text:
What is an inclusion forming unit?
What is inclusion forming unit load? I found it when reading this article.
What does this measure and what information can be gained form it? Does this represent the amount of bacteria within a person? What's the difference between inclusion forming units and colony forming unit?
I am from a mathematical background, so can someone please explain these in simple terms?

Depending on the development cycle of Chlamydia tend to appear in two forms, the elementary body and the reticulate body. As outlined in the excerpt below, the reticulate body can be found as inclusions in a cell's cytoplasm when stained with iodine. So yes, your initial guess of inclusion-forming units (IFUs) being a measurement of how much of Chlamydia spp is present in a sample (cell or tissue) is correct.
It is similar to the concept of Colony Forming Units (CFU) which is a unit used to estimate the number of viable bacteria or fungal cells in a sample. Viable is defined as the ability to multiply via binary fission ("division in half") under controlled conditions.
Applying the concept of CFU to the above an inclusion-forming unit may be understood as a unit to estimate the number of Chlamydia cells in a sample. The difference between CFU and IFU would be as follows, CFU counts are normally taken for bacteria/fungi grown in a controlled environment. CFU counts also only account for viable cells, dead cells are disregarded. This is in contrast to IFU counts as we do not have a controlled environment as such and depending on what staining method you use, IFU counts may or may not account for dead cells too.

Chlamydia may be found in the form of an elementary body and a reticulate body. The elementary body is the nonreplicating infectious particle that is released when infected cells rupture. It is responsible for the bacteria's ability to spread from person to person and is analogous to a spore. The elementary body may be 0.25 to 0.30 μm in diameter, and it mainly consists of C. trachomatis, C. pneumoniae, and C. psittaci. This form is covered by a rigid cell wall (hence the combining form chlamyd- in the genus name). The elementary body induces its own endocytosis upon exposure to target cells. One phagolysosome usually produces an estimated 100–1000 elementary bodies.
Chlamydia may also take the form of a reticulate body, which is in
  fact an intracytoplasmic form, highly involved in the process of
  replication and growth of these bacteria. The reticulate body is
  slightly larger than the elementary body and may reach up to 0.6 μm in
  diameter with a minimum of 0.5 μm. It does not present a cell wall.
  When stained with iodine, reticulate bodies appear as inclusions in
  the cell. The DNA genome, proteins, and ribosomes are retained in the
  reticulate body.

Link to Wikipedia page - excerpt was taken from there.


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What is the proper way to dispose of a medicinal substance?
Is there a protocol or a set of guidelines to safely dispose off a batch of expired drugs (as a manufacturer)? I guess the process may vary for different drugs. My specific question regarding the safe disposal of expired amlodipine; which is better — incineration or landfill or any other technique?

Usually you would return to the pharmacy of purchase for safe denaturing

@RoryM OP is asking from a manufacturer's point of view.

Chemically inactivating the drug (in a safe manner) is probably best - bleach, peroxide, other reactants that can themselves then be neutralized.

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Membrane Permeability to Pyruvate
Pyruvate seems to pass easily through the outer membrane of the mitochondrion but has difficulty entering the inner membrane (and gets in by H+ symport). I have two questions: (1) what property of pyruvate disallows it from passing through the inner membrane? Is it its charge? and (2) what structural differences are there between the outer and inner membranes of the mitochondrion that create their disparate permeabilities to pyruvate?

Pyruvate is negatively charged and quite polar, which makes it unfavourable to diffuse directly through any membrane. The outer mitochondrial membrane contains porins, which allow small molecules, like pyruvate, to passively diffuse through. Specifically, pyruvate uses voltage dependent anion channels. The inner mitochondrial membrane lacks such channels and depends on active transport by the long anticipated but only recently discovered mitochondrial pyruvate carrier (Herzig et al. and Bricker et al., 2012).

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What is the most up-to-date CRISPR/Cas9 protocol?
I am collecting literature to start a new project on CRISPR/Cas9 gene editing. I must put together a protocol to start and am intending to use the following paper as guidance:
"Genome engineering using the CRISPR-Cas9 system". Nature Protocol 8(11):2281-308 · November 2013
Could you please indicate whether this is the most reliable and recent published general protocol for the CRISPR/Cas9 system.

A PubMed search will tell you that.

Dear  MattDMo, I am aware of that. There are many papers to choose from and go through all will take large amounts of time. What I am aiming for is to collect information from experienced people and optimize my time. Thanks

Sergio - the way to do this is to search pubmed, and sort by date. Alternatively, email somebody from a lab who is currently performing CRISPR and ask them, usually people are happy enough to help with simple questions like that.

You can easily find out if it is most recent, if it is most reliable is an opinion-based question and as such out of the scope of this platform.

It really depends on what you want to do with it. Sticking to genome engineering in Human cells, Nature Protocol 8(11):2281-308 · November 2013 is the de-facto standard. One improvement I suggest is to replace the "Surveyor Assay" with deconvolution analysis of sequencing traces using TIDE.


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Rushed publications based on flawed data
In 2014 BICEP2 made a very controversial press release. It was rushed, given before any papers where published, because they feared they would be scooped by another similar experiment. In the end it turned out that their analysis of their data was flawed. It was particularly dramatic because if they had been correct it would have been a significant development.
Are there any similar cases in biology? Not necessary an identical situation, but a high profile result that was released in a hurry that later turned out to be incorrect.

This should probably be posted to http://academia.stackexchange.com.

There are many publications on severely inappropriate usage of statistics in lots of biological papers driving the results unreproducible. Google something like "wrong statistics in biology".


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Does Remdesivir cause bone marrow suppression?
According to Wikipedia, Remdesivir is a prodrug of GS-441524 which is a nucleoside analog.
I know that nucleotides are the building blocks of both DNA and RNA, meaning nucleotide analogues that prevent the creation of viral RNA can also prevent the creation of normal cell DNA, meaning they can cause problems in dividing cells. This is also reflected in the nucleotide analogue article of Wikipedia:

They are not specific to viral DNA and also affect mitochondrial DNA. Because of this, they have side effects such as bone marrow suppression.

So does Remdesivir cause bone marrow suppression?
If not please explain why.

From Off-Target In Vitro Profiling Demonstrates that Remdesivir Is a Highly Selective Antiviral Agent:

Overall, the cellular and biochemical assays demonstrated a low potential for RDV to elicit off-target toxicity, including mitochondria-specific toxicity, consistent with the reported clinical safety profile.

This isn't a very complete answer, but the wikipedia article doesn't go into detail or link references explaining the mechanism by which nucleoside analogues suppress bone marrow function. So I can't say if the assay results in my link rule out a suppression effect by remdesivir

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The reason behind red drop effect
I was reading about Emersion effect on Wikepedia, I was not able to correlate our current knowledge of photosynthesis with this effect,
First red drop effect

When Emerson exposed green plants to differing wavelengths of light,
he noticed that at wavelengths of greater than 680 nm the efficiency
of photosynthesis decreased abruptly despite the fact that this is a
region of the spectrum where chlorophyll still absorbs light

My Query is  this abrubt drop in rate of photosynthesis after 680 nm is because as PS1 absorbs wavelength greater than 680 nm till 700 nm , and PS1 does not evolve oxygen or fix Carbon dioxide? so rate of photosynthesis is very small at this point, as to reduce NADPH2 in Z scheme , photosystem 1 needed electron of Photosystem 2 , without electron of photosystem 2 it will not be able to reduce NADP, isn't it, I am very skeptic about this explanation, is it right?
Secondly it mentions

When the plants were exposed to short-wavelength light, (less than 660
nm), the efficiency also decreased.

Is this decrease in rate because of Photosystem 2 gets most activated at 680 nm and antenna molecules which broadens the spectrum as not very efficient result in decreased in rate of photosynthesis???

This graph is also adding to my confusion if PS1 active at FAR RED LIGHT only synthesizes ATP and not NADPH2 what does it have an equal bump( amplitude) like Red light(at which PS2 is active and carbon fixation in reality is happening here) So Amplitude of red light should have been greater than far red light
https://istudy.pk/emerson-enhancement-effect/ graph source

I recommend you to read taiz and zeigner's plant physiology. I read few years back it beautifully explains this concept. Right now, I'm preoccupied with some other question, if no one still answers this, I'll give a try

@biologist_jaishree hello?

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If crossing over can cause formation of new allele, can it affect Hardy-Weinberg equilibrium?
I was reading about Hardy-Wienberg equilibrium on Wikipedia  and there are seven assumptions underlying HW

It is mentioned that sexual reproduction one of the assumption and is a must for HW, but according to some answers given here on Biology STack exchange crossing over in sexual reproduction can result in exon shuffling
here is the answer I am referring to
so my question is-
1.can  exon shuffling  cause a new allele to appear in the population?
2. If a new allele can appear in the population during the cross over or due to crossing over as it is a random process that will surely change the allelic frequency so how can be sexual reproduction can be a underlying assumption for HW? it should be in the list of things that can affect Hardy-Wienberg like mutation and sexual selection
3. Does in majority of cases crossing over only causes reshuffling of allele but not the formation of a new allele? is mutation by crossing over is rare?
4. Can Independent assortment and Linkage have any effect on Hardy Weinberg law?

I'd consider creation of a new allele by intragenic crossing over a mutation.  HW was developed over 100 years ago, before the molecular nature of the gene was known, so it was based on Mendelian genetics. Normally, recombination rates within a gene will not be significant.

Reading a bit futher in the Wiki entry, "Mutation will have a very subtle effect on allele frequencies. Mutation rates are of the order 10−4 to 10−8, and the change in allele frequency will be, at most, the same order. Recurrent mutation will maintain alleles in the population, even if there is strong selection against them."


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How do I calulcate the amount of concentrated stock solution to add to get the correct dilution?
For example, how much loading buffer (6X) do I need for my PCR reaction with a volume of 25 μl?  What is the general way to calculate it?

