lot of samples over two time periods?
I've tallied the number of glands in a plant this year and last year. My full data set has about 20 plants in it (I've reproduced the data from 10 of the plants here). I want to show that the plants this year have had consistently lower gland counts than they did last year, but I don't want to bog readers down with too many data points in their faces. What kind of graph/chart should I use to best show this trend?
        Gland Count
PlantID  2015    2016
1        22.92   19.50
2        11.67   7.12
3        19.67   15.33
4        22.33   12.00
5        20.92   18.58
6        25.83   23.83
7        25.67   32.17
8        22.83   17.00
9        28.42   26.25
10       17.92   16.92

I'd highly recommend this PloS perspective article: "Beyond Bar and Line Graphs: Time for a New Data Presentation Paradigm". @Shawn is on the right lines with their answer.

IMO, this question is off-topic as it is about data visualization and not biology. I am voting to close.

@Remi.b I agree it is off-topic here,, but it might be on-topic for Cross Validated. Migrate?

@RHA This is not a statistics question either. Not suitable there as well. I am not sure which site would actually be suitable because usually questions like this are opinion-based.

@WYSIWYG "Cross Validated is a Q&A site for people interested in statistics, machine learning, data analysis, data mining and data visualization."

One solution is to plot exactly the data you are trying to describe - the delta in your values.
Consider a bar-plot (with confidence/error bars) showing the plant number along the x-axis and the y-axis showing the change in count with +ve and -ve values.
For example, using the data from your question, this visualisation shows clearly that all values bar one decreased from 2015 to 2016 (please forgive the crude diagram lacking titles etc):

Of course it would also be helpful to show a graph of the absolute values and it is obligatory to include a table of the exact values too.

Just had a few mins spare so have added a sample bar chart created trivially in Google sheets via mobile to more clearly show what I tried to describe using text. I'm willing to spend more time creating a less crudely drawn chart if this considered suitable for the OP's purposes.

Two styles of graph come to mind.

A simple 2 layer histogram showing the distribution of gland counts for each year. This is a kernel density as opposed to a histogram, but it gets the idea across.

Line graph with year on the x-axis and gland count on the y-axis, with a colored line for each plant. This would show a little more detail, and would be better if the mean gland count overall did not change much, but decreased significantly among individuals.

The line plots look great and are a very nice and direct way for showing trend for individual plants. However, care must be taken when expanding to n~20 that the graph does not become too crowded [especially when (print)size might be small].

Histograms are a poor choice here due the data not being neither continuous nor ordered (I presume the plant IDs are arbitrary and there is no "plant 1.5"). Overlaying bars could be a reasonable alternative if you can ensure the colours used clearly distinguish between the years.

I agree with the points that @tsttst raises and would add that this style of chart relies on the points/lines being visually distinct but does enable expansion to show data for a third/fourth etc year which is a definite bonus. One alteration to the example would be to also have different shapes (rather than only circles) as well as different colours to help with distinguishing which colour relates to a specific plant number.

Simple comparison of averages
The easiest and most common is to display the mean and standard error for each year.

If you have more years, you might then want to add indication on the graph corresponding to p.values of pairwise comparisons but I don't think you have more than two years.
Below is a short R code that does the job. Note that I estimated the standard error with bootstrap. You might want to switch to use Agresti-Coull method. Personally, I like bootstrap. Make sure to use the standard errors that make sense given the statistical test you performed on these data.
# Function to calculate the standard error
bootstrap_SE = function(x,reps=1e5, SEorCI="SE")
{
    means = vector("numeric",reps)
    for (rep in 1:reps)
    {
        means[rep] = mean(sample(x,replace=TRUE))
    }
    if (SEorCI == "SE") return ( sqrt(var(means)) )
    if (SEorCI == "CI") return ( quantile(means, c(0.025,0.975)) )
}

# Your data
d2015 = c(19.50, 7.12, 15.33, 12.00, 18.58, 23.83, 32.17, 17.00, 26.25, 16.92)
d2016 = c(22.92, 11.67, 19.67, 22.33, 20.92, 25.83, 25.67, 22.83, 28.42, 17.92)

# Calculate the averages
yAverages = c(mean(d2015),mean(d2016))

# Calculate standard errors
SE = c(bootstrap_SE(d2015),bootstrap_SE(d2016))

# x-axis
x = c(2015,2016)

# Make the plot
plot(y=yAverages,x=x, xlab="year", ylab="gland count", ylim=c(min(yAverages-SE),max(yAverages+SE)), xlim = c(2014.4,2016.5), xaxp=c(2015,2016,1))
arrows(
    x0=x,
    y0=yAverages,
    x1=x,
    y1=yAverages+SE,
    angle=90
)
arrows(
    x0=x,
    y0=yAverages,
    x1=x,
    y1=yAverages-SE,
    angle=90
)

Focus on systematic differences
If your goal is to insist on the existence of systematic differences for each plant, then I would recommend @kwah's solution (+1). I don't quite like @Shawn's solution (no offense), I found the graphs complicated, unintuitive for categorical variables and I found that they do a poor job to convey the concept of systematic differences in comparison to @kwah's solution.
If you're thinking at doing a paired-test, then going with @kwah's solution sounds like a clever idea.

Ensure that the visualization will not be misleading (if you intend to use visualization to argue in favor of a consistent reduction):

Count the number of plants, where the Gland Count would be lower in 2016 than in 2015 (to ensure that is lower for most plants).
Then perform a two-sided paired non-parametric test, such as the Wilcoxon signed-rank test, (to test that for most plants there was a change in the same direction), and provide the p-value.

Visualization:

Divide 2016 values of each plant by the 2015 value of the same plant, (perhaps log2-transform), and only plot the resulting values as individual dots along the y-axis, (perhaps add some background shading or line to indicate the boundary between reduction and increase of Gland Count, if it helps the visual understanding)
In case that you are preparing a publication: consider whether the limited gain of information (compared to representation by p-values or a supplemental table) is worth the space

@Jennser: With 20 individuals you could also think about a bootstrapping approach to calculate 95% confidence intervals for the means and/or medians for each year.

@tsttst. Hi. My background in statistics is not very strong, so forgive me if this question is very basic.
I performed a two-tailed paired t-test already on the data to ensure that there was a statistically significant change in gland counts between the two years. Does the Wilcoxon signed-rank test provide substantially different information from the t-test/ would it be more appropriate do use for some reason?

Hi Jennser, actually this is an excellent question (especially as Alex had hinted at your sample size, which might allow further statistical tests).  t-test assumes an underlying normal distribution of the gland counts. Unless there are safe reasons to assume such a distribution (or you can convincingly show its presence), it is better to be conservative, and use the Wilcoxon signed-rank test, which does not depend upon this assumption. -> Wilcoxon signed-rank means that there will be one thing less to worry about   (it yields p=0.06 on the 10 plants, and will likely get even better on 20)


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Why are some plants naturally yellow?
Some plants are naturally yellow. Or rather, they have yellow leaves. This is shown in the following picture, taken from my neighborhood.

I found a Quora article that explains why, but since that is not a reliable source (as far as I know), I would like to have more evidence to this claim. In short, the article claims that plants are yellow due to artificial selection (they look good, so we breed them more). Is this true? Or is there a more plausible answer to why plants are naturally yellow?
In the case of this particular plant, it is not looked after very much, and perhaps only watered once in a while. Won't the lack of chlorophyll affect the plant's ability to perform photosynthesis? I have an alternate theory as to why this plant is yellow, but I'm not sure if that is correct. This plant is very close to a backwater which is highly contaminated with pollutants (the green in the background of this photo is actually weeds and algae in the river). Could that be a valid reason why the plant is yellow?
I was not able to find any other links to this question (they were all about dying plants no matter how I phrased my Google search), but I will edit the question if I get anymore links.

The plant in your photo seems to have plenty of green. It seems that perhaps the new growth is more yellow/green, but without a clear closeup photo of the leaves it's hard to tell much.

Looks like a privet, which often has yellowish young (and old) growth for entirely different reasons.

