texts: What structural features make a molecule a potent opioid receptor agonist?

texts:
For instance, take morphine. It is used as a baseline for measuring the potency of opioid agonists. Its structure looks like this:

But then, take heroin, around three times as potent, its structure is this:

6-Monoacetylmorphine is around 30% more potent than heroin itself:

If, however, the acetyl group is bonded to the top instead of the bottom, the resulting substance is less active than heroin.
U-47700, a research chemical, has a totally different structure but has around 7.5 times the potency of morphine in animal models:

Desomorphine is 8-10 times more potent as morphine:

Oxymorphone is 10 times as potent as morphine:

The common explanation that I've heard for these substances being potent opioid agonists is that they mimic the endorphins produced in the human brain. However, Beta-Endorphin is 18-33 times more potent than morphine, and its structure is thus:

That looks absolutely nothing like any of the substances mentioned above. How can molecules with structures so radically different from those of endorphins mimic the action of endorphins? And how come U-47700 has a potency similar to the more powerful morphine analogues but looks nothing like them?

But then, there's Fentanyl:

100 times more potent than morphine, making it a more powerful Opioid receptor agonist than the body's own endorphins, and its structure looks nothing like them or any of the other ones so far. Other analogues are even more potent. So what is it about a molecule's structure that makes it a potent opioid? The only structural similarity that I can spot is the presence of a tertiary amine group in the structure. And how does U-47700 have a potency similar to the more powerful morphine analogues?


texts: Clarify pre-column pressure vs. system pressure vs. backpressure for prepacked columns used with the äkta purification system

texts:
Background: I am using the Äkta pure system for protein purification, with prepacked columns from GE-healthcare. Just to take one example, I use the HisTrap 5 mL column (IMAC: immobilized metal affinity chromatography). I understands the effects of over-exceeding the pressure limits of a column, and therefore vigorously set the pre-column pressure to 0.5MPa everytime I use the äkta. However, I am starting to question or how I should think about the different pressure, and if 0.5MPa is correct for the different columns I am using.

I was taught to always set the pre-columns pressure, which makes sense since as far as I can tell – this is the actual pressure inside the column (pressure felt by the resin). However, If I open the documentation on the HisTrap 5 mL column from GE-healthcare, I can’t seem to find much about the pre-column pressure limit. I also find the terms max-backpressure limit in the documentation for the column, and system pressure.

Questions: How is the system pressure different from the pre-columns pressure? Should I calculate the pre-column pressure myself as an effect of the size and length of the tubing leading to the column? Is there a good article or webpage that goes through this theory at a basic level?

It seems obvious, but how can backpressure be created in a system that is not closed and goes one way (or perhaps the Äkta is creating the pressure)?


texts: Do antagonist-receptor complexes get absorbed into the cell?

texts: My understanding is that normally, a neurotransmitter binds to a receptor and then that ligand-receptor complex gets absorbed into the cell and either degraded or recycled. So does the same thing happen when the ligand is not the endogenous neurotransmitter, but instead an "artificial" antagonist -- like, say, bupropion bound to a nicotinic receptor?


texts: Why do heterozygous individuals have increased resistance to malaria?

texts:
I am aware that there is such a thing called heterozygous advantage, which is due to the presence of a certain single allele, and that an example of this could be with "sickle-cell anemia".  I am quite curious as to how exactly this heterozygous advantage is created.

Could the increased resistance against malaria be due to natural resistance or natural selection?


texts: DNA complementarity against reverse complementarity

texts:
I am sorry to bother with this question (i study genetics for about few hours, because I need to understand my data) and I am really confused about these two terms, because I dont know if the books uses word "reverse" interchengeably or what is going on here.
The main problem I am totally confused about are words reverse complementarity and complementarity of two DNA strands. Since I know that strands runs in antiparallel directions and two DNA strands are complementary to each other:
i.e. sequence ACTCTG is complementary to TGAGAC and vice versa.
But my question is: are two DNA strands reverse complementary to each other? Because at least in two books I have read that two strands of DNA are. But if I would apply it to my previous example and use reversion, then no way I can get to my other strand. Is the word reverse in this context use as antiparalel (5' - 3' and 3' - 5') or am I missing something and it's true that if I take the whole DNA strand, I can use complement and reverse it and it will be my other strand?
Again I am sorry to ask this really basic question, but I am so confused about this terms.
Nice day to all and thanks if someone will have time to answer my question.


texts:
Hapten are small-molecules, that can only become immunogenic when conjugated with a carrier protein. I was wondering if all small-molecules can become haptens (eg. by synthetic conjugation).
Given that lymphocytes are filtered by negative selection, I would expect that small-molecules that chemically mimic self-peptides would not work as haptens (at least not in the sense, that they could be detected by antibodies).
Are there any examples of small-molecules that have been tried as haptens but could not generate antibodies ?
Also is there any estimate of the ratio of naturally occuring haptens and synthetic haptens. I was investigating the IEDB (https://www.iedb.org/) as well as SuperHapten (http://bioinformatics.charite.de/superhapten/) but could not find a way to filter these two types of haptens.


texts: How does a neuron know to which one of the next neurons to pass the signal

texts:
Looking into how neural networks are build in the brain, here are a couple of facts followed by some questions:

The neuron receives the signal through its dendrites and passes it to the terminal at the end of the axon.
A neuron can have as much as 1000 connections to other neurons.

As I understand the dendrites can be connected to multiple neurons, so the neuron we are talking about can receive signals from multiple cells.
Now the questions:

The terminals at the axons can be connected to just one or to multiple neurons?
If the axon terminals can be connected to multiple neurons, how does the neuron transmitting the signal knows to which of the further neurons to pass the signal next? Is it passing to all of them at once?
If the axon's terminal can be connected to only one other neuron (for the single axon neurons), how are the two-axon neurons working? How do they know to which axon to pass the signal next?


texts: Why does immunity from the flu vaccine appear only after two weeks?

texts:
It is said that immunity from a flu vaccine appears after about two weeks. However, from experience, the flu usually lasts only a few days.

If sufficient antibodies appear only after two weeks shouldn't the flu also last that long? Or is there a difference between how the body reacts to the actual flu virus as opposed to the dead one in the flu vaccine (like maybe there being more viral particles in an actual infection or something)?


texts: Why is the swelling of bread when placed in water not considered to be caused by osmosis?

texts:
Why is bread swelling up when placed in water not considered to be caused by osmosis?

Is there a property of water that should make it leave the bread instead of enter?


texts: Arthropod identification request (a spider with no legs?)

texts:
My mother sent me a picture of a creature she encountered and couldn't identify. It looks kind of a like a spider - a mostly black body, about 1cm in size, with white specks - except without any visible legs. Apparently it was hanging from a thread, descending to the ground, and still moving.
I don't know a lot about arthropods, and, perhaps unsurprisingly, searching for "spider without legs" gives no useful results, so I'm at a loss.
This is in Northern Germany, mid-March. (The background is a cork floor.)

Any info on what this could be - and whether it's dangerous or not - would definitely help put her at ease.


texts: How do paper wasp larvae not fall from their nest?

texts:
There is now a paper wasp nest hanging from the eaves of my bedroom. Not very big, I supposed about a hundred chambers and about 7 to 10 adults in total. I observe it every now and then.

It just occurred to me that when the larvae first hatch, they are so small compared to the chamber diameter. So here are two questions:

How do they not fall off, being suspended and all?
Is there any known statistics of how often larvae fall off (for a particular species, let's say)?


texts: Why do Hot/Cold drinks taste sweeter once returning to room temperature?

texts:
Now, I know this is a very bizarre question, and I tried to find a correct exchange for this, but it might relate to biology/science as it being our taste buds and everything.

I am so sorry if there is a better exchange for this, but (I hate using this excuse) I'm new to StackExchange, so please be gentle and point me in the right direction.

Now, to meat and bones (Unintended pun; meat...bones...biology hehe), over the last few days I have noticed that after my drink returning to room temperature, it is so much sweeter than it originally tasted.

Drinks

Hot Tea - I normally only add 1-2 teaspoons of sugar into my tea and it tastes just right, though after taking a sip when it had returned to room temperature, it tastes about 3 or 4 times sweeter than when it was hot/warm. (Milk)
Iced Tea (Bubble Tea) - Just today I had a bubble tea with the smallest amount of sugar possible, it was still too sweet but I stuck with it, and again when it reached room temperature, it was almost unbearably sweet. (No milk)
Slurpee - Again, after returning to room temperature, it is extremely sweet, with it being much lighter with respect to sweetness.
Hot Coffee - Come to think of it, I have also had the same experience with sugared coffee.
Coke - Also, when coke (or any other soft drink) is flat and room temperature, it also produces the same super sweet taste.

So, I tried to think of possible reasons why this happens but, I cannot think of any possible explaination other than magic.

If anyone knows why this might happen, it would be greatly appreciated since I am tripping out trying to figure out why this happens!


texts: Can ampicillin resistant bacteria survive penicillin plate?

texts:
in my molecular bio class we were asked a trick question:

If the bacteria has a plasmid with that grants it ampicillin ressistance, can the bacteria survive if placed in penicillin?

