text:
Centriole genes Knock-out Experiment in Common experimental animals?
Anyone know of any experiments that have knocked out the genes for producing centrioles in a worm, mouse, fish, fly or whatever animal? Are the genes for centrioles even identified? It has been shown that centrosomes form with out centrioles so I'm curious how lack of centrioles would effect the system of an animal as a whole.

One of the chief components of centrosome is γ-Tubulin.
In this study the authors have reported the effect of γ-Tubulin knockout in mice.
Quoting the abstract:

Gamma-tubulin regulates the nucleation of microtubules, but knowledge
  of its functions in vivo is still fragmentary. Here, we report the
  identification of two closely related gamma-tubulin isoforms, TUBG1
  and TUBG2, in mice, and the generation of TUBG1- and TUBG2-deficient
  mice. TUBG1 was expressed ubiquitously, whereas TUBG2 was primarily
  detected in the brain. The development of TUBG1-deficient (Tubg1-/-)
  embryos stopped at the morula/blastocyst stages due to a
  characteristic mitotic arrest: the mitotic spindle was highly
  disorganized, and disorganized spindles showed one or two pole-like
  foci of bundled MTs that were surrounded by condensed chromosomes.
  TUBG2 was expressed in blastocysts, but could not rescue the TUBG1
  deficiency. By contrast, TUBG2-deficient (Tubg2-/-) mice were born,
  grew, and intercrossed normally. In the brain of wild-type mice, TUBG2
  was expressed in approximately the same amount as TUBG1, but no
  histological abnormalities were found in the Tubg2-/- brain. These
  findings indicated that TUBG1 and TUBG2 are not functionally
  equivalent in vivo, that TUBG1 corresponds to conventional
  gamma-tubulin, and that TUBG2 may have some unidentified function in
  the brain.

Another important gene is pericentrin. Fibroblasts from pericentrin knockout mice show abnormal spindles during mitosis have been studied.

In agreement with a model in which pericentrin is required for correct
  spindle orientation, fibroblasts isolated from PCNT knockout mice show
  a significant increase in cells with disrupted astral microtubules and
  misoriented spindles (Fig. 2; unpublished data; Zheng, G., personal
  communication). Spindle misorientation is shown by an increase in the
  angle formed by the pole-to-pole spindle vector and the cell–substrate
  adhesion plane in pericentrin knockout compared with wild-type
  fibroblasts.

Apparently both TUBG and PCNT deletions (individually) are not lethal.


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How is incomplete dominance different from codominance?
Ok let me start with the definitions of incomplete dominance and codominance.
incomplete dominance - The situation in which the phenotype of heterozygotes is intermediate between the phenotypes of individuals homozygous for either allele.
codominance - The situation in which the phenotypes of both alleles are exhibited in the heterozygote because both alleles affect the phenotype in separate, distinguishable ways.
It is the standard textbook example of incomplete dominance to show a cross of red and white Snapdragons of pure bread. Which yields the phenotypic ratio of 1 red : 2 pink : 1 white. The standard text example of codominance is AB blood type where the A glycoprotein and B glycoprotein together produce a distinguishable phenotype apart from AA or BB.
I really don't understand the distinction between intermediate phenotypes and distinguished phenotypes. How is pink not distinguished from white and red. Consider a hypothetical example of some insect that interprets red, white and pink as distinguishable signals where perhaps red is a safe flower, white is ignored, and pink is dangerous. Say these signal recognitions have evolved based on the insects contrast against the flower pigment and the probability of being eaten by a predator because of increased exposure while getting nectar from the flower. I suppose I have a misunderstanding but wouldn't the red, white, and pink phenotypes be distinguishable rather than intermediates in that case?
So I'm probably just being an idiot but how is incomplete dominance different from codominance?

"Co-dominance, where allelic products co-exist in the phenotype, is different from incomplete or semi-dominance, where the quantitative interaction of allele products produces an intermediate phenotype. For example in Co-dominance, a red homozygous flower and a white homozygous flower will produce offspring that have red and white spots." - from the wiki on dominance

But aren't pink flowers just red and white spots at a molecular level?

I think you may find the answer you are looking for in this post

I ran across this reference for a break down of dominance in "Human Molecular Genetics 3" by Strachan & Read.
http://www.ncbi.nlm.nih.gov/pubmed?cmd=historysearch&querykey=2

incomplete dominance are more likely mean blend, like you make juice contain apple and pear by blender, you can not distinguish them.
codominance can be think as mix, like you a salad that contain apple and pear.
like the example of incomplete dominance: pink flower, pink is differ from white and red, but it related to the two color,
as the example of codominance ABO blood type, blood type AB means it contain A antigen and B antigen, we can distinguish them

Remember, the vast majority of traits don't conform to the Mendelian paradigm, even when its stretched a bit like this.  So this really is a very academic question, and neither term is applicable to a huge number of real-life situations.
To use the examples of snapdragons and blood types, an AA, AO or AB blood type all show no reaction at all to the A antigen.  If AA was protective towards A blood, but AO and AB showed weak reactivity, we'd likely call them incompletely dominant.
For the snapdragons, it really doesn't make any sense to call either allele dominant.  What's really going on there is that the "white" allele is a broken gene in the process that makes red pigment, and flowers with only one working allele don't make as much red pigment as flowers with two working copies.  Whereas one working copy of the ABO gene (that is, the A or B alleles) is enough to teach the immune system not to react.
So I'd say that incomplete dominance is usually a results of haploinsuffieicny; one allele is broken, and the other by itself doesn't do as good a job as two working copies, and co-dominance is usually two working alleles both doing different things.

incomplete dominance is when one allele is partially dominant over the other allele of the same trait.both these alleles are dominant but one is more powerful than the other .for examples a mating between a white female and black male in humans and have a colored child.
co-dominance is when two alleles are equally expressed.

I doubt your example is correct. Human skin color is polygenic inheritance.

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Codon tables and the wobble hypothesis
In E. coli, there are only 47 different tRNAs but 61 potential anticodons. This is because, from what I understand, the third base of the anticodon can pair by wobble rules.
However, it is known that there is some correlation between tRNA pools and expression levels.
So if, for example, GUA and GUG were covered by the same tRNA, why are their codon usages different in a codon table? If one were only concerned with expression level, shouldn't they theoretically affect translation rates similarly?

This is a good question as, although in higher eukaroyotes codon usage does not necessarily correlate with translational efficiency, it does to a large extent in Escherichia coli (see e.g. Boël et al., 2016). The answer is not simple, but the following may contribute.
To optimize the strength of base pairing
Although in particular circumstances ‘wobble’ allows one tRNA to decode more than one codon (see diagram in my answer to Redundancy and the Generic Code) the strength of base pairing will be less for the wobble base-pair:

It has been suggested this would generally disfavour (and hence reduce the incidence of) the degenerate codon that needs to be decoded by wobble. (In some cases a wobble interaction might be an advantage if the first two codon bases were G or C, so that the hydrogen bonding was not too strong.)
To utilize the spectrum of tRNAs able to decode degenerate codons
Although wobble enables a reduction in the total number of tRNAs necessary to decode the 61 amino-acid codons, additional tRNAs often exist that one might regard as unnecessary. Furthermore, where three codons are decoded by a tRNA with a 5'-I (inosine), the other tRNA sometimes has a 5'-G (rather than A) and can hence decode two codons. This is illustrated by the E.coli tRNAs for threonine:

Thus, the relative abundance of these three Thr-tRNAs could determine the codon usage, and Dong et al., 1996 reported that this is the case.
To reflect the overall GC-content of the genome
If the genome of a prokaryotic organism has a particular base composition, because there is so little non-coding genomic DNA the mRNA will necessarily reflect that base composition in its codon usage. Your might ask why doesn’t the base-composition of the genome just reflect that of the synonymous codons, but there are actually strong pressures on the GC-content of prokaryotic and viral genomes. In some bacteria this may reflect needs for thermal stability, but in others it seems to be random drift (see e.g. Biology SE questions on GC-content of genomes).

Codon usage is not necessarily associated with translation efficiency, as your example would illustrate. Though control of translational efficiency and accuracy is one of the well known reasons for the existence of codon usage there have been other hypotheses that link it with asymmetric mutagenesis rates and overall GC content (See "Why does codon usage bias exist?" Novoa & de Pouplana, 2012).
From the same article:

However, the search for a correlation between tRNA abundance and codon usage has been successful only in some organisms [5, 34]. In several species, including many bacteria and eukaryotes, this search has failed [35, 36], prompting the proposal that, in the latter organisms, translation efficiency might not be the primary factor influencing codon usage [36, 37]. However, it was recently reported that two distinct modifications at the wobble position of certain anticodons are at the core of this apparent lack of correlation [28].

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Why is my peripheral vision better for seeing in the dark?
I often walk around my house at night with the lights turned off and one night I noticed that looking straight at an object with very little light available made the object disappear from sight but if I directed my visual else where I could clearly see the object in my peripheral

"Peripheral vision is more light-sensitive than the central vision" written by AliceD here gives a great answer to your question.

Its down to the structure of your eyes. The eyes are made of rods and cones, which have differences in detecting light.
Now, compare the images below.

As you can see, the peripheral vision is predominately due to your rods, and your central vision is made of cones.

Measured density curves for the rods and cones on the retina show an enormous density of cones in the fovea centralis. To them is attributed both color vision and the highest visual acuity. Visual examination of small detail involves focusing light from that detail onto the fovea centralis. On the other hand, the rods are absent from the fovea. At a few degrees away from it their density rises to a high value and spreads over a large area of the retina. These rods are responsible for night vision, our most sensitive motion detection, and our peripheral vision.

