texts: MLE estimation with Mk model in ape or phangorn?

texts: When doing MLE with the R package ape or phangorn, is it possible to set the substitution model to Mk? If so, how does one do this?


texts:
I read up that CETP transfers cholesterol from HDL, which collected it from tissues, to VLDL. This VLDL is then sent back to the tissues, ultimately forming LDL internalised by cells.

What is the whole point in taking cholesterol from the tissues only to give it back? I read up that reverse cholesterol transport is for sending the excess cholesterol to the liver for excretion as bile. But LDL receptors are everywhere and not just the liver.

There also happens to be a SRB1 pathway specific to the liver but apparently not significant in humans :(

So pls help me make sense.


texts: How is the type of genetic manipulation determined in CRISPR-Cas9?

texts: I've been reading up a bit on the CRISPR-Cas9 system for gene manipulation. From what I read, it introduces double-strand breaks at specific points determined by the choice of sgRNA. But how do you get from double-strand breaks to editing genes in incredibly specific ways? As far as I read you can fix point mutations, insert whole genes or disable genes with CRISPR-Cas9. How do you specify which kind of repair mechanism is invoked?


texts: What is the estimated number of variant surface glycoproteins that trypansomes can express?

texts: In "Vaccination against trypanosomiasis" by Greca and Magez they assert that there are "innumerable" variant surface glycoproteins that the parasite can express. What does innumerable mean here? These proteins presumably have to conform to some sort of structural conditions, so I don't believe it is truly infinite. Is there an estimate of the order of magnitude of the number of these proteins?


texts: Can I dry digested protein sample over weekend in a vacuum concentrator?

texts: I have digested with trypsin the tissue protein extract for mass spectrometry, and forgot to transfer the sample from the SpeedVac to the -80C freezer. As I did this on Friday, I can transfer the samples only on Monday. Will this temper with my sample and subsequent protein identification?


texts: If bacteria with recombinant DNA molecules do not survive in gene cloning, how they can be grown into a colony after being isolated?

texts:
This is as far as my understanding of gene cloning goes. Let's say that the plasimd (vector) in the bacteria contains an ampicillin resistence gene. Through restriction enzymes, the ampicillin resistance gene is cut through and foreign DNA is inserted. This creates a recombinant DNA molecule.

Once many bacteria are introduced to a medium that contains ampicillin, only ones that have no recombinant DNA and functional ampicillin resistance genes will survive and those with the recombinant DNA won't. Through the addition of some chemicals, the surviving bacteria will turn blue and those with the recombinant DNA will turn white. Thus, bacteria with recombinant DNA can be taken and grown in their own culture, the recombinant DNA can be isolated, and research goes on.

However, if all the bacteria with recombinant DNA have been killed because they have no functional ampicillin resistance genes, how can they be 'grown' in their own colony? They're all already dead, aren't they?


texts: Is it possible to guide animals to a new breeding ground?

texts:
(This is a question for a book I'm working on.)

One of the threats to some animal species is the disappearance of breeding grounds (because of the spreading human population, or for example because of ship routes).

Hypothetically: would it be possible to encourage a species to breed on another place? Has that ever been tried? What do animals do naturally - do they seek another location, or rather keep trying?


texts: Where do I find standard tissue and cell names?

texts: I am developing specialized database on some desease microarray experiments. The initial data is retreived from NCBI and ArrayExpress databases. The problem is that sample attributes sometimes specify similar or same things but in different manners: as cell and tissue names, desease names, age, ethnicity of donor, ect. Where do I find conventions for naming experiment sample attributes?


texts: Jamaican/Caribbean insect, plant identification keys/field guides

texts:
Where can I find plant and insect identification keys and Field guides for Jamaica specifically, or for the Caribbean as a whole?

I've searched Amazon and google for Jamaican and Caribbean identification keys/field guides, to no avail. I'm taking pictures of organisms in my backyard, and I want to identify them and post them to iNaturalist. For my own sake I want to be able to identify them myself, prior to and independent of the (long) wait for a community ID to be given and confirmed.


texts: Initial population when i count backwards?

texts:
My question is dealing with how many ancestors it took to produce me:

--> to produce me it took 2 people (my parents) = ($2^1$) people = 2
--> one generation further included = ($2^1 + 2^2$) people = 6
--> in the past 500 years my pedigree chart contains 15 generations, so $2^{16}$ people = 65.532 people to produce me (-2 to be completely correct)
--> when i calculate back to 35.000 year ago I get a larger number *)
--> when i calculate to all humans 2.400.000 ago I get a ridiculous large number *)
--> when i include up to all mammal grandfathers and grandmothers 60.000.000 years ago the total number takes pages to scroll *)

*) see: http://ed.je/2L6 for the actual numbers did not want to clutter here.

*) I took 3 generations per 100 years to let the numbers be small as possible.

So, I think I'm making a mistake somewhere. Only I don't know where: to create a child you need 2 parents. And to create a parent you need 2 further parents. But somehow calculating back to "all mammals" just related directly to me would mean $2^{1.800.001}$ mammals walking around 60 millions years ago being my direct predecessor back then.

So where am I going wrong? Somehow I can't figure out where my error lies (I've not studied Biology though).

I visualize a pedigree tree (reverse pyramid) starting with me and then logically each parent needs to be born out of 2 other parents just calculating my way up.


texts: Do different chiral centers on ligands cause different confirmational changes and effects in their target proteins?

texts:
Say pathogenic bacteriaA makes toxinA, which had D-amino acids instead of L-amino aids, does this difference in chirality cause a different conformational change in the receptor or enzyme, thus leading to either deactivation of the enzyme or signal transduction pathway or activation of a different pathway?

I understand what chirality is in the concept of organic chemistry — rotating plane polarized light, ingold-prelog system etc; however I never leaned what structural feature of chiral molecules changes the way they react inside a cell.

I do NOT understand HOW changes in chirality can be associated with cellular toxicity.

links:
https://www.ncbi.nlm.nih.gov/pubmed/24752840

http://www.jomb.org/uploadfile/2014/0113/20140113053743849.pdf

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3960212/


texts:
This article about storing apples for the winter says:

  You do not want the apples' temperature to fall below 30°F (-1.1°C), however,
  because that will make them freeze and turn to mush when they're
  thawed. Their cell walls will all collapse.

  Therefore, apples are best stored somewhere around 30-35°F (-1.1 to 1.6°C), in a humid environment.

I don't understand why you should keep the apples below the freezing point of water. Why would damage only occur below 30°F (-1.1°C)?

Is the article correct?


texts: Why are VAL, MET and ALA substitutions commonly used for protein behaviour and function studies?

texts: I have seen that amino acids are commonly replaced with VAL, MET or ALA to study the effects of these specific substitutions.  Why are these specific amino acids used in particular, what are the results of these substitutions expected to show, could substitutions of other amino acids achieve the same results, and what is the source of this technique?


texts:
After reading an article, I saw expressions like "cross-immunoreactivity among epitopes", "cross-immunoreactivity among variants of virus", "immunological reactions among pairs of peptides" and so on.

I wish to verify my following understandings:

An epitope is also called antigenic determinant, and it is part of the antigen that is recognized by the antibody. An epitope, then, is a part of a virus variant. Peptides are short chains of amino acids. Thus, we can talk about the immunological reactions among peptide-pairs, because the virus variant itself is a protein, which is composed of peptides? Did I understand it correctly?

Moreover, I saw a sentence like "this antibody is against a few variants while reacting with all tested peptides", so I guess reacting here includes against? Reacting may include other situations, right?


texts: Poly-G tails in NovaSeq Paired-end sequencing from museum samples

texts:
I'm currently working with DNA samples originating from museum specimens, this means they have been stored in formaldehyde for the last 50-100 years.
The DNA I'm analysing has been sequenced by Illumina NovaSeq 6000 with paired-end sequencing.
As far as I'm aware NovaSeq uses two-colour chemistry, where Green is T, red is C, yellow (green + red) is A, and no green, no red is G. Over time and increase in sequencing cycles the green and red signal will become weaker, resulting in mistaken categorization of the nucleotides as G in the tails of reads.
This poly-G pattern is however only observed in the 3' end of the 2nd read in the pairs, which I find a bit weird.
Is this an expected pattern (only in the 2nd read in a pair) from NovaSeq or could this possibly also have something to do with my samples being stored in formaldehyde for the last 100 years, thus degrading or affecting the DNA?


texts: Phenotypes caused by mutations in mitochondrial DNA?

texts:
Will mutations in mitochondrial DNA necessarily affect phenotypes?

I have some cursory knowledge of serial endosymbiotic cell theory, and find it difficult to consider that the DNA of the former cell — now organelle — would affect anything outside of the mitochondrion itself, although I can imagine the alteration of mitochondrial processes having an indirect effect on non-mitochondrial processes associated with certain phenotypes.


texts: DNA Helicase, the enzyme that is responsible for tearing apart the strands before DNA replication, requires ATP to rip apart nucleotides. I have asked this question to several professors and they couldn't give me a clear answer. My question: What is the ATP:nucleotide bond breakage ratio? In other words, how many nucleotide  bonds can be broken from a single ATP through helicase.


texts: If you are to increase the intensity of light indefinitely, would you expect the production of oxygen to continue to increase?


texts: Link between hypoglycemic events in Type 1 diabetics and clinical anxiety?

texts:
I recognize that the scientific community is aware that the chemical stress pathway is mediated by glucocorticoids. The pathway response initializes as a result of some sort of stress (potentially chemical, such as low glucose) and the hypothalamus secretes corticotropin-releasing hormone which binds to targets on the pituitary gland. This causes the release of adrenocorticotropin-releasing hormone, which binds to targets on the adrenal cortex and promotes the production of cortisol.

In the event of hypoglycemic stress, cortisol concentrations rise everywhere in the body as a result of this stress signaling. For Type 1 diabetics specifically, hypoglycemia is a common side-effect of treatment.

I also recognize that the anxiety response is largely mediated by amygdalae activity, and the amygdalae are known to have receptors for cortisol (they are the ‘fear’ center, after all). From my research, the morphology of dendrites in this brain structure as well as other centers for mood/emotion are shifted into less functional patterns as a consequence of chronic exposure to glucocorticoids such as cortisol (Krugers 2010). Additionally, glucocorticoids cause serotoninergic receptors to become less sensitive to activation (van Riel 2003).