I gave it  a thought and said that it cant, since amp differs from pen by an extra amino acid that could harm the bacteria, the answer corresponds with the class material but amp is known as the broad spectrum antibiotic.... so should i go with the  class flow  lured by the experimental assumption and assume it dies  or persist on whether it will survive? i'm really confused at this point, any input is appreciated


texts: Why mammals don't have renal portal system

texts: I am  a high school student and I am a little confused why mammals don't have renal portal system?, some books says that because we have four chambered heart, so our blood is filtered more effectively than pisces, amphibians and reptiles but I am unable to understand how our 4 chambered heart helps us in this case and provide us an edge in blood filteration?


texts: Minimum size for a peptide/protein to be immunogenic in human?

texts:
What is the minimum size for an (injected) peptide/protein to cause immunogenic response in human?
A reference is very helpful, as well.

Thanks in advance


texts: Human Demography - Where can I find this statistic?

texts:
In "An Introduction to Genetics" by David J. Merrell, copyright 1975 by W.W. Norton + Co., p. 742, in the Chapter "Genetic Counseling and Eugenics," the author states: "... 50% of the women produce 85% of all children born in the United States."

The author provides an Additional Reading list, but I'm not a geneticist, nor do I have access to much of the listed material.  With that in mind, 1) where can one find the statistic mentioned above? and  2) has this number changed over time?

OP EDIT: In response to comment (a few examples from Reading List of 30 items):

Davis, 1970, Prospects for Genetic Intervention in Man, Science, 170 279-1283

Dubos,1965,  Man Adapting, Yale Univ. Press

Dunn, 1962, Cross Currents in the History of Human Genetics, Amer. J. Human Genet, 14: 1-13

Ehrlich, 1968, The Population Bomb, Ballantine NY

...

Lynch, 1969, Dynamic Genetic Counseling for Clinicians, C. C. Thomas, Springfield, Mass.

...

Petersen, 1969, Population, 2nd Ed. Macmillan

...

1969, WHO Expert Comm. on Human Genetics, "Genetic Counselling(sic), Tech Rept 416, pp. 1-23

I know I can find stats like average ages, etc from the Statistical Abstract of the United States, but where do geneticists find items like the one cited in the Merrell book?


texts: Is it correct to regard archeaic humans (i.e.n Neanderthals and Denisovans) as distinct species to Homo sapiens?

texts: There is increasing evidence (e.g. here) that Homo sapiens interbred with contemporary homonins such as Homo neanderthalensis and the "Denisovans". Although these homonins do show differences in their mtDNA, since a species is generally defined as a group of organisms capable of interbreeding and producing viable offspring, should we not regard humans, neanderthals and denisovans as the same species and name them as such?


texts:
I recently found this insect  near our veranda wall. What insect is this ?
Is it poisonous?

As you can see, it has multiple legs fine as hair, but it is not like a common millipede or centipede.
I searched for this insect by reverse Google image search without result.

Location: Kolkata, India

Nature: fast-moving, aggressive.

Unlike earthworms, this insect loves basking in sunlight.


texts: What would it take to recognize a deer by its photo?

texts:
I am trying to recognize a deer by its antlers or any other means.
Elaborating:
I was hoping to use their antlers to recognize them but I have heard that most deers shed their antlers every year so it would be difficult to recognize it from the last year's photo unless these antlers retain the same pattern every year.

If not the antlers, what other characteristics should I be looking for?

Is there any software that can help me in recognizing a deer?


texts: Why has evolution made neurons use spiking?

texts:
I'm going to be forward and say that I'm not a biologist.  I don't claim to fully understand the functionality of a neuron from an electrical/chemical perspective... I'm curiously gazing from the outside in as a computer programmer.

Now, the big new thing these days with artificial neural networks is simulating them with biological precision- that is, with spiking, actually placing the network in Euclidean space, and all sorts of other goodies (Check out the Human Brain Project; it's really cool.  Our own brains are computable, given a powerful enough computer.  Probably has a lot of fascinating and horrifying philosophical implications too.), but this isn't the only model that people have commonly used for neural networks.

In the past, multilayer perceptrons were the big thing; I'm not going to go deep into explaining them, but essentially, each neuron simply performs a mathematical function on its inputs and then outputs it.  There's no spiking in the sense similar to our neurons.  A neuron could be blasting its output at nearly 100% indefinitely and there isn't any objective difference between that and it being at 0% or anywhere else.

Now, I sort of went off on a tangent, but what I'm trying to understand is- why this behavior is not observed in the system of computation that evolution has produced over the many, many years?  Why do we use spiking neurons instead?  We have instead developed a strange system where spikes travel down chains of neurons in patterns we don't really understand yet to produce the behavior necessary for the creature to survive.  My question is, why has this been favored over something similar to multilayer perceptrons?  Is it more energy efficient to use a spiking model?  The brain does use a disproportionate amount of energy.  I wonder if it is more effective as a model for computation.


texts:
I have some idea about it. Is it the wasteful back flow of H+ ions through uncoupling proteins during aerobic respiration?

Thank you


texts:
What are the algorithms / methods in use for the calculation of primer dimers and hairpins?

As an example, IDT's OligoAnalyzer tool will generate these analysis given particular sequences.

The homo-dimer analysis seems to me to just be a sliding scan of two sequences across each other. I assume this doesn't take into account possible hairpin issues? or are such structures less likely compared to the myriad of other more common problems.  In addition, how are the ΔG values calculated given a particular dimerization pattern?


texts: Which sequence assemblers I can use to compare different paradigms?

texts:
I'm a high school student whose interested in bioinformatics. Therefore I chose a project which I study Sequence Assembly. My main goal is to compare different paradigms (Greedy, OLC, De Bruijn).

I have done my initial research but I don't know which assembler to use for comparing paradigms. Most of them are designed for real world usage, where there are many different factors to consider, but in my case the problem is more like a Computer Science problem: Reconstructing an array of symbols from it's fragments.

If there is no hope, I will try to implement them myself but I want to avoid that since it will very likely to be error-prone and slower than real world implementations.

Thanks!


texts:
In a comment to this question, it was said that

  Radiocarbon dating won't work. For a start the tree needs to be dead, which since you're not using the rings I'm assuming it isn't. Also the atomic testing in the 20th century completely messed up the level of C14 in the atmosphere, so radiocarbon dating can't be used for anything that didn't die 70 years ago or more.

I did not know this. So, what kind of dating techniques biologists use today? :-)


texts: Sulforaphane vs. Hyperthermic conditioning (sauna use) which would induce a greater heat shock response in the human body?

texts:
I’m curious to know which would induce a greater upregulation of heat shock proteins, consuming sulforaphane or putting the body through heat stress such as using the sauna.

Sulforaphane reference- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2975177/#!po=79.7872

Hyperthermic conditioning reference-
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3418130/

There are many more articles/studies done on these two subjects, these are just 2 references of the many.


texts: What is the length of anaerobic biodigestion stages?

texts:
I have built an experimental portable batch biodigester to process organic garbage. A 50L drum filled half with garbage, half with water and with some cow dung added for inoculation, is connected from the top to a truck tire, boxed into another, larger drum.

I consider filling the bin within a week, based on the amount of daily garbage my home is producing. After a week, the bin is filled in with water and inoculated, and connected to the gas-holder.

How long would the biodigestion take in average before I can disconnect the bin and use the remaining slurry?

I have looked at existing information regarding the biodigestion process. The stages of biodigestion are explained in Chapter 4 of the Biogas Handbook sample I have:

  Aerobic
  Oxygen will inevitably enter with the raw materials put into the generator, and so aerobic bacteria use this oxygen up,
  meanwhile doing what they can to break the materials down. CO2 is
  released, and some heat is generated.

  Extracellular enzymes
  In this stage, anaerobic bacteria release enzymes that attack large molecules which are still outside their own
  bodies (extracellular), so these molecules will be broken down into
  “bite sizes.”

  Acid digestion
  The bite size molecules (still fairly large) are absorbed by the bacteria and digested. The main byproducts of this
  third process are simple molecules such as the short chain fatty
  acids, H2 and CO2. (We’ll get into the short chain fatty acids soon.)
  It’s interesting to note that at this stage, hydrogen gas, an
  excellent fuel, is evolved. Hydrogen does not often show up in the
  final biogas apparently because it is used by the anaerobic bacteria
  (in the next stage) in making CH4, methane.

  Gas digestion
  Now comes the part we’ve been waiting for. The fatty acids are now gobbled up by the last group of bacteria, who turn them
  into H2O, CO2, and best of all, CH4.

Alas, the length of these stages is not explained. However, Biorealis suggests the length of the Acid Digestion and Gas Digestion in a critique of conventional continuous-feed biodigesters vs. the two-phased biodigester it has developed:

  Conventional single-stage digesters are not only unstable, they are
  also relatively inefficient. For example, if the system is operated at
  a hydraulic retention time (HRT) conducive to growth of acidogens (2-3
  days), any methanogens present will be washed out of the system faster
  than they can reproduce, preventing them from ever becoming
  established. On the other hand, if the system is operated at an HRT
  conducive to growth of methanogens (20-25days), the faster growing
  acidogens will be maintained at the low growth rates of the endogenous
  growth phase - essentially at starvation level.