For any question regarding volume and concentration, you should consider the equation $C_1V_1=C_2V_2$. We can use it to derive a general equation for the addition of concentrated stock solutions. We want to find the volume of stock solution ($V_1$) to add so that its final concentration is 1X. Here's what we know:

The initial concentration of stock solution, $C_1=X$
The final concentration of the solution, $C_2=1$
The volume of solution we are diluting the stock into, $V_s$

So the equation becomes:
$$XV_1=V_2$$
We don't know $V_2$, but we do that $V_2=V_1+V_s$. Subbing that in:
$$XV_1=V_1+V_s$$
Solving for $V_1$:
$$XV_1-V_1=V_s$$
$$V_1(X-1)=V_s$$
$$V_1=\frac{V_s}{X-1}$$
Then you simply need to sub in your values:
$$V_1=\frac{25μL}{6-1}$$
$$V_1=5μL$$
So you should add 5 μL of your 6X loading buffer to the 25 μL solution to get a 1X final concentration.

@biologist You’re welcome!

Absolutely correct. I leave this comment only as an aside for people who may find it unhelpful to think and visualize mathematically: a 6X buffer simply means it should make up one part in six. You add 1μl of it to 5μl of your solvent. Or add 2μl to 10μl. Or add 5μl to 25μl. Or 1 teaspoon of honey added to 5 teaspoonfuls of tea. Now that's some 6X honey.

Candianer's answer is a generally correct way of solving these problems but, in my opinion, overkill for this situation.
All Nx buffers are mixed to make your life easier, and you will generally encounter 10x, 6x, and 5x buffers. 10x and 5x seem obvious, you just put them in so they make up a tenth or a fifth of your solution, but 6x seems to confuse people. The reason it's x6 is because you are adding it to an existing solution, so as well as you're solution you're going to have one lot of whatever you're adding. This makes it (1+N)x and you can then clearly see that 6x is (1+5)x, so you need to add an amount equal to one fifth of your volume.
One fifth of 25 μL is 5 μL so that is what you need to add.

Certainly one doesn’t need to derive the equation every time; I was just showing how it’s done. It really is as simple as dividing the volume by 1-N.


text:
Can someone tell me the species of this lizard?
It's a green lizard with a silver tail, and it has pretty, bluish eyes. I saw it today, July 26th, trying to get some shade on a hot, sunny day (32 degrees) at around 18:00 in Austin, TX USA. It's been hot and dry here the past few weeks, but it rained a lot a few months back.
Austin has a humid subtropical climate. The city is characterized by hot summers and mild winter days and usually cool to cold winter nights. The geo coordinates are 30.4 (lat), -97.7 (long).
Oh, it was able to jump a good meter.
Thank you.

I know nothing about lizards, but this looks like a Carolina anole (Anolis carolinensis), also known as a green anole. Apparently they can change colour:

Yes , an anole. Very common , more than you see because they prefer to be in trees. Sometime wrongly called chameleons.


text:
What is this colourful insect with a large thorn?

Someone sent me the picture so I don't have a lot of details. Is it a real insect or is it fake?

It might not be fake, it looks like a thorn bug

As @Kiritee mentioned this is actually a treehopper, due to thier unusual shape they are of long interest of naturalists.
This is a female Umbonia crassicornis.
Here's a female with her colourful nymphs captured by
C. D. S. Molinari
.

Facts:

The females have a pointed pronotal horn (spike), the males' are blunt, with a flat top.

The adults display variation in colour and size.

The pointed pronotal horn is an adaptation as the insectivorous birds mistake them as thorns (on stem) and do not consume them.

This is a variable species as to size, color and structure, particularly the pronotal horn of males (which is more angled posteriorly than the females' and often somewhat expanded apically).
This tall, essentially perpendicular thorn-like pronotum discourages birds and other predators from eating it, if only by mistakenly confusing it with a thorn.
Typically, the adult is green or yellow with reddish lines and brownish markings.
The range of this species is from Northern South America all the way to Mexico and Florida. Its preferred hosts are ornamental and fruit trees of subtropical regions.

Parental care: The females on sensing an intruder would rush to her nymphs and would charge the offender by kicking her legs, fanning her wings and sometimes even buzzing. The females communicate with the nymphs to ensure that they are in a group.
References:
Encyclopedia of Land invertebrate behaviour, Encyclopedia of Insects and Libraries of life

Picture References:

A female with eggs.
Two males (blunt top)
Original size

Good reads:

Thornbug to Thornbug-The inside story of insect song

Libraries of life (audio clips)

Your edits really elevated this answer. Nice picture :). +1.

Wow, are the wings functional?

@AntonSherwood Yes, they are. The males are detectable when they fly from one branch to the another in search of female.


text:
Why do (almost) all energy carriers contain adenine?
Unlike this question which is specific to just ATP, this one includes all energy carriers.

When thinking of common energy carrying molecules, I can think of Adenosine triphosphate (ATP), Nicotinamide Adenine Dinucleotide (Phosphate) (NADH/NADPH), Flavin Adenine Dinucleotide (FADH2), S-adenosylmethionine, coenzyme-A (derived from cysteine, pantothenic acid and ATP), etc. Recalling exceptions, I can only think of biotin (carboxylated) and uridine diphosphate glucose. Just talking about ATP, we could have called its preference over others just a matter of chance. But when so many carriers contain adenine, there has to be some selection against other energy carriers (or adenine was so lucky?). Note that when saying 'common energy carriers', I exclude GTP, CTP, TTP and UTP since they are not very commonly used (or at least their use is confined to only some metabolic reactions, unlike ATP which finds its use in almost all metabolic reactions requiring energy).
Why do the majority of energy carrier molecules contain adenine (or its derivative) instead of any other nucleobase?

This question is open for discussion i.e. everybody is welcome to post their (scientifically backed-up) opinion as an answer while none of those answers will be selected because of lack of conclusive proofs, which are very likely to remain elusive forever.

I know questions like this are likely to get primarily opinion-based answers, but I still wish to keep it on this site since some opinions might be scientifically more sound and may get back-up references either now or later on.

What is even commonly used if  GTP is produced during the citrate cycle and is needed to synthesize every single protein that's existing in a cell?

@adjan in that sense, even CTP, UTP and TTP find uses somewhere. But I was talking about the diversity of functions, in which ATP is by far at the top. But I'll edit that point to make it clearer

@adjan — Just for the record, the GTP produced in the TCA cycle isn't used for cytoplasmic proteins synthesis as it is made in the mitochondrion. However, I do agree on its importance in protein synthesis, although, paradoxically it is not used for peptide bond formation, but is thought to be a timing device as in other G-protein systems.

@David well i did not mean to imply that it was the same GTP that was used for both, i just found these are two very essential processes in the cell.

As @canadianer comments, this question is unanswerable, and it verges on being classified as ‘opinion-based’. However, because I do not find the answer from the OP appealing, I’ve set out a few points of my own. Hardly an answer — more a list of alternatives as food for thought.
I can imagine adenine being chosen for one of the following reasons (others are welcome to suggest additions):

Functionally best suited
Was there first
Easiest or cheapest to synthesize originally (which would explain why
it was there first, if this were the case)
Random choice

Let’s look at them in turn.
Adenine functionally best suited
There seems nothing in the function of NAD that suggests the adenine ring could not have been replaced by another of the bases, and we know that the free energy of hydrolysis of the beta–gamma phosphodiester bonds of GTP, CTP and UTP can be utilized in an analogous way to that of ATP, so this doesn’t seem very likely.
However one does wonder if a purine (rather than a pyrimidine) ring conveys some sort of advantage in that the other purine-based triphosphate, GTP, is used so widely in the (ancient and essential) process of protein biosynthesis. Perhaps the greater area of contact of the purine ring favoured interaction with proteins (if you don’t argue that these came later).
Adenine was there first
One might consider that early in the evolution of life the bases (or nucleosides and nucleotides) emerged one at a time, in which case the first might have been used for NAD etc. and stuck. One might also consider whether a two-base world preceded a four-base world. If A and U (but not G and C) were in the first RNA (which may have been single-stranded, so I don’t see that the GC content of contemporary thermophiles is relevant) then it may have been a choice between A and U, which A might have won because U is subject to spontaneous deamination (or for the protein-interaction argument mentioned above).
Adenine as easiest or energetically cheapest to synthesize originally
Clearly, the first base might have been the one favoured by chemistry in relation to its synthesis. Contemporary biosynthesis is unlikely to reflect primeval biosynthesis, but it is amusing to observe that adenosine biosynthesis is the only one that doesn’t involve NAD-dependent oxidation. Of course all the contemporary biosyntheses utilize ribosyl pyrophosphate, which requires ATP in its synthesis from ribose phosphate. (Talk about chicken and egg!)
Random choice that stuck
In the absence of any more sophisticated explanation, then it could just be this. Once a choice was made and enzymes evolved to use NAD etc. the choice of adenine couldn’t be changed (or there was no strong enough functional advantage to doing so).
Postscript: When and how did NAD appear on the scene?
One of the reasons I don’t favour the OP’s answer is because it envisages NAD arising after DNA genomes and as a separate entity. I would suggest that it is likely that RNA preceded DNA and that catalytic RNA was responsible for some of the early oxido-reductions. (The first ones were probably catalysed by iron–sulphur centres, either inorganic or associated with simple proteins.) It seem feasible that the nicotinamide ring was an elaboration of a ribozyme which was ultimately almost completely replaced by protein. The adenosine was retained with the functional nicotinamide because it could interact better with the protein. Gross speculation, and it doesn’t explain why adenine was the chosen base, but an antidote to thinking NAD evolved in the fully grown form we see it today.

@tomd — Thanks. I'm pretty ignorant about that sort of thing, which is rather embarrassing seeing I proffered an answer of sorts. But it does suggest a different approach to that of the poster.

+1 although you would need to get some back up papers, like the one @tomd has suggested. I did not wish to get completely speculative answers (at least some of the claims must be backed-up in some way or the other) in which sense "contemporary thermophiles" seems more relevant than "maybe adenine came first" (although I wasn't talking about 'contemporary' thermophiles in my answer).

I think a lot of David's answer was just common sense, though. The arguments of "adenine came first" and "it was random" seem perfectly rational to me and it would be nigh on impossible to justify them with evidence.

@jam if I say "adenine is preferred because I say it is" that seems perfectly rational to me, but there is no way I can prove it either. Just giving common sense points as arguments is not sufficient, lest everything in biology can be justified by common sense. I have no problem with david's answer, I just mean I don't understand your perspective.