So my questions are:

if hypofunctioning of serotonergic receptors in the Raphe Nucleus leads to excess firing of hippocampal and amygdalae neurons, which is believed to be one of the primary mechanism through which anxiety manifests itself, why hasn't chronically high levels of cortisol, as a result of hypoglycemia, been implicated more in anxiety disorders in Type 1 diabetics? Is there a link to clinical depression from here?

SSRIs are consistently used to treat anxiety in the short term, but for diabetics, the crux of the issue seems to be the chronic exposure to high levels of cortisol. Has anyone studied or seen this in their practices/research?

Sources:

Krugers 2010
http://www.ncbi.nlm.nih.gov/pubmed/20820185

van Riel 2003
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3059694/


texts:
Here's another climber from the same garden in Araku Valley

So what is this climber?
Does it have any economical uses?


texts: Genetically speaking, are dogs exactly similar to humans and chimps both?

texts:
Richard Dawkins mentions in his book The Greatest Show on Earth that dogs are exactly similar to both humans and chimps. Supposing that a cell contains the genetic similarity between 2 species, he says

  The human/dog cell should have an identical resemblance score to the chimpanzee/dog cell because humans and chimpanzees have exactly the same degree of relation to dogs. It should be identical, too, to the monkey/dog cell and the lemur/dog cell. This is because humans, chimpanzees, monkeys and lemurs are all connected to the dog via their common ancestor, an early primate (which probably looked a bit like a lemur)

He later says that this will be found within "statistical margins of error".

Because the common ancestor of both chimps and humans was more similar to chimps than to humans, it stands to reason that chimps will be more genetically similar to the common ancestor than humans. Therefore (not a direct therefore), dogs and humans can't be exactly similar as dogs and chimpanzees are, even theoretically. Humans and apes are even more dissimilar. Therefore ape/dog cell will not be exactly same value as the human/dog cell.

Please explain where I am wrong.


texts:
I just have a quick question. I am currently studying for a test and I am confused as to what my book is saying. On the first page when learning about the gas exchange of insects it states that the insects have a large surface area : Volume ratio and this increases the rate of diffusion allowing the insects to get the oxygen they need at a fast enough rate to allow them to survive. Then on the next page when talking about the prevention of water loss it states that insects have a small surface area : Volume ratio to prevent water loss as it minimises the area at which the water can be lost. I am confused as the book states that an insect has both high and low surface area to volume ratios and because of this I'm not sure which is correct to write for the exam.

Thank you


texts:
Location: South India

Month: June

Tree:

Leaf:

Its Flower:

EDIT:
For avoid confusion about ID this species, I even added its flower now.


texts:
I took a picture of this bug while I was in Chucchilán Ecuador in June. I am wondering what type of insect this is?

It was about 1-inch long.

This was the only good photo I was able to take, sorry for the poor angle.


texts: How the size of ribosomes are calculated?

texts: When I was studying microbiology, something didn't make sense to me. We all know ribosomes have two subunits; the large subunit and the small subunit. Such as for eukaryotic cells, the large subunit has 60 S (svedberg) and  small subunit has 40 S. When they combine with each other they are considered as 80 S. Why it is 80 S instead 100 S?


texts:
My textbook( COMPREHENSIVE TEXTBOOK OF PHYSIOLOGY VOL-1 by GK PAL) says:

  Microfilaments project into microvilli present on the epithelial surface such as on the intestinal mucosa, and extend up to the tip of microvilli. They help in microvilli movement.

How far is the second sentence correct? When I searched on Wikipedia( in a page about microvilli) I found following:

  As mentioned, microvilli are formed as cell extensions from the plasma membrane surface.Actin filaments, present in the cytosol, are most abundant near the cell surface. These filaments are thought to determine the shape and movement of the plasma membrane.

So does these two imply that there is some sort of movement (due to actin) in microvilli?


texts: Lab marker for labelling cell culture plastics?

texts:
I am a lab manager trying to ask other lab biologists what brand/make of markers their labs use for labeling tissue culture plastics, which need to be repeatedly wiped down with 70% ethanol to maintain sterility. (Most "permanent" markers wash off in 70% ethanol.)

I have been looking for an equivalent to the Sharpie Industrial Extra-Fine point marker, which seems not to be on the market anymore. The supposedly solvent-resistant Fisher extra-fine point marker leaves almost no trace when wiped with ethanol.

Does anyone have suggestions?


texts: If we had children wear an apparatus swapping e.g. Red and Blue colors, would their perception adapt?

texts:
In the context of neuroscience and philosophy, one difficult question is what makes colors so peculiar and vivid if they're just signals encoding light intensity coming from certain receptors -- an instance of the "Problem of Qualia". In other words, why do perceived colors take their particular "qualitative" appearance. Experiments like color matching functions and simple mathematical properties clearly cannot fully account for this qualitative appearance -- a mathematical model like the opponent process:

can explain for instance that yellow and blue or red and green should appear to be in opposition, but it cannot explain exactly why we perceive green to be our particular green and not some other qualitatively distinct perception with the same mathematical properties.

  1) Are the "appearances" of red, green and blue the only possible
  "appearances" that satisfy the mathematical properties of colors in
  our visual system? Or more generally are those simple mathematical
  properties plus their general relation to objects in nature sufficient
  to explain their subjective appearance? (say we had a propensity to
  like and perceive blue positively because of it's association with
  clear whether)

I suspect not. Intuitively I suspect there are a number of different ways colors could qualitatively appear like that go beyond this simple mathematical model and their association with seen objects, embedded in the structure of our brain's complex neural networks. But I don't have a convincing argument to support this conclusion.

I wonder what kinds of experiments can be done to explore this subject, and what experiments have already been done.

One such (imaginary) experiment that comes to mind is swapping different colors a child sees since birth with an ocular device. If the statistical association of objects and color signals were decisive for qualitative color perception, we might expect that then color preference (the favorite which is usually blue) would shift accordingly if we swapped red and blue -- people should start preferring Red over Blue.

  2) Do we have any evidence suggesting the outcome of this kind of experiment (and the nature of perception in general)?


texts: What is the progressive evolutionary advantage that leads to flying?

texts: As far as I understand, all life started as non-flying and flying came about by natural selection. What is the evolutionary advantageous "path" to flying? Or is there something else to explain this?


texts: Hill-Roberston effects and effective population size

texts:
From this article, first page, middle of the second column:

  Even if harmful alleles do not become fixed, they can still reduce the efficacy of selection on neighbouring loci through a process called Hill–Robertson interference. This effect occurs because individuals bearing deleterious mutations are less likely to survive and reproduce, reducing the number of individuals that contribute genetically to the future population. This reduces the effective population size witnessed by a focal locus

I don't understand the link between the Hill-Robertson effects and the effective population size. Why would the effective population size be greater in absence of Hill-Robertson effects? Can you please make this link clear to me?

Here is another question on the same article.


texts: Why are the pulmonary vein and artery not like the rest of circulatory system?

texts:
I'm learning anatomy. What I learnt is that we have arteries that have oxygenated blood which appears red in color, and branch blood to arterioles to deliver blood to cells via capillaries from where de-oxygeneated blood is collected via venules into veins to go back for oxygenation. So:

artery = oxygenated
vein = de-oxygenated

However, in defining the pulmonary vein and pulmonary artery, I see the reverse of these definitions.
The pulmonary artery is for de-oxygenated blood.
Why is it so?


texts: Comparative evolutionary study: is amino acid or nucleotide comparison more useful?

texts:
I am a high school student and am currently learning about evolutionary relationship study in biology.

My teacher said that a comparative study of amino acid sequences is more useful than a comparative study of nucleotide sequences, because the genetic code is degenerate in nature — several codons may code for the same amino acid.

However, I just do not understand the logic.

Since several codons may code for the same amino acid, I (as a math person) consider the conversion of a nucleotide sequence to an amino acid sequence as a non-injective function, and thus is information-losing.

(Analogy: consider the function $f(x)=x^2$. Imagine that you have a number, and you plug it into $f(x)$ to get $1$ as the output. You would never know if the original number is $1$ or $-1$.)

Therefore I arrive at the exact opposite conclusion. Is my conclusion correct or not, and why?


texts: What is the tRNA gene copy variation between different yeast strains?

texts: I just started working on predicting steady-state protein levels from different codon usage bias measures. I have whole-genome sequences (it's NGS data) from different strains of S. cerevisiae and S. paradoxus and I began to wonder if it's possible that different strains of the same species could have different copy numbers of tRNA genes? If so, would this be detectable in the sequencing data (presumably the reads were mapped onto a reference genome so maybe this copy number variation would be lost)?


texts: Can dietary monosodium glutamate intake induce restlestness?

texts:
The question is all in the title.

More context:

I like phở soup. I have noticed that I get restless after eating the phở soup at some restaurants. The effects are similar to the ones resulting from caffeine intake. (Ingesting a cup of Turkish coffee or a couple of espressos results in my hands shaking badly.)

The phở soups which I think trigger the reaction appear to be the most savory ones. Given that:

Monosodium glutamate (MSG) is a common ingredient in phở
MSG has flavor enhancing properties
Glutamate is a neurotransmitter

I thought there was possibly a connection. (Or perhaps not. Or perhaps it's the intake of MSG together with the consumption of an herb containing caffeine or another psychoactive drug. Phở contains herbs in large quantities.)

I found this paper which states the effects of caffeine result from an increase of glutamic acid (GA) in the posterior hypothalamus which in turns triggers wakefulness.

Thus I guess what I am asking is: does dietary intake of MSG increase blood serum levels of GA and does an increase of GA blood serum level result in an increase of GA in the brain (or in some parts of the brain)?


texts: Do all plants grow roots when separated from parent?

texts:
Recently I bought my very first plant.

I thought it was doing well because it remained green, sometimes a yellow leave but all of my acquaintances which do know about plants told me not to worry, and remove the yellow leaves.

Until yesterday,
suddenly
a branch of the plant fell off,

I looked at it and it had rot through the whole stem of that branch and broke off.

Quite displeased of course,

Now, the branch is still alright, I guess, the leaves are still green,

now what am I supposed to do?