NB: I opted for a batch biodigestion system to avoid the complications mentioned by Biorealis here above and because Biorealis' two-phased biodigester is more expensive and less easy to build.

So far I have a rough biodigestion calendar of:

3 days of acid digestion
20-25 days of gas

But I still lack some information on the stages:

how about the length of the two previous stages mentioned in the Biogas Handbook?
on what do those stages depend and can I accelerate digestion somehow? (I already know about heat at 21°C, how about water ratio or anything else?)
how long does it take to digest a big chunk of food, say a 27cm² bit of carrot? (Important because I hope the garbage is completely processed before I toss the slurry in the garden as fertilizer)
in short after how much time can I confidently unplug the batch, knowing the biodigestion is complete?

Could you help me shed some light on the length of biodigestion stages? Thanks.


texts: Is there a difference in the energy produced from the hydrolysis of GTP and ATP?

texts: Is the energy produced from the hydrolysis of GTP greater than/less than or the same. I know that GTP can be converted to ATP through a pathway and so my thinking was that GTP would be less.


texts:
Which databases you know that store data on tracking of marine animals?

I am interested particularly on mammals (for which I know meop storing data on sea lions) but also on fish schools (not sure they exist though).


texts: Are animals able to plan hunts, give tasks if they do it in groups and fulfil it adapted to the current situation? Do they use unique tactics for special circumstances (e.g. based on experiences)  or they just act from instincts?


texts: How quickly can lasers of various wavelengths and powers impair human vision or cause pain in the eyes?

texts:
There is a discussion on HackerNews about how self-driving cars might be susceptible to confusion attacks using a cheap laser pointer and a RaspberryPi.

Some people argue that human drivers, too, are susceptible to attacks by laser pointers.

For lasers in the visible spectrum, I'm pretty sure that the human driver can tell he/she is under attack very quickly. But how about lasers outside the visible spectrum? Since you can't see the laser, the only way you can tell something is wrong is if your vision is impaired or you feel pain in your eyes. How quickly can that happen?


texts: Difference between Peptone, Peptide and Proteose

texts:
In my school textbook, it is given that Pepsin converts proteins to peptones, proteose and peptides.

What is the difference between the three products? On googling the terms, the definition was similar.

Peptone: a soluble protein formed in the early stage of protein breakdown during digestion.

Proteose: A proteose is any of various water-soluble compounds that are produced during digestion by the hydrolytic breakdown of proteins short of the amino acid stage.

Peptide: a compound consisting of two or more amino acids linked in a chain, the carboxyl group of each acid being joined to the amino group of the next by a bond of the type -OC-NH-.

Peptide has a different definition, but it can be applied to the other two too as all are degraded proteins but not amino acids.


texts: Application of molecular dynamics simulation (or alternatives) for the full pathways of protein interactions?

texts:
If one would like to control the biological system (e.g. to treat disease or aging/senescence) then one should introduce the drugs in the system, that initiate complex protein interaction pathways that (in final) generate the necessary proteins that induce the necessary biological mechanisms without adverse side effects from additional outcomes.

I am reading https://www.ncbi.nlm.nih.gov/pubmed/29139324 article about application of molecular dynamics simulation to the drug discovery but this article is essentially about simulation of one - target protein/molecule. My question is this: are there methods (molecular dynamics or others) that simulates the processes in the extended protein pathways that are induced by the one or more initiating molecules/drugs? It should be quite complex simulation, but nevertheless nothing less is expected from computational drug discovery and engineering.

I am quite confused. Maybe there is no need for such simulation at all? The databases of protein interactions just provide the more or less complete picture what protein interactions leads to what new proteins or structural updates of participating proteins and there is nothing to simulate - there is just empirical or predicted knowledge about what molecules leads to what other molecules/structures and one just extract the relevant pathway (starting from the drug coming close to the initial proteins) from the database and that is it?


texts: Is "reaction center" the same as "photosystem"?

texts:
I have a diagram which labelled a part of PSI (Photosystem I) as "reaction center". But I have read on several websites that the reaction centers are PSI (the whole complex, not just a part of it) and PSII.

So, which one is correct? And if the reaction center is only a part of these PSI and II complexes, what does it contain? And what does it do?


texts: Introducing novel genes to an adult multicellular organism?

texts:
Is it possible to introduce a novel gene into the genome of every cell (or at least most cells) of an adult multicellular organism? How would this be done?

Thanks,

CDB


texts:
The book, Introduction to Bioinformatics, by Arthur M. Lesk, 3rd edition; Oxford; low-price-edition; in its chapter-1 (introduction), page-no. 6 ; provided a paragraph, entitled "Dogmas: Central and Peripheral".

As-if; there exist a contrasting term for central dogma.

But while thoroughly going through that paragraph (and other chapters linked(mentioned) in that-paragraph; I couldn't found the mention of the term "peripheral dogma" or such.

From the paragraph; it looks like the term "peripheral" has been used to indicate all information-flows other-than genetic codes, and including Junk-DNA and  protein-folding-variations. No mention of epigenetic codes found.

In Web too; I could found only 1 website  used the term "peripheral dogma" in context with biology. which, too, does-not mention the definition clearly.

So, What is peripheral dogma?

P.S. this is purely a terminology question; which is looking for authoritative reference about usage of a term.


texts: What can I research for thesis on DNA data storage from math?

texts:
I'm a math researcher, I just finished a Master on Error Correcting Codes. I recently saw a presentation on DNA-based data storage that I loved.

I wish to continue my studies on (applied mathematics) in this subject.

I received a PhD offer and when I mentioned the subject, the possible director was receptive, but he is not well informed on the subject either, so he proposed that I come up with a research path ...

What do you think is an interesting research topic (and worthy of the community) about storing DNA data from the perspective of error-correcting codes?

Thanks for the help!


texts: Do pyrocalciferol and isopyrocalciferol form in vertebrate skin?

texts: I heard that pyrocalciferol and isopyrocalciferol can only be formed above 100°C/212°F, yet some images in the web depict them as forming in vertebrate skin. So, I wonder if pyrocalciferol and isopyrocalciferol do form in vertebrate skin. If they do, is there something catalyzing the thermal transformation of previtamin D or is it also a result of UV irradiation?


texts: Raising two legs together while lying on bed

texts:
Let's do some exercise(duh!)

Ok so lie on the bed. Lift your left leg. Put it down. Lift your right leg.Put it down. Easy?

Now lift your left leg and without putting it down, lift your right leg. Easy ? No.

Now try to lift both the legs together. Easy ? No.

My question : What is the anatomical reason ( arrangement of muscles around the bones etc.) which makes it difficult ?


texts: Engineered CD8 T-cell therapy for HIV infection

texts:
CD8 T-cells are effective in controlling HIV during the early phase of the infection. However by the time, the virus mutates and develops an evasion mechanism against CD8 T-cells.
Since cancer cells also develop immune evasion mechanisms, and scientists are using several technics to block those mechanism, i think it would also be possible to control "viral escape".
I made some research regarding HIV immunotherapy, however the only thing i found was antibody based immunotherapy.
My question is, would it be technically possible to engnieer custom CD8 T-cells which will targed HIV infected cells ?


texts: variation in antigen binding site of antibodies

texts: Antibodies or immunoglobulins are proteins made by the immune system in response to alien(!) molecules. Each antibody binds to its specific antigen. This great diversity and specificity is cause of diversity in Antigen Binding Site of heavy chain and light chain of antibody. Although other sections of Antibody are highly stable, Binding sites are very mutant. What is the reason for this difference in mutation rates in different parts of antibodies?


texts: How many honeybees are there, and how has the number changed across time?

texts:
How would you begin to estimate the world population of the European Honeybee (Apis mellifera)? Would recent colony collapse disorder show up as a blip? How about the spread of A. mellifera from Europe to Asia and the New World?

Ideally, I'd love to see a chart with estimates of the kept and feral populations of A. mellifera across time. I realize that this is a tall order; but given that we have available to us:

the complete genome,
current data from agricultural organizations, and
historical and archaeological records,

it seeems that with a combination of genetic and historical methods this shouldn't be impossible. Or is it? There seem to be plenty of articles arguing about A. mellifera's African or European origin, but none that I see that mention actual population sizes.


texts: Confusion on polarity and hydrophobicity of Proline, Tyrosine and Cysteine?

texts:
I will list here several sources that state differently on the polarity and hydrophobicity of Proline and Tyrosine:

From the article Amino Acid on Wikipedia, it states that Proline is a special case, Tyrosine is hydrophobic and Cysteine is also a special case.

From Khan academy, it also states that Proline is polar, Tyrosine is nonpolar and Cysteine is polar.

However,

From Pearson Prentice Hall's Biological Science, it states that Proline is nonpolar, Tyrosine is polar and Cystein is polar.

From BioNinja, it states that Proline is nonpolar, Tyrosine is polar and Cysteine is nonpolar.

On Wikipedia,

The article Proline supports Proline is nonpolar.

The articleTyrosine supports Tyrosine is polar and hydrophilic.