(Taken from: http://hyperphysics.phy-astr.gsu.edu/hbase/vision/rodcone.html)
You can read about the photorecptors of the eyes here:
http://webvision.med.utah.edu/book/part-ii-anatomy-and-physiology-of-the-retina/photoreceptors/

This is not the complete story; this answer is more complete under linked question

Because peripheral vision uses the peripheral retina,which has mostly rods as photoreceptor,while central vision uses the foveola,a central part of the retina which mostly has cones as photoreceptors.
Rods are more sensitive to light. That is why they are more efficient in the dark.

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Is this tall, white tree in central Australia a kind of Eucalyptus?
This is near Alice Springs NT, Australia, about -24°S latitude, 550m. Area is arid but it's in a maintained park.
I don't know the exact size, but the photo is hand-held from the ground and clearly the tree is quite tall.
I only have this one photo to work with (it's not mine). I've added some cropped sections of the same original image below for easier viewing.
It reminded me of the tree I saw in the linked video below, which is likely a Eucalyptus considering the koala context.
I don't need an exact species, just confirmation of my genus hunch.
Oh! No koalas were seen in the tree eating leaves at the time, which would have made a "differential diagnosis" easer.

From Koala Bears and Eucalyptus - Periodic Table of Videos at about 02:10 (Sir Poliakoff reminds us a few times in the video (himself as well) that koalas are not "bears"!)

Yes it is a Eucalyptus tree.That's known as a Ghost Gum. (All Eucalyptus' are referred to as Gum Trees) .

Thanks! I can certainly see how it got that name. I also see that Ghost Gum refers to a group of closely related species. Do you also think that this is probably Corymbia aparrerinja?

This tree is ilwempe (Corymbia aparrerinja) or  Ghost Gum. It is endemic to Central Australia where you saw it, and depicted in the paintings of local aboriginal people.
https://en.wikipedia.org/wiki/Corymbia_aparrerinja
Before the 1990's all trees of this form were in the genus Eucalyptus (and usually called gum trees), since then many have been put into the genuses Corymbia and Angophora

Wow, thank you for the new, updated information!

This is Eucalyptus apodophylla, the so called whitebark.
Further information can be found here

I'm not convinced about this ID: Alice Springs is well outside the known distribution of E. apodophylla. See Atlas of Living Australia http://bie.ala.org.au/species/http://id.biodiversity.org.au/node/apni/5194695

The tree stands in a maintained park and not in the wild...

@JulPal that's right, and is a good reminder why adding as much information as possible to a species ID question is important. Next task would be to estimate the age of the tree and the age of the park ;-)

@uhoh have you read the first sentence of the OP? I cite: This is near Alice Springs NT, Australia, about -24°S latitude, 550m. Area is arid but it's in a maintained park.

@JulPal I don't understand; I am the OP, and I wrote that sentence. My point in the comment is that we (or at least I) don't know when the tree started growing there and when this plot first became a maintained park, so we don't know if the tree first grew there by itself and then later a park was built, or if the land was first cultivated and watered, and the tree was then planted there. However, if you are more familliar with Alice Springs, perhaps you can address that specifically?

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Why do dragonflies have these special little spots on their wings?
The wings of several kinds of dragonflies I've seen here in Taiwan all have an apparently special little pigmented spot near the ends of each wing.
Does this spot have a name and a function?
below x2: Taken today in Hsinchu county, Taiwan. Note arrows. I've also asked Identify these two large dragonflies in Taiwan?
Click for full size

below left: from Identify this black dragonfly with bluish coloration along its flat top, yellow on it's mid-body and green on its head below right: from Identify this black dragonfly with a bright bluish-white band around its body
Click for full size

Pterostigma is what those spots are. Wikipedia article is at https://en.wikipedia.org/wiki/Pterostigma.
I read the summary of the technical article below.
The pterostigma are heavier than the rest if the wing, and so the insect can glide faster without a destabilising flutter beginning.
The author also believes that the pterostigma contribute to more efficient active flight.
Technical details at:
Norberg, R. Åke. "The pterostigma of insect wings an inertial regulator of wing pitch". Journal of Comparative Physiology A. 81 (1): 9–22.
doi:10.1007/BF00693547.

This is excellent, thank you very much! btw I've just asked Why this inertial regulator of dragonfly wing pitch reduces self-excited coupled flapping and feathering vibrations and improves gliding flight speed in Aviation SE. I am not sure yet if it will "fly" there or not, but let's see what happens.

That question "flew" as did this one. Thanks for your answer!


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Water snake with a yellow criss-cross on a black background?
I saw a 60 cm long, very skinny (~15 mm diameter), black with yellow diagonal criss-cross patterned snake swimming in a pond this afternoon in northern Taiwan.
It was swimming near the top of the water and I could see it very clearly, but as soon as it noticed me it dropped most of its body to the bottom of this shallow pond and just kept part of its head above water, so the photos are not very clear.
I tried to wait for it to continue but something else disturbed it and it took off.
Is it possible to identify this snake or at least narrow down the options?
First image is cropped from the large image. I have played with contrast, color and sharpness to make the pattern and color look most like what I remember before it dropped its body lower into the murky water.

sketch of pattern as I remember it

The useful relevant facts are:
Present in freshwater
Active in daytime
Yellow patterning
(photos from wikipedia)
I used the site
www.snakesoftaiwan.com/
This gives most likely candidates of:
Rhabdophis tigrinis subspecies formosanus, the Tiger Keelback.
Grows to 0.6 to 1.0 metres long.

more photos (cannot embed due to copyright) at http://m.blog.sina.com.tw/d100vs/article.php?pbgid=30839&entryid=404413
and
Fowlea piscator  the Checkered Keelback or Asiatic Water Snake. growing 1-2 metres long.

more photos at http://m.blog.sina.com.tw/d100vs/article.php?pbgid=30839&entryid=342476

These are wonderful sites, thank you very much! Yes both of these work per the information in my question and its less-than-optimial photos, and both are compatible with what I recall. I'll have to now look for a copy of A Cobra Hijacked My Camera Bag! Snakes and Stories from Taiwan by Hans Breuer as mentioned in the site. I did surprise a 2m black Taiwan cobra myself several years ago; It was pretty close and I completely froze, never thought about reaching for my camera.


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Identify this large, beige or pine cone-colored squareish beetle and/or the pine cone it's on?
I saw this large beige beetle on a large pine cone on the ground in February in Hsinchu county Taiwan.
It was about 4 cm long and 2 cm wide and the color was similar to the pine cone it was standing on. Though it was sunny it was cool (15 C) and the beetle didn't really respond when I picked up the cone.
I remember seeing a sign about (apparently) this species in November when hiking so I've attached it as well. I think the sign warns that this is a pest but I can't read it; I assume it is in Chinese.
Unfortunately I didn't remember the poster (from November) until later.
Any idea what it is and/or what the kind of cone that it's on, and what problems it can cause?

click images for full size

It is not a beetle, but a true bug. Tessaratoma papillosa, to be exact. It is relatively common in Taiwan. It can cause problems if you have a lychee tree, as it is a destructive pest to lychee trees.
Here is an image of this animal:

The nymphs look like this:

https://www.inaturalist.org/observations?place_id=7887&taxon_id=47743&view=species
https://en.wikipedia.org/wiki/Tessaratomidae#As_agricultural_pests

This is great, thank you very much! I really appreciate the extra links. I can see that February was well before the peak observation count in April. Do you know what time of year that those colorful nymphs are most likely to be seen? The Wikipedia article doesn't give any information on the seasonal behavior. I also found it interesting that this Lychee Stink Bug Lyramorpha rosea is often confused with Tessaratoma papillosa.

@uhoh Discerning what time of the year the nymphs are most likely seen is difficult because many people on iNaturalist do not specify the life stage, but it appears to be from April to May. The wikipedia article is actually for the group of insects that it belongs to as the article for that particular species doesn't provide much useful information.

This is Tessaratoma papillosa, also known as the lychee giant stink bug. It is a pest for lychee trees, this is probably the reason for this warning sign. See the image for comparision:

See also this page for more information.

This is great reading, I'm starting to see why there is such a stink being raised about them. I'm also glad that I didn't mess with this one; the defensive chemicals of tessaratomids (particularly that of Tessaratoma papillosa and Musgraveia sulciventris) are notable for being one of the most debilitating to vertebrates, probably a defense specifically aimed against birds. They can cause damage to human skin and even cause temporary blindness if sprayed unto the eyes!

See also this answer for information on the poster. I guess the pine cone is a red herring.

Can you use your mod powers to check if there was another answer here before? I don't have enough reputation to see deleted answers, but I think there was and that there was some helpful links in it, but I could be misremembering. Thanks!

@uhoh Damn, you are right. I meant to clean a flag but it seems I accidentally deleted the answer. It is mainly a repeat of the earlier answer, though.

Thanks! It seems that I was after this link in the other answer.


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Dark, long-legged spider with long mouthparts in front, long "pincers" in the back and very short 3rd pair of legs (northern Taiwan)
Just inside a doorway in northern Taiwan I found an interesting looking spider flat against the wall, pointed downward about 30 cm above the floor, sitting motionless.
Mostly dark but some patterns appear with the flash photo.
Everything is long; long mouth parts in front, long "pincers" in back, and long legs, except the 3rd pair from the front which were thinner and only about 20% of the front (longest) pair. See photo for an estimated scale bar - roughly 16 mm from mouthparts in front to "pincers" in back, over 80 mm toe-to-toe.
I assume it's just sitting there waiting for something delicious to walk by and eat, but why are the mouth parts and "pincers" so long and the 3rd leg pair so short? Are there specific activities or functions that can help explain these?
Does it always hunt like this or does it also build webs?

above: cropped, below: click for full size, the first uses a flash and is viewed from above-front, 2nd is with ambient light and top-down view.