There simply can't be one answer to this question, especially since I couldn't identify the plant from the photo. However, looking at the different possibilities can be helpful, even if it's just scratching the surface of a very large topic.
Introduction
First of all, why are the plants green? It is common knowledge that the photosynthetic pigment, chlorophyll, gives this color to leaves. This substance has maximum absorption in the red and blue parts of the spectrum, so the spectrum of light transmitted and reflected from the leaf is dominated by the green part of the spectrum. In most plants, the amount of chlorophyll present is far bigger than the amount of any other pigments, and hence we perceive the leaf/plant as "green". However, some plants have other pigments that is the dominant pigment in their leaves, and this causes the leaf to be a different color, "yellow" in this case. Let's take a look at some hypotheses as to why this can be the case.
Hypothesis 1
It should be remembered that chlorophyll is far from being the only pigment found in leaves. For example, carotenoids - which give yellow and reddish colors - are present in plant leaves. There are many carotenoids (according to Wikipedia there are over 1100 known, but that number will continue to grow). The biological roles of these carotenoids are also varied. In the course of the question, we may be interested, for example, in the photoprotective role of carotenoids. They are involved in the deactivation of reactive oxygen species (ROS). ROS can be formed during photosynthesis and can potentially be harmful to cells. Therefore, in conditions of excess solar radiation, plants can increase concentrations of carotenoids to prevent oxidative stress. It has already been pointed out to you in the comments that younger leaves look yellow - this is a common occurrence. The leaf is a very expensive organ, in the sense that the plant invests a lot of plastic substances in its development. So it makes sense that young, growing leaves get extra protection. That is, a young leaf that has not yet formed all the necessary structures (thick enough cuticle, efficient conductive system, etc.) is less efficient in terms of photosynthesis and therefore more susceptible to negative  processes of photodamage. Increased concentrations of carotenoids, among other things, can reduce such risks. If you add to this the small thickness, it is understandable why young leaves often look more yellow.
Hypothesis 2
I have already said that leaves are expensive organs. They have a high protein content, which is very valuable to the plant. If a leaf is damaged or aged, there is a threat of irreversible loss of protein, which would be a great waste. Therefore, in such cases, plants trigger complex processes of removing valuable substances from the leaves. In particular, chlorophyll begins to break down, and the decomposition products are transported to the more durable parts of the plant. This is the reason why leaves change color in the fall, before defoliation. When the concentration of chlorophyll decreases, other pigments, such as carotenoids, increasingly affect leaf color. That's why damaged and old leaves often turn yellowish.
Although, I doubt that in the case of your plant, this process is often the cause for yellow leaves.
Hypothesis 3
Again about photodamage. We have to remember that the capture of photons by chlorophyll is only the beginning of a very long chain of chemical transformations needed for photosynthesis to take place. If the plant is under unfavorable conditions (low or high temperature, lack of moisture, etc), the biochemical cycles can be disrupted. In this case, chlorophyll will continue to absorb photons and enter the excited state, but it will not be able to release this energy further into the cycle. This can be due to many reasons, like the depletion of the plastoquinone pool for example. Under such conditions, the threat of heat shock (if the captured energy is released as heat) or oxidative shock through the formation of reactive oxygen species (ROS) increases. Some plants have developed interesting mechanisms to prevent such adverse effects. In particular, mottled leaf coloration, where green areas alternate with meteolated (chlorophyll-free) areas. Such meteolated areas act as a kind of buffer storage of substances which can be used when the resources of the green areas are exhausted (I am speaking in a very simplified manner here; in fact, these mechanisms are very complicated and it is not quite correct to describe them simply as storage of substances). What is important to answer the question is that some plants can purposely form areas of tissue without chlorophyll, including yellowish coloration. In general, the leaf may look "more yellow."
Hypothesis 4
Before that, we were talking about chemistry. But leaf color is also influenced by anatomical structure. The evolution of the leaf was aimed at maximizing its efficiency as an organ of light capturing and transformation. For example, in the structure of a typical broad-leaf, we can distinguish (conditionally) 4 basic layers of tissues: upper epidermis, columnar tissue, spongy tissue, lower epidermis. All these histological layers contain cells of different shapes. When light passes through the cells, it refracts. That is, each cell acts as an optical lens. For example, the upper epidermis can focus scattered light. Columnar cells often act as photoconductors (similar to an optical cable). The lower epidermis can also act as a reflective layer (so the underside of the leaf often looks lighter than the top). In this case, the light that has passed through the upper epidermis, columnar tissue, and spongy tissue is reflected from the lower epidermis, and is forced to pass through the spongy tissue again. Then it can reflect again from the lower edge of the columnar tissue. In general, geometry and optical properties of leaf cells are also very important for effective light energy absorption. It is important that, passing through the leaf, light is repeatedly refracted and reflected. We know that photons with different wavelengths refract and scatter differently. Therefore, the very anatomical structure and shape of the leaf cells may have an effect on how different parts of the spectrum will be reflected or transmitted by the leaf. One (potential) consequence is, the leaves of some species may be more likely to reflect the yellow portion of the spectrum (and hence be perceived as yellow).
Hypothesis 5
Selection. Indeed, leaves with unusual coloration are perceived as more ornamental. Therefore, artificial selection is often aimed at selecting plants that exhibit unusual leaf color. We have already looked at several natural mechanisms that give yellow leaf color. If artificial selection (by humans) was aimed at intensifying such mechanisms, you could very well get plants with bright yellow leaves. The same applies to mottled and variegated leaves.
Conclusion
The hypotheses I have described are only the tip of the iceberg. Even though it requires a lot of research and investigation to get an accurate answer to your question, I hope these hypotheses have provided you with a general intuition as to why some plants have yellow leaves.

This is a great answer! Thanks for taking the time and effort to post  I will give you my replies to your hypotheses down below:
[1 of 6]

This is very possible. I live in a very tropical climate, and especially since the plant had very tender and soft leaves, the excess radiation would be a very plausible reason for the plant to have yellow leaves.

[2 of 6]

Not much of a chance, but thanks for the info  We don't have autumns here, so virtually all plants are evergreen.

[3 of 6]

Although this is plausible because of the high temperatures, I don't think this is the reason. The plant looks yellow throughout, and there aren't any patches of green like you mentioned, so I don't think this is the real reason.

[4 of 6]

This is very interesting! However, there isn't any way of finding out if this is true (unless you actually try refracting light through the leaves). I didn't know about this before, so thanks a lot for mentioning this

[5 of 6]

This could or could not be true. This plant was certainly not selected for or against, but the whole species could have been used for artificial selection years ago. Anyways, thanks a lot for your information, and I really appreciate it

Thanks for the edits, English is not my first language. I will try to add some links soon to make the answer "complete".

Sure, that would be great

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text:
How much of life expectancy gender gap is caused by social vs biological factors?
I can't find any data/study bringing some light to the components of the life expectancy gender gap. But this should't be difficult:

Men suffer many more accidents and suicides, these are clearly not biological factors, it should be easy to calculate life expectancy gap excluding these.

Men abuse alcohol and tobacco more than women, it should be possible to compare life expectancy for non-smokers and non-drinkers only.

Please let me know if you know of any study.

Men suffer many more accidents and suicides, these are clearly not biological factors debatable. Perhaps men have a higher 'biological' instinct to commit suicide or do risky things. Fundamentally, I don't think there's a possible distinction to be made between things which are 'purely' biological or social.

Agree with user438383. Social factors are biological factors manifested in interpersonal behaviors. If what you mean is something about physiology that intrinsically differs between men and women, somehow excluding (or at least statistically adjusting for) social factors... maybe. (This isn't a judgment on you, people in general are sloppy when they talk about this.) In any case, there are multiple studies that can be found readily, in one second of googling I found this. There are a ton of references in there.

I like your question, and it got me looking for some answers to similar questions I've been thinking about too.
I don't have the full answer; the exact disparity between specific hormones and the differences between mood regulation, but I do have a pretty good research paper that looked into this.
I'd highly recommend anyone and everyone to read it - it's free to access, and even if you only read the abstract you may hopefully take something from it.
In summary though, to answer your question, there seems to be due to (as you said) riskier decision making, but just in young men, and increased stress levels in middle aged men.
I guess the men who make it through to old age (due to socioeconomic, genetic/epigenetic reasons or just pure luck) managed to not be situated on the upper end of either of these spectrums of risk taking and physical stress response, as is most likely thanks to selection pressures. However, these high mortality-linked traits have not entirely been bred out of our populations around the world as many of these high-mortality-associated men do live long enough to pass on their genome, of which some, (roughly half, on average), will be inherited.
These physical, inheritable traits are a bit like radioactive decay: They will decline in the population over many many generations if nothing else happens, but they will never truly disappear. And the problem is that the way that society works is it does in fact exert an external force on many people, pushing them towards making risky decisions (e.g. gambling, impulse buying expensive items on a pay £0 today finance deals et cetera) and to experience much higher daily levels of stress than people can cope with day-to-day. There may even possibly be epigenetic modifications occurring in individuals that would possibly be passed down to offspring if that is the case. This, I believe, alongside the increased media attention recently on mental health, is why we are seeing much more of it these days than ever before, unfortunately.
Anyway, here's the paper: Economic Transition, Male Competition, and Sex Differences in Mortality Rates
I hope you enjoy reading it, and if you have any follow-up questions I'd be more than happy to try to answer them.

The paper is so close, yet never gives the ratio of internal to external causes.

I dug into Eurostat's Causes of Death statistics to come up with this napkin calculation. (I am not a statistician, do not take this data at face value.)

2010 Norway - all LEGG: 4.54
2010 France - all LEGG: 7.14

Minus mechanical causes: suicides, assaults, accidents and drug and alcohol overdoses, etc.

2010 Norway - all LEGG: 4.54 | non-mechanical LEGG: 3,51, decrease by 29.5%
2010 France - all LEGG: 7.14 | non-mechanical LEGG: 6.19, decrease by 15.3%

Assuming that smoking reduces the life expectancy on average by 10 yers and smoking rate among French men and women are 0.349 and 0.319 and smoking rate among Norwegian men and women are 0.17 and 0.154, I reduced the LEGG further:

2010 Norway - all LEGG: 4.54 | non-mechanical, non-smoking LEGG: 3,35, decrease by 35.7%
2010 France - all LEGG: 7.14 | non-mechanical, non-smoking LEGG: 5.89, decrease by 21.2%

It should be possible to do this for alcohol, meat consumption, and many other causes. Again, I am surprised that I can't find any such research.

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Predicting host-pathogen gene interaction networks
Background
What we have are:

~20 genome sequences for a host species that come with gene annotations
Several sequenced genomes for parasite/pathogens of these hosts

Question
What are the possible ways of predicting gene-to-gene interactions or gene regulatory networks between hosts and parasites?

About what kind of interactions do you think? Transcription factors from parasites that influence the host?

thanks for the question. at the simplest level an interaction would involve binding, e.g. gene A that expresses a transcription factor that represses gene B via binding it's promoter sequence would be considered an interaction between gene A and gene B.

there is no way by which you can predict genetic interactions based on sequence alone.. You need more information such as protein-DNA interactions, expression correlation, protein-protein interaction etc

exactly! which is why i am asking the question i suppose, you hinted at some ideas there thank you - could you expand on them?