The article Cysteine states that Cysteine is polar and hydrophobic, AS WELL AS Tyrosine.

To summarize the result, I'll put them in the following table

Please help me to clear out the confusion, why the polarity and hydrophobicity of these amino acid are not agreed with each other?


texts: What are the physiological effects of wine?

texts: I have read that alcohol in general and wine in particular can have advantageous as well as detrimental effects on human health. Is this true? What are the physiological effects of consuming wine in moderate quantities?


texts: What is this tree that displays sycamore like characteristics but appears to be too small?

texts:
I have been wondering about this tree:

It's bark/leaves make me think it's a sycamore, but it seems too puny. I don't think they'd plant a sycamore there... What is it?

The tree is in a park/residential area in Orange County, Southern California.

Reasons I think it looks Sycamorish:

Alternate leaves
3 lobes
Mottled/patchy/peely bark

https://www.thoughtco.com/identify-maple-sycamore-yellow-poplar-sweetgum-leaves-1343480


texts: If a cell has two different GPCRs, how does the cell differentiate between the phosphorylation cascade caused by each?

texts:
In my biochem course, we learned that GPCR receptors trigger a phosphorylation cascade, with the end result being a large amplification of the signal in the form of cAMP. We never studied any particular GPCR individually, but we were told that GPCRs always end in the formation of a large amount of cAMP, which will go on to phosphorylate key targets that achieve the end result.

My question is as follows: If there are two GPCRs on the same cell membrane (let's say GPCR-A and GPCR-B triggered by substrates A and B respectively), how does the cell "know" which GPCR triggered the phosphorylation cascade if the end result is the same (large amount of cAMP). In theory, couldn't substrate B bind to GPCR-B and cause a phosphorylation cascade identical to that of GPCR-A, thus triggering GPCR-A's cellular response?

Is there some deeper specialization/uniqueness to each type of GPCR receptor that we didn't cover in my course? Does each GPCR produce a slightly different cascade that ends in something similar, but not exactly cAMP? Or is there some restriction, like each cell limited to only one GPCR (I would find this surprising, if this is the case)?


texts: Do most plants need long photperiods in order to germinate.

texts:
For a plant to perform photosynthesis, it needs long photoperiods, right?

But what about for germination, do MOST seeds need long photoperiods for germination?

Thanks


texts: What is a book that goes into reasonable detail (but isn't textbook-level technical) about the origin of earth and in particular the origin of life on earth? Something intended for a broad audience, but that still covers the biology/geology and does not completely gloss over the sicence.


texts:
How does carbon dioxide from respiration diffuse out of the leaf during the night?

Do stomata close completely during night?


texts: Regulation of the TCA cycle and glycolysis by adenine nucleotides

texts:
Why is the tricarboxylic acid cycle regulated by the ADP/ATP ratio as stated in the following quote :

  Isocitrate dehydrogenase is allosterically stimulated by ADP, which enhances the enzyme's affinity for substrates.1

while glycolysis is regulated by AMP/ATP ratio as in the following quote from the same book :

  Why is AMP and not ADP the positive regulator of phosphofructokinase? When ATP is being utilized rapidly, the enzyme adenylate kinase (Section 9.4) can form ATP from ADP by the following reaction: 2

I want to check my hypothesis that it is because the TCA cycle needs acetyl-CoA ( which can come from glycolysis and other sources such as beta-oxidation of fatty acids) in order to operate, so it gets acetyl-CoA from many sources and isn't dependent on glycolysis alone, and that's why it is affected by ADP (which increases upon initial exercise) while AMP stimulates glycolysis (increases after more exercise) to give more acetyl-CoA and that's rate of the TCA cycle is faster than glycolysis?

References

1,2 J.M. Berg et al. (2002). Biochemistry, 5th ed. New York: A H Freeman.


texts: An unknown band appearing in my gel electrophoresis

texts:
I am having trouble understanding what is the source of band "2" in the following gel-electrophoresis:

In this experiment, we took an E.coli transformant colony and ran its nucleic acids in the gel, after adding a restriction enzyme which cuts the recombinant plasmid molecule into two corresponding bands ("3" and "5" ["5" is very weak in the scanned version, but is well seen in the "hard copy" )  . I know the first line ("1") corresponds to possible genomic DNA we took from untransformed bacteria, and that the fourth line ("4") corresponds to a plasmid molecule without an insert. 6 is also well understood.

My question is-
What is the source of band "2" which contains more base pairs than any of the parts of the plasmid and its insert , and in particular more base pairs than the insert?

WIll someone please help me understand this ?

Thanks in advance


texts: Can we identify an individual from their palm lines. Is there any uniqueness for palm lines among family members ?


texts: Why is active transport needed in repolarization?

texts:
During the repolarization phase of an action potential, the potassium ions diffuse out of the cell, and active transport begins.

What I do not understand is why active transport is needed when the movement of ions is not against their concentration gradient?

Since the potassium ions have diffused out in repolarization, only the sodium ions are left in the intracellular space.

The sodium/potassium pump is used to pump 3 sodium ions out and 2 potassium ions in. However, isn't there a concentration gradient as the sodium ions are moving out of the cell, where there are no sodium ions, and thus from a high concentration to a low concentration?

Is it because the active transport allows the imbalance to occur (3 out and 2 in)?


texts: I have read about basics of molecular genetics ,although its not a thorough in-depth knowledge. I would like to know about "regulatory genomics". What is it actually?


texts: Suppose we took all living humans and found the set of their mothers, mothers' mothers, etc. and then traced down as far as possible. Is there a logical reason that this tree has to converge to one 'mitochondrial eve'?


texts: What hold and inject pressure to be used in microinjection?

texts: I am planning to set up micro-injection apparatus in our lab. Normally what hold and inject pressures are used to inject DNA in fly embryo? I couldn't find in any literature as far as I've come across.


texts: How to DIY preserve pet DNA today so that it can be used in 20 years

texts:
I know that there are companies that offer a kit+storage of your pet DNA for around $2k.
My question is if there is any other option for doing this yourself with a thought in mind that in 20+ years the technology will get so advanced that even this DIY sample can be utilized.

Any ideas? Maybe drying a blood drop or mixing blood with alcohol/acetone?

Also, I read somewhere that it is better if the pet is still very young, because if you take old pet DNA the clone will exhibit mature signs even as a youngster. Is this true? If yes then what is the top age that is safe?


texts: Can cfDNA testing distinguish results in the case of twins?

texts:
A fetus can now be screened for some of the more common genetic diseases and its sex determined from just a whole blood sample from the pregnant mother. Fetal DNA is abundant enough in the systemic circuit to be able to be purified and sequences analyzed. Question is, in the case of fraternal twins, could the procedure discern between the two fetus's...

As a clearer example, can it distinguish between:

Scenario 1: if one fetus was male and one fetus female
And scenario 2: both male?

It appears the test would just look for presence of Y chromosome using certain markers. But it could then look at SNP to distinguish individuals.

Looking for clarification here


texts: Extra-mitochondrial conversion of Acyl Carnitine to Acyl CoA

texts:
Normally fatty acids in the form of acyl CoA are converted to acyl carnitine in a reaction catalysed by carnitine palmitoyltransferase I (CPT1), which is also known as carnitine acyltransferase I. This allows them to be transported across the inner mitochondrial membrane by a translocase when the acyl CoA is regenerated in a reaction that is chemically identical but catalysed by a different enzyme, carnitine palmitoyltransferase II (CPT2).

As a result of observations I have made (detailed below) I wish to known whether acyl carnitine that has not entered into the mitochondria — either present in the cytosol or blood/plasma — can be converted back into acyl CoA without entering mitochondria?

Essentially, does a reaction like that catalysed by CPT2 occur outside of the inner-mitochondrial matrix?

Elaboration

I'm studying plasma metabolites. During fasting there is an increase in plasma acylcarnitines due to increased fat utilization/beta oxidation. If the fast is broken, acylcarnitines are typically supposed to drop. Oddly, some people experience an increase in plasma acylcarnitines 0-30 minutes following eating - but then they drop after the 30 minutes. I'm confused as 30 minutes after food ingestion, elevated circulating insulin levels are still present and should be still working to inhibit the majority of fatty acid oxidation - yet the odd increase and then drop in acylcarnitines after 30 minutes of food intake still exists.

So it leaves me with the question, is there another pathway in which acylcarnitines are converted back to acyl CoA outside of the mitochondria? In short, how does the cell recall fatty acids that are destined for the mitochondria?


texts: Can two proteins sharing a few domains be considered homologous?

texts: I wonder when to say two proteins are homolog. In the current example I checked the sequence of these two proteins in pfam and as you see they have some shared domains but all domains are not shared. Can I say that these proteins are homolog? How can I be confident about my decision?


texts: How to get rid of mosquitoes in a small lake

texts:
I own a small lake. Give or take it is about 50 meters wide and 100 meters long (or 160 feet wide, 320 feet long), with a max depth of around 2 meters / 6.5 feet. One third of the lake is surrounded by forest, the rest is grass / small enclaves of tress. The lake absorbes only rainwater from the surrounding residential area. There is a small outlet towards a much larger lake close by. The lake was recently dredge to remove many years of plantlife that had almost turned it into a swamp.