From a browse through iNaturalist, I believe this is a member of the genus Hersilia also known as long-spinneretted bark spiders or two-tailed spiders. I have no idea which of the species this might be, but a Hersilia striata comes up as being present in Taiwan.
The characteristics are, unsurprisingly, the long spinnarets and long legs. I believe these will be largely ambush spiders similar to wolf spiders, using camouflage to hide and deceive prey.  I don't know if the long spinnarets play any role, nor the shortened legs.

It seems like you've got it narrowed down nicely, thanks!

I do a lot of walking and hiking - I come from northern latitudes so the much higher species diversity of Taiwan is a never ending source of discovery. I've been here 15 years and still on every long hike I photograph a new flower or two and several new insects I'd never seen before. I've seen many of these in the same general area, and always wondered if they were "really well reinforced egg cases". But I suppose it's captured, digesting prey, and those short 3rd legs and long spinnerets are just the right lengths to make these?

@uhoh yo might well be right there on the 3rd pair being the right length to fit the spinnerets. Still I wonder what the evolutionary pressure is to have such long ones.

I would venture a wild guess that it's to have a way to suddenly move forward very quickly to grab its prey without resorting to jumping and trying to land firmly on a new bit of tree without falling off. Need to find some video. If I were more adventurous I'd bring a few home, set up a tall terrarium with some vertical surfaces and a good camera and stock it with little crawly things and wait... but it seems a YouTube search is more likely.

This looks like the short 3rd set of legs are pulled under and forward and working with the mouth parts to hold prey https://youtu.be/u7VIHz9Dspc and this is just a nice, camouflaged specimen https://www.youtube.com/watch?v=OjnT-fzEV2E According to this they hunt by throwing silk, now I need to see it...

Interesting if they are web throwers - that would fit the extra long first and second pair of legs and the long spinnerets. Use the spinnerets to cast a web between all 4 pf the first 4 legs, then use these to spread and trap. The spinnerets wouldn't reach otherwise. The first two leg pairs might be too long for the mouthparts to reach and hold, so 3rd makes sense. The beauty of evolution in action! You'd need to see them at night to see the web casting, probably in a contrived set-up - that's how the doco crews do it.


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Is RNA polymerase affected by proteins bound to the coding sequence of a gene?
I am designing a synthetic gene construct to express genes in E. coli driven by either Ptet or PLacO. The construct would look like:
-Ptet-(Gene1)-PLacO-(Gene2)-
I want to express each gene using either aTc or IPTG, but I want to make sure that the transcription of each gene can be controlled independently.
Let say I only add aTc and transcription is initiated at the Ptet location, would RNA polymerase bump into LacI bound to the PLacO promoter and stop transcribing? Or would it knock-off LacI transcribe (Gene 2)? I am not sure whether or not need to include terminator sequence to make sure the expression of each gene is decoupled.

Nice question!
First of all make sure that you have multiple transcription stop / terminator sequences at the end of your first gene . This is quite standard procedure. Also in your case the phenomenon called transcription interference (TI) comes handy. Here's a review on TI. In short:

the term TI usually refers to the direct negative impact of one transcriptional activity on a second transcriptional activity in cis.

Although TI is mostly defined as two transcription events affecting each other, at the low level the basis of it is that two proteins bound to the DNA affect each other's activity. Now since LacI's function is to inhibit transcription, thus it is strongly bound to the DNA and I'd say even if a polymerase somehow slips through the polyA signals at the end of the first gene it is likely to be stopped by the LacI already bound at the second promoter.
Alternatively you could put a weak promoter opposing the first gene and drive its expression, so it would collide with the oncoming polymerase from the first gene thus stopping it before reaching the second gene. Also here is another article on TI, that proposes a gene regulation network based on TI.

PolyA addition occurs in eukaryotic nuclei, but E. coli is a prokaryote.  I think what @poka.nandor is referring to are transcriptional terminators, which are very well characterized in E. coli and its viruses.

Oh, right, my bad. I got my head wrapped around TI and stuff we work with. I 'll edit my answer immediately. Thx for point that out!


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Reliability of Sanger sequencing
Hailed as the "gold standard" of sequencing, I was wondering to what Sanger sequencing owes its incredible accuracy to. If possible, I would like a quantification of the accuracy (because I doubt it is 100%, though possibly very close).
I understand ddNTP chain termination and the strategies involved in Sanger sequencing but I lack the connection to accuracy.
Thanks!

In searching, I have located something known as "phred programs" which had provided early confidence levels for Sanger sequencing. I do not directly see the correlation though to modern Sanger sequencing

I don't think it's referred to as the gold standard solely because of its accuracy but rather because it was virtually the only method used for some 20 odd years before second generation techniques were even talked about. Chain termination sequencing is accurate though and is theoretically only limited by the error rate of the polymerase. That said, next gen techniques are also accurate.

Here's some accuracy comparisons: http://www.hindawi.com/journals/bmri/2012/251364/tab1/

Thanks for the comparisons! Personally, I have heard that Sanger sequencing is sometimes even used to confirm next gen tests, and its 99.999% accuracy is as expected. But I do agree that next gen is improving, in both accuracy and convenience

Reliability comes from the fact that in Sanger sequencing (AFAIK) the synthesis of the new strand to the template and the actual reading of the sequence is separated. As you may know Sanger seq uses capillary gel elfo. thus separating the newly produced DNA fragments on a single nucleotide difference, and the reading is done by fluorescence detectors (then base calling etc.) Now compared to this the other sequencing methods like Illumina and 454 detect each nucleotide incorporation that may produce less reliable signals. For eg. in Illumina colonies may overlap on the plate, or in 454 incorporation of multiple nucleotides at homopolymer regions cause a hard time deciding how many nucleotides have actually incorporated. Also it must be noted that quality of the singals / reads is not constant through out Sanger sequencing. The beginning and the end of the reads tend to have noisy and low quality signals, thus actually only the 100-500(-600)bp segment of the whole fragment can be read reliably. Also ABI's SOLID uses a 2 color color-space and each base is read twice and is extremely reliable (99.96% is said by the inventors). Also clever base calling and error correction algorithms may improve accuracy.
It is noteworthy to say that next gen sequencers also achieve high accuracy by taking advantage of their immerse throughput / output - due to clonal amplification of template sequences each original fragment is sequenced multiple times and errors in a single read can be corrected by the use of others.


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Common Errors For Low R Value in Bradford Assay
I've recently started doing Bradford Assays for my samples and my standard curve has been non-linear and I have been getting low R values (.90-.95). I initially thought the error was in pipetting, most likely in adding BSA while establishing the standards but I have repeated in care and somehow still get low R values. Are there any other possible sources of error?

You could be measuring outside the dynamic range of the assay (you can only add so much / so little BSA to a certain amount of reagent).
You could be outside the linear range of your spectrophotometer, usually under 1 is fine, although some old/crappy ones might not even be reliable over 0.5.
If you're fast you're measuring your different concentrations also at different times. Bradford is a little bit time-dependent, so waiting the recommended time before measuring your standards is not a bad idea.

Probably it's still pipetting though, try pipetting at least 20 uL in every dilution step and see if you're still off.


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Do these large spiders in Taiwan belong to different species?
I see both of these spiders (and others) frequently on hiking trips outside of Taipei. Their large webs are often high overhead between trees but can be right across a hiking trail that hasn't been used in a few days, which can make for some excitement.
The two individuals shown in the photos were quite large; both had a body length of about 5 cm not counting legs.
They have similar body shapes but very different color. I don't know if they are completely different species, or different sex or different age.
I mostly see "Spider #2", and usually they are around 3-4 cm in body length. I see  "Spider #1" much less frequently, and I don't think I have ever spotted a smaller individual, but that could just be due to lower frequency.

Spider 1:
I spotted this on on this plant, but once disturbed he started climbing up a vertical thread back into the threes.

Spare photos: 1, 2
Spider 2:
I see these more often than Spider #1.

Adjusted brightness, contrast, sharpness to make the structure of the web more visible:

Spare photos: 1

Bottom is definitively Nephila pilipes -- see here for example. Wikipedia mentions multiple subspecies that you might want to look into for more definitive ID of top specimen. Both of your specimens are females based on the extreme sexual dimorphism (specifically, female gigantism and male dwarfism) common in this group.

@theforestecologist that's why I put Spider #1 first, I see it less frequently than the brightly-colored Spider #2.

a 5 min search on my end didn't turn up anything that looked or was described quite like your top specimen. Definitely looks related, but not sure to what degree. Again, I'd start researching the subspecies to see if you find any leads...

The following is from Biogeography and Speciation Patterns of the Golden Orb Spider Genus Nephila (Araneae: Nephilidae) in Asia, Yong-Chao Su, Yung-Hau Chang, Deborah Smith, Ming-Sheng Zhu, Matjaž Kuntner and I-Min Tso, Zoological Science, 28(1):47-55. 2011., DOI: 10.2108/zsj.28.47 http://www.bioone.org/doi/full/10.2108/zsj.28.47
Spider 1 seems a good match for C in the images below, and Spider 2 matches A and B. So I propose that both spiders are Nephila pilipes but with different color patterns.

Fig. 1. Nephila diversity in Asia and Australia and its extreme sexual size dimorphism: (A–E), N. pilipes; (A–B), female of the common color pattern, Taiwan; (C–D), female of the darker color pattern, Taiwan; (E), male (arrow) in copulatory pose on female, Singapore; (F–G), female N. antipodiana, Singapore; (H), female N. plumipes, Australia; (I–J), female N. clavata, Taiwan. Images by M. Kuntner (www.nephilidae.com).

Both of those are variations of the Giant Golden Orb Spider, just of a different age. They might be large but they are not very dangerous. Their scientific name is Nephila pilipes if you want to do more research
Both of the spiders you have shown are females of the same species. As these spiders grow they molt and spider #1 should eventually develop the same pattern as spider #2 once it matures.

