text:
Can animals and humans be ranked in their ability to detect moisture?
One reason for insects being so successful - about 70% of all animal species - is their excellent ability to detect moisture. Take termites for instance. The soldiers boot out the flying reproductives only when it will rain within 24 hours. Because moisture will be needed to survive and make a new termite nest.
Humans by contrast are hopeless at detecting moisture; humans do not have the senses to be able to predict rain. Except by more indirect methods and science.
So my question is is there any way of ranking the different abilities to detect moisture? This is not a list question. Rather, it's steering for a formula or set of variables. Are there factors that make a dog better at detecting moisture than cat for instance, if that is the case?
I am surprised that nobody seems to have done this for something - water and moisture - that is so vital for life.

If you are going to downvote this at least have the guts to comment and say why; it seems like a valid question to me.

It sounds like you are talking about rain prediction, i.e. weather prediction of animals. And the title sounds like the ability to detect local water, like mosquitos when they lay eggs, which can be explained through scent. The phrases are more like BBQ convo than concise info statements and queries. A dog can smell water because water smells of algea and nitrogen and things. Air pressure can also predict rain, perhaps that's what termites sense. I'm not voting, I't difficult to answer a vague question. it's a cool topic to research though.

https://www.google.com/search?q=animal+sense+of+weather&oq=animal+sense+of+weather&aqs=chrome..69i57j0.5696j0j7&sourceid=chrome&ie=UTF-8

If it helps anything I have a shelf full of books about termites. I was keeping jargon to a minimum so that might sound ironically like "BBQ conco". The flying reproductives of termites are called aeletes. They have four fixed wings. I have beena round a lot of scientists who study termites.

So did you mean weather prediction or water location? Don't hesitate about to write formal, and even harvard/cambridge/academic English on this forum, it's quite a strict forum for science level. It helps others to learn good English and the ops like it.  I didn't have time to check the results for animal sense of weather prediction, but there are lots of examples and explanations of many animals.

Both if the animal is using their senses to find it.

The termites may not detect the moisture, only the pressure drop. same goes for most rain prediction in advance, the air would still have the same humiditiy.

Actually that is not true. Termite alletes will only be booted from their nest when [1] there is some increased humidity [2] the temperature is hot but not too much - 30 degrees centigrade approx, [3] little wind so they can fly better. I have observed first hand dozens of allete flights.

As a newcomer, a friendly word of advice regarding your response to the downvote (not from me). Be careful. Although I appreciate your frustration and have been in a similar situation, it is not obligatory to explain a downvote. Often, when I have done so, this had made the situation worse because the poster has objected to my criticism in an inappropriate and intemporate manner. From which you may see that an expression like "have the guts to comment" is inadvised and not in the "be nice" ethos (that the mods keep reminding me of).

Ok, thank you! It is not obligatory. But it helps.

I should have made a suggestion. You could grit your teeth and write “It would help me to improve my questions in the future if the person who downvoted me explained why”. You’re unlikely to get a response, though.

I think you simply Can't.
To design an experiment you need 2 things:
1- Something Common between Humen and Insect and can be measured.
2- Different scale to order the species.
And I Think here you just do NOT have both criteria.

One of the common factor one can use is "hygrosensation receptors" or their homologs. After that one can compare the technical properties of such receptors (like latency, sensitivity etc) to get rank list. Similar successful attempt have been made in the case of Vision. One can rank insects to humans for specific visual task based on their photoreceptors. [e.g. Visual Motion Processing (Clark and Demb 2017)]


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What is the subcellular location of synthesis of non-essential amino-acids?
What is location of non-essential amino acids synthesis in a cell? Is it some specific organelle? And what is the gene driver behind this?
I thought the whole point of DNA is coding for how to synthesize proteins and that it is the mechanism of genes expression. Triplets of nucleotides are codes of amino acids and that is the granularity that cell works with.
Now it turns out cells knows how to synthesize more than half of the 20 amino acids, in humans, and I do not see, in the web, good texts of how it is done, where, and how that is coded.
Thank you for helping to shed some light.

This is a very basic question, the answer to which is easy to find on the internet. Did you search Wikipedia for Essential Amino Acids or Amino Acid Synthesis? If that is insufficient and you need a biochemical text book chapter, Berg et al. on NCBI Bookshelf should be your next port of call. The specific section is in Chapter 24. Your expression "gene driver" is unclear to me. Read the chapter and then explain any further questions.

Hardly it is a basic question, David. I did go through the wikipedia articles but I did not manage to answer the title question. I am a computer programmer, I have no formal education in molecular biology.

Consider the response if I posted a question on Stack Overflow asking what a “for loop” was (for). Not only would I be posting a basic question to the wrong sort of site, but I would have shown a singular lack of initiative or aptitude in using the resources of the internet.

You are showing a lack, that is sure. Quite singular

I think you are almost right. DNA (in the nucleus) is transcribed to mRNA, and protein synthesis occurs on ribosomes where the the sequence of bases in the mRNA is translated into protein. Ribosomes are located in the cytoplasm or attached to the endoplasmic reticulum. (The 'mRNA story' is well told in Who discovered mRNA?)
But there is also another type of RNA that is critical to protein synthesis, and that is transfer RNA (tRNA): each amino acid is attached to an 'adaptor' molecule (tRNA) and it is this form of the amino acid that is used by the ribosome. It is the adaptor molecule (a tRNA 'charged' with an amino acid) that contains the anti-codon, which base-pairs with the mRNA during protein biosynthesis.
In order to carry out protein biosynthesis, the cell needs a supply of amino acids, the 'building blocks' of proteins. It is here  your thinking (maybe) is a little confused? The building blocks may come the digestion of protein in food, or they may be synthesized by the organism. If they can be synthesized 'de novo', perhaps starting from a glycolytic or Krebs cycle intermediate, they are (usually) considered non-essential. What amino acids are considered essential or non-essential depends on the organism. Humans, for example cannot synthesize 'de novo' the aromatic amino acids Phe, Tyr or Trp, but we can convert Phe to Tyr.  E.coli, on the other hand, can make all three of these amino acids from simple building blocks, but cannot convert Phe to Tyr (see Miller & Simmonds). Thus Tyr is considered non-essential for humans (provided that an adequate supply of Phe is available).
The biochemical pathways leading to amino-acid biosynthesis are usually quite complex, with the involvement of many gene products (enzymes). The story of amino acid biosynthesis is well told in Umbarger(1978):Amino Acid Biosynthesis and its Regulation.

There are several enzymes involved in amino acid biosynthesis. These some of thse enzymes are encoded in the human genome. You can check out KEGG for a detailed pathway in different organisms.

The green arrows denote reactions (and enzymes) that are present in a given organism (Homo sapiens, in this case). If you click on the arrows you can know the details about the enzyme.
These enzymes are present in the cytoplasm as well as in mitochondria. Moreover, the reactants for synthesis of certain amino acids are produced in mitochondria (TCA cycle intermediates). See this article on the role of mitochondria in amino acid metabolism.

  Overview of the amino acid metabolic network in human mitochondria. Shaded areas represent the cytoplasmic segments of the pathways.

I lack chemistry knowledge in order to understand the answer fully. Thank you for answering - it gives some key hints and introductions to the topic and has quite good links. One thing perplexies me still - enzymes are transcribed & translated from DNA which are to participate in non-essential amino acids sythesis, but for the translation you need amino-acid building blocks. So it might happen the same amino acid is needed,which is then a recursive task? Seems I have to read more to understand,I am also a layman in molecular biology

source: Stack Exchange

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

sort: votes


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Why is it possible to make yoghourt with lactose-free milk?
The function of the Lactobacillus bulgaricus and Streptococcus thermophilus  cultures is to ferment lactose to produce lactic acid. The increase in lactic acid decreases pH and causes the milk to clot, or form the soft gel that is characteristic of yogurt.
In lactose-free milk, all the lactose was transformed in glucose and galactose using lactase. Is it possible for those bacteria to ferment glucose and galactose instead of lactose? Or is this based on other biological reactions?

Conversion of lactose to galactose and glucose is a part of the bacterial metabolism of lactose. So digested lactose would work.
In fact, it should work for all kinds of 6-carbon sugars as lactic acid is produced from pyruvate (end product of glycolysis). See Wikipedia:lactic acid fermentation.

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


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What kind of bird is this?

Found in southwest Michigan.  It appears to have fallen from a nest.

It's clearly a heron of some kind. My money's on a juvenile Great Blue Heron, but I will need to double-check their juvenile plumage before I can be sure.

Please provide the approximate size of the bird. Thanks.

The body shape does seem to indicate it's some kind of heron/egret (12 species, of which, have been previously found in Michigan [according to Wikipedia]).
The seemingly large size from your picture (please edit with actual or best approximation of size), the tufted feathers on the head, white face, and the start of a black line on the anterior edge of the eye all suggest that this could be a great blue heron.
Great blue herons are typically grey (not the dark almost black of your specimen), but I did find some photos with nestlings /fledglings with darker plumage, including below:

 Source: Wikipedia


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Is 'disorientation event' a common term among biologists?
On the South Carolina Department of Natural Resources web page about the marine turtle conservation program it says, "When a hatchling sea turtle is attracted away from the ocean towards a direct or indirect source of light, biologists describe this as a disorientation event."
Does something like the disorientation event describing the sea turtle behavior also occur in other species?

The source you link seems to describe the term as specific to sea turtle biology. Not every biologist studies sea turtles. Are you asking if it is used in other species? Or are you asking if it is used in scientific papers specific to sea turtles?

Presumably they are just explaining a term that has been used or coined to describe the phenomenon under a more general heading using scientific or formal language, so the reader understands its subsequent use. The idea conveyed to you that biologists mutter it to one another at coffee time is incorrect and, I imagine, unintentional.

@BagiM I am asking if it is used in other species.

@Bob516 You should edit your question to clarify. As written, there is nothing in your question that implies you are asking if it is used in other species. With that added piece of information, I am also unclear if you are asking if this term is used or whether something like "disorientation events" in sea turtles also occur in other species. It's important to be precise in your questions.