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Electronic cigarettes (e-cigs), any health risks?
Background:
An electronic cigarette (e-cig or e-cigarette) is a battery-powered device which simulates tobacco smoking patented in 1963 by Herbert A. Gilbert.
It generally uses a heating element known as an atomizer, that vaporizes a liquid solution. Some solutions contain a mixture of nicotine and flavorings, while others release a flavored vapor without nicotine.
Question:
Are there any health risks uniquely associated with e-cigs as compared with normal cigarettes?

There is a really good sciam article on this in April 2014 issue.

Since the question is about risk specific to e-cigarette as opposed to classic cigarettes, what's left is the potential harm from the chemicals in refill-fluids (apart from nicotine): polyethylene glycol, glycerol, alcohol, linalol, flavours. You can find cytotoxicity experiments (e.g. http://www.sciencedirect.com/science/article/pii/S0890623812002833), that show that the most harmful components may be the flavouring compounds. Some other articles (I can't find a reference right now) point out that the moderate heating of the fluid might create harmful byproducts, differently from those in regular cigarette: acroleine, formaldehyde. The use of e-cigarette is probably too recent to have long-term studies that answer your question.

The e-cig possess potential risks for healthy people as well as for a ill ones.
It contains nicotine which still reaches the lungs and causes its negative effects as oxidative stress.
In addition, because one can smoke e-cig anywhere there is potential risk for nicotine intoxication for smokers using e-cig nonstop.
There is a risk of paradoxical conversion from e-cigs to regular ones by teenagers/beginners because starting smoking with e-cigs can increase tolerance to nicotine and raise the need to higher concentrations of it to achieve the desired sensation of "smoking", thus the user can replace the e-cigs to regular and more toxic ones.
In Feb 2014 a special article was published
Ann Am Thorac Soc. 2014 Feb;11(2):236-42. Electronic cigarettes. Potential harms and benefits. Drummond MB1, Upson D which abstract I place here -
"Use of electronic cigarettes, devices that deliver a nicotine-containing vapor, has increased rapidly across the country and globally. Perceived and marketed as a "healthier alternative" to conventional cigarettes, few data exist regarding the safety of these devices and their efficacy in harm reduction and treatment of tobacco dependence; even less is known about their overall impact on population health. This review highlights the recent data regarding electronic cigarette toxicity, impact on lung function, and efficacy in smoking reduction and cessation. Studies show that the vapor generated from electronic cigarettes has variable amounts of nicotine and potential harmful toxins, albeit at levels lower than in conventional cigarettes. The long-term carcinogenic and lung function effects of electronic cigarettes are not known. Although some data demonstrate that electronic cigarettes may be effective in reducing conventional cigarette consumption, there are no data demonstrating the efficacy of electronic cigarettes as a tool to achieve cessation. Until robust longitudinal evaluations demonstrate the safety of electronic cigarettes and efficacy in treatment of tobacco dependence, their role as a harm reduction tool is unclear."

It must be stressed that the only consensus is that "no one knows yet" how much e-cig is more/less dangerous. You cite the risk of conversion from e-cig to real smoking. Other studies show that e-cig could help smoker temporarily or permanently quit (e.g. http://www.sciencedirect.com/science/article/pii/S0306460313003304). And you are right to underline that any product containing a high level of nicotine must me considered harmful a priori.

Please source your claims. You mention a risk of "nicotine intoxication". What's that? The nicotine high is precisely the reason why people smoke. Nicotine is not in itself particularly harmful, the dangers of smoking are primarily related to imperfect combustion and the subsequent production of CO and free radicals, not to the ingestion of nicotine as such. I have read pretty much everything published on the subject and have yet to see any evidence that e-cigs are harmful and have seen a lot of evidence that they are much safer than normal cigs.

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text:
How do mosquitoes maintain telomere length?
While the vast majority of eukaryotic organisms maintain their chromosome ends (telomeres) via telomerase, an enzyme system that generates short, tandem repeats on the ends of chromosomes, other mechanisms such as the transposition of retrotransposons (e.g. Drosophila) or recombination (e.g. Yeast) can also be used in some species.
I would like to know of your thoughts on the possible mechanisms that regulate telomere lengths in mosquitoes.

It seems that the current model is that recombination is the mechanism by which telomere length is maintained in the malaria vector Anopheles gambiae. Here is an exerpt of Roth et al paper that proposed the recombination mechanism:

The insertion of a transgenic pUChsneo plasmid at the left end of chromosome 2 provided a unique marker for measuring the dynamics of the 2L telomere over a period of about 3 years. The terminal length was relatively uniform in the 1993 population with the chromosomes ending within the white gene sequence of the inserted transgene. Cloned terminal chromosome fragments did not end in short repeat sequences that could have been synthesized by telomerase. By late 1995, the chromosome ends had become heterogeneous: some had further shortened while other chromosomes had been elongated by regenerating part of the integrated pUChsneo plasmid. A model is presented for extension of the 2L chromosome by recombination between homologous 2L chromosome ends by using the partial plasmid duplication generated during its original integration.

You might also be interested in this paper: Genes required to maintain telomeres in the absence of telomerase in Saccharomyces cerevisiae and then look at whether there are mosquito homologs of the identified yeast genes that might be involved in telomere maintance.

Cheers @Gergana Vandova Do you think this mechanism of telomere length maintenance would require any specialized enzymes?

mm that's a good question. My first thought would be no, as eukaryotic cells are in general capable of  recombination. I am not really familiar with mosquitoes, but would assume that applies for them as well. But again, it might be possible that there are telomere-specific recombination enzymes. Worth looking into.

May I ask, are you a telomere biologist?

No I am not but I know the principle. You should just read this paper and try see whether you believe the interpretation of their data. Also just wait to see what other people might say about that.

Oh sorry I didn't mean to question your thinking... We are actually working on a manuscript based on genetically engineering telomere length regulation for pest control, the next stage is to carry out experimental work and so we're seeking expertise in telomere experimental work :)

I can actually help you with that! Steve Artandi (Stanford University) is working on telomeres. You might be able to talk to one of his students... Email me at gvandova@stanford.edu if you are interested.


text:
Why not use non-visual self-recognition to test for consciousness in an organism?
Background
A well-known test for consciousness in an organism is to observe its ability to recognise itself in a mirror (see wikipedia article: "Mirror test").
Question
Why haven't I come across a "non-visual" mirror test? I.e. one that involves one of the other senses?
For example, how about testing for consciousness in bats by using an "audio mirror", the premise being that perhaps bats may recognise themselves through echolocation?

(image adapted from here)

There are many ways to test higher brain function in animals. The mirror test is by no means robust. Hopefully some questions will touch on this.

Reading the page you linked, I found this

MSR test may be of limited value when applied to species that
  primarily use senses other than vision. For example, dogs mainly use
  olfaction and audition; vision is used only third. It is suggested
  this is why dogs fail the MSR test. (With this in mind, the biologist
  Marc Bekoff developed a scent-based paradigm using dog urine to test
  self-recognition in canines.[19][41] He tested his own dog, but his
  results were inconclusive.[42])

Emphasis mine.
19 Archer, John (1992). Ethology and Human Development. Rowman & Littlefield. ISBN 0-389-20996-1.
41 Stanley Coren. How Dogs Think. ISBN 0-7432-2232-6.
42 http://www.psychologytoday.com/blog/canine-corner/201107/does-my-dog-recognize-himself-in-mirror

Here are my thoughts.

An animal does not chose to emit some light while they have more control over other signals they emit and may likely just not emit it. So it would not be an easy trait to study.
More importantly, animals (almost) always receive feedback for signals they emit. When a dog barks, it can hear itself! Animals are not used to receive feedback of their appearance through a mirror and therefore they cannot evolve to respond adaptively to the signal they emitted. Any adaptive response to a new signal is either due to luck or to cognitive abilities. The advantage of the (visual) mirror is that it is uncommon and their response therefore necessarily reflects cognitive abilities. Typically, if a bat can response to the sound it produces, it doesn't mean it is able of self consciousness (Theory of Mind), it just mean that bats evolved to recognize the sound they produce.

It's got to be because optical mirrors are relatively easy to produce and field, and it's obvious that it presents a duplicate.
I would be interested in designs for a 'sound mirror' that doesn't just look like a wall under echolocation. Maybe a system to dynamically reproduce a 'sound hologram' of the bat?
A 'scent mirror' would be really difficult to build, not to mention 'ability to recognize your own smell' doesn't really imply higher brain function. Perhaps storing urine from dogs in estrus or stress or something to see if their own scents provoke behavior changes as if it was another dog?
A 'touch mirror'? A 'taste mirror'?
Nearly everything can see, and mirrors are way easier than the alternatives.

I mean a scent 'mirror' using urine from other parts of the female estrus cycle for instance might be interesting, but 'it's really hard and/or redundant' covers your question.

Most animals can see, but not all use sight as the primary way to recognize individuals.  For instance, a person with visual agnosia might conceivably be able to "see" but still fail the mirror test.


text:
What are the possible causes of Lactase persistence?
Lactase enzyme which is responsible for the digestion lactose (a disaccharide milk sugar) normally its production decreases when a young mammal is weaned but mostly Humens continue to produce this enzyme throughout adulthood, this ability is termed as lactase persistence.
What is the reason and mechanism of this phenomenon?
what are the evolutionary basis of lactase persistence?

Welcome  Dr. Uzair Ali. We are expected to show the results of our own investigations into a subject here, you can [edit] to tell us what your searches found and where the sticking points are. You should also take our [tour] and refer to the [help] for guidance as to the ways of any site you post on and see our homework-question policy. Enjoy the Stackexchange network.

Interesting question. This paper, Evolution of lactase persistence: an example of human niche construction, published in a very reliable source, argues that lactase persistence is an example of niche construction: "Niche  construction  is the  process by  which organisms construct important components  of their local environment in ways that introduce novel selection pressures. Lactase persistence is one of the clearest examples of niche construction in humans".  The pdf seems to be freely available from the journal site


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Movement of sperm to the egg

Sperm swims through semen and reaches the haploid egg in the oviduct during fertilisation.