Nephila pilipes (northern golden orb weaver or giant golden orb weaver) is a species of golden orb-web spider. It can be found in Japan, China, Vietnam, Cambodia, Taiwan, Malaysia, Singapore, Myanmar, Indonesia, Thailand, Laos, Philippines, Sri Lanka, India, Nepal, Papua New Guinea, and Australia. It is commonly found in primary and secondary forests and gardens. Females are large and grow to a body size of 30–50 mm (overall size up to 20 cm), with males growing to 5–6 mm. It is the largest of the orb-weaving spiders apart from the recently discovered Nephila komaci, and one of the biggest spiders in the world.

Just an interesting fact, in some regions people will eat these spiders once they are fully grown.

Thanks! At first glance I thought your comment said that in some regions these spiders eat fully grown people!

No they aren't that giant, but they can grow to be the size of someone's hand and eat birds or bats.

I may have some photos of a very tiny spider on the same web in proximity to one of these. If I find it I will ask about it separately and notify you here.

if they are red a few mm big and several of them hang around the big spider then they are most likely the males. In this particular species the males are the smaller of the sexes.

Sounds familliar; will take some time to dig those photos up.

Hi Joseph. Welcome to Bio.SE! We ask that answers (especially) those to species ID provide ample support. Thank you for taking the time to link-to and quote from the Wikipedia article, but your claim that both specimens are the same species comes across as an opinion ("I believe...") without having any formal support provided. Since the relation between the 2 specimen's in the OP's post is the main question being asked, I ask that you provide additional support/detail to back up your opinion. Thank you.

Have a look at Female, Cairns Botanic Gardens December 2010 here: http://www.arachne.org.au/01_cms/details.asp?ID=1627


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Would anything limit an "invasive species" T. rex introduction now besides equilibration with available prey or intervention by humans?
In the video Two-and-a-half billion T. rex roamed Earth, study finds contains a short explanation of the results in Science Absolute abundance and preservation rate of Tyrannosaurus rex by the corresponding author of the paper.
I'd like to understand better what is known about T. rex's adaptability and range of environments where it was thought to flourish. It's hard to imagine what things were like back then, so using modern flora/fauna and climate distributions as reference points will help me to understand this better.
Based on that knowledge and reference frame, I'd like to ask about the following Gedankenexperiment:
Question: Would anything limit an "invasive species" T. rex introduction now besides running out of food or intervention by humans?
Would they basically thrive over much of the Earth's surface and eat all the other mammals? Or without a supply of dead and rotting dinosaur cadavers would these giant scavengers with excellent olfaction quickly deplete a small region and die of starvation?
Currently there is not likely enough DNA to reconstruct a full genome nor a scheme to build and incubate a dinosaur egg for it (as far as I know), so we are not at any risk of this happening in the near future.

Fun question, there are too many ecology variables to give a definitive answer, perhaps T-rex was an ambush specialist... folks on a paleontology forum would know. If the oxygen levels were OK and there were many buffalo, hippos, rhinos and elephants, i'm pretty sure T-Rex would be unstoppable!

It seems that if the current earth could support terrestrial predators/scavengers the size of T.rex, there would be one already. Terror birds were around relatively recently (2 million years ago) but instead of getting larger, they went extinct

@timeskull I'd always thought that population dynamics was more complicated than that, and that there could be multiple equilibrium points or alternative stable states especially when there's been a significant change in the status of a keystone predator.

@aliential I've added a bounty.

@timeskull ditto.

@uhoh T-rex maximum speed was 20mph and a buffalo is 35mph, I think it's really one for reddit/paleontology :) velociraptor and triceratops would be more invasive... It's only recently that scientists agreed T-rex went 20 rather than 45 mph. 2 many science variables.

@aliential Who needs buffalos there are billions of easy livestock humans have confined with fences and pens a rex can step/reach over. Also remember there is decent evidence T-rex are pack hunters.

Lots of things could impact a reintroduced invasive species.

Disease/sickness: although no close relatives are present that is not a guarantee,  many diseases jump species. Parasites likewise could cause problems, especially newer parasites the dino may not have a good defense for. Even modern Fungus could pose a problem for eggs.

Predators: While an adult t-rex is predator proof eggs and newborns are not. Rats and other small mammals as well as many birds have been the demise of many ground nesting birds.

Poisons: there are plenty of animals and plants that are poisonous enough kill a t-rex that the rex may not recognize as dangerous. Remember there are a lot of things around a t-rex did not evolve with. This is more dependent on location, a t-rex dropped in Australia might kill itself with its first meal.

Human stuff: I am not talking about humans killing them. I am thinking of the things humans make killing them. things like walking into power lines, eating weird plastic human garbage, car accidents ( a car moving at speed could easily cripple a rex), even something as simple as getting hit by trains


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Will proper autoclave treatment really "inactivate all resistant bacterial spores"? If not, how widespread are autoclave-resistant bacterial spores?
Wikipedia's  says:

A widely used method for heat sterilization is the autoclave, sometimes called a converter or steam sterilizer. Autoclaves use steam heated to 121–134 °C (250–273 °F) under pressure. To achieve sterility, the article is placed in a chamber and heated by injected steam until the article reaches a temperature and time setpoint. Almost all the air is removed from the chamber, because air is undesired in the moist heat sterilization process (this is one trait that differs from a typical pressure cooker used for food cooking). The article is held at the temperature setpoint for a period of time which varies depending on what bioburden is present on the article being sterilized and its resistance (D-value) to steam sterilization. A general cycle would be anywhere between 3 and 15 minutes, (depending on the generated heat) at 121 °C (250 °F) at 100 kPa (15 psi), which is sufficient to provide a sterility assurance level of 10−4 for a product with a bioburden of 106 and a D-value of 2.0 minutes. Following sterilization, liquids in a pressurized autoclave must be cooled slowly to avoid boiling over when the pressure is released. This may be achieved by gradually depressurizing the sterilization chamber and allowing liquids to evaporate under a negative pressure, while cooling the contents.
Proper autoclave treatment will inactivate all resistant bacterial spores in addition to fungi, bacteria, and viruses, but is not expected to eliminate all prions, which vary in their resistance. For prion elimination, various recommendations state 121–132 °C (250–270 °F) for 60 minutes or 134 °C (273 °F) for at least 18 minutes. The 263K scrapie prion is inactivated relatively quickly by such sterilization procedures; however, other strains of scrapie, and strains of Creutzfeldt-Jakob disease (CKD) and bovine spongiform encephalopathy (BSE) are more resistant. Using mice as test animals, one experiment showed that heating BSE positive brain tissue at 134–138 °C (273–280 °F) for 18 minutes resulted in only a 2.5 log decrease in prion infectivity.

The statistical discussion of "sterility assurance level" and "bioburden" already seems to preclude any possibility of absolute certainty, such as "...all resistant bacterial spores..."
Question: The research cited in Is it known how some heat-resistance Bacillus spores repair their DNA after having been heated to 420 °C? (see below) shows an abrupt transition between 420 and 430 °C. Can we therefore assume that the sentence "Proper autoclave treatment will inactivate all resistant bacterial spores..." is just plain wrong If so, just how widespread are autoclave-resistant bacterial spores?
Related: Why do we use an autoclave at 121°C (250F)? (Origin)

The 2018 Extremophiles paper: Beladjal, L., Gheysens, T., Clegg, J.S. et al. Life from the ashes: survival of dry bacterial spores after very high temperature exposure. Extremophiles 22, 751–759 (2018). https://doi.org/10.1007/s00792-018-1035-6 (also downloadable from researchgate).

Turns out no, though repeated autoclaving does: here

@bob1 that's excellent, thanks!

I assume that this question stems from this recent Q&A on Space Exploration?

@MichaelSeifert if you check my previous Biology SE question I've linked to above "Is it known how some..." you can get the bigger picture; there are several.

Comment on "The research cited in Is it known how some heat-resistance Bacillus spores repair their DNA after having been heated to 420 °C? (see below) shows an abrupt transition between 420 and 430°C." An important distinction here is that this research was utilizing dry heat, while an autoclave utilizes heat from pressurized steam, which are quite different physical processes. Consider that boiling water and steam can scald human skin almost instantly at 100°C, but a brief exposure to dry heat over 250°C (i.e. reaching into a pizza oven) has almost no noticeable effect.

@MikeyC I knew there was something missing from my answer, but couldn't for the life of me work out what it was. If you don't mind I'll edit something in to my answer covering that aspect.

@MikeyC yes that's a really important distinction, thanks!

Bacterial spores in most contexts are properly called endospores, formed within the bacterial wall and are a survival mechanism, creating resistance to desiccation, heat and cold, with tolerances up to 150 Celsius (300 F).
The vast majority of bacterial spores studied are from Gram-positive species, that are medically relevant. These include organisms such as Bacillus anthracis (anthrax) and Clostridium species (colitis (C. difficile), food poisoning (C. perfringens), and tetanus (C. tetani)), which are significant pathogens of humans. The reason that they are studied is that sterility of equipment and items ued in medical settings, as well as in the food industry is a great way to prevent illnesses and not have patients getting sick in the hospital from nosocomial infections.
In the context of autoclaving, the temperatures, times and pressures have been worked out to inactivate the bacterial spores from these medically relevant bacteria, and are suitable for the vast majority of bacteria that people encounter in their every-day lives. These conditions work even for things like Mycobacterium tuberculosis, which are incredibly resistant to many of the ordinary disinfectants used in health-care settings and in the food industry.
However, there are whole classes of bacteria that survive under unusual conditions of high heat and/or high acidity or alkalinity. These organisms are known as extremophiles. It turns out that some of these are quite resistant to autoclaving, as one might expect. It seems that they are resistant to up to 3 standard autoclave cycles and some other pretty extreme conditions:

Cultures of Desulfotomaculum sp. C1A60, D. kuznetsoviiTand D. geothermicum B2T survived triple autoclaving while other related Desulfotomaculum spp. did not, although they did survive pasteurisation. Desulfotomaculum sp. C1A60 and D. kuznetsovii cultures also survived more extreme autoclaving (C1A60, 130 °C for 15 min; D. kuznetsovii, 135 °C for 15 min, maximum of 154 °C reached) and high-temperature conditions in an oil bath (C1A60, 130° for 30 min, D. kuznetsovii 140 °C for 15 min).