The lake has a large number of mosquitoes. There is also quite many frogs and a few birds that live near the lake.

What can I do to decrease the amount of mosquitoes in the lake?

For example, can I set up certain nesting boxes that will attract birds or bats that will eat a large number of mosquitoes?

Can I release certain fish that thrive on mosquites?

It is in Scandinavia.

EDIT

The shorelines are sharp and most of the vegatation has recently been removed. The lake was recently completely emptied and about 2 meters (or more) of vegatation and soil was removed. The lake has previously been contaminated which was cleaned away. I guess this means that a very large part of the ecosystem has been removed, a few fish did manage to survive, but not very many.


texts:
The brain purportedly produces very weak EM waves.

EEG is a method of measuring electrical brain activity, it has classifications for the types of brain wave it can detect: Theta, Alpha, Beta, Gamma etc.

Are these the weak EM waves the brain produces?

If not what is the frequency range of the EM waves that the brain produces and does it vary depending on mental state?


texts: About embryonic and genetic evidence of evolution?

texts:
My question here is about evidence for evolution from Embryology and from Genetics.

Mammals do have similar Embryos, but is it the case that for each species there is an embryonic development that occurs in earlier species, has such relationship been observed?
What I mean for example if we generally conceive of having species$Sp_1,Sp_2,...,Sp_n$ where each $ Sp_{i+1}$ being evolved from $Sp_i,$ then is it the case that the embryonic development stages of $ Sp_{i+1}$ contains some of the embryonic development stages of all of its ancestor species.

Similar question to 1 but regarding Genetics, is it the case that every species has a genetic thumbprint of its ancestors that lie there in the non-functional sections of its DNA, i.e. is it the case that all the genetic history of our evolution is recorded in the non-functional section of our DNA. So do human DNA have some portions of the DNA of some dinosaurs for example?


texts:
Sorry if my question is very basic for biology majors because I am not. I am trying to build a mathematical model of a particular pathway using systems of differential equations and in order to reduce the number of parameters, I need to know the total concentration of multiple enzymes. How are enzyme concentrations usually reported in the literature so I can google it? Also, this does not seem to me to be a straightforward measurement for professional biologists, so how are enzyme concentrations actually measured or approximated? Thanks in advance!
I am interested in the following pathway:


texts: What is membrane-partitioning free energy? Can it be simulated?

texts:
Firstly, is there a strict definition of the "membrane-partitioning free energy"? It is banded around in membrane biology, but I have never seen it strictly defined. The only non-scholarly site that google shows is this Q&A on quora, and the answer there even has ambiguity in what is defined as partitioning in the membrane. This seems wholly unclear.

Furthermore, is it possible to study free energy changes upon partitioning in GROMACS, or with any other molecular dynamics simulations? If not, what are the methods I would need to use to determine the free energy of partitioning?

Links and citations for further reading on this topic are encouraged.


texts:
I am extracting DNA from cicada exuviae using ethanol precipitation combined with either NaCl 6M or Ammonium acetate. After DNA extraction, my samples have quite low A260/230 ratio such as in the attached picture. I suspect this might be due to left-over salt in my samples, since I dont use kits or phenol/chloroform/isoamyl in DNA extraction protocol. I proceeded on with PCR using 16S primers but received no bands.

Could you advice what potential contaminants could appear in the samples that prohibit PCR? As well as what could I do to improve this ratio? Thank you so much!


texts: What causes fingerprints to form and why is the pattern formed unique?

texts:
I've found research that suggests that the reason we develop fingerprints is because they aid us with feeling surfaces (Scheibert, et al. 2008) and not to increase friction  and help with the gripping of smooth objects (Warman and Ennos 2009).

One thing I am still curious about is at what stage of growth the pattern is formed and why a unique pattern is created in the fingerprint of each person (including identical twins). I assume it has something to do with the mechanism by which the patterns form, but I couldn't find any detailed research into this. Any insight would be very welcome.


texts: How does dsDNA become ssDNA when binding to a nitrocellulose membrane?

texts: I would like to know how double stranded DNA becomes single stranded when binding to nitrocellulose membrane in southern blots. Does it require a special reagent? Is denaturing a special property of the membrane itself?


texts: Why doesn’t p53 cause the repair of cellular DNA that has been altered experimentally?

texts: When scientists mutate bacteria or even embryos of lambs and other animals, why doesn't the p53 reverse whatever mutation the scientists cause? I know that the p53 stops the DNA from mutating and since the restriction enzymes essentially mutate the DNA, why doesn't the p53 stop it? Does the p53 gene have to be temporarily turned off?


texts: Reason behind colour of hibiscus and sunflower

texts: What is the reason for the red colour of hibiscus and the yellow colour of sunflower?


texts: How host defends against S. pneumoniae capsule?

texts:
The host response involves at least phagocytosis and probably localised acute inflammatory response at least after the colonisation.

I am thinking how the host can defend against pneumolysin which helps the streptococcus pneumoniae invasion.

How can the host defend against Streptococcus pneumoniae capsule?


texts: What effect has changing pH and salt concentration on protein complexes?

texts: I'm struggling to find peer reviewed literature that explains the effect of changing the pH and the salt concentration on protein/protein complexes in solution. What effect does the pH and the salt concentration have and what is the physical basis behind this?


texts:
I've asked this question, specifically because i've seen this question.

As we see in this diagram , G0 phase occurs after M phase and at a specific point within G1 phase.

Is there a meaning to saying "end" in this case?
What is the checkpoint for causing a cell to enter G0 instead of continuing with the cell cycle, in case of heart cells and neurons? (what exactly is "checked"?).


texts: How are 6 "fixed" CO2 molecules joined toegther as glucose?

texts:
When we study calvin cycle, we study it with 6 molecules so as to form 1 glucose in a single cycle as:

6 RuBP + 6 CO2 => 12 3-PGAL => 1 Glucose + 6 RuMP

But if we look deep, then we know that the molecules are synthesized one-by-one & 6 cycles give 1 glucose, but:

1 RuBP + 1 CO2 => ... => 1/6 Glucose + 1 RuMP

My question: What is actually this 1/6 glucose (organic carbon fixed from inorganic carbon and how are such 6 molecules joined together?


texts:
To clarify at first, I have very little knowledge in biology and paleontology so there might be very obvious things I overlook.

According to the evolution theory, there must be a graduate evolution process over millions of years such that the skull and the horns of the Triceratops gradually appear over time. However why there is no fossil record of such "intermediate" form between Triceratops and earlier dinosaurs? I mean there must be some intermediate dinosaurs that has a short skull that almost looks like a small mountain on the neck and very short horns. However based on my internet search I can't find any information that confirms existence of such intermediate dinosaurs.

I just want to know is there any such evidence of graduate evolution among paleontologists or the evolution of dinosaurs is still much based on speculation (without firm evidence)?


texts: How are flies able to extract nutrition in feces when the originating animal wasn't able to? What makes flies more capable?


texts: What's the difference between Ki and IC50?

texts:
I have just read this post at researchgate: "How to calculate experimental binding free energy from the IC50 value"

I am not be very sure about what the difference is between Ki and IC50. Could anybody explain?


texts: Problem on finding sequence of Taq polymerase

texts:
As i know, Taq Polymerase can be found in Thermus aquaticus, so i do a search for protein list of Thermus aquaticus and have this : http://www.ncbi.nlm.nih.gov/genome/proteins/1724?project_id=55053 . After filter for 'polymerase' i found a lot of protein named polymerase :

DNA polymerase beta domain protein region
DNA polymerase I
DNA polymerase III, alpha subunit
DNA polymerase III, beta subunit
DNA polymerase III, delta subunit
DNA-directed DNA polymerase
-.....

I don't know what they mean and which is the protein i'm looking for ?

After click on one of them i have the sequence not in A-T-G-X format :

ORIGIN
        1 msgvdallll gvelsraiit aysvyaivli lggflarlpt rweervealg gsfylagvil
       61 wryyaggday dldlflrasg mallvlprlv rvvlreyggg r

What does it mean and how to working with it ?


texts:
As simple as that, lentils beans and other legumes are sold both with and without husk, and often I make beans with the husk germinate in a jar.
Do those without husk germinate as well? Or are they simply dead?
I'm asking this because my girlfriend told me she's using de-husked legumes, but that they take longer and less of them actually do sprout.


texts: Ethidium bromide and mutagenesis on cloning

texts: When performing a DNA cloning, sometimes PCR amplicon is run in agarose and it is detected by ethidium bromide marking under UV light. After that, gel is sliced, DNA extracted from gel....... until eventually you have your transgenic organism. The thing is that when doing so, you use the very same DNA sample that was "contaminated" by ethidium bromide, so does this DNA you are using for transformation contain ethidium bromide? if so, how can it affect in numbers to mutation risk?


texts: How efficient is the human body at metabolizing food?

texts:
My friend and I were having a discussion over how "efficient" human digestion is. If a human ate a 1000 calorie hamburger, how many of those calories (how much energy) does the body process into usable energy (i.e. fat or other stores). I've heard things like "it's better to workout on an empty stomach because you will burn fat instead of energy from the food you just ate" - so from this I presume that storing energy as fat is less efficient than using the energy from digestion immediately (though in all honesty I'm not sure if that even makes sense.)