Once the sperm reaches the cervix, through what does the sperm swim through to reach the egg?
Is the uterus completely filled with a fluid that allows the movement of the sperm, or does the sperm only swim through the endometrium (uterine lining)?

Once the sperm reaches the cervix, through what does the sperm swim
  through to reach the egg?

It swims through the cervical mucus. Human sperm swim in a straight path in cervical mucus.

Is the uterus completely filled with a fluid that allows the movement
  of the sperm, or does the sperm only swim through the endometrium
  (uterine lining)?

Yes, the uterus is completely filled with uterine fluid. They are attacked by many leukocytes while being helped by various contractions.
I would suggest reading the Suarez 2006 review. It has very nice information of all stages of sperm moment.


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What are the priorities of blood group that a person with AB group can recieve?
Suppose a person has a blood group of AB. I read somewhere that it is best to transfuse blood of type AB into that person, as opposed to groups A, B, or O. If AB is not available, however, it might be better to use types A or B than O. Why is that?

Blood groups are nothing but the classification of Red Blood Cells based on what particular molecules they have on their surfaces. A person with an A blood group has an A antigen (think of it as a protein) on the surfaces of their blood cells, while a person with a B blood group has a B antigen. People with AB have both the antigens, and people with O have none. The immune system produces certain antibodies that helps protect the body against foreign invaders. An antibody is a substance that helps kill foreign antigens. An antibody in a healthy individual will not attack the body's native cells. Thus, people with an A blood group only have anti-B antibodies, and vice versa. O people have both the antibodies and AB people have none.

This means that if a type A person receives type B blood, the newly introduced blood cells will be destroyed, due to the presence of anti-B antigens. Similarly a person with O cannot receive AB blood due to the presence of both antibodies in their plasma. However, AB people can receive any blood type, since they have no antibodies in their plasma. O people can donate to anyone, since they have no antigens in their RBC, but they can only receive donations from other O people.

This is why people with an O blood group are known as universal donors and people with an AB blood group are known as universal receivers.
A similar effect occurs with the Rhesus Blood Groups (+ve and -ve), where Rh+ people can receive either type, but Rh- people can only receive Rh- blood. Thus, Rh- can donate to either type, and Rh+ can receive either type. This means that O- can donate to any blood type, and AB+ can receive any blood type.
In terms of your question, suppose that a person with blood type AB needs to receive a blood transfusion. As explained above, a person with AB can only receive blood of type AB. This is why it's the "highest priority" to use blood of type AB. Although not medically recommended, A or B type blood has a better chance of compatibility with the receiver than type O, since type O has both the antibodies while type A or B only have one. Thus, the AB has the "highest priority" with type A or B having more "priority" than type O.
Hope this answer made things clear. Cheers!

Well illustrated answer - I think what the OP meant with 'priority' can be explained in the following scenario: Let's say you have a certain amount of 500 ml blood of each of the four types, the types should be prioriticed according to the blood type distribution of that country and the donor/receiver ratio - a simple mathematical formular based on availability and the blood type distribution of possible receivers in need. But that's just my assumption..

I read the question, and I think I understand what the OP meant. Suppose a person has a blood group of AB. When transfusing blood to that individual, it is best to use blood of type AB. If AB is not available, A or B might be better to use than O. I don't think it's recommended to use anything other than AB though. Perhaps it's worth a try if the condition is critical and no AB blood is available.


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Where is energy stored in a molecule of ATP?
Where is energy stored in a molecule of ATP?
How is energy released from a molecule of ATP? What specific bond needs to break
What is the difference between ATP and ADP?

Define pigment

a.  What pigments are found in plants?
b.  What colors of the Visible Spectrum do chlorophyll pigments absorb? Not absorb?
c.  What would you expect to happen if a plant was grown under a green light? Blue or red light?

Label and define the following:

a.  Granum:
b.  Thylakoid:
c.  Stroma:
4a-3 Explain how photosynthetic organisms use the processes of photosynthesis – Ch. 8-3

Define autotroph, give an example
Define heterotroph, give an example
Define photosynthesis and write out the equation for photosynthesis (both the word equation and the chemical equation – you need to be able to recognize the chemical equation)
What are the three factors that affect the rate of photosynthesis, and how does their absence or presence affect the rate?

The rate at which a plant carries out photosynthesis depends in part on its environment. Plants that grow in the shade, for example, carry out photosynthesis at low levels of light. Plants that grow in the sun, such as desert plants, typically carry out photosynthesis at much higher levels of light.
The graph below compares the rates of photosynthesis between plants that grow in the shade and plants that grow in the sun. It shows how the rate of photosynthesis changes with the number of micromoles of photons per square meter per second (μmol photons/m2/s), a standard unit of light intensity.

a.
When light intensity is below 200 μmol photons/m2/s, do sun plants or shade plants have a higher rate of photosynthesis?
b.  Does the relationship in question 1 change when light intensity increases above 400 μmol photons/m2/s? Explain your answer.
c.  The average light intensity in the Sonoran Desert is about 400 μmol photons/m2/s. According to the graph, what would be the approximate rate of photosynthesis for sun plants that grow in this environment?
d.  Suppose you transplant a sun plant to a shaded forest floor that receives about 100 μmol photons/m2/s. Do you think this plant will grow and thrive? Why or why not? How does the graph help you answer this question?
4a-4 Describe the light-dependent and light-independent reactions of photosynthesis (comparison of products in each) – Ch. 8-3

Answer the following questions regarding the Light Dependent reactions:

a.  Where does the energy for the light dependent reactions come from?
b.  Where within the chloroplast do the light dependent reactions take place?
c.  What pigment is contained within this structure?
d.  Define photosystem
e.  The light dependent reactions start in which photosystem?
f.  What are the products of the light dependent reactions?

Homework questions and trivial questions about basic biological concepts are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy.

So you just decided to copy-and-paste your test here without even trying to answer any of the questions? Lovely...

As far as I know the polyphosphate stores the energy, and the nucleoside is just a flag to know where it delivers the energy to.

The energy is "stored" in every bond. The primary bonds that break are either the first and second phosphate or the second and third phosphate creating AMP or ADP.
The middle letter stands for Mono, Di or Tri (meaning 1, 2 or 3 phosphates).

Please read our homework policy before answering questions like this.


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In Sanger sequencing, why do we resort to cloning? Why doesn't PCR suffice?
I understand that in Sanger sequencing we can clone our fragments with the help of e.g. bacteria to make multiple copies of our fragments for further analysis.
I also understand cloning can be a bottleneck in Sanger sequencing - and partly prompted the development of NGS methods.
But doesn't PCR do just that, make multiple copies?
What am I missing?

Possible duplicate of Sequencing from PCR

@MarchHo: but... that question is not about Sanger :-|

In some cases, you do not know the sequence you are looking for--functional cloning, genome projects, cloning DNA/RNA binding to proteins you are interested in etc.

In addition, PCR can amplify any sequences having primer sequences at the both ends. Sometimes, you are not sure if you get a right sequence from crude DNA mixtures.

This is impossible to answer without knowing the context of what you are trying to sequence.  But as someone who has sequenced literally thousands of exons from genomic DNA, cloning is obviously not required for every single Sanger project.  I just used PCR to amplify the regions I cared about,.

You can use PCR products in Sanger sequencing; it is very common. Using PCR products instead of cloned genes does raise a set of problems that are less of a concern than with cloned sequences, such as the presence of incomplete or incorrect PCR products, but there are standard and simple solutions for most of these concerns.

And other minor issues like eventual need for cloning, possibility of using standardized sequencing primers post cloning (like T7) etc.

The error rate of PCR is still very high in comparison to natural bacteria DNA replication of its plasmids.
Natural bacteria DNA replication has an error rate of approximately 1 in 10 billion, and the best PCR polymerase commercially available (Q5 from NEB) has an error rate of approximately 1 in 1 million.
Therefore, cloning fragments into bacteria and sequencing the cloned plasmids ensures that you have the correct sequence for further downstream experiments, since the error rate of natural plasmid replication is far lower. With PCR, you are likely to have some errors introduced due to the higher error rates. This becomes more and more likely with increasing numbers of PCR cycles as well as increasing PCR amplicon lengths.
The fact that the PCR amplicon sequences correctly does not mean that DNA cloned from the PCR amplicon is correct. Therefore, if the PCR is intended for downstream experiments, it is best to sequence the cloned plasmid instead of the amplicon.
In addition, as WYSIWYG has pointed out in the comment, having the PCR amplicon cloned into a plasmid would also allow for the plasmid's regions flanking the cloning site to be used for sequencing. This allows standard sequencing primers on the plasmid to be used, instead of having to design new sequencing primers for each PCR amplicon.
Furthermore, since Sanger sequencing requires the primers to bind ~50-100bp upstream of the region to be sequenced, cloning the amplicon into a plasmid would also allow short amplicons to be sequenced in a single read, instead of requiring a forward and reverse read for sequencing a PCR amplicon.

This is not correct; or at least, it's only partly correct.  It's true that PCR has a much higher error rate than bacterial replication.  But that is not a major concern when sequencing pooled DNA from a PCR reaction, because while each amplified strand may have errors, the average of the amplification is still the original sequence, because only a tiny fraction of the strands have a specific error in a specific place.  However, if you first amplify the DNA with PCR, and then clone it and sequence it, you have the worst of both worlds, because you may well have errors in the piece you cloned.