For now I planted the branch in the pot of the main plant,
I'm intending to get a separate pot for the branch and plant it again,

But I wonder, do all branches of all plants grow roots when put in ground?

If not it's not worth the effort to buy another pot of course,

Could someone help me out?


texts: Why is arterial pO2 normal in carbon monoxide poisoning?

texts:
Arterial blood gas measurements often show that pO2 is 'normal' even though haemoglobin is bound to carbon monoxide with high affinity.

Is this because there is still oxygen bound to some subunits of the haemoglobin? Surely the CO will displace at least some oxygen, reducing the pO2? As oxygen solubility in plasma is very low, where would oxygen be in the blood if not bound to haemoglobin if there was still high  pO2?


texts: Could someone help me identify this insect from Malaysia?

texts: Could someone help me identify this insect? My grandfather went on holiday to Malaysia and found this interesting beetle it looks like and has been trying to find out what it is, he placed it in resin to preserve it and I was hoping someone might have the answer to what it could be. The beetle itself is about two inches long and is mostly a vibrant yellow. and sorry the picture is so blurry


texts: Are there animals which produce their own colour pigments`?

texts:
After discovering flamingos natural colour isn't red, pinkish as one naively may have assumed though, I looked into the matter more deeply. I also found out that many other animals do not produce the respective colour pigments matching then their outer appearance.

Some seem to use certain optical effects like Rayleigh Scattering or applying several different layers of filters to absorb wave lengths of light from the spectrum just emitting the intended colour.

After browsing through some more cases several questions arose, which of course cannot be answer all in detail here. However most interesting to me were:

Why does it seem so difficult for animals in contrast to plants to produce their own colour pigments?
Some colours seem to be more difficult to achieve than others. For example I found that melanin and several variation of it as colour pigments are produced quite commonly by animals, however blue rather difficult. As the following post indicates, blue colour pigments seem to be in general difficult to produce: Why are so few foods blue?


texts: What does delta G refer to in primer dsesign?

texts:
It seems to be related to the likelihood of the given primer to form primer dimers and Hairpins, with a lower Delta G having a higher likelihood of these structures.

Obviously this would reduce the efficiency of the PCR.
Is this all that I should know about the Delta G for the purposes of primer Design?
I'm having trouble finding a good source for a comprehensive explanation of this value as it relates to primer design and have only been able to find tangential answers to my questions in older threads.


texts: SEREX serological analysis of cDNA expression library

texts: What is Serological Analysis of cDNA expression library? I went through this article:http://cancerimmunity.org/serex/introduction/ but could not really make out. Can someone please explain this to me in a simpler manner?(I have not studied biology since last 8 years and now I am going through it because I need it for my research. So if someone can describe it in simple language it would be very helpful)


texts: What do the intervals between groups of arrays in microarray gene expression data images mean?

texts: This can be a dummy question, but I am not familiar with microarray experiments at all. In this image, what does each of 16 big squares mean, and what are the black intervals between them are? I know each small square corresponds to a gene expression value, but I don't know what each separated group of expression values means. Oftentimes I see those separated expression values in microarray dataset images. I would be happy if someone can explain. Thanks!


texts:
I've read that homologous chromosomes are composed of one maternal chromosome and one paternal chromosome.

I want to confirm if this image is for one set of homologous chromosomes:

They have the same size, length, loci and same genes but are not identical.
They have different DNA sequences, so contain different alleles.

Still, I'm confused if it should be one maternal chromatid and one paternal chromatid.

I thought, homologous chromosomes are supposed to be one maternal and one paternal chromosome?

Can someone kindly explain if chromosomes are duplicated as to one paternal and one maternal chromosome or not??

Now is this image a homologous chromosome duplicated? So there are two sets of homologous chromosomes?


texts: I did myocardial infarction experiments on mice and I am a newbie in this area. I need to isolate RNA and protein from the remote and the border zone. Where should I cut the heart so i can separate the infarct zone, border, and the remote zone? Can anybody help me with this?


texts: Effect of Ethanol on Brain Volume Measurements

texts: I want to compare the brain sizes of two populations of fish. However, all the samples I have were fixed in 95% ethanol. As far as I know, 4% formalin is the normal fixative for soft tissues. Can I conduct my study, or do I need to obtain samples in formalin? I've scoured the literature, and I can't find any useful recommendations.


texts: Can Taq polymerase be used instead of polymerase Vent exo (-)?

texts:
Instead of using  polymerase Vent  exo (-), can I go with the usual Taq polymerase?

Do the PCR conditions change (the temperature and master mix concentrations ) in the these two conditions? Do the primers (sequence and concentrations) change if we use vent exo instead of Taq polymerase and vice versa? If the primers are designed specifically for Vent exo (-) how can I modify the PCR conditions so that I can use the same primers (meant for vent exo) using Taq polymerase?


texts: Is it worth to experiment with pro-biotics at home?

texts:
Let's assume that Joe has done some investigation on Internet and wants to see, if pro-biotics would help him. Now he goes to amazon.com and buys a pro-biotic product with excellent average rating. Note that not all of the reviews are from  "Amazon Verified Purchaser" for the specific product, but you got the point that it sound convincing that other people claim to benefit from the product.

So validity of Joe's pro-biotic experiment starts from pro-biotic supply chain. What are the steps in his pro-biotic experiment where experiment could go wrong; and what are the precautions he can take to make his experiment successful - either prove or disprove their benefits?

In the answer I seek something between lines (feel free to reuse these points to make your answer whole):

  Joe should be confident that seller is selling the real thing and not  candies. Are there any regulations that ensure that there is no fraud going on at this step from Over-the-Counter seller? How common is such fraud by sellers? Have there been any studies?
  The bacteria might die during shipping before Joe actually received his pro-biotics, for example, because of temperature changes. Obviously responsible seller should know how his merchandise should be shipped.
  Joe should probably not take pro-biotics together with other drugs or even together with other pro-biotics, because they might kill each other.
  There already could be some bacteria living in Joe's body that immediately kills "good bacteria" in pro-biotics without even making it.
  And most important - The initial hypothesis found by Joe on Internet about "good bacteria" in pro-biotics was wrong in the first place. Is there a website that I can check with convincing research that has studied how each bacteria affects our body as a whole?

Also, would it be worth to grow culture of pro-biotics at home to make sure that there is bacteria in the first place? How hard that would be? We have microscope at home.

The reason I am asking this is because a person very close to me is super excited about pro-biotics so that it starts to affect my life. I just want to get opinion from people in the biology field on how skeptical they are about DIY people doing such pro-biotic experiments at home. I am not sure yet whether I should support this person or try to talk out of this. It seems that this person has been reading a lot on Internet about this subject so it is not easy for me to argue back.


texts: Molds and fungi usually found on book pages: identifying and preventing further spread

texts:
I know I can use bleach to kill most of the spores that live on my walls. I know I have to keep humidity below a certain level and temperature above another to prevent the spread of mold. I have read tons of websites on how to treat 'wall infestations'.

It's the mold that affects my books that worries me the most.
Especially now that I've discovered a very enticing market for used books. You can find bargains but sometimes the books smell "of mold".

I would like to know more about the kind of molds (and/or fungi or other bio-monsters) that usually feast on paper. The paper that makes the pages of a book.

Can someone point me to any kind of resource with answers to the following questions?

What are the most common biological causes of page deterioration?
1b. Can they be identified without lab instrumentation?
Can they spread from one book to another, and if yes how and how fast?
Can they be neutralized in some way (stopping the spread), or should one just burn the moldy books to avoid contagion?

I seek knowledge to protect knowledge.


texts:
I'm curious as to how we "see" neurons, for lack of a better term. Is it the detection of the neuro-transmitters? Can we literally see the electricity firing and moving throughout the pathways? Is it a combination of both, or something completely different, like scanners?

What kind of technology is used to do these things?

thank you!


texts:
On the wiki page for NMDA it says that NMDA is a synthetic substance that mimics glutamate. So why does the body not use glutamate instead of NMDA?

Also how is it possible that our body can produce something that is synthetic? I thought synthetic was man-made chemicals. Does that mean the NMDA receptors it binds to are also synthetic? How did this come to be?


texts:
I'm aware that our earliest records of many major animal and plant phyla come from the Cambrian or Precambrian periods, and I'm also vaguely aware of some of the objections raised with general concept of phyla. With this in mind, I'm curious which of widely accepted biological phyla appeared most recently, and what evidence do we have of their relatively recent appearance?

I'm most interested in animals, but I'd also welcome any information about other organisms.


texts: Review paper on gene expression regulatory mechanisms

texts:
I'm a junior grad student in bioinformatics with CS background. I am involved in a project around discovering gene regulatory networks in some data, which got me curious about the gene expression regulatory mechanisms in eukaryotes. I found this page on Nature, which looks super helpful:
https://www.nature.com/collections/pfdsgqgzck
But it does have 27 review papers listed there. Are there any review papers you could suggest that sums up/introduces different regulatory mechanisms and regulatory factors (CTCF, chromatin accessibility, TFs, enhancers, promoters, lncRNAs etc) in a more global overview?
Thanks!


texts:
In human anatomy / biomechanics, what is the motion called when the arm swings sideways so the elbow moves in an arc of 90 degrees?
So e.g. if a person was to elbow somebody behind them , or if somebody had their arm out and then swung it keeping it parallel with the floor.
Like in this video
https://www.youtube.com/watch?v=IOh2-4WWzEE


texts: What is the purpose of getting a rabies vaccine after exposure?

texts: After exposure to the virus, it is already inside you and your immune system will start to recognize it. Is the vaccine then just a way to kickstart this process so the body can fight off the infection sooner? Is it just a way to introduce much more antigen to the system than would be present only a few hours post exposure from actual virus replication? Or is the boost coming from adjuvants?


texts: How does a Na+/H+ antiporter drive osmosis in this "osmotic motor"?

texts:
This recent paper in Cell describes a cancer cell using osmotic pressure to move in confined spaces. The cell preferentially inserts Na+/H+ antiporters in the leading membrane. I want someone to double-check my osmosis before I make students reason it out:

The normal Na+/K+ pumps cause an increase in Na+ ions outside the cell, but little change in osmotic pressure across the membrane.
Increased Na+/H+ antiporters will allow Na+ in while pushing H+ out at the "front" end of the traveling cell.
While this causes little net solute change, it increases water flow into the cell via aquaporins (?? this part I find mysterious)
Na+ continues to be pumped out of the cell by the Na+/K+ pump at the "back" end of the cell
Water follows the Na+ through aquaporins out the "back" of the cell, moving the cell forward

I don't feel convinced that moving ions around like this is causing osmotic gradients. Can anyone convince me?


texts:
I don't understand how to sum the changes in a phylogenetic tree.