As sort of a "teach to fish" answer, let's approach how to answer a question like this:
Google Scholar is a pretty good index of scientific literature: good enough for this purpose. If you search:
"disorientation event" -turtle
you will return all results that use the specific phrase "disorientation event" except those that mention turtles.
You can also do the search:
"disorientation event" turtle
to find the turtle papers. As of today, "disorientation event" returns 57 results; 14 also include the word "turtle", 43 do not.
Among the 43, it looks like the majority of papers are discussing human disorientation, particularly in the context of human pilots but also in the context of cognitively impaired individuals or simply lost pedestrians. There is one paper that uses the term referring to rats in a maze-like task.
Overall, these results lead me to conclude that "disorientation event" is not a common general term used by biologists to refer to non-turtle species losing their way, although I would also say that I would expect a biologist to understand the meaning of the term given sufficient context.

I'm only familiar with the bird research and it is not a commonly used term in ornithology. Birds use multiple methods for navigation which include the sun, stars and the earth's magnetic field. When biologists talk about birds becoming disoriented (usually by magnetic fields or they could appear to be disoriented after a fallout event, due to a hurricane etc) they don't refer to it as a disorientation event, as far as I know, there isn't a term to describe these events in ornithology.
I feel like I should clarify, since I used a term and then said there isn't a term...
"Fallout" or migration fallout is when severe weather prevents birds from reaching it's destination (e.g. breeding grounds or wintering grounds) and instead taking refuge in an unusual place (what we could consider unusual, as it's not their normal path of migration, not their "normal" stopover site). It's not actually referring to birds becoming disoriented, which is why I would say this is not a term to describe a disorientation event.


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Bug larvae identification
 anybody know what this might be, found in my bed. Pennsylvania, USA . Thanks

Please see the tag info for species-identification to learn how to make an answerable species-ID question.

That's a silverfish (order Zygentoma) https://bugguide.net/node/view/79 This individual is not in great shape, and probably got crushed, however you can see it had the cerci in its tail. The individual is lacking antennae, which are usually long, but the eyes  are also very characteristic. You can see a similar picture on this thread (https://bedbugger.com/forum/topic/here-we-go-againcame-home-now-and-found-this-id-please-silverfish. They are fairly common in homes and are harmless. They feed on fibers and detritus in your home.

that certainly doesn't look like any silverfish I've ever seen. Presence of prominent cerci is not conclusive evidence of a silverfish. The OP's specimen appears to be a larvae of some type, and silverfish don't have larvae as they undergo direct development vs. complete metamorphosis. Please provide stronger support for your answer. Thanks.

I stand by my ID, because I've seen exactly specimens of silverfish like that. This is just a mangled specimen, which makes sense because the OP found it on the bed. Also, I know silverfish have direct development (I'm a PhD in Entomology), but you're assuming the OP knows those finer biological details.

Ok please explicitly explain what characteristics (and /or provide image examples) you've used to make your claim. Currently, it comes across as an unsupported guess. Due to the immense amount of misinformation on the internet, Answers can't be based on expertise alone - you need to expand upon your answer. Regarding biological details, please see here. Thanks.


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What kind of weird little insect is this?
What kind of insect is this?
I found it in my work room.
I live in the city of São José dos Campos, São Paulo, Brazil

Please indicate the approximate size of your specimens. Also, if you have a clearer/brighter picture of the top of the insect, please provide that as well. Thanks.

This is probably a nymphal stage of a stink bug (aka shield bug).
Based on the roundness of your specimens, I'd suspect that they represent possibly the 1st or 2nd instar development stage.
I am unsure of the species currently, though I suspect this is an image of the adult (wrongfully labeled as a "bed bug" at its source):

 Source: Shutterstock
I will dig into the Brazilian fauna to see if I can get you a species...


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Problem with joining the gene of interest into the open plasmid when their lengths are not the same
Before the recombinant plasmid is obtained in recombinant DNA, the gene of interest is inserted into a linearized plasmid by DNA ligase.
What happens if the length of the gene of interest is not the same as that of the gap in the open plasmid? (e.g. far longer) Can the gene still be connected with the gap or are other processes needed before the recombinant plasmid can be put back into the bacteria?

From your question I suspect that you are thinking of DNA as being a very rigid molecule — it isn't.
Double stranded DNA is reasonably flexible and a useful mental model would be to think of this as being like tying the ends of two pieces of thin wire together to make a circle.
Double stranded DNA can make a closed circles smaller than 250 bp long1,2 and I don't think there is any known upper limit — for example there is a known circular bacterial chromosome 14,782,125 bp in length3.
A typical plasmid can accommodate inserts of any size up to total size of around 50 kb, but plasmids that are more than 20 kb are very difficult to work with and may require special transformation techniques.
References:
1: Thibault, Thomas et al. “Production of DNA minicircles less than 250 base pairs through a novel concentrated DNA circularization assay enabling minicircle design with NF-κB inhibition activity.” Nucleic acids research vol. 45,5 (2017): e26. doi:10.1093/nar/gkw1034
2: Shore, David, Jorg Langowski, and Robert L. Baldwin. "DNA flexibility studied by covalent closure of short fragments into circles." Proceedings of the National Academy of Sciences 78.8 (1981): 4833-4837
3: Land, Miriam et al. “Insights from 20 years of bacterial genome sequencing.” Functional & integrative genomics vol. 15,2 (2015): 141-61. doi:10.1007/s10142-015-0433-4


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Why is glycerol supplied/used as 87% solution?
While preparing glycerol stocks of my transformed bacterial cells (DH5alpha) the protocol I had to follow was that I would make one 50% glycerol stock (500µl culture, 500µl glycerol 50%) and another 87% glycerol stock (850µl bacterial culture, 150µl glycerol 87%). 87 seems to be a very specific number. Any particular reason why 87% glycerol concentration is used?

In which protocol/reference did you find the 87% glycerol?

I think my lab protocol follows sambrook russel's molecular cloning.

Yes I will try to provide a proper reference.

Glycerol is typically sold at 87%, which just pushes back the question one step. Many years ago I was told that this is because of glycerol's hygroscopic nature, such that a higher concentration would tend to absorb water from the atmosphere and dilute itself anyway. Does this stop at 87%? Figure 1 from Glycerine: an overview suggests that 50% relative humidity might lead to a glycerol concentration that is in the ballpark of 87%, but 40 or 45% relative humidity looks closer.  Not definitive, so I'll leave this as a comment.

Typically, a glycerol stock will have a final concentration of 10-20% of glycerol. Glycerol is highly viscous. Pipetting higher concentrations of glycerol is difficult (especially for smaller volumes). Therefore a lower concentration such as a 50% solution (works for me) is convenient: add 300µl to 700µl of bacterial culture.
Regarding 87%: some vendors provide 87% glycerol along with anhydrous (>99%) glycerol. The reason is probably the same: it is easier to pipette 87%.
From a vendor's website:

Glycerol is a component of several buffers, media or reagents in
  biological research. It is supplied as glycerol anhydrous or 87 %, the
  latter containing 13 % water. Both glycerols are from the same
  quality, the 87 % glycerol has the advantage of a lower viscosity.
  Anhydrous glycerol can be pipetted with difficulty only, especially at
  low temperatures.

But the question is why 87% and not 90 or 80? See Michal et al. (2017)  for a relationship between viscosity and concentration of glycerol-water mixtures.

Another graph plotted from the data given in the document mentioned by iayork in the comments. Different coloured lines denote data at different temperatures (in °C). Original data from: The properties of ordinary water substance. Compiled by N. E. Dorsey, New York (Reinhold), 1940.

So I am guessing that 87% must have been optimal beyond which the viscosity just shoots up rapidly with a small increase in concentration. I wish to reiterate that this is just my guess. I could not find a authoritative (in fact any) reasoning on why precisely 87% glycerol is (or was historically) supplied.

Thanks so much for such an well reasoned and knowledgeable reply. That ought to be the reason for using 87% glycerol stock.

I think this is more plausible than the hygroscopicity I was told was the reason, since 87% doesn't show an obvious connection with anything on the hygroscopic chart whereas it's a better match with viscosity. The vendor's comment you quote also strongly supports this. Upvoted!


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What enzyme or bacteria could dissolve plastic?
What enzyme or bacteria could dissolve plastic aside from acetone? Preferably, low-cost and environmentally friendly. Any suggestions would be helpful.
I'm targeting for thin plastic (low-density polyethylene). Environmentally friendly for me is that it follows the EPA standards from the USA. I'm targeting for around 150 USD. I'm okay with solvents that make the plastic swell, but a chemical that could dissolve it is preferable.
I asked this on the ChemStack Exchange and I'm not sure if enzymes and bacteria are allowed there so I'm asking here too. Thank you!

You should wait before the [chemistry.se] people decide that it is off topic there before posting to another SE. Don't simultaneously post on multiple websites. If it is indeed off topic there, they can migrate the question here.

Anyway, did you try searching google scholar on this topic?

Yes, I tried, but I found out that Ideonella sakaiensis works, but it digests plastics in 6 weeks. I'm trying to find a more effective way to digest bacteria. Thanks!

@JosephLopez You should include prior research in your question. It would be kind of rude if someone wrote up a whole answer about Ideonella sakaiensis and then you responded "yeah but that takes a long time I'm looking for something better." However, you should also note it seems you are asking for a bit of a holy grail here: an EPA friendly way to quickly deal with one of the biggest pollution challenges of today? Sounds like a Nobel prize, not a SE answer.

Not an enzyme, but D-limonen does a good job dissolving polystyrene. See here for example. It's cheap, and I assume about as environmentally friendly as dissolving plastic can be.

Thanks! Looking into it now with fresh eyes, my tone sounds kind of rude.... Thanks for correcting me! @BryanKrause

Thanks @theforestecologist for the suggestion!


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Does anyone know a good pancreatic-cancer metastasis cell line?
Researching about pancreatic cancer. We have mostly "main-tumor" cell lines in our lab, and I´m currently looking for cell lines originating from metastases (liver, lung, etc.).
Does anyone know a well-established pancreatic-cancer-metastasis-cell line?

Did you check this article?

Thanks, but I already know this one. Good paper nonetheless

Perhaps you should mention that and explain what different do you expect.