@iayork While it is true that directly sequencing a PCR product is doable and is frequently done, the vast majority of cloning is done to transfer a piece of DNA into a vector for expression of some kind. If you sequence the PCR product before cloning it, you will need to sequence it again afterwards, since there is risk of the individual cloned fragment being incorrect. It makes more sense to sequence a known single clone instead. From what I know, PCR product sequencing is usually done either to check that the PCR has worked, or to sequence short stretches of DNA in long vectors.

I think you have a rather limited view of sequencing; I have been using PCR for sequencing purposes since 1992, and I am far from alone.  In any case, the original post wasn't asking how to clone, they were asking whether there was a technical reason for cloning with regard to Sanger sequencing.  There isn't one; sequencing from PCR gives highly accurate sequence, and your explanation of error rates is misleading.

@iayork I added a number of technical reasons for cloning. I would consider these to be good reasons to sequence a cloned plasmid instead of the PCR amplicon directly.

You have still not corrected your misleading comment about PCR error rates, though.

@iayork I don't consider the error rates misleading. The point is to show that PCR produces errors in a nontrivial proportion of amplicons, making it necessary to sequence a number of clones derived from the amplicon if you wish to obtain an error-free product for downstream experiments. Relevant to your own answer, one "standard and simple solution" to the issue of errors in PCR amplicons is to clone and sequence them.

Yeah, but you're missing the point.  Sequencing the PCR product doesn't show the errors.  It's only a problem if you want to clone the product.  The original question is whether you have to clone in order to sequence.  You're answer is saying "You have to clone because if you don't clone, then when you clone there are problems".  Seriously, this is very basic stuff.


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Why do children prefer sweeter foods?
As we get older, we tend to lose our sweet tooth and become more tolerant to bitter foods, like vegetables. However, I never understood how this works. Why is it that children prefer sweeter foods, even some that adults may consider "too sweet"? In fact, is there any reason they would also dislike bitter foods, even when they can be beneficial to their health?
This just seems bizarre to me that the body would start out craving sweets and lose this later on. Are only humans like this? Is there anything suggesting that younger animals prefer sweet foods too, but like them less as they get older? Does this have any biological advantage or is it just random?

Your body start out craving for milk and lose this later, it often lose ability to digest milk at all. Why this should be bizarre? Human body needs change in time. Young children require a lot of energy to grow and to learn.

@Colombo explains one reason that I think is obvious. However, there has been some research done on this.
One other reason is because it would provide an evolutionary advantage in environments where calories are scarce. Also, sugar actually acts like a pain reliever. Studies show that giving sugar to babies and children during surgery act like a pain reliever.
The sweet tooth could be controlled by hormones secreted from the growing bones. Some common hormones like insulin also affect sensory centers in the brain. This explains why the sweet tooth goes away as an adult.
Reference
NPR -http://www.npr.org/sections/thesalt/2011/09/26/140753048/kids-sugar-cravings-might-be-biological

other reason is because it would provide an evolutionary advantage in environments where calories are scarce. Should't then fat taste sweet? fat = 9 cal per gram, sugar = 4.


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Why do we like music?
Music is, of course, just a sequence of sounds. Sounds are vibrations in the air, which our ears detect. So why do we find certain sequences of sounds to be appealing? What makes us want to hear these sounds (turn on a radio, for example), or make these sounds on our own (sing/play an instrument)?
Heck, why do we even move our body strangely when we hear certain music (dancing)?

Just a side info on the evolution of music appreciation: The field of evolutionary musicology is a field in the junction between evolutionary psychology and biomusicology. In evolutionary musicology (and in evolutionary psychology) empirical testing is very complicated and therefore, today we can only think and make hypotheses but we can't test them. So always take with a grain of salt what you read in those fields.

I assume our enjoyment of rhythm originates with the sounds we hear all around us (stop and listen some time!). I would also assume that lyrics originated as a useful way to pass on information and continue to be an effective form of communication. Enjoyment of harmonies and melodies must be much more complicated since they seem to be less consistent (perhaps these, too, are related to the sounds heard in varying natural environments?). Most curiously, though, is music's effect on our emotions (e.g., see Salimpoor et al. 2011).

Just a note, to say humans interpret sound in a similar way to animals, and they process music using the language and voice processing networks of the brain, and for that reason humans hear music far differently from animals.

DISCLAIMER: Usually I do research before I write. But the factual basis on this topic are pretty... meh.. So this time it was the other way around. So take note that the arguments here are just ideas. If you find references to empirical studies that support/deny these claims please leave a comment!
Turns out that I wrote a whole frickin' article in a short time. But I think this topic deserves it.
Short Answer:

Music is a primitive form of language. Both are sound patterns meant to convey information. Humans are drawn to music just as they are drawn to language.
When compared to visuals, noises are harder to localize and can't be back-checked. It's essential for survival to get the most information out of very little sound. That maybe explains why humans are so easily fascinated/obsessed with even slightest details in melodies and rhythms.
Mothers share their emotional state with their baby via endorphins, stress hormones etc., and that baby may associate these emotions with her heartbeat in the womb, learning a sense of rhythm.

Long Answer:

What came First? Talking or Singing?
What is singing? Singing is like talking, but with a melody. And when singing, we don't really care that much what words are used. That makes singing an easy way of conveying emotions between each other, much like a "primitive" form of language. Look at the asian language: Words shift their meaning when changing pitch.
So I had this idea that our complex language must have evolved after we began to sing. And it turns out that I am not the first (this article).

Even Charles Darwin "talked about our ancestors singing love songs to each other before we could speak articulate language," Patel says.

I think this makes it clear that our love for music is deeply rooted in our love for language.
This article also claims music is deeply rooted in evolution:

Music making seems to occur, in some form or another, in all human societies. Although musical behaviour varies in sophistication, music itself seems to be universal across all human cultures and plays a key part in rituals of all varieties, and the origins of these practices seem very ancient.

Detecting Sound-Patterns Is Like Learning a Language
Human hearing however, is unique among to animals. We have evolved to learn and speak a ridiculously complex language. And toddlers do not seem to have any issues by learning that language all by themselves. When mommy's lips move, sounds come out. And at some point they recognize a patterns of speeds, noises, repetitions, etc. They all represent and define things that we see around us. And learning these definitions is fun, because it helps them getting exactly that thing that they want right now.
My point is: Music is basically noises arranged in a complex pattern. But other than language, these patterns have no specific meaning. Still, that does not stop our inner child from trying to learn those patterns. After all, those patterns might tell us something.
Small Sounds Must Elicit Big Emotions
Hearing is essential to survival. Hearing must elicit an emotional response in the right situation in order to regulate our behavior. A hissing sound in a bush means "don't stick your hand in there". Screaming means problems. Yawning means sleep. Whispers mean secrets. Laughing means happiness.
But the problem with sound is, sounds can not be perceived a second time if we want it. If we see eyes looking at us from between the trees, reality allows us to look again and check. Noises however are harder to localize, so they are often singular events. And they can easily be missed or ignored. And that can have dramatic consequences. That’s why I think that the control of hearing over our emotional state must be so strong, so that even small sounds are allowed to override our current emotional state. It’s essential to survival, being able to instantly switch from e.g. relaxing at the campfire to standing up and checking in on the sound of branches breaking.
And I think that this idea goes even deeper. It’s not just branches breaking that should freak us out, but all those sounds that humans make. After all, the only dangerous „predator“ left to humans are humans. And humans can be hard to read. What did he say? How did he say it? Is he lying..? Did I say something wrong? Does he/she love me? And to read a human successfully, we must be able to discern even the slightest shifts of volume, pitch, tone, speed, etc.
My point is: We love hearing details, since it has always helped us to survive. And Music is full of details that are just waiting to be over-interpreted.
An Unborn Child may Associate Heartbeats with Emotions
But how do we learn to enjoy music in the way that we do? Why do minor chords sound sad, and major chords happy? I don't know the answer, but I might explain why we are able to associate different rhythms with emotions.
The first sound we ever hear is the heartbeat of our mother. It can be fast or slow. And that has a meaning. When mommy's heart is beating fast, she's also getting warmer. Also, the levels of hormones (Stress hormones, endorphins) in her blood change. In other words: A mother shares her emotional state with her baby. In fact, a mother's stress can change fetal heartrate, too (Monk et al. 2000).
And I presume that the child is able to associate different heartbeat frequencies to stress/happyness in the womb already. That might be the reason why we perceive slow rhythms are calming and faster rhythms as exciting.

As a musician, I find it difficult to explain this empirically. However, there are certain mathematical avenues one can take to analyze why exactly certain combinations of notes sound consonant- Andrew Huang has an excellent introduction video to this concept. If you're interested on why certain intervals, like the diminished 5th, sound grating, while octaves or perfect fifths are more pleasing to the ear, read a bit about natural harmonics. This, however does not serve to explain why music is so enjoyable to us.
I personally hold the belief that it is a largely cultural thing. There are many Muslims who are repulsed by music of all forms- their religion forbids it. while I may tap my hands in rhythm to a song played on the radio, someone from a muslim background may attempt to turn the music off. Our enjoyment and understanding of music is based entirely off of our expiriences, culture, and beliefs.
To expand on this, there are different systems of music, as well! Eastern music theory is far different from Western theory. While Western music often uses a 12 tone scale, (12 notes per scale), Eastern music, particularly Arabic music, utilizes microtonal scales that may sound displeasing to a western-trained ear. In my mind, this cements the concept that the expirience of music is a largely cultural thing. For more information on this, you can read about the Oud, an arabic microtonal instrument. there are plenty of youtube videos that exlpain this in an easy to digest manner.


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Can cancerous cells reach the Hayflick limit?
This may be a stupid question, but I've been wondering. Each time a cell divides, the telomeres on the chromosomes shorten. If this goes on for long enough, the chromosomes will no longer have telomeres and the chromosome will deteriorate. Thus, the average cell will divide between 50-70 times before cell death.
Cancerous cells divide uncontrollably fast, of course. But can they reach the Hayflick limit? Considering how quickly they multiply, it shouldn't be impossible, right?