I’ve added a postscript which is even more speculative than the main part of my answer. @another'Homosapien' asks for “claims to be backed up in some way” — this isn‘t a claim, it is a set of ideas explored in the context of what fossils we have of the chemistry of early life. It‘s not for the poster to accept or reject either — that‘s not what questions here are for — it‘s for interested parties to read (and vote for or against if they wish). In fact the development of oxio-reduction in general is probably a more fruitful area, although my own chemistry is not really up to it.

@david I meant just backing-up any of your claims if the speculations in your answer can be related to it (knid of "I know we ppssibly had A [see this], so I speculate A -> B -> C and C is the present scenario"). I appreciate that you brought up another possibility in your answer, and I know you can't back it up.

One of the reasons why adenine is by far the most common component in energy carriers might be its less utility in DNA. Naitoh (2008) also describes this opinion. Keeping in mind the conditions on earth when first life would have evolved, this becomes easy to conceptualize. Naitoh (2008) compared RNAs of many different species of hyper-thermophiles and found that it contained a larger percentage of guanine and cytosine instead of adenine and uracil. They suggested that this could be because guanine and cytosine form stronger base pairs than adenine and uracil. Thus, while guanine and cytosine were being preferred as the constituents of DNA and/or RNA, adenine and uracil found place in other processes. While uracil would have become usable in polysaccharide generation reactions, adenine would have been a preferred choice for energy carrier molecules. PS: we could also apply the same hypothesis with a dsRNA virus which might have evolved GC rich RNA and left more AU content in its host. In this manner, this process seems more likely to cause AU buildup in the host.
To give a better idea of what might be happening, suppose there is a unicellular organism with the following DNA sequence:
5'-GCATGCATGCATGCAT-3'
3'-CGTACGTACGTACGTA-5'
and some free nucleotides, suppose 5 GTP + 5 CTP + 5 ATP + 5 TTP. Now, since G and C are being favored because of the greater stability they provide to the DNA, they would eventually replace some of the A and T in DNA, which would later become:
5'-GCGCGCATGCGCGCAT-3'
3'-CGCGCGTACGCGCGTA-5'
giving some free nucleotides as 1 GTP + 1 CTP + 9 ATP + 9 TTP. These extra ATP and TTP could be preferred in other reactions over GTP and CTP because of higher availability. Now, it could be mere chance or better functionality of adenine (as another answer says) due to which it was chosen over thymine (or uracil).
For why many other energy carriers contain adenine, the following is just speculation. Beginning with the assumption that nucleotide triphosphates were the first energy carrier molecules (since they are the precursors of genetic materials), they would have been derived for many other processes. And in some such processes, they would have got incorporated in another molecule in such a way that the formed new molecule would have acted as an energy carrier molecule too. For example, NAD+ (Nicotinamide Adenine Dinucleotide, although it is technically a hydride ion i.e. H- carrier) biosynthesis requires ADP ribose as a precursor (Wikipedia). See the diagram below for the biosynthesis pathway (from PNAS):

Flavin adenine dinucleotide (FAD) is also synthesized in a similar manner. See this diagram (from Wikipedia):

From this, we can suggest that ATP once acted as a substrate in a reaction whose product (or intermediate) was NAD+/FAD. This molecule turned out to be a useful energy carrying molecule. We could also explain the occurence of adenine in other energy carriers through this hypothesis.

So why not NUDH? In my opinion, this doesn't really answer the question (which is actually unanswerable).

@canadianer because UTP is preferred in polysaccharide synthesis reaction and ATP would be the only carrier left to react with NaMN (as I say, this is purely speculation). And who says this question can be answered? If it could be, then there would be no need for a discussion post. And obviously, your own opinion is most welcome as another answer, which I have already made clear in the question ;-)

Also NUDH does exist, at least in vitro :P

because UTP is preferred in polysaccharide synthesis Okay, but the question is why? Truthfully, the only reason why I didn't vote to close this question is because you are an experienced user, which is perhaps an unfortunate double standard which I think others are following as well. Certainly the answers will be opinion based, which is explicitly off-topic on this site. I'm also not sure that this question is sufficiently different from the one you linked to to justify it.

@canadianer I know the question is primarily opinion-based. All I wanted to have was a discussion post just to know the different theories and opinions present out there regarding this. This is what I have tried to make  clear in the question itself: none of the answers posted will be selected since none of them can be proved true. Its much similar to "why some bad traits evolve" question: simply because they do, there's nothing stopping it, same thing here. And yes, why 'adenine' is a component of many energy carriers is certainly different from why 'ATP' is preferred energy carrier ;)

Are you arguing that if early genomes were high GC, there would be a surplus of adenine? If so I don't follow this argument.

@david honestly (no hard feelings, if it seems so) I hope you know the difference between argument and speculation. Nobody can prove it, all we can do is criticism. BTW if you and @ canadianer have another theory in mind, why not post it as answer? I am waiting for more responses :)

I have just posted my own answer, but wanted to be clear about your answer. I'm not criticizing it as speculation, but I want to be clear I understand it before criticizing it on (speculative) scientific grounds. For example, if there was little need for adenine, I don't see why it would be made in excess, as I understand (or misunderstand) you are speculating.

@david suppose you have an RNA as 5'-GCAUGCAUGCAUGCAU-3' You replace some As and Us with Gs and Cs (what evolution might have done) and you have 5'-GCGCGCAUGCGCGCAU-3' + 2 A + 2 U which can be used elsewhere. This is my speculation. I'll comment on your answer...

OK. Now you have clarified, let me put forward my criticism of your hypothesis. My main reason  is that I do not see why the synthesis of adenine would not be regulated by demand, i.e. by some sort of feedback inhibition. It would seem that you would have to postulate that regulation hadn't developed then, but as you reproduce detailed contemporary pathways, this seems special pleading. In any case I think that if an RNA world preceeded a DNA world,  I would expect NAD to have arisen in the RNA world  — for which the adenine of NAD seems to me the smoking gun. The DNA world seems too late.

Another reason which might have played a crucial role in preference of adenine could be its greater stability over other nucleobases.
Dividing nucleobases into purines (A, G) and pyrimidines (C, T, U), lets first look at the pyrimidines. It is a well established fact that pyrimidines are more prone to damage, especially damage caused by UV radiation. It is known that due to UV radiation, pyrimidines form dimers, such as cytosine dimer, thymine dimer and uracil dimer (see Wikipedia). Also, researches have concluded that once the aromaticity of a pyrimidine is lost, its C4 position becomes a hotspot for a tetrahedral intermediate, whose degradation can cause major problems including DNA strand breaks (Lin et al, 2014).
Coming to purines, it has been shown that guanine is more prone to covalent attack than adenine. It could be due to the differing electronic charge distributions in the two bases. The sites O6, N7 (in major groove), N1, N2 and N3 (in minor groove) are the preferred sites for covalent attacks (Neidle, 2002). This point also gets support by the fact that the most common modified purines, xanthine and 7-methylguanine, are actually the modified forms of guanine (see Wikipedia), again meaning greater stability of adenine over guanine (although hypoxanthine is made from adenine, but the reaction is multi-step and requires many enzymes).
Why talk about stability?
The most obvious question which arises now is why are we talking about stability? If a nucleobase is more stable, it should be a preferred component of nucleic acid (which contradicts my own claim in another answer). To answer this part, we are talking about stability in different contexts in different answers. In this answer, we talk of the stability of the nucleobase itself, while in the other answer, we talk of the overall stability that the nucleobase provides to the nucleic acid. If a nucleobase is modified in a nucleic acid, it can be repaired easily through different repair mechanisms (think about repair mechanisms of strand break and dimers). On the other hand, if a free nucleobase (in the form of NTP or dNTP) is modified, it can cause serious damage to other components of the cell. Another point is that when a nucleobase is modified, its structure changes. This modified structure can prevent other proteins from recognizing this molecule. For example, if guanine would have been a component of NADH (which we would call NGDH), it might get modified to xanthine (forming NXDH...?). Now the NGDH binding sites of different proteins would not be able to recognize this molecule, and since this molecule is not a part of DNA, repair mechanisms would not help here much either. Hence, the most stable nucleobase (adenine) gets preference as the component of different energy carriers because of its stability too.
P.S.: the point of stability can also explain why GTP is also used in some crucial metabolic reactions, like protein synthesis and TCA cycle, since guanine is the most stable nucleobase after adenine.

Do free pyrimidines form dimers in solution at an appreciable rate?

@canadianer thats a nice point, although I could not find any papers regarding this (maybe nobody else has thought about this). I suppose the rate would not be appreciable (but would surely be detectable). But, the point here is that dimerization is not the only way 'active' pyrimidines could cause damage.


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Extremely rare occurence of Heart cancer?
The occurrence of Heart cancer (similar, but not the same as Rhabdomyosarcoma) is extremely rare, about 1 per year according to MayoClinic. The reason for this rarity is explained to be the post-mitotic nature of cardiac muscles. Since they stop dividing early in the life cycle of humans and grow only by increasing in volume, they are very less prone to oncogenic activation events caused due to mutation as a result of an error in DNA replication (since they do not replicate their DNA as they do not divide).
Although I am not an expert in tumours and cancers, I think that malignant tumours in nervous tissue, i.e. brain tumours are fairly common, at least more common than heart cancer by several orders of magnitude. But neurons constituting these tissues are also permanently in interphase and hence do not divide.
 Moreover, secondary malignancies in Brain and nervous tissue is also much more common than secondaries in heart (rare) though metastatic secondary tumours, I believe, do not require oncogenic transformations in the host tissue. A metastatic fragment of a primary malignancy transported by blood is enough to cause secondary tumours.
How then these tumours (primary and metastatic-secondary) are more common in nervous tissue than heart, though both are post mitotic, i.e. permanently in interphase?
Here and here are a few links which give some basics of cardiac malignancies, though they don't address the question quite directly. The study here provides possible explanation of lack of cancer due to high oxygen content.

THe tumors in brain are mostly glioblastoma. Neuroblastoma is rare.

@WYSIWYG That is true, but, if I am not mistaken, the rarity of Neuroblastomas is lesser than the rarity of heart malignancies.

neuroblastoma is more common in infancy and early childhood when there are a lot of neural progenitors. I guess it is not an oncogenic transformation of a mature neuron. Glioblastoma is also not so common; the therapy is more difficult.