While this is interesting, and a real problem for those working with them, none of these sorts of species are medically relevant (as far as I know, I would love to be proved wrong!), so the fact that these are resistant to autoclaving is not a problem for the vast majority of us.
As a note, language is inherently difficult and to be scientifically certain that something is so, is almost impossible. This is particularly so with bacterial species, where it is estimated that there are about a trillion species and we can culture only about 3250 of them, so for the rest we know next to nothing about how they grow, their physiology or anything beyond a genome. This means that we have no way of determining if autoclave resistant bacteria are actually found almost everywhere or if they are as rare as the proverbial hen's teeth.
Basically what I am saying is that the Wikipedia article is incorrect and imprecise in its use of language. If it had said something along the lines of "inactivates all medically relevant spore forming bacteria", then it would have been correct and much more precise.

"I would love to be proved wrong." I would prefer it if you were right and all medically relevant pathogens could be destroyed by autoclaving.

@WaterMolecule - I was talking about these extremophiles being medicallt relevant here, but since you raise it; which medically relevant bacteria aren't sterilized by autoclaving? Note that I deliberately didn't use the term pathogen. I know in terms of pathogens prions aren't generally destroyed, but they aren't bacteria, so not in the scope of this question.

It would be very difficult for extremophiles to be medically relevant, as the extreme conditions that they need to grow/reproduce are not going to exist in the human body. Therefore, even though we have not exhaustively sampled all extremophiles and can't be scientifically certain, we can make a pretty good logical argument that there is no reason for concern.

@CodyGray - my point entirely. Though we do have environments in the body that are highly acidic (stomach) where bacteria such as Helicobacter pylori can thrive. I think you could easily classify H. pylori as an extremophile and pathogen. There's also the gall bladder (alkaline), anaerobic environments (e.g. appendix, prepuce), dry environments (skin) and environments which undergo rapid changes in salinity and humidity (skin) - all of these are colonized by a range of bacteria that may or may not be pathogenic.

@bob1 I never thought about myself as a host for extremophiles (beyond H. Pylori), yikes!


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how many spores are needed to "infect" a wall?
There's cardboard box in my room that used to be in another room that had mold all over the walls and it still smells moldy. This probably means the air in my room is polluted with mold spores.(right?)
If only a few spores stick to my wall could this "infect" the wall?
How many spores are actually needed to start infecting the walls in my room?
I threw that cardboard away, but I still wonder about the remaining spores

How big is this "wall" and what is it made of? Does it have a lot of moisture? There are multiple parameters here and hence your question is broad.

Yes, the box likely had many fungal spores attached to it since it smelled “moldy”. This doesn’t mean that your room will definitely be contaminated because spores often wait for ideal conditions to germinate. There are fungal spores in the air we breathe all the time, so if those haven’t already colonized your wall then adding the ones from the box are unlikely to cause any problems.
If you do see spots appear, they can be easily removed with a damp paper towel, generic home cleaner, or diluted bleach.


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Edman method to identify peptides with Phenylisothiocyanate (PTH)
We all know that in this method the PTH reacts with the first amino acid (aa) from the N-terminal to the peptide and separates from it giving PTH-aa so that we can know the amino acids sequence in the peptide.
The question is what prevents the PTH from reacting with the second amino acid after it separates with the first amino acid in the same time and phase? Because if it does we can't distinguish between the first and second amino acid residue in the sequence.

Welcome to Biology SE! Just to improve your wording here - if we all knew what Edman did you wouldn't need to explain. Don't expect everyone to be a Biochemist working on proteins. also - prevent acronyms like aa. Don't apologize. Just ask the question.

And isn't the answer linked to the chain termination methods in DNA sequencing like the Sanger method? http://en.wikipedia.org/wiki/Sanger_sequencing

The short answer is that the Edman degradation is a multi-step process. The Wikipedia page has a decent picture of the mechanism. In practice, the peptide is reacted with phenylisothiocyanate (PTH) under mildly basic conditions to give a thiourea, which is stable. The excess PTH is separated from the thiourea intermediate. The thiourea is then treated with acid to cleave the N-terminal residue from the peptide. The PTH is no longer present, so there's no concern about reacting with the second residue.


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How does the body respond to blood donation; are there any possible risks?
Can blood donation cause any harm to the donor? I have been told so, but cannot find any references supporting this claim. I have also learned that our body will replace the lost fluids within 24 hours and the RBCs within weeks. Can blood donation still cause health issues for our body?
This is not a personal medication question, and I mainly want to know how the body responds to blood loss and what mechanisms that monitor the altered levels of blood volume? To me, it would also be unethical by medical doctors to withhold the possible risks of blood donation to prospective donors, but it might also be seen as unethical to discourage a person willing to donate blood from doing so, so there might be a conflict of interest here.

If this is not a personal medical question, you should remove all references to yourself. Also, medical ethics specifically prohibits hiding information from patients.

@canadianer:I have removed

I don't understand your question. Do you want to know if blood donations are harmful for the donor?

@Chris: Yes thats what I am looking for !

Tried to clarify your question. Feel free to roll-back if you disagree.

@fileunderwater: Thank you, now it looks like a question !

How do you come to the conclusion that doctors hide risks from donors? Have you ever donated blood?

@chris The poster was encouraged to remove all personal details, so the part saying that he/she is a donor has been removed (see edit history). The last sentence on ethics is secondary to the question though, and I thought about removing it.

@Chris: I haven't concluded that doctors hide the risks, I rather inquired about it. Yes I have donated blood.

As biology and medical science have some common relationships, but medical ethics have nothing to do with biology. But this question bears biological origin and question about ethics is a bonus :)

found on internet: After blood donation, it generally takes a day or two to replenish the fluid volume in the body and three months for the regeneration of red cells to donate more blood. The total amount of blood circulating in our body's cardiovascular system is about 5 liters. Of this amount, only about 350 ml. is bled from the body during blood donation. The human body replenishes this amount of blood donated within about 48 to 72 hours of donation.

My answer below directly (and solely) addresses what I think is the main gist of the question: Are there any adverse effects on one's physiology as a direct result of donating blood?
Blood donation, at the amounts typically taken (200~500mls), will not harm you. A healthy human being produces approximately 100,000,000,000 (one hundred billion) NEW hematopoietic cells DAILY to replenish short-lived blood cells and platelets. All of these ultimately derive from the hematopoietic stem cells residing in the bone marrow within one's long bones.
As you can appreciate, with such a huge amount of turnover daily, the body is constantly churning out new blood cells. Thus, any depletion in blood cells one will experience as a result of blood donation is a fraction of what will be lost normally in daily homeostasis anyway and thus will not affect a healthy individual.
And then there are the knock-on benefits suggested by epidemiological studies, some of which are alluded in this layman article: http://news.health.com/2014/06/13/4-unexpected-benefits-of-donating-blood/
[source: I'm a hematologist]

How much amount of blood loss is considered as fatal ?

If you lose > 40% of blood volume (~2.5 L for a 75kg healthy adult male), it is most likely fatal. However, one will probably start to feel the effects (classed as hypvolemia) after >15% blood loss. As you can see, even at maximal amounts of blood donated, it is a tiny fraction of total blood volume and certainly not going to be fatal. You seem to be excessively concerned about a safe procedure that has been routinely done for over 5 decades. The biggest harm is not from donating, but from NOT donating!

Your answer and comment seems awesome and I am glad that you are worried about by excessive concerns :)

@Cantona Collar What on earth? You can start feeling the effects of blood loss (hypovolemia) after 15% blood loss? At 2.5L for a healthy adult male 15% is 375ml and you say they take 200-500mls. Seems to me from these numbers they take so much blood it approaches the quantity of blood loss which is approaching hypovolemia already.

@Zebrafish, I think you need to re-read what I wrote before typing. The total volume of blood in an average healthy human is ~5L (https://www.webcitation.org/mainframe.php)

@Cantona's Collar Right, I misread your comment. So taking 200 - 500mls of blood from a healthy adult male is taking between 4 and 10 per cent of their blood. And you say the effects of hypovolemia can be felt at 15% loss. That still seems close to the threshold to me.


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Relationship between leaf structure and Photosynthesis rate
We can see numerous leaf structures in plant kingdom. As the leaves are designed for photosynthesis, their structure must be a factor for any optimization in photosynthesis or chlorophyll distribution.
This link describes many leaf structures but I cannot find what I am looking for in anywhere.

I think taxonomy of plants deals with the flower structure but is their any relationship among plant species that we can describe with leaf structure ?
Do the leaf structure is optimized for maximum photosynthesis rate if so then why these different structures ?
Any other advantage for these diverse leaf structures ?

Two comments: 1) plant taxonomy takes multiple types of morphological traits into account + molecular information. Linneus original sexual system for plants was however based on flower morphology.
2) Leaf morphology is based on tradeoffs between many different functions, and besides the efficiency of photosynthesis you also need to take e.g. water loss (desiccation), nutrient/water transport and stability into account. Hence the diversity of structures.