Most tumor cells express telomerase, which rebuilds lost telomere sequences. Coincidentally, this is also how undifferentiated stem cells divide forever.

@MattDMo -- why didn't you make that an answer?

@JennD. I might when I have time.


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Polar bodies fertilization
Suppose a sperm fertilized a 2nd polar body( haploid) is there a chance of somewhat normal development?

The 2nd polar body contains almost no cytoplasm, so if only this body is fertilized it contains no maternal genes to guide the development and moreover not enough nutrients. So this wouldn't work. "Source"
Moreover, there wasn't reported even any case of "twin" resulting from the fertilization of 2nd polar body according to this article
There was reported case of twins formed by a mass of fertilized ovum and fertilized (diploid) first polar body. Source
What could happen is that if both polar body and oocyte are fertilized, these two cells merge and form tetraploid embryo. Which is sometimes able to form fetus (sometimes just ends as mola hydatinosa), but definitely not able to produce a viable child in humans.

Mpribis is 99% correct, except that the polar body does indeed contain the same amount of maternal genes as the secondary oocyte (remember, it's the product of the second division--from diploid to haploid). But like Mpbris said, since the second polar body is nutrient-poor, and lacks full complement of organelles, the odds of it remaining viable if it were fertilized are vanishingly small. Such "polar body twinning" is theoretically possible, but has yet to be documented as of the the time of my writing this.


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Conjoined twins formation theory
is it theoretically possible to take two fertilized mammalian eggs and push them together to make conjoined twins? How about forming non-identical conjoined twins?

The more generally accepted theory for conjoined twins is fission, in which the fertilized egg splits partially. So I don't think that what you said is possible. Not seen this happening before... even the conjoined twins share same placenta indicating they originate from same fertilized egg.


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Is it safe to consume foods that are hot enough to scald your skin if you touch it with your hands?
Coffee is usually served at temperatures that would burn your hands if it spilled on it.
Is the inside of your mouth not affected by the same biological process as that which causes your skin to burn?

I think this is more of a physics question: the volume of a single sip (about 20ml) is so small that it cools down before it damages the lining of your mouth. If you put a couple of drops of coffee at the same temperature on the back of your hand it wouldn't burn you either, but if you dipped your hand in it would be a different story.

But when you sip it, the first second of contact the water doesn't have a chance to cool yet. I don't think 20 ml of 180° won't burn you

To be honest 20ml was probably an overestimate (caused by not yet having had my coffee) - when drinking very hot drinks I suspect a sip is considerably less than 5ml. And I frequently burn my mouth on hot coffee despite this.

(Ha ha) But the question is about water temperature that your mouth feels comfortable with but is still nevertheless too hot to touch. Are you, or why aren't you, damaging your mouth


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Would gargling with salt water every day increase blood sodium levels?
Would gargling and rinsing with salt water every day for a few minutes increase your blood sodium levels? Considering the fact that sublingual medication is a very effective way for introducing substances straight into your bloodstream very quickly.
Below's a link to a study on Pubmed about this issue. Does anyone here have access?
https://www.ncbi.nlm.nih.gov/m/pubmed/3474267/

Do you think this question would be more suited for the medical science stack exchange?

Personal medical questions and health advice are off-topic on Biology.

@David it's a general question about sodium levels with regards to gargling salt water


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Do pigeons have the smallest legs-to-body ratio of any bird?
Proportional to their size, do pigeons have the smallest legs of any bird?

What measure do you want to use for size? There are likely different answers depending.

Here's data on body mass and limb length for 163 species of birds (including pigeon):

The information you really want is the ratio of the two. The shortest legs per mass are not quite all flightless birds:
                             Common Name   Hind   Mass Leg_per_kg
1                                Ostrich 1256.7 94.210   13.33935
2                           King Penguin  326.2 13.650   23.89744
3                                    Emu 1036.1 40.670   25.47578
4                           Whooper Swan  405.0 10.675   37.93911
5                       Macaroni Penguin  197.7  4.819   41.02511

whereas the longest legs per mass are:
159            Yellow-Bellied Flycatcher   51.3  0.011 4663.63636
160                   Common Treecreeper   41.8  0.008 5225.00000
161                 Whiskered Flycatcher   51.2  0.008 6400.00000
162        Southern Beardless Tyrannulet   47.5  0.007 6785.71429
163            Ruby-Throated Hummingbird   21.8  0.003 7266.66667

The pigeon falls somewhere near the middle:
106                        Scaled Pigeon  108.7  0.260  418.07692

Swifts are actually down near the bottom:
153                        Chimney Swift   49.9  0.023 2169.56522

While they do have tiny legs, they are actually quite long for their body mass.
Of course if you chose a different measure of size, then these relative numbers would be all different.

Length per kg in my opinion is a really really bad measure. In general, body length increases with the cube of mass. This measure just tells you the biggest bird. Pretty obvious if you look at the leg length of on ostrich - those are long legs, almost half the height of the bird, even when including a very long neck. That doesn't seem to be at all what OP was asking for.

Technically it's exactly what the OP asked for ("proportional to their size ...") but I agree it's probably not what they actually wanted to know. I upvoted for the interesting chart, but was tempted to downvote again because there's no reference. Where do the data come from?

@iayork I collected the data from the Museum of Comparative Zoology (Cambridge, MA).

@BryanKrause Agreed, which is why I said that if you picked a different measure of size, you would get different results. I can think of good reasons not to pick any of the other obvious possibilities: wing length (penguins, ratites), trunk length (penguins, loons), mean vertebral length (swans, geese, herons, etc.), synsacrum breadth (Anseriformes). So given the tradeoffs of picking any proxy for size, mass is as good or as bad as any other, as long as you interpret the results in that context.

That achievement probably belongs to the Swifts, specifically known for their short legs. Their name Apodidae derives from the word for "footless" in Greek.


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Can high energy photoelectrons damage cell membranes?
I've read that in addition to ionizing radiation causing damage to DNA through direct absorption, but DNA can also be damaged through photoelectrons with enough energy.  The thing I was wondering is what kind of energy (in electron volts) would or might photoelectrons need to damage or penetrate the cellular membrane (like if x-rays excite photoelectrons outside of cells)?


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Clarification of the brightness of bioluminescent proteins
One basic thing I'm not too clear on, which I would like to be clear on, is the brightness per mass unit of GFP or luciferase.  I was having trouble finding a resource that would state the brightness at least for standard GFP or luciferase per gram, for example.  Is there a basic rule for the maximum brightness for either of them?  I'm aware this might end up being a vague question, but I could use help clarifying this.  I found brightness as a product of the extinction coefficient and quantum yield but I wasn't sure how to translate that to watts.

Search quantum yield

So I understand that the quantum yield is the ratio of photons emitted to photons absorbed, but I still don't know what's generally the maximum brightness of at least certain kinds of GFP under a sufficiently bright light source, if that question makes sense.


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Acoustic characteristics of thoracic diaphragm
I am looking for any kind of information about the acoustic characteristics of the thoracic diaphragm. In particular, I'm looking for characteristics which will allow to differentiate it from other muscles using ultrasound, MRI, CT, etc.
References to the literature are especially welcome.

One identifies the diaphragm on ultrasound/CT by thinking about the anatomy and appearance (e.g. on ultrasound it's a thin hyperechoic structure between the liver and lungs). I'm a bit unsure what you're asking as unless you get close to the body wall there's not many other muscles in that area to confuse it with.


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How does one find the corresponding SNPs in the pair of chromonosmes in a FASTA file?
You might say I'm an amateur bioinformatician, or trying to become one.  I have a BAM file, from which I have succeeded, using UGENE , in extracting consensus data in FASTA format.  I now see a single series of nucleotides, and their complements, for each chromosome.  What I don't see is two corresponding sequences.  SNP data (e.g., SNPedia ) cites (if I understand it correctly) the SNP at the same site on each chromosome in the pair.  I don't know how to determine my variation, since I see only one nucleotide at any given site, not the pair.
Pretty sure I'm missing something fundamental here.  Thanks for any help navigating this jungle!

"Two corresponding sequences": corresponding to what? What SNP data? What SNP should be on both chromosomes? The link you gave seems to be for a SNP that can be either hetero- or homozygous. Why are you assuming it is homozygous in your data? What are your data? Please [edit] your question and clarify, it is very hard to understand what you're asking at the moment.

Sorry if I'm not expressing myself well... I'm kinda new to all this.  I am, in effect, talking about what I should expect to see in the case of a heterozygous SNP.  The question is simply this: If the particular genome I am examining happens to have a heterozygous SNP at some site, let's say (C;T), then how/where would I expect to see this in my data?  A consensus reflects the more prevalent read at that site, but, in this case, I would expect about 50% of the reads to be C, and 50% T... so the consensus isn't useful.  Am I wrong?

If you are looking for simple one off queries it might be better to load the BAM file and a relevant reference genome into a browser like IGV and simply navigate to that specific position.
For some data I had lying around a heterozygous SNP would look like the picture below, there has been an A to G SNP and a C to T:
For longer lists of queries I would take a look at BEDtools: https://bedtools.readthedocs.org/en/latest/content/bedtools-suite.html
If this does not help you, I recommend you ask your question on https://www.biostars.org/ There you will find help from true bioinformaticians.

Right, so I've been looking at the BAM file, but I've yet to find any instance of a site where I see 50/50 reads of two nucleotides (e.g. 50% C and 50% T).  Is this what I should expect to find in the case of a heterozygous SNP genotype?  If so, then should I just ignore the consensus and just look at the BAM file?  I'd just like to validate that I am on the right track here...