SUIT-2 cell lines are derived from the liver metastases of Pancreatic Ductal Adenocarcinoma. The subline S2-007 is highly metastatic. The other sublines are S2-013, S2-020 and S2-028 which have decreasing metastatic capabilities.
You can probably refer these articles for more info :
1. https://www.ncbi.nlm.nih.gov/pubmed/3102439
2. https://link.springer.com/article/10.1007/s10585-017-9840-3


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What is the use of having a surrogate mother in animal cloning?
In animal cloning, an ovum is collected by an animal and processed to form an embryo after fusion, which is going to be inserted to a surrogate mother. So my question is that why can't the embryo be inserted the animal that gives the ovum as they are both maternal?

Seems trivially obvious, doesn't it?  Presumably the goal of cloning would be to produce many identical copies of the cloned individual, therefore you need many surrogate mothers.

It would make the result at least a little ambiguous. How would you establish with high confidence that the offspring was the results of your implanted cloned ovum and not a naturally fertilized one? DNA testing would have to be quite extensive to establish that offspring was a clone and not the result of an ordinary pregnancy. If you use a surrogate mother, the offspring will have DNA quite distinct from the surrogate.


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Bug Identification: Tiny Bugs
I have seen these on my hands recently and I am wondering what they are. Urban Setting. South Central Pennsylvania.

Please comment about whether you have any animals (especially birds) living in or around your home. Thanks.

Related: Tiny white very hard cell bug! Please help to identify!

@Erik K Looks like maybe you have two accounts..You can merge them together if you'd like. See here for instructions. Let me know if you have any issues

This appears to be a bird mite (or possibly rat mite) in the genus Ornithonyssus of the parasitic family Macronyssidae.

 Credit: user Aewills on bugguide.com
Identification:
From Central Exterminating Co.:

The mites are distinguished from most other common, structural species by the very long legs and very long mouthparts. These long, pointed chelicerae and palps stick well out in front of the head region. The 8 legs are very long and well separated, allowing for good mobility by these mites. The body is oval, with the thorax and abdomen combined to a single segment without separation. The color is light grayish in unfed mites to reddish orange in mites recently having had a blood meal. The fowl mites often seem to have a patchy, mottled appearance of dark areas.

Distinguishing between species is difficult.

As for knowing the specific species, citybugs.tamu.edu suggests:

Distinguishing between different species of Ornithonyssus mites to determine whether birds or rodents are the likely source is difficult and requires special expertise.

Blaine Mathison mentions the following features useful for identifying these mites to lower taxonomic levels under magnification [source: bugguide.com]:

chelicerae shape
dorsal plate breadth and degree of dorsal coverage
spiracle present between legs
genitoventral plate width
sternal plate shape and presence of setae

(see the linked post for pictures and more detail).
You can see videos of these mites crawling on people here and here.
Regarding their affects on humans:
From Penn State Extension:

Bird mites have piercing mouthparts that enable them to take blood meals from their
bird hosts. Although the mites will inadvertently bite people, they cannot reproduce without their bird hosts...

As the mites search for an alternative host, they will crawl onto the skin and conduct an exploratory bite to test the appropriateness of the host. The mite will move on, possibly trying the host again, but will not feed. These bites are felt as a “prick” and a resultant rash and itching, sometimes intense, will occur. Some individuals are apparently capable of sensing the crawling of the mites on the skin. The irritation produced by the bite is enhanced by the injection of the mite’s saliva that can cause a localized histamine
response.

Management:
Remove birds (and especially nests) from on or near the building. Check for any holes in your building that could be large enough to allow birds inside. Again, these mites need birds to reproduce, so if you eliminate the birds eventually these will disappear. See PSU Extension and Central Extirminating Co. for more suggestions.

Congratulations, you have baby cockroaches!  I have lived with many.  Their shape and coloring changes with age.  Your organism walks too fast and is too big to be a parasitic mite.  So this is good news.

You are more likely to get a positive response to your answer if you explain why your identification is correct. Specifically, please [edit] your answer to add discussion of key features that led you to this conclusion and supporting references or at least validated images. Without this your answer is indistinguishable from opinion. In particular you are disagreeing with someone with a well-established reputation for excellent answers — they could be wrong, but you really need to demonstrate that rather than making unsupported assertions.


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Bug Identification: Tiny Bugs in Fairport NY

We have been finding a ton of these tiny bugs (pin head size or smaller) outside on our patios, outdoor tables, on the grill, etc.
What are they and how do we get rid of them?

Related posts: Can Anyone Identify This Insect?, What are these tiny, swarming, jumping bugs?, Help identifying tiny jumping bug, Taxonomy: Categorising Collembola, What kind of small insect is this?, Unknown aquatic larvae

These bugs are a type of hexapod called springtails (subclass Collembola). Springtails are often very tiny and hard to see without a lens, so I have to say you did a good job grabbing a fairly detailed picture of this one. Specifically, your specimen appears to be some species in the order Entomobryomorpha.
According to Wikipedia:

They can be best distinguished from the other springtail groups by their body shape...The Entomobryomorpha...contain the slimmest springtails [with]...long bodies. [They also have] well-developed furculae

Specific species:
Usually, IDing springtails is very difficult, but I believe your specimen matches a fairly widespread species called Entomobrya nivalis (aptly named the cosmopolitan springtail).

 Source: Wikipedia; photo credit: James Keith Lindsey
The description of this species matches yours fairly well. From Wikipedia:

The cosmopolitan springtail measures about 2 mm in length. Its color consists of a yellow or white background with dark pigment forming transversal bands along the third segment of the thorax and the segments 2 to 6 of the abdomen. The fourth segment of the abdomen has a U- or 11-shaped pattern that easily distinguishes this species from others in the genus Entomobrya+

Somewhat true to its name, this somewhat cosmopolitan species is found in temperate and polar regions across North America and Europe+. Adults typically live among lichens and trees (whereas young live in leaf litter), however, according to NC State Extension:

Rarely springtails may become exceedingly abundant and may congregate in heaps several inches high on driveways, sidewalks and poolsides.

So what exactly is a springtail??
In general, springtails usually feed on decaying matter, and -- you guessed it -- they're known for their ability to jump!

Springtails are so-called because they have a unique structure, the furcula, that allows them to jump for considerable distance relative to their tiny size. [source].

 Springing mechanism of a generalized springtail. Credit: Marianne Alleyne [Source]

+ Wikipedia cites Katz, A.D.; Giordano, R.; Soto-Adames, F. (2015). "Taxonomic review and phylogenetic analysis of fifteen North American Entomobrya (Collembola, Entomobryidae), including four new species". ZooKeys. 525. doi:10.3897/zookeys.525.6020

Those are Collembola, something in the line of this genus https://bugguide.net/node/view/91878. They are harmless to humans, usually live in the leaf litter and I don't know if there's really anything you can do to control them. Let's see if any expert in Collembola chimes in.


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Species identification. Is this a leech?

The pictured creature, shown at the bottom of a glass, was attached to a friend’s child after he was swimming in the Ottawa River today. It stretches out to roughly an inch in length but in this “resting pose” was around half that length. Below is a shot of the mark left behind:

It looks like a leech to me, but I thought I’d ask the Internet.

Welcome to Bio.SE! What attempts to answer this question have you already taken? We ask that all question posters here attempt to search for an answer to their own question and explicitly indicate what research they've already done, what they learned, and what is still confusing or unknown to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thanks!

Thanks, I'll try to do better next time.

Yes this is a leech. It appears to be a species in the family Glossiphoniidae, or the freshwater jawless leeches. This family of leeches is relatively flattened with a poorly defined anterior sucker.
According to The Canadian Encyclopedia, there are about 45 species of leeches found in or around Canada.
Langer et al. (2018)1 provide a more limited selection of Glossiphoniidae leeches they ascribed to Ontario. Of the ones they list, yours most looks like a specimen from the genus Placobdella.
See, for example, this image of Placobdella phalera from de Carle et al. (2017)2 found in Ontario, Canada:

 Source: Figure 1, de Carle et al. (2017)

1  Langer, S.V., Vezsenyi, K.A., De Carle, D., Beresford, D.V. and Kvist, S., 2017. Leeches (Annelida: Hirudinea) from the far north of Ontario: distribution, diversity, and diagnostics. Canadian Journal of Zoology, 96(2), pp.141-152.
2  de Carle, D., Oceguera-Figueroa, A., Tessler, M., Siddall, M.E. and Kvist, S., 2017. Phylogenetic analysis of Placobdella (Hirudinea: Rhynchobdellida: Glossiphoniidae) with consideration of COI variation. Molecular phylogenetics and evolution, 114, pp.234-248.


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Easy Hardy Weinberg Equilibrium

Hi
My friend and I get 2 different answers to this question. I would like to know how to calculate the value of q. My friend says that 500/1500=q because there are 500 recessive alleles in the population and there are 1500 alleles in total. I say that p2= 500/1500 and P is the square root of that value and  q+p=1 but we both get different answers.  Please let me know which way is correct. Thank you guys in advance

P=(250 × 2 + 500)/1500 = 0.66
Q=500/1500 = 0.33
Your friend was right, you miscalculated P because forgot to add the alleles coming from the heterozygotes.


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What would happen if VEGF was injected into a person?
Couldn't VEGF help with ligament recovery? I looked it up and found some studies in rats, but nothing on people. VEGF inhibitors tend to be used more often then VEGF.
Why isn't VEGF being used in people? What would generally happen if VEGF was injected into a person?
EDIT
Here is the one study that examined injection VEGF in rats for increasing skin viability.
Also I am not really asking about the effect of VEGF on ligaments. I just figured that because there is little vasculature surrounding ligaments (and cartilage), VEGF could in theory improve recovery of such injuries. The bigger question is why aren't people ever injected with VEGF?

VEGF is a family of growth factors that promote angiogenesis and vasculogenesis.
Vascularization is a key step in the progression of cancer, so the VEGF family has often been a target for suppression: preventing vascularization of tumors can stop their further growth.
That said, your premise that VEGF hasn't been tried clinically is false: there have been several clinical trials of VEGF (and no doubt more that I didn't find).
Hedman, et al 2003 used catheter-based VEGF gene transfer at the time of angioplasty/stenting, though they found it did not prevent restenosis they did see increased perfusion (it seems to me that further research didn't show sufficient effects on long-term outcomes). Ripa, et al 2006 used VEGF gene transfer as part of a treatment for ischemic heart disease. It seemed like the treatment was safe, but the efficacy was limited. Ropper, et al. 2009 attempted VEGF gene transfer for the treatment of diabetic polyneuropathy. They found some improvement of pain, and report a fairly high rate of adverse events but their control group also experienced adverse events.
It seems like a similar VEGF plasmid is available in Russia as Neovasculgen for use in limb ischemia; the company developing the drug is in the process of beginning to get approval elsewhere.
VEGF as a topical application has been studied under the name telbermin, for example Hanft, et al 2008.
There may be others, but I stopped my search there. https://clinicaltrials.gov/ is a good place to start looking for what research has been done in humans if you have trouble finding journal articles at first.