@WYSIWYG Whatever may be the rarity of neuroblastomas or glioblastomas, what about secondary tumours?

Well.. i dont know the answer myself; thats why I commented. I am looking up. It is an interesting question.

In case of secondaries, one reason could be that the brain is static (immobile) while heart is dynamic (mobile). It's very difficult for a embolus of tumor cells to adhere to a constantly shrinking and expanding structure viz. heart as compared to a very immobile organ - brain.

This is a specific version of the great cancer question: "Why are some cancers more common than others?" The answer is either "Some have more common causes", and (or) "Some are cured spontaneously more often". So now all you are asking is "What causes cancer?" and "How do we cure it?"
Given that, I don't expect a general definitive answer will be forthcoming. A specific answer might be possible, but I doubt there will be any existing experiments that address this. With the obvious caveat that only experimental or statistical results can really answer your question, here are a couple of off-the-cuff hypothesis for consideration:
1 - Differences in stem cell populations.
Apparently, differentiation can actually be targeted as part of a treatment in some neuroblastoma cases - see the section on "Differentiation therapy" in this page from Sloan-Kettering. Cardiac stem cells seem to exist, but a difference in relative population and turnover rates between brain and heart might be related to the relative frequencies of these types of cancers. @WYSYWIG referred to neural progenitors in his comment above.
2 - A filtering effect due to a more extreme selection pressure in the uniformly stressful environment of the a beating heart.
Although there is a relation between elevated levels of oxidative stress and cancer causing mutations, it could be that this only matters in a punctuated stress environment, where cells have down time to recover. A sustained stress environment might actually helps prevent cancer. The path from normal to cancer cell requires multiple mutations, and I would not expect most pre-cancerous cells to be more fit than correctly wired ones. The extra stress of the cardiac environment might produce an elevated mutation rate, but also produce an even higher rate of apoptosis in early "sick" cells before they accumulate enough mistakes to become become cancerous, resulting in a net decrease in the rate of cancer.
Both of these ideas fit with heart cancer being less common and with metastasis from elsewhere being more common in heart than primary cancer, but unfortunately, a higher rate of clearing of sick cells would necessitate a higher rate of replacement from stem cells, so these two hypotheses partially cancel each other. Again, hypotheses without experiments are not really answers.


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Water potential in plants?
The concept of water potential in plants tries (and succeeds) to explain various movement and transports in plants. I have learnt that it can be though of being composed of various components like the solute (osmotic) potential, Matric potential, gravitational potential and the pressure potential. I know how to quantitatively determine the osmotic pressure and have worked with the chemical potential of water in solution and pure state. Can someone help me develop an intuitive understanding of all these components quantitatively? I am comfortable with basic thermodynamic treatments of chemical potential and already have an intuition of the osmotic component. Here is the basic definition regarding water potential. (Since this pdf is quite old, I am not sure whether the same definitions operate or rather are used now.)
EDIT:- As an example, we can derive the lowering of chemical potential of pure water on addition of solute and for the ideal case, the lowering turns out to be $RTln(X_a)$ (where $x_a$ is the mole-fraction of solute, $R$ is the gas constant and $T$ the absolute temperature) and this is defined as the osmotic potential or the solute potential. Next, the gravimetric component. We can intuitively understand that the water must flow from higher gravitational potential to lower and hence flow downwards. But I want to understand how can we assign a quantitative basis to our arguments in terms of chemical potential for differenf heights. Same way, how can we ascribe a mathematical (or chemical) basis to all the components of water potential including the turgor pressure and the matric components.

sadly this paper is behind a paywall - any other references?

I have a copy but I dont think we can share without uploading. Nevertheless, (http://en.wikipedia.org/wiki/Water_potential) wikipedia provides some minimal non rigorous definitions. See if that helps provide some quanlitative clarification of this concept.

could you add a couple of questions or issues you have - what sort of phenomenon or math puzzles you about water potential?  again there's several ways to go here.

Added in the edit

Ok let me try to tackle this one - still could be off - let me know.
The book Chapter from UCDavis that is linked from your wikipedia page is a good reference I think. Overall the term 'water potential' will try to estimate an energy function that describes the behavior of water in a chemo-mechanical sense.
$\Psi_{total} = \Psi_{reference} + \Psi_{solute} + \Psi_{pressure} + \Psi_{gravitational} + \Psi_{humidity} + \Psi_{matrix}$
It looks a lot like a Hamiltonian expression of total energy that tries to see the water as a fluid.  The water potential is not the same as an energy equation for fluid dynamics which tries to understand the motion of a body of liquid and does not typically take into consideration chemical changes like solute in the behavior.
So first we are looking at a set of behaviors that the fluid experiences.  some of them treat the fluid as a body ( pressure, gravitational) others look at the potential for evaporation or diffusion (solute and humidity to some degree).  wetting of surfaces and surface tension (matrix).
The water potential is an equation broken down into a set of measurable or approximately measurable energy terms.  But like a lot of Energy equations, when  you are looking at a biological system, it is more often qualitative than a quantitated entity.  The general observation that surface tension decreases when temperature goes up, or when the solutes have higher concentration is used to make arguments of the mechanism of say physiology
Generally speaking looking at the magnitudes of the various terms you can see how influential they are and then try to focus the hypothesis into a test that can make a distinction about the mechanism with specific measurements.  The actual overall measurement of a water potential or any total energy is almost always intractable.  The difference in energy is what you might be able to measure, but in the case of the water potential, the measurement will usually be an observation, with some uncertainty that water is moving from point A to B and not elsewhere.
Take a look at this paper describing Drought Stress in Arabidopsis.  The water potential is cited as a critical element of drought response - and of course it should be.  But all this work here, with all the proteins acting to change the physiology of the cell, adjust the chemical potential (and therefore the osmotic potential) of the cell membrane, its hard to imagine how measuring a root system at all points would be possible.

Physical properties of the cell wall play a crucial role in the response of plants to water deficit (Bacon, 1999). Transcriptome analysis of pDr showed the repression of many expansin genes (Bray, 2004), while mild osmotic stress revealed the induction of expansin genes (Skirycz et al., 2010). Cell expansion in response to drought was characterized in the maize (Zea mays) root system as an adaptation to low water potential (Wu and Cosgrove, 2000).


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Need help distinguishing between a primary and secondary source
I am trying to figure out if the following article is a primary or secondary source.
I'm leaning towards secondary but here are my cases for both.

Primary: Published in a peer-reviewed journal.
Secondary: It seems to be mostly a summary of other works so it might
  not be original research.

Can anyone confirm this for me? Thank you!

probably better on Academia?

This would be a better fit on academia.stackexchange.com

Too long for a comment: Although this is a review article which summarizes the findings of other researchers, considers this as a primary article. The author gives you all the resources he used in the reference section of this article and summarises their finding. Additionally, review articles in renowned journals (and Genome Research is definitely such a journal) are peer-reviewed. Primary vs. secondary sources would be more the comparision of research articles and news articles. In my observation, news articles hardly ever name the sources or the original articles about which they report. Plus they sometimes have problems of getting the message wrong.


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What tree is this?
Can you please help me to identify this mystery tree. I have been trying to identify it for four years (Leafsnap app didn't help). Here are a few things about the tree.

All the leaf veins are parallel. They remind me of a dogwood tree, but it's not a dogwood tree.
The leaves are very small, about 3 cm in length, 2 cm wide.
Here is a ripped leaf.
The leaves grow together from a joint point.
Here is another picture:
There are some flowers, but they don't look like flowers. They look like tiny green buds. They smell like honey (or this is just my imagination), but no petals ever show up. The flowers are extremely tiny, all grow from a joint point.
After blossoming (if you can call it this way) there are no berries or fruit. All the seeds mysteriously disappear.
The bark is black.
The tree is not tall. It equals an apple tree in size.
It is growing in Eastern Europe, but it was planted by someone. It is not a native plant and there are no plants like this around.
It's deciduous. The leaves are gentle and soft, not like apple or pear tree leaves. The leaves are not shiny.

I am attaching pictures of leaves and flowers. If you need a picture of a tree trunk, let me know, I can take some as well.

Where is it from?

Right now it is growing in Eastern Europe, it was definitely planted by someone, but the tree is definitely not native species. It's the only tree like that I have ever seen my whole entire life.

Okay, I will take one soon and post here.

It's deciduous, of course.  The leaves are very soft and gentle.

I added a picture of a ripped leaf. It is a zigzag clean break, no stringy strands.

It looks like a Purging Buckthorn (Rhamnus cathartica) - Native to Europe and North Asia. It is the food-plant of the Brimstone butterfly.

See Woodland Trust
If it is isolated from others perhaps it is rarely pollinated and never produces berries.

From http://www.sussex-butterflies.org.uk/conservation/allotments/
It is unusual to see such a large specimen but here is a photo taken in Oct 2016 at Kingley Vale National Nature Reserve in West Sussex, UK. The vale has many Purging Buckthorn of a mature age and size as shown in middle of the photo with people to give some scale. Well worth a visit if you ever get a chance, it is one of Europe's most impressive yew forests.

https://en.wikipedia.org/wiki/Kingley_Vale_National_Nature_Reserve
See also http://www.hainaultforest.co.uk/5Purging%20buckthorn.htm

I too suspected this species but its leaf size is larger than OP's leaf  (if 3cm is not an average lower limit). Size

Maybe it is undergoing senescence and its leaf size is naturally diminishing?

If this is Rhamnus cathartica, it must be one of the biggest ones I have ever seen. I only know it as a small shrub, up to 5 meter max. Can't it be another Rhamnus species?

Added a photo of Kingley Vale where there are many large Purging Buckthorn 'trees'. Of course, yes it could be something else.

First and foremost I want to thank you for trying to identify this tree. I believe you are on the right track and it is most definitely some buckthorn. The only two things that puzzle me are: 1. the leaves are very tiny. Like 2x3 are the biggest leaves out of the bunch.

I never saw it fully bloom. Like those little green buds stay there for a week and then they mysteriously disappear. The buckthorn in your picture has flowers. Could my be male? Also, my tree looks like an actual tree where buckthorn is more like a shrub.  Wiki says buckthorn is spiny. "My" tree does not have any thorns. Thank you for your guess. It's nice to know that somebody actually can identify this tree. You are amazing.