I adjusted the answer to include a picture. Hopefully everything is more clear now

I wouldn't necessarily expect regions of heterozygosity to be apparent from a consensus fasta.  I'd eyeball if you know some potential sites, or run your .bam through something that will call SNPs.


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What is the risk of permanent brain damage and/or long term cognitive effects from a single exposure to extreme altitude?
I have read some of the papers on the subject of the permanent brain damage induced by high to extreme altitude (5000m-8000m) climbing. The evidence seems contradictory. One paper (Fayed 2006) found significant post expedition MRI findings including white matter hyperintensities but this finding seemingly is in doubt for lower altitudes where studies other than this one have only picked up more temporary changes (usually in white matter fraction). The evidence for 8000m+ climbs seems clearer, in that it is clearly more damaging.
I would consequently be interested in any views based on the available evidence of the risk of permanent damage of a single 'normal' sojourn to 5000m to 7000m if acclimatisation profile is reasonable and HAPE / HACE do not obviously manifest.
The brain is evidently highly sensitive to hypoxia and there is some well evidenced impact on cognition whilst at high altitudes but do mountaineers exposed to these sub 8000m altitudes risk longer term damage?
Some relevant papers:
Fayed et al 2006 paper that was extensively picked up in the media but did not do pre expedition MRI: https://www.semanticscholar.org/paper/Evidence-of-brain-damage-after-high-altitude-by-of-Fayed-Modrego/f182e5c8a73b505e66e50bcb671ee8cf86c0f6f5
Fan et al paper on reversible abnormalities https://www.nature.com/articles/srep33596
Kotke et al paper finding limited evidence of structural damage (Morphological Brain Changes after Climbing to Extreme Altitudes--A Prospective Cohort Study) https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0141097
Dr Peter Hackett study on Denali - https://www.boulderweekly.com/adventure/this-is-your-brain-this-is-your-brain-at-altitude/

Your references aren't contradictory. The papers you cited (and others) all show the risk of permanent brain injury is obvious. (The Nature article showed persistent changes.)The pre-/post-HA MRIs study supports the Nature study. Brain changes at lower altitudes were observed in the late 1890's and in Fayed's later papers. The answer is most likely "high"). But does this brain damage manifest in permanently diminished post-climb capacities? That would be my question.

I do think the evidence is unclear e.g. Kottke et al (up to 7000m). No white matter hyperintensities nor grey matter atrophy but a decrease in brain WM fraction. Foster et al 2015 (3 weeks at 5000m) observed a GM reduction, while WM was unchanged.
Zhang et al (6200m): "disturbances mainly in cerebral WM, showing compromised fiber microstructural integrity".
Hackett study detailed here (https://www.boulderweekly.com/adventure/this-is-your-brain-this-is-your-brain-at-altitude/) found increased WM volume and subcortical climbers in 6% of climbers of Denali (6300m); the rest normal on MRI

So one paper found a decrease in grey matter but no decrease in white matter. Other papers found a decrease in white matter but no decrease in grey matter. Some papers found largely normal MRIs except when obvious severe AMS developed. Some papers found certain cognitive functions (e.g. motor or memory) had been affected, others found nothing. Is neuroscience always like this?!

@Anothercanary Yes, science with small samples is always like this. Those results need not be contradictory as they seem.

From my limited reading of the literature, it seems fairly clear - even with the small sample sizes - that permanent brain changes (call it damage if you will) do occur at lower altitudes, especially in novices. Do they occur in everyone in the same way? No. Do they matter? You'd need longitudinal studies (neuropsychiatric evaluations at intervals for years) to answer that. The longer the study, the more confounding issues result, muddying the conclusions. @BryanKrause, you're a neuroscientist, no? am I missing something?

Thanks, that makes sense. It's a shame there is no definitive view as it makes individual decision making about HA trips difficult as you're missing one side of the risk-reward equation. This study hypothesises: "There may be various reasons for these inconsistencies: different high-altitude experiences of climbers, manifestation of neurological disturbances during or after the expedition, [or] the use of different MRI techniques." https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1468-1331.2008.02243.x


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Telomerase and End Replication in Eukaryote
Here is a picture of using telomerase in solving end replication problem (Courtesy: Molecular Biology of the Cell, Alberts, Garland Science Pub.)

Now lets consider the $3'$ end here, we are extending this end, and then using DNA Pol we extend the $5'$ end, even though the $5'$ end would still be truncated w.r.t $3'$ end but the original strand would be maintained. Now we know that this Telomerase enzyme is active in stem cells but NOT in somatic cells. So far so good.
Now if I consider the above layout in more detail: Lets consider what happens after the above replication cycle:

This is because in the 1st replication cycle, we have added more nucleotides to $3'$ end, as well as possible few more nucleotides to $5'$ end as well. Now this would create overhangs on each $3'$ end of my DNA. And I am confused on these overhangs. Either the replication machinery deletes these overhangs ( which I am not sure whether it happens), OR the second replication would start on these overhang DNAs. A possible issue with the second approach (i.e replication with overhangs intact) is that the length of each strand would keep on increasing with each replication cycle as we are keep adding new nucleotides to $3'$ end in every replication cycle!!
Can someone shed some light on how the second cycle would happen, and whether the overhangs would get deleted or it would remain (in this case strand length would keep on increasing)?

The overhangs are needed for telomere function and maintaining chromosome stability, so they aren't deleted. This is an active area of research, so the amount of detail you need to know depends on your level of study. They undergo processing instead of being deleted, involving nucleases. Note that DNA polymerase is filling in most of the gap. It will continue doing this in subsequent replications, so the slight single-stranded region left over won't grow. I'm assuming you mean "single-strand length" by "strand length." If you mean overall telomere size, then it depends on if the cell is somatic or not, which you pointed out.
(The 3′ overhangs can also form structures called T-loops, where the single-stranded overhang "invades" the double-stranded telomeric DNA. This helps protect the chromosome ends from being recognized as damaged DNA, maintaining genome stability.)


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Must one autoclave LB medium after it has been made?
Is it necessary to autoclave LB medium after it has been made?


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Is it possible to distinguish between coding and template strands from the sequence?
Let’s say you have the following DNA sequence fragment:
5’-ACCAGTACTTCGT-3’
3’-TGGTCATGAAGCA-5’

Is there any way to determine which strand is the template strand and which is the coding strand for RNA synthesis solely from the above information?

There are two main problems with your post. First it lacks any sort of context: why this sequence, is it eukaryotic or prokaryotic, are you looking for promotor sequences, is it a homework question and what research have you done yourself to try to answer your question? It sounds very much as if you don't really know what you are asking and have made no effort to read about the topic, otherwise you would know that the answer is No. The second problem is terminology. Template for the mRNA transcript of a gene meaningful, but unusual terminology;  coding strand is ambiguous. Please clarify.

For reference, this question has been the subject of discussion on biology.meta

Given a DNA sequence alone, you can annotate open reading frames (ORFs) in order to identify the coding strand, with the caveat that not all ORFs are genes.  ORFs are sequence segments that begin with a start codon (ATG, though see my note below) and end with a stop codon (TAA, TAG, TGA) when read from 5' to 3' in 3-base codons.  There are no start or stop codons in either strand of the short sequence you provide, so I've appended a new example sequence:
DNA :

    5' - AGGATGCAGGAGTGGTACGATTTATCCTAGGAACCT - 3'  <-- Coding strand
            ^^^                     ^^^
            Start                   Stop
    3' - TCCTACGTCCTCACCATGCTAAATAGGATCCTTGGA - 5'  <-- Template strand

RNA :

       5' - AUGCAGGAGUGGUACGAUUUAUCC - 3'

Note that the start and stop codons given are part of the standard nuclear genetic code shared by eukaryotes, and there are alternative genetic codes used in prokaryotic and mitochondrial DNA transcription.

I don't know about your specific example (perhaps look for triplets that code start codons?), but machine learning has been used to predict promoters from sequence information (from promoter regions, you get downstream initiation of transcription of DNA to RNA). You would probably need more sequence to predict a promoter with more certainty. Cites: https://en.m.wikipedia.org/wiki/Promoter_(genetics) and https://academic.oup.com/bioinformatics/article-abstract/35/16/2730/5270663

The answer is simple : promoter
the promoter is a non-coding sequence of DNA found on one strand of the DNA when reading from (5'->3') which is to be the template strand .
For example the (TATA) box is found in prokaryotic cells DNA (also named  prinbow) and in eukaryotic cells DNA .In eukaryotes, It has the following sequence (5'...TATAAA....3') and is centered (-20-30 bp/20-30 bp upstreaming away from the coding sequence of the gene)  it is the sequence to which the transcription factors  and RNA polymerase II bind initiating the transcription process.


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What placement of plasmid parts makes the most sense?
If you want to express the largest amount of a certain or a few proteins using a plasmid, does it make sense for the antibiotic resistance gene to come after genes for proteins you intend to synthesize?  So that the promoter and RBS/origin of replication would specifically come before the proteins intended to be synthesized and the bacterium would put less resources into its antibiotic resistance?  But would that be canceled out by bacteria not surviving as much as if the antibiotic resistance gene is downstream of the other proteins?  Or is it roughly the same in either order because they're both being synthesized anyway?

The relative placement of genes on a plasmid should not affect their expression.
Both will be expressed and to what extent is dependent on the strength of the promoters and a few other factors like codon availability.
However where you ultimately plan to express these genes can be an important consideration in plasmid design. For example, if you are designing a binary vector for agrobacterium mediated transformation of plants then positioning the plant resistance cassette next to the left border is a sensible move.