Hanft, J. R., Pollak, R. A., Barbul, A., Gils, C. V., Kwon, P. S., Gray, S. M., ... & Breen, T. J. (2008). Phase I trial on the safety of topical rhVEGF on chronic neuropathic diabetic foot ulcers. Journal of wound care, 17(1), 30-37.
Hedman, M., Hartikainen, J., Syvänne, M., Stjernvall, J., Hedman, A., Kivelä, A., ... & Närvänen, O. (2003). Safety and feasibility of catheter-based local intracoronary vascular endothelial growth factor gene transfer in the prevention of postangioplasty and in-stent restenosis and in the treatment of chronic myocardial ischemia: phase II results of the Kuopio Angiogenesis Trial (KAT). Circulation, 107(21), 2677-2683.
Ripa, R. S., Wang, Y., Jørgensen, E., Johnsen, H. E., Hesse, B., & Kastrup, J. (2006). Intramyocardial injection of vascular endothelial growth factor-A165 plasmid followed by granulocyte-colony stimulating factor to induce angiogenesis in patients with severe chronic ischaemic heart disease. European heart journal, 27(15), 1785-1792.
Ropper, A. H., Gorson, K. C., Gooch, C. L., Weinberg, D. H., Pieczek, A., Ware, J. H., ... & Kirchmair, R. (2009). Vascular endothelial growth factor gene transfer for diabetic polyneuropathy: a randomized, double‐blinded trial. Annals of neurology, 65(4), 386-393.
Simovic, D., Isner, J. M., Ropper, A. H., Pieczek, A., & Weinberg, D. H. (2001). Improvement in chronic ischemic neuropathy after intramuscular phVEGF165 gene transfer in patients with critical limb ischemia. Archives of neurology, 58(5), 761-768.

These are interesting articles. However, they all appear to be utilizing gene transfer therapy methods rather than hormone therapy. Are you sure you found studies that utilized VEGF and not VEGF plasmids?

@JHouseman That seems to be the typical approach. The Hanft paper is VEGF itself rather than plasmid, you can find more searching telbermin. As you'll note in the cardiac work, part of the point is to have VEGF present where needed, such as the site of angioplasty, and also the desire to have VEGF present over a long time period, hence the use of plasmids. It may be easier to inject VEGF directly in an animal study where the animal is always in the lab, but not really feasible for human use.


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Is this spider venomous?
I found this spider in bathroom. Just wanted to know more about it.
Location : India(South India,Hyderabad)
Temperature : 30°C
Humidity : 74%

Hi Sumeet. Please provide an estimated size for your specimen. If you have additional photos, clearer photos of both the top/bottom of the spider are useful. Thanks!

I think with the legs, the length is around 4-5 inches.

Please [edit] your post to include the size information. Thanks.

perhaps 4-5 centimeters rather than inches?

Your spider shows an apparently large size, a large round cephalothorax, with smaller and thinner abdomen, very long and sturdy legs, with a long 'foot', and is a general brown color, with some darker markings on the legs.
This is consistent with one of the larger varieties of spider found in the warmer areas of the world, and trading under the name of Huntsman Spider, or Giant Crab Spider.  There are a number of species of these spiders in the family Sparassidae.
As it happens, the most common variety of Huntsman, Heteropoda venatoria, is found pretty commonly in southern India (reference link example included: http://www.southindianspiders.org/south-indian-spiders2.htm ), and I'm quite confident that this is what you have there.  Here is an example, from the US website Bug Guide, of this species:

Like almost all spiders, this spider is venomous, but like almost all spiders, its venom is not particularly troublesome to us humans.  A bite from a spider this big would be moderately painful simply from the large fangs, and the venom doesn't appear to usually add too much to it.  Here's a short but amusing discussion of such bites, from an Australian website: http://sciabc.us/IL2pR
These are sort of the spider equivalent of Geckos - commonly foraging in human homes for the various critters that like to make pest of themselves (cockroaches, mice, etc.) - but they never try to sell us insurance.

I don't know the species (could be a wolf spider), but I am certain they are not dangerous. I have seen these all over my bathroom, dining room and bedroom before. They are all over in South India. No one in my family seamed concerned by them. I am quite certain I even had one crawl on me once.

Hi J Houseman, and welcome to Biology SE! Please take the [tour] and carefully read through the [help] to learn more about the site, including How to write a good answer. In general, anecdotal comments such as yours can be added as comments if they are not chatty but instead provide insight. However, such anecdotal comments are unfit as answers because they do not provide reputable support (e.g., through links or citations) for claims made. As such, your answer will be downvoted and deleted. Please add support to your post to avoid this


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Unknown Lamiaceae plant identification
A while ago I received a pack of seeds described as Pycnanthemum Pilosum / Mountain mint. The seeds are small (below 1 millimeter) and brown:

Plants grown out of these seeds are around 40 centimeters high and spread widely. Leaves are bright green and smooth, around 3 - 4 centimeters long:

with strong minty smell (though quite distinct from let's say Mentha × rotundifolia or Mentha spicata).
Stems are square, with very short hairs.
Recently plants started to flower:

producing clusters (around 1.5 cm in diameter) of small (3 - 4mm long), slightly  flowers along the stem. Flowers are white, with light shade of purple. with no spots or other marks.
The plant started to flower in the first year after sowing (the plant is around 4 months old, planted outside, in Central Europe).
The plant doesn't really resemble Pycnanthemum pilosum descriptions I found online (for example this or this), which, among other differences, describe long and narrow leaves.
I wonder if someone can help me identify it. Thanks in advance.

I guess I'd like to know which characters don't seem to match.

@BryanHanson Not sure if I get your comment. Could you elaborate? Thanks in advance.

Your edit helped.  So, chief discrepancies are the leaves are too broad, and, it's not hairy. I looked up some pictures a colleague of mine took here in Indiana, which we ID'd as P. pilosum and it's definitely not your plant.  Given the similarities of many mints I think one has to start fresh and attempt an identification.

Can you say more about the flowers? Size? Color?  Spots?  In the one pic they look pretty pale off-white.  Any odor to crushed leaves?

@BryanHanson I've added another picture of the flowers - they become more prominent since I've posted the question (sorry for the quality, I have access only to a phone camera, and it is not great. I'll try to take another one, when the lighting is better). There are small, whitish with a shade of pink / purple, and the color is uniform (including stamen).

That's a pretty great picture actually, and the flower color rules out my answer below.  Do the leaves smell strongly minty?

@BryanHanson They do, which makes me think (following the source you've shared in your answer), that it might be Mentha arvensis.

That's where I was headed if you answered with minty smell.  Will revise my answer for posterity.

I'm going to take a stab at this. If your plant is not particularly aromatic, I feel pretty confident it is Lycopus uniflorus.  There are good descriptions here and here.  In particular, the description of the flowers at the Minnesota site, as having 2 purple-stemmed exserted stamens seems to match your flowers.  Apparently this species should have a tuber (should you end up digging yours up), while Lycopus virginicus which is probably a good second guess does not have tubers (see the differential description at the bottom of the Minnesota page).
Updated and Revised Answer
With additional pictures of now more mature flowers, which are clearly lilac in color, and the info that the leaves are strongly minty smelling, we'll revise the answer to Mentha arvensis, which fits all the available info. More here.


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How evolutionarily conserved are UTRs?
Coding sequences of genes have a certain degree of evolutionary conservation, so that comparisons based on sequences (BLAST, HMMER etc) can be informative. Generally speaking, the more two species are phylogenetically close to each other, the more their genes will be similar to each other. To add to that, different genes will have different degrees of sequence conservation - for instance, histons are very conserved and so on.
Do these considerations hold true for untranslated regions of genes (both 5' and 3')? To what extent can an alignment of UTRs be meaningful? Are there any very conserved UTRs as there are very conserved CDS? I know that there are some conserved motifs in 5' and 3'UTRs, but what about the overall sequence?

Depends on the gene but, in general, less than CDS

Can you please clarify what you meant by "for instance, introns are very conserved"?  Did you mean exons?  Introns are generally less well conserved than exons.  Also, introns are parts of genes not genes so this doesn't seem to be a relevant example to give.

@tyersome Oh sorry, I meant "histons", not "introns". I just wanted to make an example of a very conserved gene.

I assume you mean histones not histons. In which case why don't you download sequences of human and mouse histone mRNAs from Genbank and compare them by one of the many online programs available to do so? The overall conservation is likely to be low (it is for actins), but this does not preclude more subtle conserved features.

@David ...yes, sorry, English is not my first language so I get confused. I'm not interested in levels of conservation in histone sequences, I'd like to know how conserved are UTRs at a broader phylogenetical level. I found this article (https://bmcgenomics.biomedcentral.com/articles/10.1186/s12864-018-4821-8#Sec10) about 3'UTRs in cichlids and non-cichlids, but not much more.

This is a question specific to the organism, assembly, and genes of interest to you. You can answer this yourself with a bit of elbow grease.
You could measure mean phyloP or phastCons conservation signal over UTR-annotated intervals, and compare it against the background mean conservation signal over random, mappable regions of the genome of similar length (i.e., calculate the mean and variance in UTR length and sample mappable regions of the genome for intervals with the same distribution).
At a very basic level, you could perhaps apply either the U-test or Wilcoxin rank-sum test, depending on your assumptions of dependence, whether your background does or does not include UTRs.
One source of phyloP and phastCons signals for various genomes and multi-genome alignments is UCSC Goldenpath. For example, here are phyloP 100-way alignments to hg38. You might get UTR annotations from Gencode, assuming you are working with human or mouse. To do interval overlaps and mapping/statistics operations, you might use gff2bed, bedops, and bedmap in the BEDOPS toolkit(*), and then use R to do statistical tests.
Disclaimer: I am one of the authors of the BEDOPS toolkit.