@treehugger Buckthorns can lack spines.

Then most likely it's a buckthorn, just a very old one.


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Do non-green flower colors have any functional interactions with the sun?
I always hear the pseudo-evolutionary claim "plants are green because they need to use red and blue light".  If this premise to my question is true,
What (if any) other functional relationship occur between the color of the blossom of the flower or the color of the leaves in the fall, and the spectrum of the sun.  Could it be said that plants are actively absorbing a particular spectrum for a particular purpose by expressing particular colors other than green?

I was thinking someone with experience with proteins like opsins would have a better chance of answering the question.

Some functions of non-green flower colors:
#1: plant-animal interaction. Flower colors act as signals received by animals with eyes (e.g., pollinators, which many plants need to attract in order to reproduce).
However, it sounds from your question as if you're looking for other physiological effects. Two that come to mind are:
#2: heat. Flower color and opacity have a great effect on flower temperature.
This can be especially important for arctic and alpine flowers. Many of these are not only shaped like satellite dishes, but even pivot to follow the sun. This creates a warmer micro-environment which can be important to attracting pollinators and to increasing/speeding seed production. (See, e.g. Mølgaard 1989)
#3: UV protection. Certain pigments can be more effective at filtering UV.
I work in the alpine and occasionally encounter "glasshouse" plants, which have translucent floral parts that act to create warmer microenvironments, with the same effects as above. In addition, these floral parts have been shown to be more effective at UV filtering than green floral parts (Tsukaya 2002)
*edit: as these papers are behind paywalls, I'll also point out that the Wikipedia pages on Heliotropism and Rheum nobile contain similar information.

 Mølgaard P. 1989. Temperature Relations of Yellow and White Flowered Papaver radicatum in North Greenland. Arctic and Alpine Research 21: 83–90.
 Tsukaya H. 2002. Optical and anatomical characteristics of bracts from the Chinese “glasshouse” plant, Rheum alexandrae Batalin (Polygonaceae), in Yunnan, China. J Plant Res 115: 59–63.


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What mechanism suppresses melatonin release in humans?
I'm looking at melanopsin, a photo pigment in the human eye. One of its actions is to trigger suprachiasmatic nuclei SCN to suppress melatonin release. I'm interested in learning what is the exact mechanism that actually suppresses melatonin release. Is it another hormone or some way of modulating the pineal gland function?

Is this not answered within your own previous question?
http://biology.stackexchange.com/questions/3614/how-are-melatonin-levels-measured-in-humans?rq=1
"melatonin release is suppressed by blue light with peak suppression occuring at 420-480nanometer range.
This light is registered by Melanopsin, a photopigment in the eye.
Melanopsin signals the Suprachiasmatic Nucleus, the master clock of the human body.
Suprachiasmatic nucleus makes a decision to suppress melatonin release in response to blue light observed."

So you're interested in the nature of the signal between melanopsin and the SCN?

To clarify: I know that SCN makes a decision to suppress melatonin. What interests me is what takes place during the actual process of suppression. What physically ensures that pineal gland stops producing melatonin. Is it another hormone that is released?

From Kalsbeek et al 1999 Neuroscience (link 1, link 2)

"retina-mediated photic activation of suprachiasmatic nucleus neurons
  induces the release of GABA from efferent suprachiasmatic nucleus
  nerve terminals, resulting in an inhibition of melatonin release by
  the pineal gland."

So it appears that GABA is key. When the retina is stimulated by light it results in activation of the neurons within the SCN which then release GABA. There is much more detail within the article and this is not my field so you may get more from reading that rather than my summary attempts.

Take a look at this (especially page 938): Coordination of circadian timing in mammals by Steven M. Reppert & David R. Weaver Nature 418, 935-941 (29 August 2002) | doi:10.1038/nature00965

Sodium-dependent action potentials provide the primary means by which
  the SCN transmit circadian outputs to other brain areas and are
  essential to its role as a pacemaker1.
Signalling molecules from SCN efferents include neurotransmit- ters
  and secreted factors. An output role for secreted factors comes from
  the results of SCN transplant studies that suggest that the
  alternating activity of SCN-derived ‘inhibitory’ and ‘activating’
  factors drives locomotor activity rhythms (and hence rest/activity and
  sleep/wake cycles) in rodents

There was also a mention of per/cry gene expression.

Welcome to Biology SE.  It would be helpful if you could summarize the findings in your own words: you cannot count on everyone having access to the journal, or the link even working in the future.

Sure, will do :-)

Thanks for a great article! It does not explicitly state how the pineal gland is affected though.


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What are the variables that control/influence the color of oranges(Citrus sinensis)?
I hear that Oranges cultivated in tropical areas of the world tend to be greener when ripe, is that correct?
Even the same type of Orange differs in color if cultivated in California or Florida. I hear that's because of the climate (colder nights == oranger oranges)
But, at the same time, oranges tucked in between the tree leaves tend to be greener, for they need more chlorophyll to make the most use of less access to sun rays.
Could someone correct my assumptions? Also, if possible, list the pigments and processes involved?

Naturally, ripe orange skins are usually green-yellow. In colder climates, they will turn orange over winter, since in the cold the chlorophyll will start degrading and stop masking out yellow/orange carotenoids in the skin. If the fruit is picked in fall (and not let ripen or degreened) they will have green color.
Ehtylene gas, which is a natural plant hormone, is sometimes used to give them more uniform, orange color (degreening). Also, some oranges cultivated in the US are dyed with Citrus Red 2 to make their peels orange.


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Does the molecular composition of human body change after a period of time?
I was discussing change in human biology over time and my two in-laws charged in saying, "we're molecularly different after x". I didn't pay attention to what time period they exactly mentioned (hence x).
I am familiar with how mainstream media warps research data to be entertaining. So would serious researchers and scientists consider bold statements such as "we (humans) are completely different after 6 years!" as nothing more than anecdotal?
I'm not talking about decomposition after death but rather about processes in the live body.


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Species identification please - Bug is a plague for Italian Stone Pines (Pinus Pinea)
They hangout on the top of Pinus pinea and spray a sticky substance all over the place. Size is about 2mm (head and abdomen) may be 4mm including antennae and legs. Could you please help me identify it and understand some of its habits and biology? I took the photos in a coastal town in Southern Spain. Thanks!!

That's and aphid (Hemiptera:Sternorrycha). Most likely, it belongs to the genus Cinara, which is common on trees. https://en.wikipedia.org/wiki/Cinara


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When contracting a muscle will the muscle spindle stretch or contract?
When you contract your muscle, will your muscle spindle stretch or contract? And why? I was always under the impression that it was contracting your muscle spindle, but now I am not sure.

Welcome to Biology S.E.! If you need additional advice on asking or answering questions, please visit The Help Center.


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By what mechanism does Risperidone swell breast tissue?
There has been much talk of the anti-psychotic drug Rispeirdone causing un-natural breast tissue growth as well as galactorhea (milk production). Especially in young men and boys.
What is the mechanism of this drug that is causing this? Is it actually introducing some amount of female hormones into the male's body or is just causing increased production of them?

There is a class-action lawsuit against the makers of this drug (a.k.a. Risperdal) because of it causing breast development in men and boys. So the answer is yes.

The edit is much better. +1 and retract close vote.

Risperidone prevents dopamine from acting on the pituitary gland by blocking dopamine type 2 receptors. One of dopamine's effects on the pituitary is to suppress prolactin production. In patients taking risperidone, prolactin production thus increases and prolactin levels in the body are higher than normal. In younger males, this can result in abnormal growth of breast tissue and even milk production.
See e.g. Melkersson, K. I. (2006). Prolactin elevation of the antipsychotic risperidone is predominantly related to its 9‐hydroxy metabolite. Human Psychopharmacology: Clinical and Experimental, 21(8), 529-532.

Could you add a reference for this?


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How does the drug MBC effect the depolymerization of microtubules in eukaryotic cells?
I have tried to look for the mechanism of how methyl benzimidazol-2-yl-carbamate affects microtubules in eukaryotes, but what I found wasn't very useful:

Quilan et al 1980 assert that it acts by inhibiting polymerization of microtubules rather than by directly depolymerizing them.
In "The Cytoskeleton: A Target for Toxic Agents", it is mentioned that

..strains of Aspergillus that were resistant to the drug had a lower affinity for MBC in a binding assay, whereas super-sensitive strains had a higher affinity for the drug.

Any references would be appreciated.
In Summary: I would like to know how the drug MBC effects the depolymerization of microtubules in eukaryotic cells. I would also appreciate any scientific references.

Welcome to Biology Stack Exchange! I made a few edits to your post, you are welcomed to change it back to the original if you feel it better describes your question.

Carbendazim inhibits microtubule polymerization by directly binding to tubulin, preventing subunits from interacting. Therefore, mytotic spindle malforms and potentially causes aneuploidy in affected cells. Mechanisms of resistance are often shown to be changes in membrane permeability to the compound.

CARBENDAZIM (addendum)


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8 abdominal muscles but 10 pack

Simple question, how is it possible that there are people who appear to have 10 pack abdominal muscles while the human body has only eight?

While each muscle has a single "belly", many have multiple "heads". That is, portions of the muscle attach at different locations. These attachments follow, as separate bundles, down into the belly of the muscle. Biceps, for example, have two heads. I suspect it's possible these may appear as different bulges in a well developed gym rat.

The only "way" someone can have a 8-pack or 10-pack is due to genetics. Across the rectus abdominis muscle you have either 3 or 4 tendinous bands going over it, consequently resulting in either a 8 or 10 pack.