So, to summarize: how many calories of food does your body turn into usable calories via digestions? Percentages would be nice.

Bonus question: If the body does not process at 100%, does the FDA take this into account when labeling food products on their calorie content? If my Basal Metabolic Rate is 1800 calories a day, do I need to eat more than that since my body won't process all of the calories into usable energy?


texts: What is the correlation between hand and neck flexibility?

texts:
I am trying to understand this statement in the book, Mudras, Yoga in your Hands by Gertrud Hirschi:

  There is a direct relationship between the hands and the neck since the nerve paths run through the vertebral foramina in the arms, hands, and fingers.

Furthermore it is stating that neck flexibility is correlated to hand flexibility.

Where is the vertebral foramina and what is it?


texts: What is the difficulty with cloning and genetic engineering in humans?

texts:
I asked this question many years ago and was told by my molecular biology professor that humans were (simply) more complicated than goats.

So, I didn't get a straight answer, but supposing he told the truth, what's the problem? Or are people really more complex than goats, from an engineering or genetic standpoint?


texts: If we change our breathing rate so easily, then what is the point of measuring it?

texts:
When we are self-conscious of our own breathing, its rate changes very easily. Therefore, if it changes so easily, what is the point in measuring it?

Thank you for your time and effort


texts: Can a dividing cell that skipped DNA replication become cancerous?

texts:
Let's assume that a cell fails to replicate its DNA during the S Phase of the cell cycle. Let's also assume that the appropriate CDKs are inactive (perhaps due to mutation or lack of cyclin proteins etc.) and the G2-M checkpoint fails.
2 questions:

Will the Spindle Checkpoint fail due to not having duplicated DNA, or can mitosis complete and form aneuploid daughter cells?

More to the point, if mitosis can complete after a cell fails to replicate its DNA (irrespective of the answer to question 1), can the resulting cell (if viable) lead to a neoplasm or cancer?

My thought is no because the odds of having subsequent generations of cells experience similar losses of DNA via mitosis of un-replicated cells would eventually lead to mostly non-viable next-generation cells and the "uncontrolled" division would cease.

Though, admittedly, this assumption is dependent on the assumption that the original cell has a heritable issue that "disables" the appropriate checkpoints (vs some random fluke event) allowing the uncontrolled cell line to continue duplicating with un-replicated genomes.

I'm also not sure how ultrafine anaphase bridges (see Moreno et al. 2016) can be informative for this question.

I found a paper (Deshpande et al. 2005) that discusses cyclins and cdks in development and cancer, but their paper focuses on the transition form G1 to the S phase and stops short of discussing mitosis of un-replicated cells

Note: this might sound like a homework question, but I'M the one writing the assignment! In fact, it's an exam, and I'm trying to cover my bases for the answers I provide for a different cancer-related question to ensure there are not multiple correct answers.


texts: Do antibiotics attenuate immune response on subsequent exposure to same bacteria?

texts:
A healthy immune response to a bacterial infection includes "memory" to permit the body to thwart subsequent exposure to same bacteria.  What are the dynamics of using antibiotics on initial exposure to the bacteria regarding a possible degradation of the quality of this "memory" and thus the body's possibly compromised ability to fight a repeat exposure to same bacteria ?

I am not speaking of vaccines ... focus here is on bacteria


texts: I am wondering if there is any new information on which cells HPV is able to infect. Is it still limited  to squamous cells or are there other cells such as columnar cells it is able to infect?


texts: Why can't a human regenerate limbs like some other species?

texts:
When a person's arm is amputated, the arm will no longer be able to grow back. However, in salamanders, the arm actually grows back.

In comparison to a human, what is really happening to the cells in the wounded area in salamander ?


texts:
In early October I was on a holiday near the equator and got tanned. Now, roughly 3 months later, the tan on my face and arms has gone almost entirely where my belly, chest and legs are still moderately tanned. It seems that body parts that are exposed (to light) more than others seem to loose the tanning effect more quickly. Why is this? Or is there another reason?

I am not a biologist so I would appreciate an answer that is articulated in a way non-biologists can understand it.


texts: Growth hormone and insulin like growth factors are diabetogenic, so I assume that people with high growth hormone (say due to pituitary tumor) may be at high risk for diabetes.  Has any correlation been established between these two? I know that diabetes is a multifactorial disorder and so only a correlation may be established.


texts:
What tools are available to estimate the function and purpose of a gene ? I think the right approach is to find similar sequences of genes that we know the function of.

All the information I have on a gene is (for example):

KXN84633.1

and

>lcl|Query_208731:23119-24312
CTACAGACATATCCCATCCAGAAGAAATCTTTATCTATCGAATACCTTCGCGATAACGCGTATCTACGCG
CTCGAACAGGCCAAATAGCTGCAATGTTAAGGCTGAGGGATAGTATTTCCAAAAACCTATCCCGGCATTT
TGAGGTACATTTACTTTCTTCCGTATCTGGCCTGACTAAAAATCCTGCGTAGTCTCAAGGGTTTACATAT
ACTCATACGCCTATAATAACAGCTAGCGATTGCGAAGGCGCAGGCGAAGCATTTCGCATATCACCTATCC
AACCTACCACCCCCTCTCTCTCAAAAACTGACGCAAGTTCAGACGCAAATACCCCTATAGAGTTCTTTTC
ACGTCCTGCATATCTCACAGTCTCGCATCAACTTCATCTAGAATCCTTCACCACGGCTCTCTCTCGCGTG
TATACCCTTTCACCATGTTTTCGTGCGGAACGATCTATGACTGGACGACATCTGGCCGAGTTCTGGATGC
TTGAGGCCGAGTGGAACCTTGCAACGCGTTGCGATAGCTTAGAAGAAATTTGTGCCTTTGTGGAAGGCTT
AATTCGGACGTCGGTAGATCATGAGTCGCAGGATGTCAAGGCTCTGTGGGCGGAGAAAGGAGCGGAAGTA
GAGGAATTCAAGATGTTTCGTGCCGCATTTGACAACGCTCAGCCTTGGAGGCGATTAACATACTCGGATG
CAGTCGAGGCGTTGAGCACGGCTTATGTCAACGGACATCCTTTCGAATTCAAACCTGTCTGGGGCGAATC
ACTCTCGAGCGAACATGAACGTTGGCTGGCAGAGGTGTACGTTGGTGGACCAGTGTTCGTGACAGACTAC
CCTATCAAACTTAAACCGTTTTATATGCGGGTCAACGAAGATGGGAAAACCGTTGCGTGTTTCGATTTGA
TTGTACCTCATGCTGGTGAACTTGTGGGTGGAAGTGTGAGGGAGGAGAGATGGGATGTCCTCTCAAAACG
GATGGCAGAGCATGGATTGTTGCCTCACCCTGACCAGAATGAGGGTGCCCCAACTGATTCGACATATGAA
TGGTATCTGGATTTACGCAAGTATGGTGGAGCGCCGCATGCAGGGTTTGGTCTTGGGTTTGAAAGGCTGG
TGAGCTGGGTTGGAGGGATTGACAATGTGCGAGAATGCATCGGCATGCCTCGGTGGACTGGGAGAATGAT
TATG
>lcl|Query_208731:22646-23071
ATGCTCCTTCGCAGGTTATACTCGACTGCTGCACATCCTGCCAGGTTCAAACTACCGCCGACAATCAAAC
AGGTGCTTTCAGCTAATGGCAGCGAAAGTTCAGCGACATCAGTGACTGGCTGGATTAAATCTATCCGTAA
ACAGAAAAACATAACCTTCGCTGTAGTCAGTGATGGTACAACACCAGAGGGCCTGCAAGCAGTTGTGTCA
AAAGAACAGGGTACTTCCCCAGAAATGTTGAAAAGGTCAGTTCATCTCTCACAGCTCGAAACCGGAACAC
TCACCAATTGAAGACTTACGAACGGTACAGCAGTGCGGCTCACAGGAAATCTAATTCAGTCTCCTGGCCG
AGGTCAAGAATGGGAGCTTGTCATTCAAGAAGGTGACAAGAACGCTATCGAAATCCTCGGCGACTGTGAT
ATTGAC
>lcl|Query_208731:c22559-22323
ATATCACATTCAACATCCAGGGTAATGACATCGCCATGTCGCTAGACAGCGTCGACAATGACTTCCAAGA
AACACTCGTTCCCATCTCCACTGGAATCTCTCTGGAACTCGATCTTATCAAACCCCGTCAACCGCAAGAG
CAAGAGTCCAAACTAGCAATCTGTCTTCACCCCTGGTCTCGACTCGGAGGACGCAAAAGCGACCCGTGCG
GTGTCTTATTCCACGAGCTCAGGTCGA
>lcl|Query_208731:c23949-23902
CACGAACACTGGTCCACCAACGTACACCTCTGCCAGCCAACGTTCATG

obviously I am new to this :)


texts: What is the reason behind studying seroprevalence of a disease?

texts: Scientific literature on viral disease, specifically ones like Zika and Dengue, contains seroprevalence data. What is the reason behind understanding seroprevalence?


texts: As someone working with sequencing data and sequence files I was wondering whether is there a compression method / format for sequence / read files? Of course one can use general compressors like rar or zip to compress a fasta file, which is suitable for transferring data, but reading the sequence out of it is infeasible. Also I'm aware of BAM file format which is a block copressed gzip file of a SAM file, but as far as I know it is mainly used in alignments. But is there a compression for plain fastq(-like) files for storing millions of reads or a collection of sequences while being able to get sequence and quality info directly from the file?


texts: What winged insect is in this photo? Is it Axymyia furcata?

texts:
Posting on behalf of a neighbor who asked:

  Can anyone identify this insect? It's about 3/8" long. There are, it seems, hundreds flitting low over our lawn. There were none 2 days ago.