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Insect identification, UK, 07-19
Can anyone identify this insect found in the North East of the United Kingdom, July 2019. About 3-4cm long.
Could this be a wood wasp?
Thanks.

If by "wood wasp" you mean order Hymenoptera, family Siricidae, the answer is yes; as for which wood wasp, I'm on the wrong side of the Atlantic to go deeper (though I know the genus Sirex is among your possibilities).

It is definitely a Siricidae and looks like a Urocerus gigas (sometimes called Greater horntail), which is also found in the UK.
In the Nordic countries this is one of the more common species of sawflies, and I suspect the same is true for the UK. The picture below and some info on their biology can be found at species.nbnatlas.org:


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Is it tautological that all living humans descended from a single male and single female human ancestor?
Many popular science articles cite high sequence conservation of mitochondrial DNA and the Y chromosome among living people as evidence that all humans are descended from a single male and single female human ancestor.
Is sequence evidence necessary to make this assertion, or does it follow tautologically from the definition of speciation? What would a speciation pedigree look like for a species that does not pass through a single-individual bottleneck?

Can you give an example of an article making this claim? The way you are describing it is not an accurate representation of what mitochrondrial Eve or Y chromosome Adam means.

@J-- Why are you talking about speciation while dealing with a single species?

@J-- It will be true for any non-recombining sequence (which is the case of mtDNA and most of the Y chromosome) that all individual living at some point in time will coalesce into a single individual, yes. This is predicted by coalescent theory and is a rather intuitive consequence of any pedigree. Evidence is still good to confirm our theory though and evidence is mainly about dating the common ancestor rather than anything else.

Possible duplicate of Do all living humans literally descend from one ape?

The assertion is not tautological because the definition of speciation does not involve single individuals.1
From Wikipedia:

Speciation is the evolutionary process by which populations evolve to become distinct species. [emphasis added]

Speciation is a process of populations, and it is not necessary for only a single pair of sexually reproducing organisms to be the sole ancestors of a species.
There did exist one female ancestor, dubbed mitochondrial Eve, who is the most recent matrilineal ancestor of all living humans. Because mitochondria are passed from mother to offspring, and do not recombine, that individual's mitochondrial DNA is the ancestor of all human mitochondria.
Similarly, there existed one male ancestor, Y-chromosomal Adam, who is the most recent patrilineal ancestor of all living humans. The Y-chromosome is passed through the father, and most of it does not recombine, so that individual's Y-chromosome is the ancestor of all current human Y-chromosomes.
Note that mitochondrial Eve and Y-chromosome Adam do not have to and almost certainly did not live at the same time.2
The age estimate for mitochondrial Eve is about 150,000 years ago.
The age estimate for Y-chromosomal Adam is about 200,000-300,000 years ago.
These time frames are around or after the origin of anatomically modern humans, so it is correct to call these ancestors humans. (This is didn't necessarily have to be true, it's possible these individuals could have predated the separation of humans from other species.)
Finally, is sequence evidence necessary to make these assertions? For knowing the existence of mitochondrial Eve or Y-chromosomal Adam, no; their existence is a logical consequence of constructing a pedigree (see coalescent theory). However, for dating these ancestors and being able to claim they were human, some examination of the DNA is necessary, and DNA sequencing provides the most precise estimates.

1 We'll ignore asexual organisms, where the definition of species becomes especially difficult.
2 I will add these additional cautions from the mitochondrial Eve page, that equally apply to Y-chromosomal Adam.

Caution: This does not make Mitochondrial Eve the first woman, or the first human, or the first member of a new species. Further Caution: This does not mean that other women alive when Eve was do not have descendants today; they simply do not have living descendants who are descended only through female links. Yet Further Caution: If a person were to be discovered whose mtDNA showed a pattern of mutations of greater time depth, then the status of Mitochondrial Eve would be reassigned to the most recent female ancestor shared by both that person and the person we now call Mitochondrial Eve.


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Which hardware specification should one be looking for to optimize the visualization of a tendinopathy through ultrasound?
The 2019 study {1} reports that hip abductor tendon pathology is better visualized by 3.0 Tesla MRIs than by 1.5 Tesla MRIs.
The 2014 study {2} also mentions the usefulness of high teslas for tendon analysis:

MRI of tendons and ligaments benefits from high spatial resolution. Stronger magnetic fields lead to higher signal-to-noise ratios and improvements in image resolution; for this reason, 3-T MRI may be more sensitive than 1.5 T for detection of partial thickness tears [26]. Alternatively, higher resolution may be achieved by using a local surface coil [27]. Imaging with shorter echo times improves sensitivity to tendon changes, although this may come at the expense of specificity [28,29]. T2 weighted images are helpful for identifying fluid signal in tendon or ligament tears (Figure 5) as well as for demonstrating changes in the surrounding tissues [30]. If the orientation of a tendon changes over its course, magic angle effects may be problematic; it may therefore be helpful to acquire images with a sufficiently long echo time to avoid these artefacts.

Which hardware specification should one be looking for to optimize the visualization of a tendinopathy through ultrasound?

References:

{1} Oehler, Nicola, Julia Kristin Ruby, André Strahl, Rainer Maas, Wolfgang Ruether, and Andreas Niemeier. "Hip abductor tendon pathology visualized by 1.5 versus 3. 0 Tesla MRIs." Archives of Orthopaedic and Trauma Surgery (2019): 1-9. https://www.ncbi.nlm.nih.gov/pubmed/31243547; https://doi.org/10.1007/s00402-019-03228-1
{2} Hodgson, R. J., P. J. O'Connor, and A. J. Grainger. "Tendon and ligament imaging." The British journal of radiology (2014).
Harvard ; https://scholar.google.com/scholar?cluster=16366672343955449638&hl=en&as_sdt=0,22 ;
http://www.birpublications.org/doi/full/10.1259/bjr/34786470

Why do you give background on MRI while asking a question about ultrasound?

@BryanKrause to give an example of an important hardware specification for another imaging device also commonly used to non-invasively visualize tendons.


text:
Have humans evolved to live longer?
Do people live longer only because of better hygiene, medicine, society etc or also because they're slowly evolving to live longer under same circumstances?

There's going to be mostly opinion in answering this.  Technically, the title and body are asking slightly different questions; the latter probably can probably be answered (medicine/vaccines more important) but, again, is likely going to be just opinion-based (as is this comment).

There is an article about it here: https://www.abroadintheyard.com/ancient-teeth-reveal-30-made-you-old-aged-30000-years-ago/ it hints at cultural changes based on teeth.

Yes and no.
According to this paper, great apes and our ancestors had a life expectancy at birth of about 13 years (chimpanzees). Over a few million years of evolution, human life expectancy rose to >30 years in the 18th century. Industrialization and improved nutrition, hygiene and medicine resulted in a jump to >60 and now around 80 years in developed countries in just 200 years. The paper compares data from Sweden, but if you look at the data from gapminder.org, you see that this trend holds true for all nations (especially developing countries like India and China, who doubled their life expectancy in just 50 years).
So, while humans have evolved to live longer (as you asked in the title), due to a lower mortality and resulting increase in the age of maturity as well as the likely benefit of "grandmothers" (older, infertile females helping to feed their grandchildren) (discussed in this source), the recent increase in life expectancy in just a few generations is unlikely due to evolution.
While humans are still evolving, we have reduced the selective pressure. There is no benefit to the survival of the offspring when we live past 80-100 years. And comparing countries with lower standards in hygiene and medicine (I totally recommend playing with the gapminder tools), their life expectancy was still pretty low in recent years, only increasing with access to clean water, food and medicine. Comments on extending the lifespan usually refer to medical interventions to cope with the effects of aging.

There's no evidence that any of the changes in life expectancy you've cited are due to evolution.  Reducing infant and young-child mortality is the major cause of increased life expectancy.

@Amory: The recent changes in life expectancy are due to improvements hygiene, nutrition and medicine and not evolution, as I have stated in my answer. Nevertheless, without these improvements human life expectancy is longer than for our ape ancestors, which is one of many things that changed in human evolution.

I would say that humans have not developed to live longer. There have been many harmful changes. One is that humans have lost the ability to produce their own Vitamin C.
Vitamin C
Hygeine has been a huge factor in humans living longer, especially drinking water being clean. For instance the American Public Health Association campaigned since the 1870's for antibiotics, clean water separate from potable water, immunisation and other health measures to be freely available. Their positive effects are discussed at causes of longer life

This is just an opinion and not really an answer. Please provide an explanation suitable to the main point of the question and include appropriate references.

Humans didn't lose the ability to synthesize Vitamin C; that change happened long before, in an ancestor of the group which includes monkeys and marmosets as well as apes.

Yes. My answer is opinion. But the OP is very broad opinion and 2 questions. Unlike some other people I don't downvote.


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How to integrate transcriptomics data with kinetic metabolic models?
I have created a convenience kinetics† model. Now, I want to integrate the transcriptomics data with my convenience kinetics model for altering/weighing the kinetic parameter values. I have read some publications related to this work but can’t get a satisfactory idea of how to do it properly.
Details
I've got a pancreatic model for the study on type 2 diabetic patients. It has a few compartments and the reaction pathways; the species are metabolites. All the reactions are convenience kinetics based. Enzyme is a constant factor, so its production and regulation is not considered. From my model, I'll get the Vm values for all the reactions and then I'm supposed to get the Vm (Vmax of Michaelis-Menten kinetics) values for the type 2 diabetic patients by somehow integrating the transcriptomics data with it. I was asked to use the fold change values but I couldn't find any relevant publication on this topic (my PI has suggested me these but hasn't worked in this area before).
Any leads or references will be highly appreciated.

† You can call convenience kinetics rate laws as approximate rate laws or you might have heard about "modular rate laws", they are more or less the same. We use this approximate rate law approach in cases where we don't have the experimental data for all the true rate law parameters.

Anyway, I have come across people who have been trying to incorporate transcriptomics data in flux balance models. I'm not sure how much that improved the accuracy of the predictions. There are problems at multiple levels. I don't know much about what are the parameters that can be incorporated in FBA but I am a bit familiar with kinetic models. If you can present a minimal model with the details on how you are planning to write the equations and so on, I may be able to give some suggestions.