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What buffer should I choose for IEX chromatography for purifying IgY
I will use ion exchange chromatography with an anion exchange column to purify chicken IgY. Prior to this I did dialysis to remove salts from previous purification steps, is it possible after this step to just change buffer system?
The pI of IgY is 5.6-7.6, and so, what buffer should I use for the chromatography? I know I want the IgY to be negative, so I would want pH in start buffer to be higher than pI?
I bought a column but it has not arrived yet. Does it come with recommendations on preferred buffer system for the chromatography or can I use any one I want? And also, what buffer should I use to elute my protein?
Do you have any recommendations?
In previous steps, prior to dialysis, I used phosphate buffered saline with pH 7.
Thanks in advance

Your column manual will probably come with buffer recommendations (these manuals are also often available online). You can also search for publications that have purified IgY by anion exchange chromatography and use their procedure as a starting point.
Some generalities to keep in mind for buffer selection:

Buffers are most effective when the desired pH is close to their pKa. A rule of thumb is to choose a buffer with a pKa within 1 unit of the desired pH.
For anion exchange, the pH should be higher than the pI of the protein so that it carries an overall negative charge and will bind to the positively charged column. Another rule of thumb is to keep the pH about 1 unit above the pI. If the pH is too low, the protein will not bind. If the pH is too high, the protein will require more salt to elute, which can cause instability/precipitation.
For anion exchange, the buffer itself should be neutral or positively charged so it does not bind to the column. This can affect binding of the target protein both by its ionic strength and localized changes in pH.
Choice of pH depends on whether your column is "strong" or "weak". The charge on the functional group of a strong ion exchanger will not appreciably change over a wide range of pH whereas the charge on a weak ion exchanger is only maintained over a relatively narrow pH range.
This may go without saying, but make sure that your protein is stable in the buffer and pH you select. You may also want to keep in mind the buffer requirements of any downstream applications and choose one that is compatible to simplify purification.

Elution is generally done with a salt gradient, though a pH gradient can also be used. In a typical setup, you would have two solutions, both with the same buffer and pH but one with high salt (let's call it B) and one with no salt (let's call it A). The sample is applied in buffer A and then a gradient from 0 to 100% buffer B is applied to the column with fractions collected periodically. The most commonly used salt for ion exchange is sodium chloride (so the counterion for anion exchange would be chloride). Since relatively high concentrations of salt are often used for elution, in general you want to avoid counterions like sulfate that have a stronger salting-out effect.

You're simply the best!


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What type of spider is this that just decided to stop my plans of sleeping

This tiny little spider decided to stop my plans of sleep at 1am, since I have no plans of getting to sleep any time soon may someone tell me what type of spider could be this monsterous!

Welcome to Biology SE! Please provide more information about the size and location of "the beast" so that we can help!

It is a male Steatoda, probably S. grossa (picture below).  These spiders are often called False Widows, since the females are generally a large purply black and look similar to their cousins the Black Widows. Steatodas are pretty harmless, though, although a couple of species (in the UK/Europe) are known to sometimes produce bite effects like a mild Widow bite.  Not at all dangerous, but a little disquieting if you're the one that gets bitten.  Presuming that you're in North America, though, you're fine.  Steatodas are Theridiid ("cobweb") spiders common in and around houses, and the harmless males are often encountered when they wander around looking for love as adults.
Bug guide has a good section on S. grossa, including lots of images of male spiders like this one.
https://bugguide.net/node/view/6932
Information on Steatoda envenomation is broadly available, but not in great detail.  The Wiki entry appended below covers the ground as well as any of them.
https://en.wikipedia.org/wiki/Steatoda

A spitting spider. Neat little spiders that I get in my house quite frequently. They're harmless and one of the few types of spiders that have six eyes instead of eight. Here's some more info.
https://imb.uq.edu.au/article/2017/11/spitting-spiders-natures-strangest-hunters
https://en.wikipedia.org/wiki/Spitting_spider


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Identification of that red and black bug
Found in France countryside, few hours ago, on a bushlike plant in direct sun light.
There is dozens of individuals, by groups of 5-ish, everywhere on the plant, along aphids, maybe sucking the plant's sap.
Looks like a stink bug, with unexpected colors. Some of them were attached two-by-two by their bottom (mating, probably ?).
Sorry for the bad photo quality.

This looks like Graphosoma italicum (aka G. lineatum; it is a stinkbug):

Graphosoma italicum had been regarded as either a subspecies, or a mere synonym to G. lineatum.
G. italicum can reach a length of 8–12 mm (0.31–0.47 in). The body is almost round, with a large shield. The basic color of the upperside of the body is bright red, with wide black longitudinal stripes. The pronotum has six black bands. The antennae are black. Also the sides of the abdominal segments (connexivum) are red with many small black spots. The legs are black.
Wikipedia

I think you are right that they are mating. Here is another picture of the species mating:

ibid

(Despite it saying that the legs are black, they are clearly striped in some specimens, like in your picture.)
It's found in France, according to Honeyguide.


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How can autoimmunity be selective?
Vitiligo is a skin disorder where the pigment disappears. More on Wikipedia. This is believed to be caused by autoimmunity and has made me interested in autoimmunity in general.  I am still very much a layman, however.
One of the characteristics of vitiligo is that it is uneven. Some patches of skin look normal, others are completely albino-like.
If the immune system has decided that skin pigment is an enemy, why doesn't it destroy all the skin pigment?
I understand that little is known about vitiligo, so I will accept answers describing similar effects in other autoimmune disorders.

Your supposition is incorrect, the immune system does not destroy pigment


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What differences in effect does fast repetitive exercise have compared to slower muscle-building exercise?
As a drummer who likes to play high-energy music (fast, aggressive metal) it's safe to say I burn a fair amount of calories when doing so. But I've been drumming for over a decade and despite the amount of it that I've done, it hasn't really had any (visible) effect on muscle growth. Every time I drum I try and push the limit of how fast I can go until I start to ache, so I'm definitely doing something to the muscles in my arms and legs, but it definitely isn't building mass.
I remember reading somewhere that speed based exercise can actually reduce muscle mass as the body tries to make itself more efficient, but heard no evidence to support this or an explanation of how.
Can someone please explain to me how exercise such as fast drumming affects muscle growth and development in relation to traditional muscle building exercise like lifting weights?
I am looking for a explanation of the biology behind this by the way, not fitness advice.
Clarification - for non-drummers, the "speed exercise" I'm referring to is what are called blast beats, where the aim is to keep an often inhumanely fast repetitive beat going. It's common in more "extreme" music such as death metal. While trying to maximise efficiency by minimising the amount of effort required is the goal, the muscles required are undergoing a rapid contraction-release cycle, often sustained for minutes at a time, and sometimes for an entire song.

That's an interesting question +1. Just as a comment, body building is typically done by using weights/force and to increase the weights/force over time. Those drumsticks are too light. Although it consumes energy, it doesn't need muscle mass to do it. It needs endurance to complete an hour or two of intense practice, but no muscle mass per se. Further, I worked for a long time unloading trucks. Day in day out lifting ~15 kg boxes for months on end didn't do anything either.

With that in mind, what factors determine a muscle's endurance?

I think that's an entirely different question altogether. Muscle building is akin to body building. Endurance quite another. Do you want muscles or endurance? Perhaps a clarification in your question proper is appropriate.

what do you mean by "speed based exercise?"

In this case I mean what drummers would call blast beats, where the aim is to keep a continuous but very fast beat going (some would refer to it as a wall of noise). Usually the aim is to minimize the amount of movement required because of the extreme speeds, so it's really about efficiency. But even though the movement is as minimal as it can be, the fast "back and forth" can still tire you out.

Your body creates muscle after an exercise through a process where it fuses muscle fibers together to form new muscle protein strands called myofibrils. these myofibrils increase in size as workout intensity increases, leading to muscle growth. Muscle growth occurs when muscle protein synthesis happens faster than muscle tissue breakdown 1.
Since you are never really increasing the amount of strain on your muscles(i.e. by adding more weight to a workout) there is no incentive for your body to create more myofibrils, rather it will just replace the ones that were torn during your drumming.


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Yellow dandelion-like flowers emerging from beach in early spring
What are these yellow-flowered plants?

The yellow flowers look similar to dandelions, but the stalks are much thicker.
No leaves yet, just flowers.
March 30, 2024. Unusually warm winter this year.
Lake Ontario beach. 50ft from the lake. 5ft from grassy embankment. Port Hope, Ontario.
Flowering at the same time as snowdrops and Cornus mas in my garden in a nearby town.

Not certain, but it looks pretty well like it could be Tussilago farfara (colt's foot or coltsfoot). It's a common invasive plant in your area.
https://en.wikipedia.org/wiki/Tussilago
https://www.fs.usda.gov/database/feis/plants/forb/tusfar/all.html

this plant deserves a longer answer with more details,like it is one of the first plants to flower in spring and it is able to increase it`s internal temperature to well above ambient temperature,it makes the flower survive even when there is frost during the nights in spring.

Tussilago/colt's foot is a fascinating plant, and I'm glad you identified it properly. I was unaware of its invasiveness. I was glad to see a patch on my property years ago and sad to see it disappear over the years. (Glad because at the time, I was interested in medieval herbal medicine. Tussilago is one that actually worked. Alas, it's a carcinogen, too.)

@trondhansen - More is nice, but the OP asked for ID. They can learn more by looking at the links, or if you like, you can post a more informative answer.


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For how long would a flu-contaminated parcel be an effective disease vector?
A parcel has been delivered and contaminated by a person who has the flu.
For how long would the parcel be an effective disease vector?

Is spraying it with a 10% solution of bleach, letting that sit for 10 minutes really not an option?

Are we talking about actual influenza here? Most people, when they say “I have the flu” mean “I have a moderately serious cold”. The symptoms are somewhat similar but the pathogens causing it, as well as the severity of the disease, are completely different.

@swbarnes2 Rubbing alcohol or hydrogen peroxide also make good disinfectants, if bleach is not readily available.

@KonradRudolph true, and to a certain extent, both of those things ("I have the flu" means I have a respiratory virus, and most non influenza respiratory viruses are less severe) cancel out. In a community where confirmed influenza cases have spiked, the sensitivity of "complains of flu like symptoms" is high (which is what you want), and the specificity is higher than you'd think.

Worth noting, you can avoid this kind of concern in the future by getting your flu shot.

@Maxander you should avoid people with flu-like symptoms and practice good hygiene regardless. The flu shot is beneficial in a number of ways, but does not replace these measures.