This is the Northern California Bay Area Peninsula.


texts: I found a purple mushroom that looked like this on a nature walk in South Carolina, USA today. This is not my picture, but one that looks exactly like the mushroom I saw. I have searched the internet, but I could not identify it. Does anyone know what this could be?


texts: What is the use of crystallized Photosystems from cyanobacteria?

texts: I read a lot of articles about techniques for the crystallization of Photosystem I and II from cyanobacteria. My question is what is the reason for that and what can you do with Photosystem crystals?


texts: Phenotype choice for one of a MZ twin pair in a genetic association study

texts:
I was having a discussion with a colleague and this question came up...

It is commonplace in molecular genetics studies to only genotype one of a pair of monozygotic twins (and then implicitly impute the other's genotype by assuming the pair is genetically identical).

My question is this: assuming a quantitative trait study, what should the phenotype be? Should it be the phenotype of the genotyped twin OR should it be an average of the two twins' phenotypes?

Example:

I genotype Twin A
Twin A has a phenotype score of 4
Twin B has a phenotype score of 6
Should Twin A's phenotype for the genotype-phenotype test be 4 (the individual's phenotype) or 5 (the average phenotype of the genome)?

Answers from experience and from theory welcome!

Thanks!


texts: Can creatures that can see color in completely different visible spectrum exists?

texts:
From wikipedia - "The visible spectrum is the portion of the electromagnetic spectrum that is visible to the human eye."

So humans can see the light from 400-700 nm and this is because our eyes can interpret/sense this little portion of the electromagnetic spectrum.

I wonder - could somewhere out there exist a creature which is possible to see different part of the spectrum ? I know that on Earth a creature can have a different visual spectrum "flavour" but I do not know whether it is possible the visible spectrum to be completely different - e.g. on some other planet can creatures exist that can say to see light in lets say  1500-2000 nm ?


texts: What kind of spider is this? It was very friendly and shy, we spotted it inside our house and we carefully took it to the forest. Hope it will be a nice environment for this kind of spider... One of my kids loves to play with spiders and I would like to be advised on what kind os species he can approach or not. Thanks in advance.


texts: design and assessment of qPCR primers for COVID19

texts:
I read the False Negative of qPCR test for COVID19 is high compare to CT scans.

https://pubs.rsna.org/doi/10.1148/radiol.2020200642

I was curious if experts can comment on why and what makes it difficult to design more accurate PCR given the genomes is out there.


texts: Why must the alcohol decolorizer be used for 30 seconds or less for Gram staining?

texts:
I had today a class in microbiology and my teacher said that the Decolorizer component is the critical one and cannot be more than 30 seconds.
The decolorizer has alcohol in high concentration, my lecturer says 95%.
I know that alcohol dissolves the lipid membrane, more exactly here for RBC which should be a similar situation here, not completely sure however.

What component is the critical one that you cannot keep alcohol on your bacteria samples more than 30 seconds?


texts: This plant is quite common in vegetations near swamp areas in Bangladesh. I have included multiple picture hope that compensate for the bad quality.


texts: After how many generations descendant is not more related to ancestor, than to a random individual in an ancestral population?

texts:
Descendant of n generation has on average 1/2n DNA of ancestor. (For example children have 1/2 DNA of parents and 1/4 DNA of Grandparents, After 10 Generation 1/1024 DNA and after 100 Generations 1/2100 DNA).

Is there a point (value of n) when descendant is no more related to ancestor and is similarly related to random individual from an ancestral population.


texts: Blood serum transfusions - could vaccines against the anti-A/anti-B etc. antibodies be derived, at least in theory?

texts:
People with the AB-positive blood type have all three of the A, B and RhD antigens present on their red blood cells, and no antibodies to these in their blood serum (aka blood plasma.)
This means that they cannot receive blood serum transfusions from people of other blood types, as their serum does contain these antibodies. In general, a person's blood serum contains antibodies for whichever of the A/B/RhD antigens are not on their blood cells, and no others.
Otherwise, an acute haemolytic reaction would occur.
The most-upvoted answer to another question on Biology.SE used a quote from Dean's "Blood groups and red cell antigens", chapter 5 to explain why these antibodies were present:

ABO antibodies in the serum are formed naturally. Their production is stimulated when the immune system encounters the "missing" ABO blood group antigens in foods or in micro-organisms. This happens at an early age because sugars that are identical to, or very similar to, the ABO blood group antigens are found throughout nature.

In a hypthetical future situation where the demand for blood serum transfusions was high, would it be possible to vaccinate young AB+ children against these antibodies? I'm thinking of injecting proteins similar to the antibodies, to train the immune system to produce "anti-antibodies". The memory-B cells would hopefully produce these fast enough and in large enough quantities to destroy the original antibodies and prevent ill-effects when a transfusion was given.
Would such a vaccine be feasible?
If not, would an immunisation relying on very small quantities of the actual antibodies (not enough to damage/agglutinate significant numbers of red cells) be viable?
I'm aware that if/when such antibodies pass through the placenta, they can lead to haemolytic disease of the newborn, so a newly-born child might be too young to receive such a vaccine. I'm imagining a situation where the number of such antibodies would not be high enough to cause these complications, or where the fake antibodies would not bond to the red cell antigens.
Source:
Dean, L. (2005). Blood groups and red cell antigens. 1st ed. Bethesda, Md.: NCBI.


texts:
Why can't mutated RAS get inactivated by GTPase?
Why don't we have any inhibitors for RAS-GTP binding?
Why is RAS undruggable?
How can mutated RAS be inactivated?

I had been researching on the topic and had a lot of doubts in the regard. Please provide me direction, as to where can I find answers to the questions and continue the research "how can mutated RAS be inactivated?"


texts: I've been reading about brain cancer lately, and something I've noticed is that the tumors seem to start in all tissues, except neural tissue. Am I missing something, or is there an explanation?


texts: Why even if all requirements for natural selection are met, it may not happen?

texts:
In the book written by John Endler Natural Selection in the Wild p. 4
it says that even if condition a, b and c are met, evolution by natural selection might occur,

  [...] , but not necessarily, [...]

See last paragraph of the image.
Endler, J. A. 1986. Natural Selection in the Wild. Princeton University Press.

I’m wondering in which case it’s possible that everything is in place for natural selection to occur, but is not having any effect.

It seems to me that if every condition of natural selection are met, there will absolutely a change in the phenotypic distribution? Why does the text say evolution is not guaranteed to occur?


texts:
I met this beautiful fellow when I was choosing my socks this morning. It seems I had found her cozy place. A stowaway, supposedly sneaked into my bag while camping, and me taking her all the way home. She just sat there for about a minute (probably just as tired as me, thinking "Duuuuuude, why did you wake me?"), then stretched her neck and and set off, searching for a calm spot to get her 5 more minutes.

Ca. 3 cm long. At home in Austria/Southern Germany.

I searched the internet a bit, and I think it's a female wasp, possibly Dolichovespula because of the pointy snout(?). I don't think it's a commom wasp, due to its size. Also no median wasp queen, because there's no red.
Maybe a tree wasp?

TL;DR: Can you help me identify this buzzer?

End of story:
After a lot of buzzing on her side, me chasing her with glass and cardboard in hand, and she dozing off two times in very uncomfy places (I was a bit embarassed about how un-hospitably dusty everything was), she settled for a box of clothing and snuggled her way into my shirts. I praised her sense of Cozyness, but then carefully emptied the box piece by piece outside and found her inbetween a flowery garment. She slowly stuck her head out from the folds ("DUUUUUUDE, again?!") and flew around the terrace for a while. I hope she's found a snug place out there.


texts: Definitions and examples of some math-releated ecology branches

texts:
I would like to have an example of application and a brief description/definition (two or three lines) of the following fields. I would like to understand the exact differences between them. Other related informations are also extremely appreciated e.g. if these are fields in growth, the name of the best researcher in that field, best institution etc.

Computational Ecology;
Mathematical Ecology;
Numerical Ecology;
Statistical Ecology;
Ecoinformatics.


texts: How can you stabilize enzymes in pellets made from microcrystalline cellulose?

texts:
I want to make pellets consisting of mainly the following:

microcrystalline cellulose
saccharose
rice starch
ascorbic acid
glycerin

and an enzyme as active component.