I've added that information in the question now. Can you please tell me about those researchers/labs who have worked on their integration? Maybe provide me with the links to their webpages or the publications that you're referring to. It'd be of great help.
Regarding the approach, I myself have no idea and have been stuck here from the past week, and have been asking around people at different labs. So, any kind of lead will be appreciated. @WYSIWYG

I am assuming that in your model, the reactants and products (species) are metabolites and each reaction denotes conversion of one metabolite to another.
From transcriptomics, you will get the relative expression levels of different genes.
When you have two samples from different conditions you can calculate the differential expression.
A model can be as complex as you can make it but we can start with simple assumptions. As you said, enzymes are assumed to be constant with respect to metabolites and are not dynamically changing. I also guess that you are not considering genes other than enzymes to be affecting the metabolic reactions (you might actually want to consider the solute transporters). Also, you are assuming Michaelis-Menten kinetics for all reactions.
In that case your Vmax (i.e. maximum rate of a reaction) would be kcat × E0 where kcat is the turnover number and E0 is the total amount of enzyme.
E0 can be approximated using the transcriptomics data. However, transcriptomics data is relative and not absolute. If you need absolute quantification, you must have at least one reference whose absolute mRNA copy number is known. Another issue is that the ratio of protein and mRNA expression would not be the same for all genes and it is basically the amount of active protein you need to know. So proteomics would be one step closer.
When you are comparing two conditions, you can use the differential expression (fold change values) to adjust the parameters between the two conditions. For e.g. if you know that phosphofructokinase is 2 fold downregulated in diabetes (compared to healthy case) then you can reduce the Vmax of the corresponding reaction by 2 fold in your diabetes model. However, it all would make sense only if the parameters of your "healthy" model are reasonably close to the biological reality.
Moreover, you still need to know kcat. It cannot be obtained from high throughput studies. You may have to either make some guesses or check out papers/databases. Also, your rate is not always Vmax. To estimate the dynamic rate you must know KM too (when the substrate is in excess you can ignore KM). BRENDA may have some information about these constants for different enzymes.
At a very crude level, you can remove the reactions whose corresponding enzymes have zero expression.

These are some articles on integration of transcriptomics data with FBA (not kinetic models):

Blazier and Papin (2012)
Machado and Herrgård (2014)
Guo and Feng (2016)

Machado and Herrgård actually claim that integration of transcriptomics data does not improve their model predictions:

Also, it is observed that for many conditions, the predictions
  obtained by simple flux balance analysis using growth maximization and
  parsimony criteria are as good or better than those obtained using
  methods that incorporate transcriptomic data.

Another alternative is to model Transcription data as very sharp hill function with some fitting parameter. This will essentially mimic Boolean Model and have used successfully in generating regulatory networks. Lot of Eric Davidson's reviews have explained this. For example, Bolouri and Davidson 2002


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What percentage of the human genome hasn't been sequenced yet? If percentage estimates aren't precise, why is it difficult to estimate?
What percentage of the human genome hasn't been sequenced yet? I have read different estimates, e.g.:

https://www.genome.gov/human-genome-project/Completion-FAQ (mirror): "In the April 2003 version, there are less than 400 gaps and 99 percent of the genome is finished with an accuracy rate of less than one error every 10,000 base pairs"
https://www.statnews.com/2017/06/20/human-genome-not-fully-sequenced/ (mirror):  "Church estimates 4 percent to 9 percent of the human genome hasn’t been sequenced. Miga thinks it’s 8 percent."

If there isn't a consensus on the percentage of the human genome that hasn't been sequenced yet, why is it difficult to estimate?

Why do you care if it is 5% or 6%? What are you going to do with the number, which in any case will probably have changed in 12 months time. That isn't an interesting scientific question, which is why you are unlikely to find a "consensus" — people aren't discussing it. What is interesting is nearer to your last question. Why it is difficult to estimate is subsidiary to the question why the remaining gaps are difficult to fill. I suggest you search for info on that (perhaps even here on SE Biology) and come back with a modified question if necessary.

@David's comment may be a bit harsh, but I think the recommendation to focus on the last sub-question as the actually interesting bit is good. Although you say there is not consensus, "4-9%" and "8%" are estimates in complete agreement with each other because 8% is in the range 4-9%. The second article you link specifically explains why this is different from the "99%" or "complete" number in your first link (99% is relative to the amount that "can" be sequenced with the technique used).

@BryanKrause I don't think that's correct: The 99% estimate and the other estimates essentially refer to the same. They are simply vastly different and contradictory estimates. In particular, the amount that “can” be sequenced and assembled has been sequenced and assembled to exactly 100%.

@KonradRudolph Further evidence that the interesting question is the one David suggests rather than the title.

This is likely related to long repeating sequences of DNA which are unlikely to be sequenced with current sequencing techniques. Essentially we cannot determine the number of repeats and thus we have to estimate how much of the DNA that remain unsequenced.

I answered a related question here that may be helpful.
Some initial notes:

Your first bullet point ("99%") is to my reading talking about not the total genome size but the data that they actually assembled- e.g. for 99% of nucleotides, we are 99.99% that the nucleotide at that position is not some other nucleotide, but there may be other positions not included in the denominator that are simply not in the assembly in the first place. In other words, the existence of the position in the assembly and our confidence of the accuracy of a nucleotide call for such a position are two different (though related) phenomena.
Also, you are comparing a 2003 estimate to a 2017 estimate. We learned a lot in those 14 years.

To answer the last and most specific question about why this number is hard to know, there are a variety of reasons why:

There is no single number that is the "actual" true sequenced percentage of the human genome. In this I strongly disagree with commenter Konrad Rudolph (technological change is now giving us telomere-to-telomere assemblies of human chromosomes! The question is not how much it's possible to sequence and assemble but more whether it's the worth the time and expense to do so.). No two genomes are exactly alike, and that means not only that the nucleotides are different but that the positions are different. So even if we sequence 100% of your genome, that may only include 99% of my genome. These variable regions are, as suggested in the comments, largely repetitive regions but also just big chunks that are missing; to learn more about this google "structural variation" (here is an older review on the topic).
As mentioned already, technological advances have changed how we view the linear sequence of the genome. Earlier estimates were limited by available technology of the time; now that we have 3rd-generation sequencing tech like nanopore and pacbio, we are learning more about the extent of our ignorance. In that sense, it is unsurprising that the denominator has changed/increased.
As commenter Jeppe Nielsen states, all of these are statistical estimates based on available data. As available data increase and the statistical models that we use to estimate change, thus do the estimated outcomes change.
Related to (1): Different populations have different chunks of genome that are unique. The initial sequencing project selected a small number of humans, who were not representative of all human diversity. Efforts to fully characterize the human pangenome are ongoing.
Sometimes contaminants sneak into genome assemblies, which have to be removed. So for every sequence in the human genome assembly, especially if it's fragmentary or recently added, there's a nonzero chance that it's not actually part of any human genome.


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Fructose vs glucose
I was watching a video on the dangers of fructose and comparing it to alcohol and all of this stemming from the fact that the liver can not break down fructose like it can glucose.  But then I was reading an in depth depiction of glycolysis the first step in glucose catabolism and one of the steps is converting the glucose to a specific kind of fructose so my question is why would our cells convert the glucose to fructose in order to change it to pyruvate if it’s so dangerous?

Fructose as such is not dangerous, but excessive fructose intake can contribute to the development of fatty liver, for example. There are several articles about fructose on Biology, Medical Sciences and Skeptics SE, so you may want to ckeck those first.

I don't have much time now, so only as a comment, which I can make to a full answer later on. Without having seen this video, this is with high likelihood sensationalism without much reason. The metabolism of fructose from dietary sources is almost entirely done in the liver, which can lead to fatty liver syndrome if permanently too much fructose is contained in your diet.

Related: https://biology.stackexchange.com/questions/82478/detrimental-effects-of-fructose-in-fruit-on-the-liver , https://skeptics.stackexchange.com/questions/34808/is-fructose-the-1-source-of-obesity-in-the-united-states-today , https://medicalsciences.stackexchange.com/questions/8681/eating-fruit-is-not-so-healthy , https://medicalsciences.stackexchange.com/questions/19476/is-consuming-fruits-and-veggies-particularly-high-in-fructose-unhealthy

Fructose will be converted to Fructose 1-Phosphate while glucose will be converted into primarily Fructose 6-Phosphate during metabolism. The position of the phosphate determine the pathway used for metabolism.


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Never caught this fish before

After catching a bunch of mangrove snapper using live shrimp, my son caught this fish in about a foot of brackish saltwater water off a dock near a rock wall in  Vero Beach at around 10:00 AM  on July 5th. Fish was about 6 inches long and had a wide mouth with  small pointy teeth and what appeared to be two small horns/bumps that protruded from behind its eyes. Never encountered it before.

Juvenile snakehead?

Looks like a sculpin (Cottoidea, Cottus). Hard to pin down what kind as there are a bunch, but that very wide head is pretty distinctive.

Expanding my comment into an answer as no one else has jumped in-
This fish closely resembles a sculpin of some kind. This is a very large and diverse family, but many of them share distinctive features. The quite wide head and horns that you describe and show are common in this family. Where I am from (Northwest USA), the Red Irish Lord / cabezon is a gamefish sculpin that can grow to be quite large, and closely resembles this picture of yours (a rather small specimen shown in Figure 1).

Figure 1.
Based on where you are in Vero Beach (Florida?), I have looked a little bit and there is a chance that it is a Gulf Toadfish (Figure 2) based on its appearance and where you caught it. Here is another fisherman's account (with pictures) of a similar fish.

Figure 2.
Hope that helps.

My best guess would be that it is a Enophrys bison. Some of the pictures similar to the one you have caught that I found are:

The presence of the horns is one of the indicators similar in both images(mine and yours). Another similar image is:

Also about its habitat I found this:

Might explain why you caught it where you caught it(in a shallow brackish,rocky place). You ought to crosscheck it as I am no expert.

Could be wrong but this species appears to be specific to the Pacific Ocean according to your species range quote? The OP caught the fish in Florida (Atlantic Ocean).

Yes I saw that issue and had deleted this post. But then un-deleted in case there is some connection.


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Does vitamin D affect melanin concentration?
I am aware of the affect on vitamin D production by melanin (in sunlight) but I can not find any information regarding a reverse connection.