To the close voters, this is not a "personal medical question", as defined and used here. It could be edited to depersonalize, but unlike personal medical questions, you need no personal clinical information to answer this one. When I was in clinical practice I would much rather someone find this answer on a website than bother my nurses with "how long should I wait before handling a package". The correct answer here is is not "go see your doctor"

OP, I've edited your question to make it more clearly on topic here and keep it focused on your question of interest, which is about the package itself. I disagree with the close votes you were getting, but your most recent edit included more text about your personal exposure history.  Please roll back or tweak the edit if you'd like. Be aware, though, that the more the question is "am I personally at risk for the flu" and less it is "what is the biology of flu transmission via fomites", the more likely it is this question will be closed.

Thing to note: postal packages might also have been contaminated several times due to being handled by infected or contamintated postal workers, or by being in contact with other infected packages, etc... And not only by flu, but other infections too. Actually, chances that any package you receive is sterile is practically nonexistent. So just practice good hygiene always (wash your hands, do not put them in mouth/nose/eyes etc)

@DeNovo I've simplified the question. What do you think of it?

@Wilson personally, I think it's less fun now, but my preference for fun questions might be a minority preference :)

How long should I wait before handling the parcel to avoid contracting the virus?

If you use gloves, or don't touch your face and just wash your hands after opening, you don't have to wait at all.  If you don't use gloves or want to pick your nose, rub your eyes, or fiddle with your beard while opening the package, wait 24 hours if the package is nonporous, and 2 hours if it is not. Generally, whether contaminated or not, don't lick, eat, inhale, or rub your eyes with the package :)
Influenza and similar respiratory viruses are transmitted by large droplets, aerosols, and fomites. Your package is a fomite, an object that can be contaminated and transmit disease. There is some debate about what mode of transmission is most significant for influenza, but fomites definitely do transmit influenza and similar viruses. In a study of homes and daycare centers with children who had an active influenza infection, 59% of home objects that were tested were positive for influenza. It's reasonably likely that your package was, at least at some point, contaminated.
@LDiago's answer is useful here, but deserves some clarification. The UK National Health Services information cited in that answer comes from this seminal study. I'm not entirely happy with the wording on the NHS website, though. Virus survives on nonporous surfaces for 24-48 hours. Virus is transferred from nonporous surfaces to hands in detectable amounts for 24 hours. If your package is paper, the relevant test is transfer from cloth or paper. Virus survives for 8-12 hours, and is measurably transferred to hands after 15 minutes to 2 hours. In any case, virus transferred to hands from a fomite survives for only 5 minutes.
Infection from fomites, however, requires virus to be transferred from the fomite to (typically) the hand, and then from the hand to respiratory tract epithelium. Inoculation of nasal passageways is sufficient for infection in laboratory conditions. Conjunctival and oral inoculation may also play a role. You can read more about this in Cecil Medicine Ch. 372 and Murray Medical Microbiology Ch 59.

i am sorry. I agree with you. I didnt checked the relevence of this study.... So thank you for your answer :)

+1 for the excellent advice of not inhaling mail order parcels!

"wait 24 hours if the package is nonporous, and 2 hours if it is not." - dang, that double negative is really tripping me up. So, you mean, "wait 2 hours if the package is porous, and 24 hours if it is not"?

@cell0 I rolled this back because the appropriate usage here is "Virus survives", not "the virus", and "the relevant test is transfer", not "transferred". The test isn't transferred, the test is transfer (of virus). I appreciate your editing efforts. Please try to evaluate whether you've changed the meaning of a phrase by editing it, though.

From the UK National Health Service:

Flu viruses capable of being transferred to hands and causing an infection can survive on hard surfaces for 24 hours. Infectious flu viruses can survive on tissues for only 15 minutes.
Like cold viruses, infectious flu viruses survive for much shorter periods on the hands. After 5 minutes the amount of flu virus on hands falls to low levels.
Flu viruses can also survive as droplets in the air for several hours; low temperatures increase their survival in the air.
Parainfluenza virus, which causes croup in children, can survive for up to 10 hours on hard surfaces and up to 4 hours on soft surfaces.

Any idea why the virus can survive 24 hours on hard surfaces, but only 15 minutes on a tissue?

How does the tissue kill the virus in 15 minutes?  It doesn't have anything that can break down the virus afaik.

@Nelson, dehydration.  Most viruses (and bacteria) are quite susceptible to being dried out.


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Red flower with yellow star in center with fig-like leaves
This plant has red flowers with a yellow star in the center and has fig-like leaves.

Location: Toronto
Size: 4ft tall by 3ft wide
Date: July 25th, 2020

What is it?

They are common hollyhocks, they come in many colors. As a little kid from Chicago , I was impressed by flowers taller than me when visiting rural Wisconsin . Then the standard for hiding/decoration outhouses.


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Does dormant poison ivy contain urushiol in the above-ground portion of the plant?
I recently had a run-in with poison ivy (late spring; Canadian shield).
The poison ivy plants had not yet leafed-out so I failed to identify them as a hazard.

I think I must have either trampled and broken the stems of the plants, or dug up and broke the roots (or both), and therefore was exposed to the poisonous sap.
While the plants had not leafed-out, they were also not truly dormant (it wasn't the middle of winter).

Question:
I'm wondering if there is a time of year when the above-ground portion of poison ivy plants would not contain urushiol.
In other words, in the dead of winter, when the plants are dormant, do poison ivy twigs contain the poisonous sap?

Let's tackle your second question first. Yes, leafless poison ivy still contains Urushiol, and still can give you a rash. Here are three sources supporting this statement: a first-aid sales company, a newspaper, and a non-peer reviewed infosheet from a university. Be careful with poison ivy all year.
Your first question has slightly more nuanced implications. To know if there is a time of year where above-ground poison ivy doesn't contain Urushiol, first we have to think about when and where the urushiol is produced in the plant cell, where it is stored, and how it degrades. Some studies have shown that Urushiol and like compounds are present throughout the plant. In this older article, they extract it from both the leaves and the twigs, but more current advances have been able to focus on urushiol in just the stem. I have seen no evidence that it reduces at any time of year, and very little publication on how it is produced biochemically, although people are working and have worked on the topic. I am interested to learn more about this aspect from other answers to this question.
(An aside: you can also pick up a Urushiol rash from some cheap furniture, so this compound can stay poisonous on a wood surface for quite a while. Unfortunately, I'm speaking from first-hand experience, which is backed up by this informative article about Urushiol!)

Thank you. That clears things up. And the Japanese furniture thing is quite interesting/horrifying!


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Why is the spinal cord shortened in some vertebrates (cauda equina) but not in others?
Hodos, 2009, mentions that the "spinal cord tail" that humans have is not present in most vertebrates. This page mentions cauda equina is not present early on in human embryonic development, but forms later on because vertebral column gets longer. Hodos mentions anglerfish (Lophius piscatorius) also have a "spinal cord tail". What does it look like across other species, like, wolves, gorillas, tigers, crocodiles, dolphins, elephants? Mainly, instead of going species specific, is there any pattern to why some species develop a cauda equina while others do not?
Edit: I can add that according to Uehara, teleosts in general have a spinal cord that extends along the entire vertebral canal, while tetraodontiform fishes have a shortened spinal cord with a cauda equina. This corroborates Hodos claim that most vertebrates have a spinal cord runs the entire length of the vertebral column (teleosts account for 50% of all vertebrates, so... ) Have looked up that dogs have a cauda equina. But, have not been able to understand exactly why some species develop a cauda equina while others do not.
Edit: more context, from Uehara, 2015, "the spinal cord in the majority of the teleosts, the urodelan amphibians, and the reptilian sauropsids and birds extends through the entire vertebral canal, but in the anuran amphibians and mammals is significantly shorter than the vertebral canal."
Edit: more references giving good overview of phylogeny and shortening of spinal cord, but, not really a definitive cause. Nieuwenhuys, 1964 and 1998, and Kuhlenbeck, 1975.
References
Hodos W. (2009) Evolution of the Spinal Cord. In: Binder M.D., Hirokawa N., Windhorst U. (eds) Encyclopedia of Neuroscience. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-540-29678-2_3171
Uehara, M., Hosaka, Y. Z., Doi, H., & Sakai, H. (2015). The shortened spinal cord in tetraodontiform fishes. Journal of morphology, 276(3), 290–300. https://doi.org/10.1002/jmor.20338
Nieuwenhuys, R. (1964). [Progress in Brain Research] Organization of the Spinal Cord Volume 11 || Comparative Anatomy of the Spinal Cord. , (), 1–57. doi:10.1016/s0079-6123(08)64043-1
Nieuwenhuys, R., ten Donkelaar, H. J., & Nicholson, C. (1998). The Meaning of It All. In The Central Nervous System of Vertebrates (pp. 2135–2195). Springer Berlin Heidelberg. https://doi.org/10.1007/978-3-642-18262-4_24
Kuhlenbeck, H. (1975). The Central Nervous System of Vertebrates, Vol. 4 (Spinal Cord and Deuterencephalon) || VIII. The Spinal Cord. , (), 1–287. doi:10.1159/000395633


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Beautiful blue enigmatic insect (mantid?) in Kenya
This beautiful insect was found in Kenya today - and we don’t know what it is. We think it may be a mantid of some sort?!
Nairobi kenya, croton trees, cape chestnuts, bougainvilliea, there is quite a lot of lichen on the trees.
Despite looking to be the size of someone's arm, it's about 2” long!
Needless to say, no-one had a good camera at the time. Just phones!
The colour of the insect is very similar to the lichen on the trees (hence the mention above).
Someone suggested it was a 'grizzled mantid' Gonatista grisea (Fabricius), but we didn't think they are found native to Kenya - and likewise, we don't see a protuberance on the back of grizzled mantids... Still hoping for an answer.
You can see it also has very small wings, which I hear is a feature of some mantids - micropterous mantids.
I don’t know anything about these - someone said ‘some sort of bark mantis’.
Further update - The pronotum of Tarachodes spp females has two conical tubercles. The males are mostly fully winged, whereas the females often have shortened wings.
So it's probably a female Tarachodes species found in Kenya (or thereabouts).

I don't have time at the moment for a full answer, but Patel, S., Singh, G. and Singh, R., 2016. A checklist of global distribution of Liturgusidae and Thespidae (Mantodea: Dictyoptera). Journal of Entomology and Zoology Studies, 4(6), pp.793-803. might be a helpful resource here.