1) Your understanding of taxonomy is outdated by a few hundred years. Linneaus' original system was based on flower morphology, but we since realized that the most effective taxonomy takes into account many different traits. In today's times, we mainly use DNA sequencing to determine relationships between organisms.
2) The leaf structure is not necessarily only optimized for maximum photosynthesis rate. For instance, the leaves of cacti are spines: thin and pointy to minimize water loss and defend the plant. In fact in cacti the stem is the photosynthetic part of the plant, not the leaves. More generally, leaves may be thicker or thinner to cope with drought. You can check out the wikipedia page for Specific Leaf Area for more information.
Long story short: different plants grow in different environmental conditions, so the optimal leaf shape for any one plant depends on conditions like drought and shade.
3) There are many advantages that can be conferred by leaf shape. One example is how leaf shape can affect what is known as the boundary layer of the leaf. The boundary layer is thicker in larger, uniformly-shaped leaves and thinner in dissected or compound leaves. The intro on this webpage seems like a good resource
Overall, good question. You have to keep in mind that any trait is going to be the product of many different factors; no one factor can entirely determine a trait's morphology. For leaves, it's many different factors including photosynthetic rate, drought, shade tolerance, defense against predators, etc. that determine the shape of the leaf.


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Why MHC class I antigen presentation exist in normal cells?
The book "Kuby Immunology" states that normal infected cells might present antigenic peptides on their surface via MHC class I, but these can't activate naive CD8 cells. Only infected professional antigen presenting cells have the necessary co=stimulatory signals to do so. This is why cross presentation happens.
But then why does the process of antigen presentation on normal infected cells happen then, if it is of no use?

"This is why" cross presentation happens - is not my understanding. This is why presentation happens, by the professionals (APCs). Your question refers to presentation  by APC in contrast to normal body cells that are not part of the immune system, right? Cross-presentation is a special form of presentation by "antigen presenting cells" - APC. It occurs to me: normal cells present antigen, however may not be called antigen presenting cells. And, please correct: normal cells do not present on MHCII, hence do not cross-present.

It is of use. They're saying that naive T cells cannot be activated by normal cells because the latter lack the appropriate co-stimulus, namely B7. However, activated CD8+ T cells can recognize antigens presented by normal cells and form a response. This is how cytotoxic T cells are able to eliminate transformed or infected cells.


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Specificity of the immune system
We know that the adaptive immune system recognizes foreign particles when their proteins are expessed of the the surface of T-cells, complexed with MHCs. But MHCs present only short peptides of length 8-11 amino acids long. How is it that every antigen has one characteristic 8-11 residues long stretch in some protein of its which none of the host's protein has. Conversely, how is it that this 8-11 amino acid long peptide, which the body is recognizing as foreign is not found in any protein of any cell of our body?

For starters, your conception of antigen presentation seems a bit off, but that's not the crux of your question. There's around 10^15 different sequence permutations for a peptide 11-mer. Despite that, it's actually likely that highly conserved regions of some proteins will be present in both the pathogen and the host. T cells will not recognize them, however, as they are negatively selected in the thymus.

This is not completely true. One part of the adaptive immune system actively recognizes and tolerates own oligopeptides.

@inf3rno Which component is that?

http://en.wikipedia.org/wiki/Regulatory_T_cell "Regulatory T cells are involved in shutting down immune responses after they have successfully eliminated invading organisms, and also in preventing autoimmunity cells." - Ofc. most of the self-reactive T-cells are destroyed by negative selection, or probably (I guess) transformed into regulatory T-cells. I have to read more in the topic, but it's too complex, I have to write a program, which can maintain a knowledge graph.

Another part of the puzzle: http://en.wikipedia.org/wiki/Regulatory_B_cells

@inf3rno I don't think Tregs can be said to be actively recognizing self antigens. It seems that Treg recognition of self is an exception rather than the rule.

I would rather say that your model is coarse-grained, while this one is fine-grained, but you are right, most of the T cells do not behave that way. +1

@canadianer yea, it should be APCs, wrote T-cell by mistake. One more thing, how did you arrive upon 10^15?

@Bio_geek24 Very rough rounding of 20^11

The immune system is the most beautiful, complex biological process that operates on a scale that it can be termed as engineering.
MHC polymorphism:
MHC's have two particular properties that give it flexibility in the face of the antigen: Its polygenicitcy (it contains several different MHC class I and MHC class II genes with different ranges of peptide-binding specificities) and secondly, MHCs are polymorphic (having multiple variants of each gene within the population).
Note: MHCs are also called HLA (Human Leukocyte Antigen)

So as you can see, there is a lot of possible variation possible. I'd recommend reading through this:
http://www.ncbi.nlm.nih.gov/books/NBK27156/
From the source above:

The outstanding feature of the MHC molecules is their extensive
  polymorphism. This polymorphism is of critical importance in antigen
  recognition by T cells. A T cell recognizes antigen as a peptide bound
  by a particular allelic variant of an MHC molecule, and will not
  recognize the same peptide bound to other MHC molecules.
This behavior of T cells is called MHC restriction. Most MHC alleles
  differ from one another by multiple amino acid substitutions, and
  these differences are focused on the peptide-binding site and adjacent
  regions that make direct contact with the T-cell receptor.
At least three properties of MHC molecules are affected by MHC
  polymorphism: the range of peptides bound; the conformation of the
  bound peptide; and the direct interaction of the MHC molecule with the
  T-cell receptor. Thus the highly polymorphic nature of the MHC has
  functional consequences, and the evolutionary selection for this
  polymorphism suggests that it is critical to the role of the MHC
  molecules in the immune response.

While a good explanation, this does not address the question.

@canadianer Apologies, misread the question. Editing the answer now.


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If a given DNA oligo is an aptamer, will the corresponding RNA oligo with the same sequence be an aptamer aswell?
Functionality of aptamers depends upon the oligo's sequence and secondary structure. So, if I take a DNA aptamer and make an RNA oligo of the same sequence (T replaced with U obviously), will this RNA oligo also act as an aptamer?

There is at least one known case where both the DNA and RNA versions of the same aptamer sequence bind the same target (Lauhon and Szostak, 1995).
But you can't generalize this, there are two differences in structure between RNA and DNA, the Uracil/Thymine change and the missing 2'-OH in DNA. Those differences can affect the binding and overall structure of the aptamer.
It is possible that the RNA version of a DNA aptamer binds the same ligand, but this won't be always the case.

But does the backbone really play role in ligand binding for the aptamer? I mean had the backbone been playing any role, aptamer sequences wouldn't have been as specific as they are, because every oligo has the same backbone and hence would have had atleast some amount of affinty for any given aptamer ligand.

@Kunal24 Not just the backbone, the tertiary structure varies between ssRNA and ssDNA with same sequence. The tertiary structure is crucial for aptamer function.

@WYSIWYG: Oh I wasn't aware of the fact that tertiary structure of ssDNA and ssDNA are different. Could you please cite some informative sources for the same? Thanks a lot!

@Kunal24 that may be a question in itself; can't cite all the references in comments. The backbone flexibility (search persistence length) is different. RNA forms GU wobbles too. For wobbles you can see my answer here.


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Parameters for Fitzhugh-Nagumo model of Action Potential
I'm a high school student who's currently in AP Biology, so my background in biology is quite limited. I'm interested in mathematically modelling action potentials.
Doing a quick google search, I discovered the Fitzhugh-Nagumo model, a simplified case modelling the voltage of the cell during an action potential as a second order differential equation $ C \frac{d^2V}{dt^2} + \epsilon(V^2-1) + \frac{V}{L} = 0$. I want to solve this equation numerically, but I can't find the numerical values of $\epsilon$, $L$, or $C$ online. What are some reasonable parameters for this model for a human neuron?

A high school student would wants to solve a differential equation numerically. Woah. I definitely did not have your level in math and programming when I was in high school. +1.

I didn't know about the Fitzhugh-Nagumo model. I quickly scrolled down this paper and this scholarpedia article. Maybe you can indicate where your differential equation come from and link to some info about the meaning of the parameters $\epsilon$, $L$ and $C$.

This is actually not the Fitzhugh-Nagumo model of the a neuron, however it is highly related to it. I believe the the Equation you have there, is capable of oscilations for any positive values of $\epsilon$, $C$, $L$. I generated this graph with the parameter values all set to 1.  Note how it is very similar to a sine wave.

I believe you where trying to write Van der Pol's equation here:
$$C\frac{d^2V}{dt^2} +\epsilon (V^2-1) \frac{dV}{dt}+ \frac{V}{L}$$
Note the subtle difference of multiplying by the first derivative.
Here is again a image with all parameters set to 1

The Fitzhugh-Nagumo equation can be found on wikipedia here and on peer reviewed  scholarpedia here. For reference it is a two state model described by the equation:
$$ \frac{dV}{dt}=V-V^3/3-W+I$$
$$ \tau \frac{dW}{dt}= V + a -bW$$
A common value for the parameters are $a=.7$,$b=.8$,$\tau=12.5$ $I$ can be anything really, I used $I=.5$ to generate the graph below. Also note that the model wont spike if I below a certain value. The Fitzhugh Equation is is slightly more general, but does simplify to the Van der pol under the assumption $a=b=0$. Here is the graph of it with the constants I described.


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Value of mathematical models in biology
Sorry if this is too much of a soft question or if it is too broad for this site.
As a person who has much more experience with math than biology, I've always been really interested in the mathematical side of biology. As I study math in biology, however, I am left with the question of "how is this actually useful?"
What kind of unique insight can mathematical models give us about biological systems that we couldn't just find experimentally?

Experiments are challenging. Thus all sciences model experimental results, often mathematically, so that future study can be simplified.