Here for example: http://www.med.nyu.edu/rcr/rcr/course/phylo-cladistic.html

How do you end up with 8 for the first and 9 for the second ?


texts: Is COVID-19 claimed to get less deadly over time? If so, why?

texts:
From a TV news report of a press conference from (I think) the German Robert Koch Institute, I remember hearing an expert declare that he was expecting COVID-19 to get less deadly over time.  Unfortunately, I don't know what press conference it was (I'm not sure if it was the Robert Koch Institute — it might also have been the Charité university hospital) and cannot find such a stated expectation on the internet.

Why would an expert express this expectation?

Is it because we're heading toward summer (at least where most COVID-19 cases have been reported), or is it a standard pattern, perhaps either due to people's immune systems or due to the virus evolving and becoming weaker?


texts: Does a neuron ever generate an action potential without stimuli?

texts:
Most accounts I read involving action potentials and synapses and the like tend to focus mostly on the action potential as a mere automatic reaction to another similar event happening upstream.

From a more theoretical point of view, it would be nice to know if (and under what circumstances) a neuron would be able to generate an action potential, in the absence of an upstream neuron firing first.

I suspect that the nervous system, at least in higher animals, is not simply a relay system that processes and transmits information from senses to actuators like the limbs. The relay system picture is fine for short-timescale, reactionary behavior but it is hard to imagine any longer-timescale learning processes happening this way. This is what motivates my question.


texts: Plasmid harbouring subunit S of type I R/M system

texts:
We have an assembly of a genome of a Lactobacillus species. The genome also contains a 7.5kb plasmid.

Aside from the "usual plasmid genes" the plasmid contains:
 - toxin/antitoxin system
 - Subunit S of type I R/M system (No R or M subunit)

Now, to me this seems like an interesting case. It looks like the plasmid is "exploiting" the R/M system of the host (Bacterium seems to have type I R/M system indeed).

This could have the effect that the plasmid is increasing the fitness of the host (and itself) by making the R/M system more flexible in terms of target sequences by the R/M system (Phages, etc.).

My questions are now:

Does anyone know an example of such a case. Did not find any.
Do you think it works the way I suspect.
Could this be interesting for Biotech applications since phages in diary food environment are a problem.
How would you test if this plasmid has this effect?


texts: Do plant cells recycle carbon dioxide from their respiration during photosynthesis?

texts: It seems one of my colleague's biology textbook claims that plant cells, with presence of light, feed back 100% of carbon dioxide molecules from their respiration into photosynthesis. Can you say that carbon dioxide molecules, gas or dissolved, get transferred from the mitochondria to the chloroplast?


texts: Late control mechanisms of blood pressure (arterial) level?

texts:
I first covered the fast and moderate control mechanisms which I think are

  Fast control: Baroreceptive reflex (tonus), Chemoreceptive reflex
  (CO$_2$).
  Moderate control:  Bicarbonate
  (ECF), Phosphate buffer (ECF), Proteins (ICF).

then late control mechanisms about which I am unsure

Capillary fluid shift mechanisms
Stress-relaxation of the vasculature
RAA

What are the late control mechanisms of blood pressure?


texts: Luciferase promoter vector over p-AcGFP1-C1 vector

texts: AcGFP1 vector can emit light by itself, whereas in case of Luc vector a substrate is needed for the reaction. Nevertheless, Luc is said to be more specific or better than AcGFP1. Why is this so called? What are the advantages of Luc vectors over AcGFP1?


texts: Will neurons live after the death of a human? If so, how long?

texts: I don't know if this is correct or not, but I have heard this from a friend and I want to get a clear explanation about this.I hope there is some one who can help me.


texts: Do edible vaccines exist, and if yes, what is their mode of action? Are there any edible vaccines commercially available now?


texts: What Would Happen To a Human Who Died In Space And Stayed There For a Prolonged Period of Time?

texts:
Last night I was watching a documentary regarding the Apollo space program, and it spoke about how Apollo 8 orbited the moon 10 times then came back to Earth. It said that while the ship was in orbit no one really knew whether the ship would break orbit or continue to orbit the moon where the astronauts would eventually die.

I thought then that at some point in the future NASA would have maybe recovered the ship and returned them home. If they did this I then wondered what would have happened to the astronauts' bodies during this time? Would they decompose like they would do on Earth, or because of the lack of atmosphere would they not decompose?

There are two scenarios to this. The first scenario is that the ship ran out of oxygen and the astronauts died through asphyxiation. The second scenario would have meant that the astronauts were involved in  a decompression, so that the astronauts were then in a vacuum.


texts: Why doesn't the rest of the body have something like the "blood-brain" barrier to protect itself from pathogens?

texts:
According to Wikipedia:

  "The blood–brain barrier acts very effectively to protect the brain from most pathogens".

This is because the pathogens cannot pass through the tight junctions of the endothelial cells lining the inside of the blood vessels delivering blood to the brain through BBB.

But if so, why don't tissues/organs in the rest of the body employ the same barrier, and thus avoid pathogens from ever entering those tissues/organs through the bloodstream?


texts: Conservation Genetics - Book recommendations

texts:
Can you please give me some advice for a book in (evolutionary) conservation genetics that offers an in-depth review of the mathematical formulations used in this field.

I read the book Evolutionary Conservation Biology (Ferrière and Dieckmann, 2009) and I really liked it. I'm seeking for another book of the same kind that goes further on the part A (Theory of Extinction) and especially on the concern of the importance of population structure and the genetic load. I am also interested in landscape genetics.


texts: How are individual neuron firing rates characterized?

texts:
I'm reading this paper that the Human Brain Project published in Cell and I'm confused how they recorded the firing rates shown in the firing below:

In the publication, they mention that they use the Petilla convention. However, upon reviewing that publication, I was unable to determine the procedure of characterising neuronal firing rates. How are they able to isolate a neuron's firing behaviour away from the network it is usually contained in? Where do they measure the outputted firing rate?

I am aware that usually to characterize a neuron in a network, Spike Sorting or single-neuron recording can be used, however this doesn't seem like a valid way to characterize the physiological properties of an individual neuron.

If you consult the experimental procedures section of the paper, you can find that they used methods previously established in three papers. However, upon reviewing these papers, it appears that the neurons were stimulated while still inside the tissue, but after the tissue had been sliced. However, this seems so absurd that I must be misreading it.

How were the electrophysiological properties of these neurons characterised?


texts: What's the (or some of the) minimum(s) amount of atmospheric carbon dioxide needed by plants?

texts:
We currently have a problem of increasing $\ce{CO2}$ in the atmosphere.  But assuming we find a way to carbon sink it, what is the minimum $\ce{CO2}$ we need to leave in the atmosphere to provide a source for plants to photosynthesize?  I'm assuming this may vary per plant, and that we could choke plants so they're less productive - but at some point they will starve to death if we remove too much $\ce{CO2}$.

Where does this point lie?

Approximations, or a specific data point (say for one plant, or one type of plant) would be an adequate place to start.

Current atmosphere composition is $\pu{0.035\%}$ carbon dioxide.  In the past it has been higher (has it ever been lower?), which in theory has resulted in higher plant growth - but I've seen some contradictory statements about higher Carbon Dioxide.

(related: What is the effect of a pure-oxygen environment on a plant?)


texts: Fst Differences Between Mature Trees and Seeds

texts:
For a single co-dominant locus in two populations of blue oak, I am given genotype frequency data (genotypes are AA, AB, BB) for adult trees (at least 150 years old) in both populations (pop 1 and pop 2) and from sampling of seedlings taken in fragmented woodland from the same populations (pop 1 and pop2) very recently. I am asked to detect any difference in Fst among adults and seedlings, and propose a hypothesis explaining how any difference observed could have come about.

To tackle this question, I calculated the Fst value between Pop1 and Pop2 using the adult's genotypic frequencies and then Fst between Pop1 and Pop2 for seedlings using the respective genotypic frequencies given for the seedlings.

The Fst values for the adult's was 0.004 and the seedling' was 0.113.

Clearly there is genetic differentiation between population 1 and 2 in seeds, but not much in adult trees.

I'm mostly stuck on the explanation for why this would happen. My gut response was that there is some selection against certain adult genotypes in population 2 in that they are unable to produce seeds? Or maybe that adults in population 2 are mating non randomly and therefore produce seeds that do not match the genotypes of the adult population?


texts: Are more animal species edible than plants?

texts:
While grocery shopping I was thinking that we restrict ourselves in regard to which animals we eat. I surely don't want to eat spiders and ants, for example, but I know that this is just because of my upbringing. But a lot of plants are actually inedible. So, is my idea correct that we can eat far more animal species than plant species? And if so, why? The reasons why certain plants are inedible seem to me also as rather diverse, like most plants
developed their own special molecule(s) to avoid being eaten by us. :)
I would be interested in some more educated opinion on this thought than mine. Thx in advance.


texts: How does loss of the electrochemical gradient result in heat production?

texts: As far as I understand, uncoupling of the flow of protons and ATP-synthase  provides a bypass for protons between the outer and the inner membrane of mitochondria so that the protons don't have to go through the ATP-synthase on their way to the matrix. I see how it results in loss of electrochemical gradient. But why is heat produced?


texts: I found this insect in Utah, USA. What is it?

texts:
I keep seeing this insect around my house. What is it?