Actually, the above might be less useful since it looks like some taxonomic reorganization occurred in 2015. I'd recommend exploring Epaphroditidae

@theforestecologist - thanks! I went and checked the references you gave, but supplied photos of those species all looked like mantises, whereas this one doesn’t so much!

It's indeed nearly the same as a gonatista grisea family Liturgousinae / Liturgusa, perhaps you can msg a mantid forum.

@aliental, until yesterday I didn’t know there were so many mantids, let alone forae that specialised in them!!

I'm converting my numerous comments into an "answer" -- I don't currently know the exact species, but I can at least explain some of my thoughts more completely.
Your specimen looks a lot like Gonatista grisea, a tree mantis that mimics a lichen -- as you mention in your post. However, G. grisea, is native to the southeastern USA. I could find no evidence of any reports finding this species in Africa, so we will rule it out.
If we examine some other species of the Gonatista genus (e.g., G. jaiba, G. major, G. phryganoides, and G. reticulata) we find that they are all neotropical and not found in Africa. Therefore, let's look elsewhere.
So, I would recommend examining other close members in the same family that are found in Africa.

I originally recommended reviewing Patel et al (2016) because they provide a checklist of the global distribution of other members of the Liturgusidae family. Using this guide, we could examine known African genera.

They list Dactylopteryx, Majanga (Madagascar), Theopompella, and Zouza as African genera.

However, I had not realized that there had been some taxonomic rearrangements, and Gonatista is now in the family Epaphroditidae.

The other genus in the same subfamily as Gonotista, Gonatistella, is monotypic, and G. nigropicta is not your species.

The other genera in this family, Epaphrodita and Callimantis, (as well as the now-moved genus Brancsikia) also do not seem to contain any species I could find that are morphologically similar to yours.

So maybe we should look elsewhere in the previous Liturgusidae...

Subtribe Humbertiellina in the Gonypetidae  family are just one example of another group perhaps worth investigating because it too was once contained within the original Liturgusidae family along with Gonatista and because some online evidence suggests some members of this subtribe (e.g., Humbertiella and Theopompa) share some similar physical characteristics to Gonatista.

Some non-reputable sources (e.g., here for Humbertiella and here and here for Theopompa servillei) show specimens similar to yours with labels as one of these two genera. I couldn't find consistent imagery or reputable sources with imagery to support either one as correct...
(Also, Patel et al. (2016) suggest these genera are recognized as Asian genera, and so they may be geographically unlikely anyway like Gonatista).

However, perhaps trying to solve your unknown specimen using taxonomic and trait-similarity approaches could be misleading.

According to Rivera (2010): "Whereas the monophyly of Mantodea is well supported, the evolutionary relationships within the order are still contentious. Several classification systems for mantids have been proposed...However, the natural affinities among supraspecific taxa have been extremely difficult to discern due to the highly variable and derived morphology of these insects."

According to Schwarz & Roy (2019): "As already noticed by previous authors, external morphology is highly homoplastic and does not provide useful systematic tools above subfamily level."

Schwarz & Roy (2019) do suggest that the morphology of male external genitalia may be useful for relating individuals as these traits tend to be fairly congruent with more recent molecular phylogenies. You could start there for further research.

(I myself can't discern meaningful detail of the genitalia in your photos, nor am I any type of expert on mantises, so this route of inquiry might be too much in the weeds for me...)

If you find a good key for your region, you might want to check out Brannoch et al (2017) for a "Manual of praying mantis morphology, nomenclature, and practices" to help you with all the mantid jargon. [it appears to be a very thorough and excellent resource!].
I will update this post if I find anything more definitive for you...

Citations
 Brannoch, S.K., Wieland, F., Rivera, J., Klass, K.D., Béthoux, O. and Svenson, G.J., 2017. Manual of praying mantis morphology, nomenclature, and practices (Insecta, Mantodea). ZooKeys, (696), p.1.
 Patel, S., Singh, G. and Singh, R., 2016. A checklist of global distribution of Liturgusidae and Thespidae (Mantodea: Dictyoptera). Journal of Entomology and Zoology Studies, 4(6), pp.793-803.
 Rivera, J., 2010. A historical review of praying mantid taxonomy and systematics in the Neotropical Region: State of knowledge and recent advances (Insecta: Mantodea). Zootaxa, 2638(1), pp.44-64.
 Schwarz, C.J. and Roy, R., 2019, March. The systematics of Mantodea revisited: an updated classification incorporating multiple data sources (Insecta: Dictyoptera). In Annales de la Société entomologique de France (NS) (Vol. 55, No. 2, pp. 101-196). Taylor & Francis.

Looks like a Bark Mantis. Genus Tarachodes.
https://www.inaturalist.org/taxa/570572-Tarachodes
Here is a description of the features within the Genus from the link above and why I believe your picture reflects this genus. To narrow down to species appears more challenging as there are many species in the genus:

The bark mantises and ground mantises (genus Tarachodes) are praying mantids now placed in the family Eremiaphilidae[1] that are native to the Afrotropics. They are generally light brown but more silvery on the wings. The wings are attractively reticulated, and the veins may be mottled dark and pale.[2] The head is wider than the pronotum, which is rounded anteriorly, and doesn't overlap with the rear of the head. The pronotum is depressed, with its sides more or less parallel, and only a weak supra-coxal bulge is present.[3] The anterior tibia are flattened and greatly expanded longitudinally, and the tibial claw does not fit into a pit between the 1st and 2nd external spines of the anterior femora, as in a few mantis groups.[3]

You are more likely to get a positive response to your answer if you explain why your identification is correct. Specifically, please [edit] your answer to add discussion of key features that led you to this conclusion and supporting references or at least validated images. Without this your answer is indistinguishable from opinion and thus inappropriate for this site.

While this link may answer the question, it is better to include the essential parts of the answer here and provide the link for reference.  Link-only answers can become invalid if the linked page changes. - From Review

And also, the link points to an proposed identification. It’s definitely in the same area as the OP (Karen) but I am unsure there has yet been a species ID offered. I am pretty sure it is a mantis of some sort - but that is where my quest ran cold!


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What is Mycoplasma Lyo medium?
Used for instance in this article

The role of genital mycoplasmas as pathogens - - are
  generally neglected by diagnostic laboratories in the United Kingdom,
  possibly due to the lack of a suitable commercially-available culture
  medium. We have evaluated the bioMerieux Mycoplasma-Lyo system using
  qualitative and quantitative studies and have found it to have
  suitable qualities and practical advantages for detection of
  Ureaplasma urealyticum and Mycoplasma hominis.

What is Mycoplasma Lyo medium?
I think it is some sort of anaerobic solid medium for all other mycoplasmas except M. pneumoniae (strict aerobe).

i think your guess is right as lyo means a solution [ref:lyophobic-meaning feared of other solution] and more over the site also has column to comment in where you can comment your question and you might get your direct answer over there

Lyo could just mean the medium is lysopholized. I've checked the company that makes this stuff and not found an answer yet

@rhill45 Did you mean "lyophilised" as in freeze-dried? I don't know of "lysophilised" as a term.


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Why do people have darker skin in sunnier climates?
I don't understand why darker skin is advantageous in hotter climates. Wouldn't it absorb more of the heat? I have heard that it reduces the incidence of cancer, but I would think absorbing more radiation would increase the risk?

One of the important pigments that the earlier answer hinted at is melanin.  Melanin is a brown pigment with photoprotectant properties.
As you correctly identified in your question, exposure to EM radiation (particularly UV and shorter λ waves) is damaging (indirectly) to DNA, which can cause mutations and therefore possibly cancer.  Melanin production is one of the defence mechanisms the body has evolved to deal with this threat.
When DNA is damaged by the UV-B radiation, melanogenesis (the increased production of melanin pigment) is induced.(1)  Therefore, people often exposed to more UVB (i.e. in sunnier climates) are likely to have more melanin in their skin, which makes it appear darker in colour.  It is likely to be the increased incidence of melanin proteins in your skin which leads to the formation of a tan.
Melanin and its derivatives work as photo-protectors (protecting the body from the damaging effects of ultra-violet exposure) by absorbing UV-B photons and converting them into much less damaging infra-red wavelengths (heat energy).  It does this extremely rapidly by internal conversion and extremely efficiently - efficiency in excess of 99.9% has been reported.
As the melanin removes the danger posed by the UV within a few femtoseconds (x10-15 s), the more melanin that is present in skin tissues (and consequently the darker the skin), the lesser the chance of the UV damaging molecules in the skin so the lesser the risk of developing skin cancer.

I heard one proposition that has to do with cancer, and the other side of the coin is related to vitamin D and calcium. If I remember correctly, living in a sunnier climate can affect your skin and cause cancer. The trick is to produce pigments in the epidermis so that the radiation is absorbed by the pigments and doesn't go further inside into the dermis, where it could cause DNA damage to the living dermis cells. The epidermis is constantly shedding dead cells out, so apart from absorbing more heat, there is no problem in absorbing radiation in the pigments at the epidermis level.
Having lighter skin in cloudier climates favors the absorption of sunlight, which is necessary for the production of Vitamin D, which in turn is necessary for the regulation of the levels of usable calcium in the body. Not having enough calcium is associated to all sorts of diseases.
The claims for VitD/calcium/sunlight are sometimes also associated to lactose tolerance in adults. The scene we see in pictures where someone wakes up in the middle of the night, opens the fridge and downs a gallon of fresh milk is actually not applicable to most of the human populations. We are lactose tolerant during our infancy, but for most of us, lactase production slowly shuts down when we grow up. The claim related to calcium metabolism is that human populations living in cloudier climates became adapted to lactose tolerance in adulthood so that they could make use of the calcium available in milk, and that extra calcium would contribute to a balanced calcium metabolism given that there is not much sunlight in their climates.

Totally disagree with the first paragraph of this answer. It is the skin which is most susceptible for malignancy from UV radiation. For the epidermal cells to be shed constantly it has to be produced constantly. This happens at the basal and parabasal layers where there is constant cell division occuring to replace the cells that are shed. As far as any ionising radiation is concerned it is the cells that are dividing which are most susceptible for DNA damage. The cells of the dermis are mostly quiescent and its DNA damage has far less consequence.