This is actually broad. There are a lot of applications of mathematical models in biology and there have been many books written on this topic.  See this related meta post

I also think this is too broad and unspecific. Mathematical biology is a huge topic with many different types of applications. However, these two questions might be useful to you: What physics knowledge can be applied to biology of organisms and ecosystems? and When are population dynamics models useful?.

This question is broad.
There are plenty of uses of mathematical modelling in biology.
Wikipedia
You may want to read the wikipedia article: Mathematical and Theoretical Biology.
Books
There are tons of books on theoretical biology. I am personally working in the field of population genetics, a field where much of the theory has been expressed mathematically. Here are book recommendations for this particular field.
On Biology.SE
We have a tag for mathematical-models (you used it in your post). You may want to see what kind of posts are tagged for mathematical-models.
To repeat @fileunderwater's comment, What physics knowledge can be applied to biology of organisms and ecosystems and When are population dynamics models useful? are examples of posts you may want to read.
What prevents predator overpopulation? will give you an example of an easy and classical mathematical model to describe population dynamics of predators and preys.

Personal historical/philosophical note: At some point physicists have started to describe the laws of nature with mathematical expressions and at that time many physicists didn't quite like the idea that physics could be described by math. Biology has gone through the same phase but much later. Early mathematical biologists developed the modern science of statistics (Francis Galton, Karl Pearson, Ronald Fisher). Biologists used existing mathematical tools such as diffusion processes (Kimura). Note that part of the work in the field of diffusion equations have been done by physicist (Einstein solved the 2D equations for diffusion processes). Note also that the dynamic of diffusion processes called brownian motion have been named after a biologist. Today, biology produces massive amount of data that require good computational skills to treat. The time when biologists had only to know how to recognize species is over, now there are few biologists left that aren't able to code in at least one programming language.

Models are often used to calculate the probability of certain biological outcomes. Such predictions are great help for prioritization of further studies or making other decisions.
Example: EPA uses an array of in vitro assays for fast and cheap analysis of thousands of potentially toxic environmental compounds (ToxCast and Tox21 projects).
Next, they use the obtained data to build mathematical models to prioritize chemicals for further more expensive and slow animal studies or to decide on administrative actions to restrict usage of high priority (most dangerous) chemicals. Their prioritization models integrate toxicity data and complex exposure models (including manufacturing and usage logistics, possibility of accidental exposure etc).


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Which pair of primers should be used to amplify the ORF in PCR?
So I want to choose the correct set of pair of primers to amplify the ORF of the gene that corresponds to amino acids in a protein. The start and stop codons are underlined. (I know that these need to be synthesised by the primer also for correct PCR technique)

The boxed sets of nucleotides are the primer options I have at hand. I know that the DNA synthesis can only carry out from 5' to 3' and there is a forward and reverse primer. The forward primer should be easy enough but non of the options seem acceptable? Could someone please explain to me how to go about this problem?

So you've identified the ORF by marking the start and stop codons. You'll want a primer on either side of the ORF. You said none of the options seem ok, but why do you think that?

First of all, if this is a homework question, add that tag to it. And show what work you have done so far.
Secondly, primers for amplifications should lie on opposite strands. Primers are typed in 5'-to-3' direction (aka left-to-right on leading strand).
Appropriate primers will be: primer 4=GTG... and primer 5=GAA.... Note how those primers are always in 5'-3' orientation. That is how you order those.
Again, if this is homework (looks like it) it is very bad taste to just ask question without any work shown. It displays laziness and usually not respected behavior when asking for help.


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What causes the localization of myoglobin in turkey to regions of muscle tissue?
I've read that myoglobin localization is responsible for the darker colour of leg muscles in turkeys. Why does this localization occur in terms of any of cell biology, molecular biology, or biochemistry? I'm not looking for bigger picture explanations at the levels of physiology or evolution, although I understand that they'll be connected to this question.

"Localization" is probably the wrong term, but I think I know what you mean... It more has to do with "expression."  While the exact mechanism to my knowledge is not elucidated, it has to do with the type of motor neuron innvervating the fiber.
This has been demonstrated by studies where they cross-inervated; that is, they took the neurons which usually innervate Type I muscle fibers and innervated Type II muscle fibers with them and vice versa.  The Type I fibers took on fast glycolytic properties, whereas the Type II took on the slow oxidative features (such as higher levels of mitochondria and myoglobin that you're talking about).

Source:
Sherwood L, Kell R. Human Physiology, First Canadian Edition. pp. 282-283.

"Localization" refers to describing, predicting, or determining the location where something is or occurs. It can also refer to the fact that something is located in particular places. I am referring to the description of where myoglobin typically occurs in turkey muscle tissue.

I'm mulling your answer over. That's quite interesting.

I think it qualifies as an answer mainly under cell biology. I'm accepting it.

Yeah it's just at least in cell bio when we talk about "localization" of a proteinusually we're talking about where it's moved to; the point of the distinction that I was making was that it's not that the myglobin is produced ubiquitously and then localized in certain cells; it's expressed at higher levels in certain types of muscle tissues.  Just semantics; sorry.

That is semantics, but it is not just semantics. That is jargon within a specific domain. That jargon applies to this context, so I understand your desire to use it here. However, the existence of applicable jargon in a particular domain doesn't invalidate the use of more generic usages. Jargon is a fine tool, but not the only hammer. There's no universally accepted rule for deciding whether to use generic vs domain-specific language, though opinions abound, so I'm sympathic to your clarification.


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Evolutionary distance between Canidae, Felidae, and Rodentia
Comparing the families Canidae and Felidae, which have the shorter evolutionary distance to the order Rodentia? Less sophisticatedly put, are cats or dogs more related to rodents?

I just wanted to reiterate what Remi.b said that neither cats nor dogs are more closely related to rodents: they are exactly the same phylogenetic distance apart

I guess this might depend on the definition of "evolutionary distance". If you count something like "number of generations since nearest common anchestor", I guess the family with longer (average) generation length would win.

Online Ressources
Here is exactly the kind of question where tolweb.org is your best friend. tolweb.org is one of the most updated phylogenetic tree online. It also contains tons of reference, very useful to understand controversy over some nodes. onezoom.org is another online source that offer you to seek through the tree of life. Also, onezoom shows only the tetrapods (incl. mammals, birds, amphibians, lizards, snakes, turtles). However, onezoom has an awesome display and is a great tool for displaying diversity (they use the total length (in years) of all branches within a clade) within a clade and the threaten index (IUCN (red list) categories).
Dogs, Cats and Rodents
You will find the placental mammals here (tolweb). As you can see, the cats and dogs are both carnivora, while a rodent is a Rodentia (as you said). This means that cats and dogs have a more recent common ancestor than does either the cat or the dog with any rodent. Stated differently again, cats are not closer or further to rodents than dogs are. There is exactly the same distance between cats and rodents than between dogs and rodents.
One onezoom, the carnivorans is presented as a sister group to the ungulates. I have no idea what representation is the most correct but in any case, cats and dogs are carnivorans and share a common ancestor that is more recent than the common ancestor shared by carnivorans and rodents. So again, there is exactly the same distance between cats and rodents than between dogs and rodents.

»Please note that this tree has not been updated since 1995« ... is this really the most updated one?

The tree of the main branches of the placental mammals hasn't been updated since 1995. Seems pretty old indeed. In general, tolweb is a often updated, great source of information on phylogenetic relationship. If you seek for more updated and more accurate representation I think there is no better option than seeking directly through the literature.

Another very good source of knowledge on the subject is onezoom.org (I edited my answer to add oneZoom) but I can't tell if onezoom is more updated. Also, onezoom cannot support polytomy and will therefore not represent doubts. If I am not mistaken onezoom also don't offer list of references. However, onezoom has an awesome display!

Wrong.. You can actually have polytomies in onezoom. Actually looking a bit more at onezoom, I realize that it actually really is a very cool tool. It also offers great visualization of threaten statues!


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What are layers in the Blue Brain Project?
I was watching Bedlewo: Topology meets neuroscience when the lecturer mentions that data is available here. I might find it an interesting challenge to do some exploratory data analysis, but I want to ensure I understand the jargon.
The download page has some of the data broken down by layers, but I am not sure what a "layer" is in this context. They have a glossary of terms, but layer is not explicitly defined here.
I found the SE post L1 - L5 layers of the brain that looks like it might answer my question, but I have also been burned by jargon for different things coinciding (kind of like a hash collision but for words). Since neuroscience is outside my background, I would rather not assume.
What are layers in the Blue Brain Project (specifically the Digital Reconstruction of Neocortical Microcircuitry)?

One interesting part of the brain is called the neocortex. In the human brain, the neocortex is the largest part of the cerebral cortex, which is the outer layer of the cerebrum, with the allocortex making up the rest.
The neocortex is formed of six layers, numbered I to VI, from the outermost layer I – near to the pia mater, to the innermost layer VI – near to the underlying white matter. Each cortical layer has a characteristic distribution of different neurons and their connections with other cortical and subcortical regions. There are direct connections between different cortical areas and indirect connections via the thalamus.
This wikipedia is a reasonable start point for a neuroscience beginner.


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Is there a published calibration between footprint measurements to body length in moose?
I am in the early stages of designing a study involving a moose (Alces alces) population.
An often-true heuristic is that body parts of an animal monotonically increases in size. There likely exist counterexamples for certain choices of animals and body parts, but I think in the case I am interested in there is likely stochastic comonotonicity.
Assume that we see a moose's tracks (e.g. INat 112977489, INat 112971980, and INat 112971692) without the presence of the moose itself. The prints in the snow can collapse and distort footprints, but I am willing list those problems as limitations of the calculation. It is also the case that in the snow I do not necessarily get a flat print, which could lead to difficult-to-measure tracks either because it is hard to measure the depth of the toes as holes or that the toes appear shorter than they actually are. In some cases I will apply interval arithmetic to any calculations when I think the size of the track is roughly guessable. Often the front hooves are measurable, and rarely the posterolateral dewclaws. Anyway, my point is not to go through all of the problems, but just to show you that I am aware that even on the face of it this is an analysis that requires assumptions and tentativeness.
What I am looking for is a published mathematical function that I can plug measures on the footprints into and get estimates of the body length out.
$$\operatorname{Body Length} \approx f(\operatorname{Footprint Measurements})$$
Such a relation would probably be dependent on whether the moose was a juvenile, an adult female, or an adult male. But even a marginal relation might be useful. I don't care if the relationship is in a particular choice of units as long as I can convert back to metric.
Has anyone fitted (and hopefully evaluated, etc) such a model?