Darker skin, as opposed to common belief, probably did not develop as cancer protection. Cancer is usually something that attacks the body in a subsequent life. Even pale individuals under the sun are likely to survive far beyond their reproductive era before they are wiped off by skin cancer.
Instead, it is believed that folic acid manufacturing is the highest selection pressure causing darker skin. Folic acid (vitamin B9) which is used all over the flesh, especially during pregnancy and childhood, will decompose in sunlight.
So the skin tone tries to discover the ideal equilibrium between vitamin D and minimal folic acid breakdown.
As a consequence, if you genuinely have enough vitamin D in your diet, there is no need for lighter skin (and further proof for the vitamin-d hypothesis). That is why the Inuit have lighter skin than expected for their extreme location: the intake of vitamin D is large, so the folic acid part of the equation "wins" and pale skin is not preferable. This is why Inuit individuals do not need so much sun.
Source:
scienceline.org/2007/06/ask-dricoll-inuiteskimos/
pnas.org/content/107/Supplement_2/8962

This is not true. Skin color is highly correlated with UV-radiation, with the highest pigmentation present in areas where the radiation is the highest. This is said in both references, we also know that the skin cancer rates are much lower in people with high pigmentation. Melanin is a very effective protection for your skin. Folic acid is not mentioned in your sources, so please edit them.

@Chris I don't claim to be expert in this area (hence the question) but nowhere did I claimed the absence of correlation of skin color and UV, quite the contrary. Also, nowhere did I dispute, "skin cancer rates are much lower in people with high pigmentation." or "Melanin is a very effective protection for your skin. (regarding cancer)."

@Chris Ctrl+F yields following two paragraphs from each source:

@Chris "The possibility that photolysis of folate by sunlight was a determining factor in the evolution of dark pigmentation was first explored (24) before the full importance of folate in DNA biosynthesis, repair, DNA methylation, amino acid metabolism, and melanin production was recognized. In 2000, we advanced the theory that dark skin pigmentation in humans had evolved primarily to prevent reduction of fertility due to the photolysis of folate present in cutaneous blood vessels (7). We ..."

@Chris "Ultraviolet, or UV rays, from the sun are responsible for activating the melanin. As melanin levels rise and our body’s natural pigment darkens, protection against the sun’s rays increases. Too much UV exposure can deplete vitamin B folate –used by the cells to create DNA. On a smaller scale, the rays can also cause painful sunburns, with too much exposure leading to cancer."


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Evolution experiment for kids?
What would be a good plant to show the process of evolution to a small kid? Obviously it's a long term experiment, and preferably a fruit or a veg that is edible (like tomato?), and what characteristic would be (size, colour) good to select for?

How old is "kids" in this question?  I could imagine a thorough answer would address different suggestions for ages 4-5, 9-11, and 16-18, say.

You are going to need an organism that has a very short generation time to make an evolution experiment. Fruit flies, yeasts, E.coli. are classic examples. It is going to take a few years to have only a moderate response if you use tomatoes. Also I doubt you can really control tomatoes reproduction.

What exactly are you trying to demonstrate? Just the response of the mean phenotype to a threshold selection you would make?

Kid is 4, run the experiment for a decade. I thought (likely wrongly - this is just a layperson's wish to encourage science in the kid!) initially in the 19th the experiment was done with some kind of pea? I wish to demonstrate selection pressure - choose for a characteristic, see the result in the future. (If I'm being dumb tell me, I'll delete the question! :) )

@IlyaGrushevskiy 10 years is probably a bit long for the attention span of a 4 year old. :) I think if you change your question to demonstrate natural selection then there are some easy experiments that can be done on the order of an hour or so and are a bit more hands-on than waiting for plants to grow.

I'd say you will be better off writing a computer simulation (e.g. a very basic  genetic algorithm) with the child. This will demonstrate the same process and will expose the child to programming and some light maths. Both things are good to be exposed to at an early age. A 4-year old child is perfectly capable of understanding the maths behind basic random processes and computer code.

(you can check out the game I suggested here: https://biology.stackexchange.com/questions/54106/pen-and-paper-game-to-explain-the-theory-of-evolution/54107 - that question was closed at the time for being too broad, though. Similar to yours, it's a bit broad to focus on 'evolution' in its entirety)

If this option suits you, I can write a short example as an answer.

This Scientific American article may be of interest: https://blogs.scientificamerican.com/psi-vid/an-evolution-animation-unlike-any-youve-seen-before/.

This is for an animal, not a plant. But, when I was in school, the Peppered moth was used as an example of rapid evolution from the 19th century. Its white coat made it very noticeable against soot-stained surfaces so it had a rapid selection pressure to become black. If you can organise a trip with your kid to a natural history museum, you might be able to find some specimens.


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Can birds touch their wing tips together either in front or behind (not above and below)?
Can the tips of a birds wings touch so that it would form a ring if view from above or below? I suspect it might be a bird of prey and at the moment it is picking something up from the ground but I can't find a good photo.

Please [edit] to clarify your question. Are you asking if it's possible for a bird to touch its wings together, or are you asking for an identification of a species that you see doing this??

Black herons (Egretta ardesiaca) can overlap their wing tips in front of them while doing what is known as canopy feeding.

Oooo, just saw this! Great example!

Thanks! I think I knew some herons must do this because of "canopy feeding" by the Reddish Egret — happy new year!

Cool, I never knew that. Happy New Year to you, too!


text:
RE: Fasting gastric pH vs Normal gastric pH
If fasting gastric pH values are more acidic then why is it recommended to eat no more than three hours before bed time to prevent reflux. It seems at some point during sleep the stomach would become more acidic therefore make reflux worse.

Food only partially buffers the pH of stomach contents and acid is not the only esophageal irritant present in the stomach.
The goal, therefore, is to have as little as possible present in the stomach when lying down (supine) to reduce risk of gastro-esophageal reflux (GER) through the lower esophageal sphincter (LES) into the esophagus. Avoiding meals just before bed, especially fatty meals (which delay gastric emptying), may help in this regard perhaps by avoiding supine position while there is a low pH layer, formed in response to the meal, lying atop the stomach contents.
Weight loss and smoking cessation are frequently recommended to reduce GER symptoms, with some evidence to support this advice. Use of tobacco or alcohol may relax the LES and tends to be associated with GER symptoms, though trials of counseling to reduce their impact have not significantly reduced those symptoms (and another study).

It is good idea to add few scientific references to your answer.

(done - thanks for the suggestion!)


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Why does bed bugs not carry disease?
Whenever I look up this topic, all I get is articles that say "Bed bugs don't carry disease...", but they never explain why?  Is it something in their saliva that kills microbes?  Something in their gut maybe?  When they are crawling over the floor wouldn't it be logical that they would carry microbes, I mean cockroaches do?

It's not entirely true.
For example, a 2014 study demonstrates bed bugs can transmit Chagas disease. From Penn Medicine News:

The bed bug may be just as dangerous as its sinister cousin, the triatomine, or “kissing” bug. A new study from Penn Medicine researchers in the Center for Clinical Epidemiology and Biostatistics demonstrated that bed bugs, like the triatomines, can transmit Trypanosoma cruzi, the parasite that causes Chagas disease, one of the most prevalent and deadly diseases in the Americas.

(I'll update with more details when I get off the road)

When bed bugs crawl about, presumably they must be coming into contact with microbes and then they crawl on humans.  How is it they don't pass those microbes onto us?  With cockroaches they crawl about and transmit those microbes, what is so different with bed bugs?  Is there something on their legs that make the microbes fall off before they get to us or what?

@Travis I would want to be seconded but my guess is that bedbugs don't live in dirty places or rotting substances therefore don't catch a lot of harmful microbes.


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What advantages could there be for using the unseen variant chosen by He Jiankui instead of the naturally occurring CCR5-∆ 32 mutation?
Jennifer Doudna mentioned in https://youtu.be/9Yblg9wDHZA?t=2566 on 2019-02-21 that  He Jiankui introduced an unseen variant of the CCR5 gene when gene editing the twin humans Lulu and Nana. What advantage might there be for using that unseen variant instead of the naturally occurring CCR5-∆ 32 mutation?
Figure from the above-mentioned YouTube presentation showing the CCR5 gene and some variants:

I have crossposted the question at:

https://qr.ae/TWtxdj
https://www.youtube.com/watch?v=9Yblg9wDHZA&lc=UgwInhQJsw8lhfQBVlJ4AaABAg

Interesting question, but this seems very opinion based and speculative — I suggested some edits to try to overcome this, but they may not pass muster ...

@tyersome Thanks for the edit! Understanding the impact of gene mutations on the phenotype is an important scientific question, and I assume that He Jiankui has some scientific grounding for his choice.

You're welcome!  He likely thought he had good reasons, but considering how poorly thought out his experiment seems to have been I wouldn't count on it!

@tyersome George Church, who reviewed He Jiankui's 2 papers regarding this experiment, mentioned that it seems to have been carried out quite meticulously (put aside the ethical discussion). E.g., the genome was sequenced a few times after the edit to ensure that the edit went as expected.

I don't think we can put aside the ethical issues or even completely separate them from the technical.
For example my understanding is that mutation of CCR5 may put the girls at increased risk of other diseases including: Breast cancer — https://ascopubs.org/doi/abs/10.1200/jco.2015.33.28_suppl.17; Immune system hyperactivity — https://www.ncbi.nlm.nih.gov/pubmed/23250822.

Possibly He Jiankui was using Cas9 without a template DNA.  If so, this generates double-stranded breaks that are repaired through processes such as non-homologous end joining (NHEJ) that often produce small indels (deletions and insertions) 1.
This is consistent with the apparently random small deletions and insertions around the cut site seen in both girls.
An additional, unflattering possibility is that this way he could prove that these were his edits and didn't happen spontaneously.
Useful starting points for understanding how Cas9 works can be found at the Addgene website and on Wikipedia.

Reference:
1: Brinkman, Eva K et al. “Kinetics and Fidelity of the Repair of Cas9-Induced Double-Strand DNA Breaks.” Molecular cell vol. 70,5 (2018): 801-813.e6. doi:10.1016/j.molcel.2018.04.016


text:
House sparrow or something else?
These little flying fellows seemed to have made themselves a small nest in the crevices of the roof of my house (I live in Poland). I don't know if this makes a difference, but I do live near a small park.
I'm wondering if this is a house sparrow or something else.
On one of the photos I could swear these look like common sparrows, but on another (the one where the wings are apart) it seems like a different species. It also seemed larger than a sparrow, but is hard to tell due to the distance at which I've seen the birds and the photos were taken. One other notable feature was that they seemed very loud...
Any help?