Placement can alter protein expression. You could for example make a synthetic operon, and proteins located closer to the promotor will usually be expressed more. You could include your resistance marker in this, and probably get some interesting effects.
However, the resistance marker is usually not such a high metabolic burden that it makes any difference. Increasing expression would be needless. Decreasing expression would free up some resources, but it's extremely likely that your expression is already limited in some other way. Probably promotor strength, plasmid copy number, protein solubility or toxicity.


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If someone's arm is cut off, how does that affect blood circulation throughout their body?
Essentially what I'm asking is that if someone's arm is amputated, doesn't that cut off a significant part of their blood flow because the blood vessels that normally flowed up to the hand of the amputated arm and back can't anymore?  If it heals, does that mean the body has to grow more vessels to sort of complete the circuit again?  Does the body just compensate by putting more stress on the rest of the body's blood vessels?

Is it in reference to surgical amputation?

If I understand your question correctly, you ask how does the body deals with released blood volume after the removal of part of blood vessels?
The simple answer is the body decreases the blood volume. Our body is able to alter blood volume significantly in response to different factors.
For example, take a look at this paper: Blood volume changes in normal pregnancy. It states that:

A healthy woman bearing a normal sized fetus, with an average birth weight of about 3.3 kg, will increase her plasma volume by an average of about 1250 ml, a little under 50% of the average non-pregnant volume for white European women of about 2600 ml.

So, after the arm cutting, an organism will decrease its blood volume. Although it will take some time, blood volume altering is more probable way than new vessels generation.

Amputation of a limb or more will cut off both the arteries and veins to and from that limb. The body will compensate by reducing the amount of the circulating blood in it in order to maintain normal blood pressure. The best analogy I can provide would be electrical circuits: In amputation you are removing a circuit that is connected as a parallel circuit, not as a series circuit, therefor there is no need to create new connection after amputation to allow the circuit to complete, you just need to block the loose ends (ligate the main artery and vein to the amputated limb).
Amputation does not lead to increased stress on the remaining part of the system, in fact it has the exact opposite effect. The heart as a pump becomes more efficient as the "piping system" is now shorter with less resistance, and people with cardiac failure report feeling improved cardiac symptoms after amputation, and those with high blood pressure require less medication to control their blood pressure. In fact, the functional efficiency of all other vital organs like the kidneys, pancreas and liver improve as a result of reduced body mass (they now need to service and detox less cells). If the person was diabetic, their requirements for external insulin reduce, and people who suffer kidney failure might no longer require dialysis as the remaining kidney function -although compromised- becomes sufficient to filter the smaller amount of blood which includes less -waste chemicals- due to reduced muscle and fat mass.

I'd like to see references for the core statements (blood amount is reduced in response to limb loss, and improved heart function after limb loss), but the main point is correct: our circulatory system consists of thousands of smaller parallel circuits that branch off the main vessels in the trunk. As soon as blood clotting has taken care of the actual leakage, the rest of the system goes back to stable.

There are limited references in peer reviewed journals in relation to this subject. Studies related to amputees are very limited due to this area of science being too specific as amputees represent a relatively a small percentage of the population. However, total blood volume is generally calculated based on the person's weight as the main predictor, and limb amputation clearly reduces weight leading to reduced circulating blood volume: https://reference.medscape.com/calculator/estimated-blood-volume https://www.medicalalgorithms.com/blood-volume-after-amputation

Fair point about blood volume. I was still wondering about the improved heart function though, and I haven't been able to find evidence for that. To the contrary, when looking at the risk of heart attacks, it seems patients who lost a limb due to peripheral vascular disease have an even increased risk, and patients with limb amputation for other reasons have no change in risk (https://jneuroengrehab.biomedcentral.com/articles/10.1186/s12984-018-0400-0). For leg amputees, cardiovascular complications seem to be increased generally (https://academic.oup.com/qjmed/article/101/4/251/1544580).

Cardiac function improvement refers to the immediate improved efficiency of the heat as a pump following amputation, due to the reduction in the vascular tree this pump needs to service, while the cardiac muscle remains unchanged, and still at a high risk of further clots leading to future deterioration of cardiac function. Unfortunately I couldn't find references to support this statement, but if you ever meet a vascular amputee I expect you will be able to confirm that it is true.

You are absolutely right about the increased risk of cardiovascular complications following vascular amputations, but this is different from "improved cardiac function following amputation".Vascular amputees had narrowing in the main artery leading to the limb, and this is usually part of the systematic vascular problem. These people will continue to be at high risk of vascular complications in other organs following a vascular amputation, and statistically speaking, a vascular amputation is considered a predictive risk factor for further vascular problems in other organs.


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GFP brightness calculation
So this question is part math, part biology, but I'm asking about the biology part here (or maybe the chemistry part).
Basically I'm asking about my attempt to calculate the possible brightness per unit mass of GFP, and I'm asking if it makes sense.  Here's what I've done:
(I'm ignoring the quantum yield which should be 0.8):
GFP molar mass=27,000 amus (27 kDa)
1 mole weighs 27 kilograms
therefore 1 gram=(6.02*10^23)/27000=2*10^19 molecules of GFP
Assumption that I'm asking about; I'm assuming in this calculation that GFP releases light from one excited electron (roughly 2.5 electron volts).  How many electrons are excited in GFP fluorescence?
(2*10^19)/(6*10^18), (the number of electrons in a Coulomb/amp)=3.3 amps
Brightness=2.5*3.3
=8.25 joules per gram
From Researchgate:
" The time constant of the fast, pH-dependent chemical process decreases with pH from 300 microseconds at pH 7 to 45 microseconds at pH 5..."
Given that's the case, that's roughly 3000 emissions (or 3333) per second (at 7 Ph), so
1 gram of GFP would have a maximum brightness of 24,750 watts, if there was enough UV light, or 25 watts for a milligram.
That sounds plausible, although high.  Does that make sense, or what part of this calculation was wrong?

According to https://www.jic.ac.uk/microscopy/more/T5_9.htm , only 80% of photons absorbed lead to photon emission. (It's "quantum efficiency".) In practice, numbers might be far lower for some other reasons. I recall that even one gram of eGFP was less bright than a 30 W fluorescent light bulb. I suspect that I could not excite all the GFP molecules as often as needed. They are quite sparse in solution, even at "high concentration".

But perhaps it could be brighter than that if the efficiency was maximized (i.e. the protein was spread out over a thin surface and completely concentrated, in theory, since it would have to be in some solution unless it was in powder form)?


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Do macrophages engulf material in the epidermis?
This question comes from how tattoos work.  From what I understand, the ink particles are something like 100 nanometers in size, which is too big for macrophages to remove them in the dermis.  What I would like to know in that case is are macrophages able to go into the epidermis, or is that too far for them?  In other words, would material in the epidermis just leave the body after that part of the skin grows out?


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What exactly are the gates in Hodgkin Huxley model?

Hodgkin & Huxley found that a model with 4 gates in series produces a good fit to the S-shaped curve of the potassium current during the action potential.

Upon reading about the structure of potassium channels on the wikipedia article, I still wonder whether it is correct to  imagine these four gates in series as an entrance with four doors in series that all have to be open in order to pass? The article always talks about the potassium channel as being a single tetrameric protein. What are the four variables in the HH-equation that are independent and have to be open (or active if they are not actually gates) in the actual potassium gate? And since there are many potassium gates in a membrane, shouldn't the equation account for the actual number of gates, i.e. the parallel ones?

The HH model was from long before the structure of the actual gates was known; now the structures are well known. I'd suggest the wikipedia pages on the HH model or the individual channels (voltage gated sodium and potassium channels) which will talk a lot about the gating.

Looks like you've added a bounty without doing any more of your own reading :(

I did this by accident. I appreciate your comment and I think it did this question justice. I have another open question which I wanted to be answered, but clicked the wrong one. Is there a way to correct this?

No, it's not possible to move a bounty (not even a moderator can do anything about that). I think this is still a good question, I just think it would be improved with a bit of focus on what you know and where the gap in understanding is, hence the comment.


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Can anyone identify this woody plant
They were cut a while ago and have paper like bark, the newer bark is a reddish colour and the old is almost black, the leaves are long and slender and it had some yellow flower buds
https://i.sstatic.net/uaYM4.jpg
https://i.sstatic.net/ARWuG.jpg
https://i.sstatic.net/mCPum.jpg

Hello LIam! It would be helpful if you added the location of where you found this plant. Also, I use the iNaturalist app regularly-- and it's auto classifiers are pretty good at helping me identify a plant (immediately), and in my area they are usually followed up by a crowd-sourced (human!) identification within a few days. Plus, these pics can hopefully be used for science! You can add the app to your phone and use in real time. Check it out here: https://www.inaturalist.org/

This one has been bothering me, I keep coming back to it. I'm sure I've seen the plant as a non-native in the UK, perhaps a botanical garden or the like. Bookmarked in case it comes to mind.

This one has been bothering me as well! Perhaps a neighbor has it in their yard? I dropped the picture into two different online databases (https://identify.plantnet.org/ and https://plant.id/ and did not get the correct match. If you have a location, that would help!

Leaves and flowers bring to mind Australian and South African (fynbos) plants. The flower is odd though,

Almost got it, I reckon:
I think that this is one of the Hakea species, but it could be another of similar genera, such as Grevillea. Hakea are moderately diverse group of Australian plants in the Proteaceae. They are hardy and are like places that reach very high temps in the summer, and I think all need fire to open their seed pods. This group of plants have very distinctive flowers, with the stamens sticking out and curling around (OP's second image).
I think this is probably Hakea arborescens, as this has yellow flowers and strap-like leaves, whereas most of the other species have white flowers. H. arborescencs is also one of the more commonly planted species in those areas where it is used as a garden plant. There's also Hakea nodosa with yellow flowers, but it has stick-like leaves.