Here is another image:


texts: Are there nuclei with "real" interneurons?

texts:
In Kandel's "Principles of Neural Sciences" in the chapter about the anatomical organization of the brain one reads (p. 323, 4th ed.):

  »Although a variety of [relay] neurons are involved at each stage in information processing, these neurons generally fall into two functional classes: principal (or projection) neurons and local interneurons. The axons of principal neurons convey information to the next stage in the system. Interneurons may receive inputs from the same sources as the principal cells, but they contact only local cells involved in the same processing stage [(relay)].«

This means: All neurons of a "relay" (= functional unit) receive external input, but only some give external output. I wonder if there are examples of functional units (nuclei, cortical areas, etc.) with significant numbers of

interneurons receiving input only from local cells
principal neurons receiving input only from local cells

If there were, there would also be distinguished input neurons, receiving external input but not giving external output.


texts: Difference between mutation and DNA damage

texts:
What is the strict difference between mutation and DNA damage?  As far as I understand it, a mutation is an alteration in the genetic sequence, having "tricked" the repairing machinery and thus getting replicated in the future.  DNA damage, on the other hand, is any alteration of the DNA molecule including breaks, chemical alterations of the molecule, etc.

Then, are mutations considered a type of DNA damage?  I would thank the strict definition of both concepts.


texts: Can PCR duplicates have complementary sequences?

texts:
It is common when analyzing paired-end whole-genome shotgun sequencing data to check for and eliminate PCR duplicates. The reasoning is that the probability of sampling a fragment of the genome of the same exact length from the same exact position in the genome multiple times is extremely low. Therefore, if you see multiple read pairs with the same exact sequence in both pairs, these don't represent independent events but are multiple copies of the same event.

My question is whether PCR duplicates can be reverse complements of each other. All the PCR duplicates I've observed myself have been exactly the same sequence on exactly the same strand. Is there a technical reason why this is the case, or is it possible that PCR duplicates could not be on the same strand as each other?


texts: Cloning DNA fragment - at least trying to

texts:
I`ve been trying to clone a fragment (about 1.6 kb) using pGEM system, unfortunately it was not succesful. Then, I moved to pJET, and guess what? Again, very low transformation efficiency. Now I am moving to pENTR. However, I am think about why I am struggling to clone this fragment.
I have tried to increase insert:vector proportion; plate a higher # of e. coli cells; left my ligation reaction overnight, but nothing is very helpful. Does anyone have any guess or suggestion about it? Does anyone think that the fragment is too long?
Thanks :)


texts: Effect of testosterone hormone on cell signalling and behaviour?

texts:
A steroid, testosterone was injected in female body which led to development of secondary sexual characters but these characters were not developed over night (Response was very slow). What could be possible explanation of this phenomenon

a Steroid hormones produce a slow response because they do not have secondary messenger
Slow response is due to lack of cell membrane receptors and amplification enzymes
Movement of this hormone is very slow in blood
None of the above

I think option 3 is correct because steroid hormones are hydrophobic in nature and cant be transported in the blood without the help of any carrier protein so this may be the reason but I am not sure about this..


texts:
Klenow fragment does not seem to have 5->3 exonuclease activity, but it can still displace nucleotides in front of him - How? How would this displacement mechanism differ. My first guess is that exonuclease activity actually digests upcomming strand into single nucleotides, but how come the displacement activity not get in the way for lab work? :
"The 5' -> 3' exonuclease activity of E. coli's DNA polymerase I makes it unsuitable for many applications. "

Why doesn't the 5->3' displacement activity make the applications troublesome then? What would those applications be.

I've spend a long time looking for these answers, but unfortunately I've found nothing.

Maybe someone has any idea:)

Cheers!

References:
Image - http://www.vivo.colostate.edu/hbooks/genetics/biotech/enzymes/klenow.html


texts: Does eating antacid (such as Magnesia) before meal have any impact on digestion?

texts:
During an anatomy lecture I heard of the importance of the acidity of gastric acid (e.g., killing microorganisms, dissolving food, being a factor for triggering further processes). If a healthy person would eat a tsp. of Magnesia [Mg(OH)2] suspension before a meal (lets say at least 30 min beforehand) and then eat normally, would it have a significant impact on the digestion? Like being unable to extract or produce certain products? Or having a higher risk for a yeast infection?

This question also applies to proton channel inhibitors such as Omeprazole and other drugs like Ranitidine

(Background: The lecture was just a introduction to anatomy for informatics. We never went into greater details.)


texts: Change of phase from juvenile to adult in plants

texts:
I tried googling this but couldn't get much information on this. Most of the articles were about induction of flowering.

I am more interested in knowing what factors influence the conversion of juvenile phase to adult phase in plants and not the induction of flowering.
Can a plant survive if it is artificially kept in a juvenile phase ?


texts: Can a neuron make a synapse onto itself?

texts:
I was wondering if a neuron can make a synapse to itself? I suspect that it would be extremely unusual for a neuron to do this. Anyway, has anyone seen even a single instance of this?

Is the process by which a neuron 'knows' not to make a synapse onto itself is known?


texts:
Surveys show that 0.6 percent of the US population has an allergic reaction to peanuts. This prevalent allergy has even prompted some to ban peanuts from schools altogether.

I am completely unfamiliar with the topic, and can't seem to find any specifics in the literature. Thus my question is:

What specifically causes the the allergic reaction associated with peanut consumption, and why is it so prevalent in comparison to other foods?


texts: PBST vs. TBST buffer in western blotting

texts: What is the advantages and disadvantages of using either PBST or TBST in western blotting, or while working with proteins in general? Are there other buffers which are also used for western blotting, or washing steps while working with proteins?


texts:
What is meant by drug tolerance?

This question is in my biology textbook for IGCSE and I have no idea what drug tolerance is. It would be very helpful if someone could clarify. Thank you.


texts: Henry Fingerprint Classification System Disrepency Among Articles

texts: I know that the formula for fingerprint primary classifications is [1+(even finger value sum)]/[1+(odd finger value sum)]. So according to this formula and the Henry Classification System finger values, if a person has whorls on all ten fingers, then the classification ratio would be (1+31)/(1+31), which is 32/32. But some of the articles I have read say that it is actually 31/31 for a person with whorls on all ten fingers. Here are two articles that say that: article 1 and article 2 while other articles such as article 3 say 32/32. To me, the first two articles did not add the +1 to the numerator and denominator. Which is correct?


texts: Are freshwater jellyfishes really jellyfishes?

texts:
Articles from the aquaticcommunity.com and the Nature Conservancy suggest that freshwater jellyfish, Craspedacusta sowerbyi, are more closely related to the Genus Hydra. From the Nature Conservancy article:

  It should be known that though Craspedacusta sowerbii is touted as a
  jellyfish, some argue it is more   related to the family Hydra than a
  "true" jellyfish. Many researchers still call it as such, but others
  may simply refer Craspedacusta as a jelly. The main difference between
  Craspedacusta swerbii and "true" jellyfish is the presence of a velum.
  Its velum is a thin, circular membrane around the cap that helps
  propel, or move, the jelly forward.

An articles from the US Geological Survey (USGS) states that Craspedacusta sowerbyi is a hydrozoan that can take the form of a jellyfish. From the USGS:

  Craspedacusta sowerbyi is a hydrozoan (Phylum Cnidaria, Class
  Hydrozoa), which is most easily identified when it takes the form of a
  small, bell-shaped jellyfish, known as a hydromedusa.

The Merriam-Webster dictionary defines a jellyfish as follows:

  a free-swimming marine coelenterate that is the sexually reproducing
  form of a hydrozoan or scyphozoan and has a nearly transparent
  saucer-shaped body and extensible marginal tentacles studded with
  stinging cells

This definition, to me, seems to suggest that Craspedacusta sowerbyi is a jellyfish, however there must be some other reasoning that I'm missing that makes others believe that they aren't. Any clarification would be greatly appreciated.


texts:
Wikipedia says :

  The kidneys secrete a variety of hormones, including erythropoietin,
  and the enzyme renin.

Can a substance be both an enzyme and a hormone ? Why is renin both an enzyme and a hormone ?


texts: Blinded sphinx first instar caterpillars not eating

texts:
I've got several freshly-hatched Blinded Sphinx Moth caterpillars (ID'd the mother), but they don't seem interested in any of the host plants I've offered. I had birch and basswood ready, and so far it's only basswood that's even gotten a nibble. I have access to cottonwood, willow, and aspen, and will probably go pick some up soon.

My question is-- is there a reason a caterpillar would ignore a plant that is a known host for the species?

Thanks!

Cal


texts:
My shin splints are clearly tied to running. Though the pain level doesn't seem to correlate  to my running intensity. So what is it about running that causes shin splints?

My real hope is that if I understand the cause clearly enough I can adjust to fix them.


texts: Are hormones biotic or abiotic? I have tried reading different articles, and  I've found that it is both, but can that be true?


texts: I've seen Taq polymerase being marketed as either "native" or "recombinant". I understand that the recombinant version is produced by specially modified Escherichia coli strains that have the gene for polymerase production spliced in them, but I am wondering about the "native" variant. I imagine that Thermus aquaticus is rather difficult to culture in a medium; is it thus true that the archaeans have to be extracted from the springs they came from for producing "native" polymerase?


texts: I am always so confused whether to do a chi square test or a t test in the sums given by my biostats teacher. Does anyone have a simple rule to decide this?


texts: I've read that female mules can sometimes have offspring, but that male mules are incapable of doing so. Why is that the case? Is their sperm not capable of entering the egg or is their a genetic reason?


texts: about the direct intervention of a child's gender

texts:
Can we determine the gender of a child now,I mean,not randomly?
There are equal amount of sperms with X chromosome and Y chromosome.
Can these two kinds of sperms be distinguished easily?
If yes,we can choose the kind of sperm to meet the ovum,then the gender of the child can be determined.


texts: What is the current theory of sexual orientations in Biology?

texts: What is the current explanation of what causes the different sexual orientations in humans.


texts: In what reaction of mitochondrial respiration is hydrogen peroxide an anomalous product?

texts: I understand that hydrogen peroxide is produced in an anomalous manner during mitochondrial respiration, which also produces other by-products or free radicals. Does anyone know the details of the specific reaction in which hydrogen peroxide is formed and what is the normal product(s) of the reaction?


texts: Why does a broad-leaved evergreen (Mahonia aquifolium) has red leaves?

texts:
To my knowledge, oregon grape (Mahonia aquifolium) is purportedly an evergreen shrub? Deciduous broadleaf plants lose their leaves in autumn usually and before that as the leaves die they oxidize and turn shades of yellow and red as carotenoids and anthocyanins are expressed.