Based on your image I would rather identify it as an Eurasian Tree Sparrow. They are pretty similar to the House Sparrow, but have a distinct black spot below their eyes which is missing for the House Sparrows (image from the Wikipedia):


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Reason behind colour of hibiscus and sunflower
What is the reason for the red colour of hibiscus and the yellow colour of sunflower?

Welcome to Bio.SE! What attempts to answer this question have you already taken? We ask that all question posters here attempt to search for an answer to their own question and explicitly indicate what research they've already done, what they learned, and what is still confusing or unknown to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thanks!

Flower color is result of reflection of light due to various color pigments. Evolutionary such pigments were selected due to various reasons like to attract pollinators (Dyer et al 2012). There are two major types of flowers pigments

Carotenoids (produces yellow, orange and red colors)
Flavonoids (produces red, purple, magenta and blue colors)

However, flower color is affected by various other factors (e.g. other pigments, metal ions and its chemistry etc.) along with above pigments.
Hibiscus' dark red color is outcome of Anthocyanins which is water soluble flavonid (Grajeda-Iglesias C et al 2016). However, this pigment is highly unstable and depending on pH of the surrounding it can be red, purple, blue or black. (More details in this book). Hibiscus contains majorly delphinidin-3-O-sambubioside (Dp-samb) and cyanidin-3-O-sambubioside (Cy-samb) as the major anthocyanins (DU and Francis 1973). Chemical reaction responsible for generation and utilisation of these pigment is shown below (borrowed from Grajeda-Iglesias C et al 2016)

In above image, at low pH values $AH^+$ produces red color while  and $(A)$ produces purple/blue, which is thermodynamically unstable. In addition to that co-pigments like Hydroxylatedbenzoic and cinnamic acids, hydroxyflavones (which all are colorless) are also responsible for not only stabilizing these chemical products but enhances the color (Grajeda-Iglesias C et al 2016).


text:
What kind of spider is this? First time I have ever seen one

This was taken 07/06/19 in Cape Breton, NS, Canada.
I would say that it is about an inch (2.5 cm) in length and seemed to be pretty uniformly grey. The belly was the same colour as the legs, it had a few small brown spots but I couldn't tell if that was an actual marking or maybe just environmental.
It was just hanging out right beside the handle of the door exactly where you don't want a spider to be.
In usual spider fashion it has dipped and is now...somewhere :(

It appears that you have a leafcurling sac spider:

They are observed all over east and west north america:

Here is the eye arrangement from bugguide:

I labeled with arrows the two thin dots at the top, which are eyes that point upward, which are easily visible in your picture. Would need a front-facing photo to see the rest of the eyes.
The spinneretes out the back of the abdomen are also diagnostic of clubionids.
The colours can span dark yellow to light brown, and the jaws are dark and sometimes the entire front face is dark as well.
A gallery of clubionids filtered on only Canadian observations is here:
https://inaturalist.ca/taxa/121774-Clubiona/browse_photos?quality_grade=any&place_id=6712


text:
How to do desalt reaction by passage through a Micro Bio-spin 6 column?
I want to perform the bisulfite sequencing on rRNA to detect the 5-mC. I followed this protocol
•    DNA-free™ DNA Removal Kit (Invitrogen)
•    Purified RNA, Treat RNA according to manufacturer's instructions.

Adjust DNAse-treated RNA to a volume of 10 μl.

2.Sodium Bisulfite Treatment of RNA EpiTect Kit (Qiagen)
•   DNAse-treated RNA preparation
•   PCR thermal cycler
•   Micro Bio-spin 6 columns (BioRad)
•   GlycoBlue coprecipitant (LifeTechnologies)
•   Cooled microcentrifuge
3.Transfer DNAseI-treated RNA solution into a PCR tube.

Add 42.5 μl freshly made bisulfite solution (EpiTect kit) and mix thoroughly by pipetting.
Add 17.5 μl DNA stabilization solution (EpiTect kit) and mix thoroughly by pipetting.
Place samples in a thermal cycler and run the following program to deaminate RNAs:

•   70 °C: 5 min
•   60 °C: 60 min
•   Repeat steps (i) and (ii) two to six times (depending on target RNA abundance and predicted secondary structures)
•   25 °C—hold
7.Desalt reaction by passage through a Micro Bio-spin 6 column according to manufacturer's instructions.

Add 1 volume (70 μl) of 1 M Tris–HCl (pH 9.0) and incubate at 37 °C—30 min for desulfonation.

9.Precipitate RNA by adding sodium acetate (pH 5.2) to 0.3 M, 15 μg GlycoBlue coprecipitant and 3 volumes of 100% ethanol and incubate at − 80 °C for ≥ 1 h.
10.Pellet RNA by centrifugation at 4 °C for ≥ 30 min at top speed.
11.Wash RNA pellet with 75% ethanol.
12.Air-dry ≤ 5 min at room temperature.

Store deaminated RNA pellet until further use at − 80 °C.

In the step-7 I got stuck. i do not know whether do I have to use flowthrough or do i have to elute from the column.
Ref. https://www.sciencedirect.com/science/article/pii/S0076687915002335?via%3Dihub

Did you read the manufacturer’s instructions?

yeah, but it is confusing for me. The Manufacture's link...http://www.bio-rad.com/featured/en/desalting-column.html

That link does explain the basis of separation, and tells you the relative order of elution. You can take a look at the manual for more explicit directions.

Since it's a desalting column, without reading the instruction manual you could guess that the column will bind the RNA while you wash it with a new buffer. You will want what you elute at the end (RNA in elution buffer). The flowthrough will be the small salt molecules that wont bind to the column.

That’s not how a desalting column works...

@canadianer perhaps you should answer the question or if you think it is trivial (or needed more effort from the user, which is what I feel), you can VTC.

Maybe you can take a look at this. I found it through google when searching for the manual as well.
http://www.bio-rad.com/webroot/web/pdf/lsr/literature/4006051.pdf


text:
If coelocanths are more related to humans than groupers -does a Coelocanth's DNA literally have more sequences in common with a human than a grouper?
Would a coelocanth and a human still have more sequences in common than a coelocanth and a grouper? Would the coelocanth and human dna basically "look" more similar than either would to a ray-finned fish based on sequences?

This question is unclear.  Are you asking about comparing the coelacanth-to-human distance to the coelacanth-to-grouper distance, or are you comparing the coelacanth-to-human distance to the grouper-to-human distance?

Yes, in virtually every way. In terms of pairwise distances, measured in percentages, humans and coelacanth are closer to one-another than coelacanth would be to any ray-finned fish. In terms of individual genes, there would be genes that humans and coelacanth share with their common ancestor, but are not found in any ray-finned fish. Remember, humans are bipedal terrestrial fish.

Thank you, it just seems so odd to me because groupers and coelocanths have such a similar morphology and lifestyle. Is this true of pretty much any more closely related taxa compared a less closely related outgroup? i.e. are the sequences always closer among more recently diverged groups compared to groups that diverged farther back?

@KarlKjer Good answer. Would be great to have the statistics for the # of pairwise differences between Coelacanth and a ray-finned fish species and between coelacanth and humans.


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what will be the effect of cockroach bite?
I know the cockroaches are creepy for humans. But I want to know why humans are afraid of cockroaches and what will be the effect of there bite on my body. Can I touch them or if they walk over my foot is safe for me!

Are they toxic like snake or scorpion?
How they bite us?
What will be the effect if more than one cockroaches bite me?
Do I still get any disease if they don't bite me but present in my house?

There is already a question related to cockroaches bite on this form but it's about cockroaches lay eggs or not while biting and it doesn't explain the possible effects of the bite.

hmm... I don't think cockroaches "bite" people. I have heard of having eyelashes nibbled on as you sleep, but not sure if that's real or an urban legend.

I have reared cockroaches by the thousands, for years. Three species, but mainly the infamous Periplaneta americana which I am sure everyone has at least heard about (see picture at the end).
First of all: Cockroaches do bite, and they have powerful mandibles. This is in the paper below:
https://doi.org/10.1371/journal.pone.0141226
Many people think they won't bite because they have never handled cockroaches. In fact, cockroaches are amongst the most common insects scavenging dead bodies, and they'll pester sleeping individuals when they're starving (e.g. in crowded infested buildings or ships).
In the case of large P. americana, males are way more prone to biting than females, especially when they're flying around. I have been bit three times by these cockroaches, and it hurts. Once I was wearing latex gloves and seized a large male, and it bit me through the glove. Because of the pinch, I pulled it off with my other hand, and the glove teared open. Last time, I was bit about 1.5 year ago on the shoulder in my sleep by an adult female P. australasiae. The pinch was enough to wake me up (so I could kill the bloody roach) and left a red mark that lasted for 2 days.
There are numerous reports of cockroach bites going infected, specially around lips. Linked paper is referenced as: http://dx.doi.org/10.1590/S1413-86702006000100006
Finally, they're not poisonous neither venomous insects, as they produce no relevant toxins. However they may carry many pathogenic microbes, so laster effects from contact with cockroaches may develop.

Hope this was clear enough!

Your answer would be much improved if you focused on the Prado paper rather than your personal experience: we don't typically allow appeals to authority here, rather we prefer experts to use that expertise to supply proper citations. Also please add references in text form and preferably with a DOI, the link to a journal page may very likely die sometime in the future.

@BryanKrause There is a DOI paper there. I will try to make it more conspicuous

@Scientist your answer give much info about cockroach bite but there are some technical terms in your answer like pathogenic microbes and lasting effects as I am from the CS field so I had to google them. If you explain these terms then it will be more helpful :)

Millions of people live with cockroaches and there are nearly zero cases of hospitalization, thousands of times more people are admitted for wasp/spider stings, putting marbles in their nose, knife injuries etc.
They may cause damage to food, like rodents, without any serious illnesses unlike rodents.
Here is the only roach attack hospitalization that I can find, versus thousands of bee and wasp incidents, a normal and sober person would sneeze and wake up. Apparently she did not suffer a bite:
https://newsinfo.inquirer.net/868535/doctors-remove-live-cockroach-from-indian-womans-skull