Related: https://biology.stackexchange.com/questions/107876/how-much-does-dry-moose-scat-weigh-and-vary-in-dry-weight

And this paper? https://www.jstor.org/stable/1937779?seq=3

@bob1 I am getting a 404 Error with the link to the thesis.

I think I found it based on details in the URL: Lundmark 2008

Correct. Lundmark is the one for that. I've deleted the comment as it turns up 404 for me too. Worked when I copied and pasted, don't know what happened in between.

Yes - I found a paper published in 1978 by Franzen et al "Alaskan moose measurements and weights and measurement-weight relationships" 1
In this paper they looked at a number of parameters and found that they were all correlated with body weight:

A total of 1329 Alaskan moose (Alces alces gigas) were measured for total length, 1340 for
chest girth, 1317 for hind foot, 618 for shoulder height, and 1219 for ear length. Five hundred and
four moose were weighed.  ...

...All body measurements were significantly correlated with weight: total length, r (correlation coefficient) = 0.94; chest girth, r = 0.90; shoulder height, r = 0.87; and hind foot, r = 0.81

There are some nice tables and plots with data over age (in months) and separated by sex, as well as combined data.
1:  Albert W. Franzmann, Robert E. LeResche, Robert A. Rausch, and John L. Oldemeyer. Alaskan moose measurements and weights and measurement–weight relationships. Canadian Journal of Zoology. 56(2): 298-306. https://doi.org/10.1139/z78-040


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Liver - Regeneration in Cirrhosis
Liver is the most resilient of the human organ (on par with or next to skin). A very interesting experiment on liver regeneration is here. Even if two-thirds of the liver is removed, the remaining liver would regenerate to recover the full volume and function.
Cirrhosis of liver is a condition where excessive fibrosis occurs shattering the architecture of the liver. The blood vessels and the parenchymal cells of the liver get constricted into narrow spaces causing portal hypertension and fall in the Liver Function Test parameters (albumin level falls, clotting factors fall leading to spontaneous bleeding, bilirubin level rises causing jaundice, etc...). It can be either congenital or acquired. Cirrhosis is considered an end stage liver disease.
In the end stages of cirrhosis the only treatment option available is liver transplantation.
Question:
Why is partial hepatectomy (removal of part of liver) not a treatment option for end stage liver disease (cirrhosis of the acquired variety)?

The answer lies in the question. Liver cirrhosis constrains hepatocytes into small fibrous spaces limiting regeneration, hence the nodular pattern.
However,fibrous degeneration occurs in specific patterns. It can be located mostly around portal regions (centrolobular pattern) or diffusely through the whole lobule.
So basically, it is all good that hepatocytes can regenerate, but the limiting factor is not that. It is the structural impairment of the liver lobules and drainage system that will impair regeneration.
Moreover, most cirrhotic patients could not tolerate halving of their residual hepatic function. Not to mention the extensive surgery required. It would kill them swiftly.


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A good introductory book to histology?
Like the title says, I am looking for a good introductory text to histology. It would ideally cover

sample preparation
microscopy
staining, and
several example experiments

Suggestions?


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Like size and colour constancy, why does the brain not maintain focus constancy?
I have progressive myopia. I grew up with perfectly normal eyes but slowly started getting myopic.
The thing is, my brain knows (or should know) what the world looks like -- it knows that far away objects do not suddenly blur. So when the input from the retina changes, why doesn't the brain correct it in perception?
I'm assuming here that this should work by the same principles as size and colour constancy. In both cases the input from the retina is different but the brain doesn't perceive it as an actual change in size or colour.

The input is a blurry signal, what shall the brain do with it?

Interesting question. I concur with @Chris. Color constancy and size constancy are neural mechanisms and can therefore be imposed on visual input from the retina. In contrast, a blurry input cannot be neurally improved. As an analogy: Visual perceptions are processed and rendered by the brain and therefore represent "photoshopped" perceptions. In other words, perceptions are subjective representations manufactured by higher-level visual processing. However, focus is determined by optics. An out-of-focus picture, to push the analogy, cannot be fixed by fotoshop, nor the brain.

Ps: sorry to hear about your visual disorder. Good luck.


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Do gibbons have a monogamous sexuality?
the question is already in the title. If possible, it might be extended to:
Have animal taxa (mammal) who tend to live in a family structure have a monogamous sexuality? Or are there cases of these taxa, where the sexual partner is not the social one.

Regarding gibbons, yes. According to National Geographic:

Gibbons are monogamous and live in family groups consisting of an adult pair and their young offspring.

There isn't a generalized answer for "family living", although specific family types are indicative of relationship type. Nuclear families (parents and children) tend to be monogamous, families with multiple males and one female tend to be polyandrous, and families with one male and multiple females tend to be polygynous. See this page on primate social structure for more information.


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Using Canonical Correspondence Analysis on matrices with missing data
I have a matrix of sites where not all the environmental variables I want to assess were sampled. In other words, there are sites with the whole set of variables sampled, and there are other sites where just some variables were sampled. Does Canonical Correspondence Analysis work with missing data for the environmental variables? If it does, what would be the effect of not including the missing values?

this question might best be asked in cross validated (http://stats.stackexchange.com)

I had a quick look over there. I think ecologists might be more familiar with CCA than 'conventional' statisticians.

I though I should mention it since there is a chance it could get a close vote since this is still a stats/sampling based question!

I've had mixed luck posting ecologically-motivated statistical questions on CV. I was surprised that the word 'ordination' is not well known outside of ecological stats :p

First, you cannot fully analyze pair-wise correlations between your environmental variables with NA values, and therefore cannot fully discount including covarying variables. If this is the case, you will not be able to know which of the covarying variables is responsible for any trends in your data.
Second, I don't believe CCA will work with NA values -- you will either have to eliminate the observations containing those missing values or fill them in with column averages. However, both of these methods will have an impact on your results, so move forward cautiously.
Third, I wonder if CCA is even the way you want to go. nMDS (non-metric multidimensional scaling) is much less constrained than CCA. Additionally, it doesn't suffer from as many assumptions/limitations as CCA.
From McCune & Grace (2002):

The following two questions can be used to decide whether CCA is appropriate: (1) Are you interested only in community structure that is related to your measured environmental variables? (2) Is a unimodal model of species responses to environment reasonable? If, for a specific problem you answer yes to both of these, then CCA might be appropriate

However, missing environmental data is still a problem in nMDS.


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How non-invasive blood glucose concentration measurement work?
Diabetes patients need to conduct the “fingerstick” a few times a day. One of the mechanisms of "fingerstick" is to take small amount of blood sample and put it onto a test strip. The enzyme on the test strip reduces the glucose and the electronics of the glucose meter detect the redox species produced. However, this method is painful and increase the risk of infection.
Photonic sensing technology opens up a new method for non-invasive blood glucose concentration. According to an article of medGadget in 2013 (The link follows http://www.medgadget.com/2013/10/non-invasive-measurement-of-blood-glucose-levels-using-glucotrack-interview.html ), the non-invasive kind was invented. By simply clipping onto the earlobe (without puncturing the skin), the blood glucose concentration could be measured. Does anybody knows the working principle for that? Or, suggest a paper describing that?

Just saw a talk by Mark Arnold, who does some of this research with NIR spectroscopy. Might be a good place to start.

This is not a new thing, by checking the articles about non-invasive glucose level measurement, it started in the early 90's.

Near-infrared (NIR) spectra of the human inner lip were obtained by
using a special optimized accessory for diffuse reflectance
measurements. The partial-least squares (PLS) multivariate calibration
algorithm was applied for linear regression of the spectral data
between 9000 and 5500 cm−1 (λ = 1.1-1.8 μm) against blood glucose
concentrations determined by a standard clinical enzymatic method.
Calibration experiments with a single person were carried out under
varying conditions, as well as with a population of 133 different
patients, with capillary and venous blood glucose concentration values
provided. A genuine correlation between the blood glucose
concentrations and the NIR-spectra can be proven. A time lag of about
10 min for the glucose concentration in the spectroscopically probed
tissue volume vs. the capillary concentration can be estimated.
Mean-square prediction errors obtained by cross-validation were in the
range of 45 to 55 mg/dL. An analysis of different variance factors
showed that the major contribution to the average prediction
uncertainty was due to the reduced measurement reproducibility, i.e.,
variations in lip position and contact pressure. The results
demonstrate the feasibility of using diffuse reflectance
NIR-spectroscopy for the noninvasive measurement of blood glucose.

1993 - Noninvasive Blood Glucose Assay by Near-Infrared Diffuse Reflectance Spectroscopy of the Human Inner Lip

There are multiple approaches, mostly spectroscopy, but dielectric properties (e.g. conductivity) can depend on glucose levels too. Saliva can be used to measure glucose levels as well.

2014 - Non-invasive glucose monitoring using impedance spectroscopy

2014 - Broadband Tissue Mimicking Phantoms and a Patch Resonator for Evaluating Noninvasive Monitoring of Blood Glucose Levels

2014 - A paper strip based non-invasive glucose biosensor for salivary analysis

The details of each technology you can find of wikipedia.