For what reason does M. aquifolium turns red in the fall given that they DON'T drop their leaves? Does it somehow benefit the plant? Is it because oregon grape's ancestor used to drop leaves?


texts: What happens to the human brain when unconscious?

texts: What part of the brain gets affected and does it harm the brain? Thank you I just needed some extra info for a video I'm making.


texts: Parts of Brain Active for Dreams | Right Hemisphere or Cortex

texts:
I found a research that states cortex is responsible for the contents of the dream. Contents could be people, place, objects etc.

The cortex is responsible for the content of dreams, including the monsters we flee from, the people we meet, or the experience of flying. Since we are highly visual animals the visual cortex, right at the back of the brain, is especially active, but so are many other parts of the cortex.

While the other says right hemisphere is responsible  to create the dream.

The right hemisphere of the brain actually creates and displays the dream

And another source

the dream contents have their source in memories and impressions stored within the right half of the brain.

While there is another research that states posterior cortical hot zone that are responsible for our dreams.
Question: So what part of the brain is it? I know a coordination of various parts of the brain makes dreams possible but what part of the brain is responsible for main contents of the dream or major contributor to the dream?


texts: How does the immune system distinguish between commensal and pathogenic bacteria?

texts: There are billions of bacteria living harmlessly in our gut, and in fact most are helpful to us, aiding digestion, producing vitamins and maintaining gut health. The immune system is able to suppress immune responses against these organisms, avoiding killing such beneficial microorganisms in this way. However, it is still able to detect and mount an immune response against those microorganisms that are or would be pathogenic. How does it distinguish them?


texts: Role of Fbx15 in ES cells and its use in assaying for iPS cells (Yamanaka paper and others)?

texts:
I am trying to understand the assay for iPS cells in the Takahashi & Yamanaka 2006 paper.

They inserted a beta-geo cassette, which contains the neomycin resistance gene, into the Fbx15 gene.  The idea is that the beta-geo cassette will be expressed when Fbx15 will be expressed, thus conferring G418 resistance to only those cells expressing Fbx15.

They say that "Although specifically expressed in mouse ES cells and early embryos, Fbx15 is dispensable for the maintenance of pluripotency and mouse development."  Does this mean that Fbx15 will be expressed in induced pluripotent stem cells, and won't be expressed upon differentiation? (What is special about Fbx15 that will distinguish iPS cells from somatic cells, including those that might derive from iPS cells, as when pluripotency is not maintained?)


texts: Why don't we see life form again and over again?

texts: If life formed on earth by natural laws, why can't we observe the formation of life from matter today? Is it because this is a rare phenomenon? It seems just after formation of earth life formed on earth and around 2-3 billion years has passed. It must be enough time for life to form several times from scratch.


texts: How much blood do we have when the heart first starts to beat?

texts:
How much blood do we have when the heart beats for the first time?

It should be between the third and fourth week of embryonic life.


texts:
While I was studying Cellular Respiration: Harvesting Chemical Energy, I found this question:

An organism is discovered that consumes a considerable amount of sugar, yet does not gain much weight when denied air. Curiously, the consumption of sugar increases as air is removed from the organism's environment, but the organism seems to thrive even in the absence of air. When returned to normal air, the organism does fine. Which of the following best describes the organism?
A) It must use a molecule other than oxygen to accept electrons from the electron transport chain.
B) It is a normal eukaryotic organism.
C) The organism obviously lacks the citric acid cycle and electron transport chain.
D) It is an anaerobic organism.
E) It is a facultative anaerobe.
Answer: E

I wonder why the answer is E not D. How can I know that it is a facultative anaerobe? Do anaerobic organisms die in air?


texts: Why does increasing the space constant increase conduction velocity in myelinated neurons if nodes of Ranvier are constantly spaced?

texts: If depolarisation at one node of Ranvier triggers, by passive conduction, an action potential at the next node of Ranvier, why does increasing the space constant increase conduction velocity? Surely the locations of each action potential are pre-determined by the sites of the nodes of Ranvier? Is it simply the rate of the passive conduction that changes?


texts: Estimate mutation rate in UVC treated cells

texts: I am wondering how to get a coarse estimate of the number of mutation I obtain doing UVC treatment on eukaryotic cells (microalgae) starting from information such as the survival rate, genome size, number of genes or gene density... I heard about a similar estimation for EMS mutagenesis (I don't remember the exact details but it was a correlation between number of colonies surviving the treatment and the number of point mutations per kb of genome). I cannot find the source of this kind of estimate so I really appreciate any help!


texts: Is Canine teeth enough evidence to prove that one is a Carnivore?

texts:
This question does not assume that we are meant to be carnivores in the first place; In fact I have no idea to which category we belong to anyway! There are several posts online indicating that classifying humans as carnivores and pointing to our canine teeth as evidence might be fallacious.

Also, the fact that Hippos, the largest canine teeth of any land mammal, are herbivores indicates there are exceptions to this view. A couple of other animals like the Gorilla are also herbivores with big and sharp canines. I have also read about the lack of cellulace production in humans as a counterargument to the above.

To what category would we fit in to? What evidence is required to support this idea? Do scientists agree upon a common theory?


texts: Plasticity between excitatory and inhibitory neurons?

texts:
All that I've learned about synaptic plasticity only concern the synapses between excitatory neurons. For example, all pyramidal neurons (excitatory) in the cortex have plastic synapses between them, but as far as I know there are no plastic synapses between pyramidal neurons and their inhibitory interneurons.

So I am curious, are there any plastic synapses between inhibitory and excitatory neurons?


texts: What's the difference between male and female?

texts:
As long as we only look at humans the differences are clear: males have chromosomes XY, produce sperm and don't get pregnant. Females have chromosomes XX, produce egg cells and bear babies. But when you consider other species, things are more complicated: in birds, it's females who carry the Y chromosomes. In pipefish and sea horses, it's the males who get pregnant. So maybe the only reliable criterion to tell if an animal is a male or a female is looking at its reproductive cells, and decide if they look like spermatozoa or egg cells. But then there are male and female plants, where none of the methods above applies.

So how do you tell, in general, who's male and who's female in a species? Or is the distinction arbitrary?


texts: How can sequence analysis establish whether a genomic sequence is a functional gene or a pseudogene?

texts: BLASTX of a query gene shows 5 hits in my subject, how can I find out which of these are expressed and which are pseudogenes (using DNA sequence or by sequence analysis)??


texts: Why do we define anaerobic respiration as not requiring oxygen, while utilization of the Krebs cycle and electron transport chain both require oxygen?

texts: We have an electron transport chain with the final e- acceptor as SO4 2-. We say this is an anaerobic process, or specifically a case of anaerobic respiration. Elsewhere, as with fermentation and glycolysis, we have anaerobic processes that do not require oxygen. Would it be more appropriate to call these processes with the final e- acceptor as anything other than oxygen to be pseudo-anaerobic?  I say this as it seems misleading to call a process anaerobic that inherently is composed of aerobic processes.


texts: How much fat can the body absorb? Implications for daily fat distribution

texts:
This question is named analogous to this research: How much protein can the body use in a single meal for muscle-building? Implications for daily protein distribution http://ncbi.nlm.nih.gov/pmc/articles/PMC5828430

How many grams of lipids can the body absorb in one sitting? (I ask because a strict vegetarian or vegan diet is characteristically low in fat. Therefore, I consume extra virgin olive oil and nuts.)

Most of the research on pubmed.gov is about oral lipid drug administration/absorption. This work that seemed to come close is over my head and just doesn't seem to specify:

Intestinal Lipid Absorption and Transport by C T Phan 1 and P Tso

PMID: 11229876 DOI: 10.2741/phan

https://www.bioscience.org/2001/v6/af/A612/fulltext.htm

Image sources: Cronometer.com and Jackedonplants.co.uk


texts:
I just saw this insect collecting polen from bougainvillea blossoms on the Greek island of Skyros, in the Aegean sea. For future reference, this is in the middle of August and the sighting was at around 17:00.

I posted all 4 photos I took since the rude little thing didn't have the decency to sit still to let me get a clear shot. I'd say it was about 2cm long, certainly no more than 3.


texts: Example of well understood/modeled biological mechanism

texts:
I am working on modeling psychiatric disorders, where multivariate time series data - which I think is necessary to do any interesting modeling - is only broadly available recently, due to the availability of surveys via mobile devices.

To get into the dynamic systems modeling literature, I would like to look into a biological mechanism, which is well-modeled, by which I mean that the error/misfit is negligible for many applications. Basically, I am looking for a (historical) example, where I can follow the steps that were taken to get from the observed (maybe experimental) data to a good model, with the hope that I can learn some lessons for my own work. Ideally, it would be an example with about 5 < p < 20 variables.

Any hints and suggestions are greatly appreciated and my apologies if this is a too trivial question.


texts: How to inactivate trypsin permanently by boiling?

texts: I have to perform a hydrolysis of BSA with the enzyme trypsin. As a control I want to inactivate the trypsin enzyme. Can I inactivate it permanently by boiling (100oC) for 10 minutes, or does it it require 1 hour of boiling? After inactivation, I have to do a test (with an active enzyme) and a control with BSA at 37oC). At this point the inactivated trypsin (the control) should not be re-activated. So my questions are (1) whether I can irreversibly inactivate trypsin by boiling, (2) how long I have to boil it, and (3) if the boiling process will irreversibly inactivate the trypsin.


texts: Some books says the dominant plant form in tropical rainforest biome is broad leaved evergreen trees. Other books say it is broad leaved evergreen trees and deciduous trees. What is the most accepted way (or the truth)? Also how do you explain the deciduousness adaptation in tropical rainforest (e.g., when do they shed leaves)?


texts: What is the difference between these terms: clade, monophyletic group and taxon?

texts:
Wikipedia definitions for these terms are pretty similar:

http://en.wikipedia.org/wiki/Clade
http://en.wikipedia.org/wiki/Monophyletic_group
http://en.wikipedia.org/wiki/Taxon

They sound like the terms are synonyms. Why there are separate articles for them then?

Is it true that every person is a reptilomorph and an eupelycosaur just like he/she is a mammal?

Bonus question: what is the difference between a cladogram and a phylogenetic tree?

PS Please don't just give definitions and/or quote Wikipedia. Point out the differences, if any. Even better, provide examples that can be considered one but not the other.


texts: Were nicotinic acid/amide or flavin nucleotides ever part of primary RNA sequence?

texts:
NADH and FADH2 redox reactions are built deep into our biochemistry.  For example, pyridine nucleotides are involved in >500 enzymatic reactions.  When we look at the structure of deamido-NAD+, it is strikingly symmetrical:

The same is true for FAD, a two-headed monster of a nucleotide

in which we can recognize the two heads, belonging to xanthosine (a purine nucleotide) and alpha-ribazole 5'-phosphate, the latter of which is produced from flavin in the course of B12 synthesis:

The phosphoribose can be swapped between alpha-ribazole 5'-phosphate and nicotinic acid.
Given such enticing hints, it is tempting to speculate that one or more of these nucleotides might be so fundamental because it was actually part of some ancient RNA primary sequence, giving RNA containing this code the power to do serious catalytic chemistry with acid and amide groups, powerful options for redox and methyltransferase activity and more.
I know this is a hard question to answer, but is there any evidence that weighs in, or could weigh in, on whether this happened?  For example, if these functional groups are too unstable in regard to intramolecular reactions on a strand of RNA, or if there is no way to envision a potential base pair that would be reliably distinguished from the known base pairings.  Or if RNA editing sometimes creates them in some organism.  Or if aptamers made from these subunits show improved catalytic possibilities.  (That doesn't seem so easy to look up, since many papers look for aptamers binding these as prosthetic groups, rather than incorporating them)  It would be useful simply to have a notion of what evidence for such an idea would look like.


texts: By what mechanism does elevated homocysteine level accelerate thrombin formation?

texts: It has been stated that elevated homocysteine level accelerates thrombin formation. By what mechanism does this happen?


texts: What are the max angles of human eyeball rotation?

texts: How much can our eyeballs rotate towards the nose, away from it, towards the top and bottom?


texts: Found this on the wall of my house in Kuching, Sarawak, MALAYSIA It is a tiny black triangular shaped insect.


texts: Can someone explain what exactly each score of the BLOSUM62 matrix means?

texts:
The descriptions that I've found say it's the log odds ratio (observed/expected) where expected is the assumption that there is no correlation between amino acids.

I'm slightly confused as to what this means? Do we have a database of sequences and if there are 10 A's out of 1000 amino acids is it's expected simply 10/1000 * sequence length for all sequences?

What is the observed? Is the observed different for every sequence so there is a different BLOSUM matrix for each sequence? And can someone explain how this table represents 62% of "kept identity"?

Sorry if these questions seem nonsensical or vague, I'm not of a biology background.


texts: How is DNA testing used to differentiate between different species?

texts:
How is DNA testing used to determine that specimens belong to different species, rather than being subspecies, or members of the same species?
Usually the definition of species is about the ability to produce fertile offspring under natural conditions. How are markers chosen that indicate individuals are different species?

Or does this process occur the other way around? Are species identified as being different, then DNA used to identify which members are which?


texts: Are the brains of any herbivorous animals capable of utilising ketone bodies as an energy source?

texts: I ask this question because earlier today I heard from a lecturer at my university that a sheep's brain cannot utilise ketone bodies as an energy source and hence with insufficient glucose supply for their brains they die.


texts: Which organism has the smallest genome length?

texts: Which animal/plant/anything has smallest length genome?


texts: What is the physical reason that a weak muscle means that its antagonistic muscle will tighten?

texts: I've read online (probably from these two sources Athlean-X and Mike) that when one has a tight muscle that the antagonistic muscle tightens up as a defense mechanism. What I am trying to understand is why the body does this. From my intuition it seems that tightening up just makes the tight muscle vulnerable to wanting to stretch it and snap it, so I can't imagine how tightening is a good idea biologically. Furthermore, even if I choose not to stretch it (which is the instinct) it doesn't inform me what the real issue is nor does it seem as a way to defend anything. Thus, how is tightening up defending anything? How does this (perhaps from an evolutionary perspective) make sense? Why does this happen?


texts:
I know cyanide inhibits complex IV in the electron transport chain, but I don't understand why this makes it so toxic. If cyanide is bound to the complex, can't the electrons just bypass it   and reduce oxygen directly? That way fewer protons would be pumped out of the matrix, but most still would, and aerobic respiration would just be less efficient, rather than stopping entirely.

Essentially what I'm asking is what causes the electrons to get "stuck"?


texts: Does the nature of nervous impulses give us a finite number of things we can perceive?

texts:
This is a subject that is very disturbing to me and one that I've been obsessing over for years. I warn you now that this is probably not the sort of thing you get asked on this website and I'm not even sure if I'm explaining it very well but please bear with me.

I have, or at least used to have, a great passion for art and have always been a very creative person. But years ago I began obsessing over the idea there are only a finite number of possible images that we can perceive. And therefore everything I have ever created or will ever create is part of a predetermined, limited set of possibilities.

The amount of knowledge I have about how perception works is that when light hits a photoreceptor in the eye it fires electricity into its connecting nerve cell, this triggers the nerve cell to zap the next one and so on until it reaches the brain. The brain has a memory of where each chain of nerves is connected to and so it identifies that otherwise indistinguishable zap as coming from a particular photoreceptor in the eye. That each chain of nerve cells simply transmits it is on or off and nothing else. I worried that meant our perception works exactly like am LED screen, meaning that when light shines on the grid of photoreceptors, the image that gets sent to the brain is made of dots of exactly one solid colour and the only reason we don't notice it because the brain smooths the edges. This would mean that, if eyesight works like a digital camera there is a finite limit of things that we can possibly see because there is a finite number of images you can possibly create with a digital camera.
I even found an article on the Internet that claim that's exactly how it works, they even have a diagram:

Eventually I found a way around it when it turned out that the eye is constantly making microscopic movements even when holding still.

But what about hearing? I know we have sensors in the form of hairs that trigger a nervous impulse to the brain when they are stimulated. But as I understand it, each one can only send that on/off binary signal when they are triggered by a very specific level of sound. What happens if there is a sound that is in between two hairs? Do you simply not here it? Is the same true for all the sensors we have?

I know that the brain processes a lot of what is sent. I know that there are things outside our range of perception such as ultrasonic and UV light. And I know we all have our personal reactions and even perceptions. But none of that matters to me.

What I want to know is, can our senses cover a continuous spectrum? Or, is everything we perceive a number of discrete and finite possibilities made up of digital, pixelated, quantised information? Can we only perceive image A and image B with nothing in between, or can we perceive image A.012744 and A.064212454 And A.24545157845?


texts: How can enzymes be immobilised on glass?

texts:
I’m studying a hypothetical model for urease activity, which involves fluorescence measurement, hence the need for an optical window to which the enzyme urease is immobilised.
From my previous knowledge, immobilisation of enzymes on a solid surface is done through the covalent bonding of the enzyme (outside its active site) with a functional group on the solid surface capable of covalent bonding.
My question is, isn’t glass supposed to be inert? How can enzymes be covalently immobilised on glass? And if they can’t be, are there other materials that could be used instead of glass for an optical window?


texts: Is there a way to measure ATP usage in the brain similarly to fMRI?

texts: Is there a way to measure ATP usage in the brain (or anywhere else) similarly to how fMRI works (measuring changes in iron resonance in oxygenated/deoxygenated blood)? Is there some sort of similar signal that can be used for ATP?


texts: What is the biological mechanism underlying caffeine intolerance? (CYP1A2 or other?)

texts:
As far as I can tell, caffeine metabolism occurs primarily via the CYP1A2 enzyme. I am curious as to whether mutations in the CYP1A2 gene are associated with caffeine intolerance.  Some site that is not necessarily reputable suggested that caffeine intolerance is due to absence of the enzyme to metabolize caffeine. I am having difficulty finding evidence either supporting or contradicting this claim.

Does anyone know if there is evidence that suggests mutations in CYP1A2 (and therefore inability to properly metabolize caffeine) are associated with caffeine intolerance, or if there is another proposed mechanism for caffeine intolerance?


texts:
In the video "What is Life? Is Death Real?", the subject of mitochondria is raised at 2:58. At 3:12, the narrator says "[mitochondria] are not alive any more: they are dead."

What currents of thought lead to this affirmation?

When I search for mitochondria are dead on Google, I get many links about the role of mitochondria in cell death, but I don't see anywhere that the assertion in this video is discussed.


texts: What portion of America needs the Flu vaccine for herd immunity effects to become substantial?

texts:
I've been looking at the effectiveness of Flu vaccines, which are in my subjective opinion abysmal, and the concept of herd immunity.  I see many articles which argue that we all need flu shots to help support the weaker individuals via herd immunity.  However, I see very few documents actually indicating how effective this process is.

Most of what I have found on the topic is interested in the Herd Immunity Threshold (HIT), which appears to be the point where vaccinations drive the Rq of the disease (reproductive rate in the presence of the vaccinations) below 1 such that the disease spreads to fewer and fewer people with each generation, like removing the heat from a fire such that it cannot sustain itself.

There are two particular aspects of this which I believe are required to answer the question which I cannot seem to find a good answer for, which have been preventing me from answering my question:

What is R₀, the basic reproductive rate, for influenza?  I have seen estimates ranging from 1.2 to 3.  As best as I can tell, even a poor vaccine would be very effective if it was 1.2 but it seems like it would do very little against the higher R₀ values.
How substantial of a knee in the curve is there regarding the number of immunized individuals vs. the herd immunity effects?  If there is no substantial knee in the curve, that should indicate that there are valid herd immunity arguments for influenza even if the vaccines are substantially ineffective.  If the knee in the curve is sharp, then herd immunity arguments would only be valid if we could reach that threshold.

It appears some of these questions may have been answered in "The vaccination coverage required to establish herd immunity against influenza viruses" by PedroPlans-Rubió in 2012, but I do not have any access to Preventive Medicine, the journal it was published in.


texts: How does carcinoma enter into blood or lymphatic vessels？

texts:
When carcinoma begins to metastasize, it enters into blood vessel or lymphatic vessel to migrate to the site of metastasis. In that case, although I think breaking down the basement membrane is necessary for epithelium such as carcinoma to enter into them, I can't find out the reports.
Are the basement membrane actually broken down in the first step of metastasis？What are the molecular mechanisms in which carcinoma enters into blood or lymphatic vessels？


texts: Is "aggregate percentage" still a valid term in ecology?

texts:
Martin et al. 1946 define "aggregate percentage" as a metric that describes the mean percentage contribution of a group to the total mass/abundance of all samples. The metric is useful in datasets that are plagued by outliers and non-normality, something that is a commonplace with most ecological community and diet studies in my experience. Aggregate percentage is calculated as follows:

$AP_i = \frac{100\%}{N_y} \times \sum\limits_{j = 1}^{N}(\frac{a_{ij}}{\sum a_j})$

Where i is the i$^{th}$ taxon, j the j$^{th}$ sample, N total number of samples, a$_{ij}$ the abundance or mass of i$^{th}$ taxon in j$^{th}$ sample, and $\sum a_j$ the summed abundance or mass of all taxa in j$^{th}$ sample.

Martin et al. 1946 illustrate this as follows:

I am sure that "aggregate percentage" is a standard method in ecology, but I cannot find many studies using this term by googling. Probably the method has synonyms and there might be a more accepted term for the method nowadays. My question is what is the valid term to use for the method?


texts: Contribution of major nutrients to energy in the human body

texts:
What is the contribution of the major nutrients -- glucose, fat and protein -- to the human body's energy requirements, in normal conditions?

For some tissues, the fuel preference is known qualitatively -- the brain runs on glucose, the heart preferentially oxidizes fatty acids, etc. I'm looking for quantitative data on the consumption (oxidation) rate of the major nutrients, on the whole-body level. Molar amounts per unit time, or energy per unit time, or relative contributions to the total.

To get a rough idea, I looked at glucose and triglyceride turnover in blood. This article estimates blood glucose turnover at about 8 g / hour, or 190 g / day. If we assume that blood glucose transport equals amount of oxidized glucose, then this corresponds to 3200 kJ / day, or about 1/3 of the daily energy requirement. Similarly, this article estimates blood triglyceride half-life at about 1h; with a blood triglyceride content about 5 g, this yields about 90 g / day, or 3300 kJ / day from fat.

So with this rough estimate, sugar and fat appears about equally important, but about 1/3 of the daily energy requirement is missing. And I would imagine my quick calculation is inaccurate in many ways... Anyone know of better estimates? Some literature on the subject?

(I'm aware of the the dietary reference intake data, but diet composition may not equal the proportions of nutrients oxidized due to all sorts of interconversions.)


texts: Dopamine receptor count: Role and Measurement

texts:
Can the Dopamine (DA) receptor count take a significant drop over the course of life or does it stay constant? I read that low D2 (Dopamine receptor type 2) receptor count does not cause Parkinson's Disease (PD) and has some interesting effects instead, but what abut low D1 (Dopamine receptor type 1) receptor count? What are its effects? All I found is this. Is D1 receptor only related to motor activities?

I found some research papers on how to measure the DA receptor count, but are those tests publicly available and affordable? Is there any indirect way to determine D1 & D2 receptor count?

Disclaimer: This is not a self-help question, and PD is not my focus. I am trying to form a theory that requires easy way to measure DA level plus D1 and D2 receptor count, but sadly I am not part of any university with biology department to go seek advice from.


texts: Do presynaptic neurons and postsynaptic neurons have different compositions of neurotransmitter receptors and transporters?

texts: For example if certain neurotransmitter is released, will there be neurons that won’t be even potentially affected, because it doesn’t have such type receptors?


texts: MOL2 to PDBQT conversion via OpenBabel and MGLTools removes hydrogen atoms


texts: Is it possible to create a restriction map using python?

texts:
I have some fragments of DNA from single and double digests using three different restriction enzymes. I'm trying to construct a restriction map of a linear fragment of DNA. The map needs indicate the relative positions of the restriction sites along with distances from the ends.

Can this be done using python at all?

DNA Sizes of Fragments (bp) - uncut DNA = 900

DNA cut with EcoRI = 500, 350, 50

DNA cut with HindIII = 600, 300

DNA cut with BamHI = 400, 300, 200

DNA cut with EcoRI + HindIII = 350, 300, 200, 50

DNA cut with EcoRI + BamHI = 300, 250, 200, 100, 50

DNA cut with HindIII + BamHI = 300, 200, 100


texts: Why is gynodioecy common and androdioecy rare?

texts:
Gynodioecy is when a population features individuals that produce both male and female gametes and individuals that produce just female gametes. Androdioecy is when a population features individuals that produce both male and female gametes and individuals that produce just male gametes. The former is "not uncommon" and the latter is "virtually unknown."

Charlesworth 1991 states that this is common because cosexual populations would normally evolve a male sterile mutation first, causing gynodioecy, and then female sterility mutation(s) will build up leading to dioecy.

Why should it be so much more common for male sterility mutations to evolve first?

(I think the answer lies within articles cited in the above paper, Charlesworth & Charlesworth 1979 Proc R Soc B, and 1987 Evolution which I'll try to read this weekend, if it is I'll post a self-answer but in the mean time...).


texts:
Every cell has its division limit. But plants cell looks like don't have it (like Sequoia sempervivens D.). I searched a little for it but what I have found didn't help to answer my question. I found a paper http://epsce.com/wp-content/uploads/2016/02/EMBRYONIC-PLANT-EXTRACTS-EXTEND-THE-HAYFLICK-LIMIT.pdf, which states that plants cell have something call EPE. Which seems to me like super telomerase ( Just kidding don't take it seriously).

My question is: How do plants slow their aging process? Have they different limits for cell division? Are phytohormones related to this phenomena?


texts: What degree of influence do SNPs have on activity of ligands at receptors?

texts:
I know that generally, evolution tends to evolve towards having some wiggle room in respect to effect of polymorphisms on binding of endogenous ligands, but with synthetic ligands, especially modern structurally-unrelated molecules, does the same continue to hold true?
I've been particularly wondering about this in respect to biased agonists with selective functionality for some pathways activated by a receptor over others - wouldn't activity of that degree of selectivity be particularly vulnerable to disruptions by SNPs?
Hypothetically, would a ligand preferentially activating therapeutic pathway A but not a highly hazardous pathway B of an ABC receptor be a viable drug at all? Or would it be prime "expect it to kill somebody sooner or later" material?


texts: What specific markers does a Covid-19 PCR test look for?

texts:
I've done a search and can't find anything as to what specifically makes a Covid-19 positive that identifies it as unique. I would expect to see something like this:
https://madridge.org/journals-admin/uploads/fulltext/MJV/images/mjv-118-t002a.gif
or
https://i.stack.imgur.com/423Ay.jpg
Instead I find this:
https://communitymedicine4asses.files.wordpress.com/2020/05/2020-05-07-17_38_07-covid-19-testing-what-you-should-know.png?w=624
and
https://myrepublica.nagariknetwork.com/uploads/media/PCR_20200513092900.jpg


texts:
Kimball Biology 5e says

  Coelom is the main body cavity of many animals. It is lined with an epithelium derived from mesoderm.

Gilbert Embryonal Biology 9e says

  Coelom is the space between the somatic mesoderm and splanchnic mesoderm that becomes the body cavity. In mammals, the coelom becomes subdivided into the pleural, pericardial, and peritoneal cavities, enveloping the thorax, heart, and abdomen, respectively.

Then my lecture materials and the research site say

  Coelom is the secondary body cavity.

Finnish Wikipedia says that Coelom is only with invertebrates.
Again the Wikipedia page about peritoneum suggests that human has abdominal cavity and no coelom, and other mammalians coelom.

Does human have Coelom?

The confusing thing is the use of the word "OR", since I am not sure whether people are using it in different pages like "XOR" or like "AND" in normal speaking.


texts:
Melanin is a natural pigment that is categorized into two main forms, eumelanin and pheomelanin. It's well documented in the science literature that increased eumelanin levels reduces the risk of developing skin cancer, whereas it was recently reported in Nature that pheomelanin may itself be carcinogenic. So my question is:

Does pheomelanin have a useful biological function?


texts: Does a DNA sequence has its own derivation tree or pattern?

texts:
I am new to bioinformatics and natural language processing. In linguistics, they have Treebank - derivation/parse tree for each sentence. For example, a sentence "Sara sleeps" can be visualized by a tree: Sentence -> Subject Verb, Subject -> Sara, Verb -> sleeps.

I've heard about Genbank, a database for nucleotide sequences. Does a DNA has its own derivation tree, or is any pattern in a DNA sequence already known with current technology? I only heard about repeats.


texts: What's the role of bromelain in pineapple?

texts: Bromelain refers to one of two proteases found in pineapple and its relatives. Like other proteases, many believe it has therapeutic uses and it's the subject of a lot of research. But what role does it play in the pineapple itself? Why does pineapple (or papaya, for that matter) generate large quantities of protease when other plants do not?


texts: Needing help in order to infer the statistical hypothesis tests performed in an old paper

texts:
I am in great need of help in order to infer the statistical hypothesis tests performed in an old paper. However I need to make some reasonable guesses only from the abstract of the paper since the original text is in chinese which i can not understand (after extensive search i was also unable to find the original text even in chinese)

The title of the paper is:
“Detection of sister chromatic exchange in workers exposed to coal tar pitch and to coke oven volatiles"

The abstract of the paper (which was published in 1998 is the following):

In order to know the changes of genetic toxicological effects on workers occupationally exposed to polycyclic aromatic hydrocarbons (PAHs), sister chromatic exchange(SCE) was detected by the methods of peripheral lymphocyte culture in 23 workers exposed to coal tar pitch (CTP) and in 19 workers exposed to coke oven volatiles (COV) and 12 normal controls. The results suggested that the SCE in occupational workers was significantly higher than that in controls (11.31 vs 6.37, P < 0.001). The SCE in workers exposed to CTP and to COV was higher than that of control (10.27 and 12.58 vs 6.37) respectively. In workers exposed to CTP and COV, there were no differences of SCE for smokers and nonsmokers (P > 0.05). It is indicated that CTP and COV caused strong genetic toxicity and injury to chromosome.

In your opinion how do you think that the above reasarch was organized

For example: a) What types of statistical hypothesis testing was performed by the reasearchers b) What kind of data was collected and used for each statistical hypothesis test c) What methods were employed for the each hypothesis test ?