Is it furthermore necessary to add protease inhibitors or other stabilizers to remain the activity of the enzymes for a periode of at least one year OR is the dry environment conservation enough?

The enzyme is called histaminase and is extracted from kidney cortex through a series of centrifugation, filtration and dialysation. To be more precise, it is a liquid protein extract containing small amounts of this enzyme. No buffer etc. is added to the protein extract so far. The whole purification process is done at 4°C. I don't know how long the enzyme is stable without further preparation. Probably not that long because some proteases should remain in the natural homogenate from porcine kidney cortex. The other components of the pellets are of pharmaceutical quality. The aim of this experiment is to feed the pellets to dogs with digestive complaints. For this purpose the pellets will get a enteric coating to survive acid environment of the stomach.


texts: Can citric acid be used as fungicide in banana based fly (Drosophila melanogaster) food?

texts: I am experimenting with a banana based fly food for better larval synchronization. Instead of propionic acid, I am going to use (added) citric acid as fungicide. Is there any downside to this approach?


texts: Why and how does complexity usually tend to increase through time?

texts:
The question of complexity is classic in the very first lectures of evolutionary biology where the teacher usually tries to tell the students that complexity does not necessarily increase and that humans are not more complex than other organisms.

My questions are:

Why does complexity tend to increase through evolutionary time?
What are the different hypotheses to explain this pattern?

When writing "Mass extinction" on google image, we find many graphs displaying the number of families (or other taxa) through evolutionary times with the five mass extinctions. What would it look like to draw such graph replacing the family richness in the y-axis by :

Mean complexity among all living things?
Complexity of the most complex taxon?

I suppose that anyone who wishes to answer to this post will necessarily need to define the words "complexity". He or she might define it in terms of number of genes, number of metabolic pathways, length of DNA sequence, number of cell types, some kind of index taken from information theory. When asking my questions I had in mind a definition close to "number of genes" or "number of metabolic pathways".


texts:
Touching an object activates a nerve - something that can be observed by scientists.
Scientists can also trace the resulting "signal" through your nerves to your brain. They may know which portion of the brain is activated.
The next step is to think about the thing you just touched.
Does this process generate something physical that scientists can detect? Or is though, so far, "invisible"?
To put it another way, do scientists know what "thought" is made of?


texts: How do scientists know what part of DNA does what?

texts:
There are many genetically engineered foods and animals and I was wondering, how do scientists know which part of a DNA to cut in order to produce the desired result. For example I want to make a tomato more durable and to do that I cut the durability part of the DNA of something long lasting and put in the tomato. I'm not sure, but I guess that's not how things work. If I wanted to make a human with tiger arms, I'll just cut the arms DNA part of the tiger and put it in the human DNA, no? I'm sure it's much much more complicated than that.

P.S - I'm just 16 and interested in biology, I do not posses any university/professional academic knowledge.


texts: What can give rocket salad (Eruca Sativa) a fish smell?

texts:
I bought an 'already washed' plastic tray of rocket salad (arugula, or Eruca Sativa) enclosed in a sealed plastic bag. It has been kept in the refrigerator for four days. When I opened it, some 12 days before the "best before" date,  I noticed a strong smell of fish.

I am a regular consumer of this sort of vegetable, I also have some in my garden, so I know how it smells. Yet, by searching on the net I realized that other people have lamented this fish smell in their pre-washed arugula salads.

I am wondering now where does this fish odor come from? Can it come from the plant itself, or is it a side-effect of industrial washing? What exactly is giving this smell? Bacteria, molds, natural decomposition of the plant's essences, or something else?

(Following my instinct I threw the salad away, but I did taste a few leaves and it did not taste 'bad' or 'foul'. It was just the smell that was off.)


texts: Is it possible to have action potentials in cells lacking both dendrites and axons?

texts:
I'm reading Kandel. Chapter 3 states the following:

  Because the initial segment of the axon has the highest density of voltage-sensitive Na+ channels and therefore the lowest threshold for generating an action potential, an input signal spreading passively along the cell membrane is more likely to give rise to an action potential at the initial segment than at other sites in the cell.

I know it is possible to have dendritic spikes, which is an action potential given a much stronger input to open enough Na+ channels. But can there be a different action potential, not axonic nor dendritc, given that enough Na+ channels locally open in the cell membrane?

I've seen some papers talk about "somatic action potential", but its meaning and how it works I don't understand.


texts: How to inhibit formation of specific antibodies (to antisera)?

texts:
Is there a way to inhibit an antibody response to a specific antigen using immunosupression? I am interested in reducing the anti-antibody formation to animal antibodies such as murine antibodies in antisera.

I have read that there are ways to decrease the immune response to antisera but haven't found a detailed paper on how they work.

Update 12/3/2014: Would this work? http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2374127/pdf/0100491.pdf
Although it is streptavidin, could a similar process be used for antibodies?


texts: Do transposons usually jump from one chromosome to another?

texts: If it is usual occurrence, does it mean that my one gene can change its location from one chromosome to another?


texts: What are the microscopic mechanisms of plant branching?

texts:
For a long time I've been idly interested in how the shape of a complex organism gets determined during development at a microscopic level. Recently I've realized that plants could be a good place to start trying to understand that, because the structure of even a quite complex-looking plant can sometimes be described by a few simple behaviors. Here are some examples.

My radish plants have a single base where all foliage grows from. After it's first two seed leaves, it grows some number of large rough leaves which all descend to the same point. No other branching ever takes place.
My pea plants have only one long stalk, which grows symmetrical pairs of leaves at regular intervals. Occasionally, the base of a leaf pair spawns a mini-stalk, never more than 3 or 4 leaf-pairs long, ending in a "claw" of three tendrils. Most of the time, one of the three tendrils will split again in three (always the one aligned with the "top" of the stem, as determined by leaf orientation)  .
My fennel plant has thick bases to its stems which each extend a few inches before branching starts. At that point, it branches at regular intervals in symmetric pairs of fronds, which in branch the same way. Those third-layer fronds branch at regular intervals but alternate sides, and there are always exactly four layers of branching no more and no less.
My basil plants seem roughly able to grow branches in any advantageous spot, with no rigid rules or geometric behaviors like the other examples.

My background is in mathematics, and all my knowledge of biology is dated to high school. I've always been confused by how DNA is presented as a "list of proteins", when it is clearly so dynamical and not static: each cell type only produces some of those proteins, and those proteins can in turn determine what proteins it's children produce, I guess, and this can create a rich (non-linear) hierarchy of tissue differentiation out of a linear list.

For a really complex organism like a mammal I guess that our understanding of how DNA gets actualized is phenomenological (i.e. we can tell that gene X correlates with macroscopic trait Y, even if we have no idea what the signalling mechanisms are behind it and which cell types produce a relevant protein and when.)

But is this true also for plants, or do we have a deeper understanding of what proteins differentiate, for instance, the four stalk types of a fennel plant, and why each type can only produce the next one? I think simple animals like sponges and nematodes and cnidaria probably would be as helpful as (or more than) plants, but as a gardener I see these plant geometries every day and am fascinated by them.

Does anyone know of a good reference, book or online, that discusses these topics? I'm okay with something a little out of my technical depth - I'd prefer a difficult answer to an incomplete one.

EDIT: Leaf architecture is also interesting, and probably inseparable from branch architecture on some level, but I focused on stalks and branches probably because I don't have the terminology to meaningfully describe leaf architectures.


texts: Does cortical nephron has just thin ascending loop of Henle?

texts:
Guyton and Hall , South Asian edition states that, in Table 76-1 that ascending limb of loop of Henle has thin segment only. But, none diagram in book or internet explain this.
Can any one explain this difference in text and diagram please?

Note: AK Jain Textbook of physiology 6th edition. states on Table 55.1

The descending limb of loop of henle contains a thin segment whereas ascending limb contains a thick segment.

This does explain diagram a bit.
This makes Guyton contradictory.
Edit: From comments, no where the table states part of loh in medulla.


texts: Query for gene upregulation in cBioPortal

texts:
there! Could anyone help me with some biostatistical problems using cBioPortal.

We are looking for cell lines with upregulation of certain genes on cBioPortal. My supervisor is teaching me to use this website because I have no prior experience. She is using EXP >= 0.5 to define upregulation. Although I am of no bioinformatics background, my opinion is that 0.5SD away from the average is not strong enough to define an upregulation. I think it better to use EXP >= 2 or 1.5. I have discussed this with my supervisor but she insists using EXP >= 0.5.

Does anyone have any experience with this issue since I am still not convinced by what I was told. Thanks a lot!


texts:
Trees in a forest, alongside the fungi, animals and plants that live there in, capture atmospheric carbon dioxide and store it inside their tissues and in the soil as humus.

It is possible to estimate the amount of carbon stored in some portion (say 100 square meters) of a climax forest?

This should depend on the specific biome, for example Eucaliptus and Pine forests seem to contain less organic matter than broad-leaved tree forests in temperate regions.

PS: A slightly more speculative aspect of this topic is to evaluate weather reforestation can contribute to lower the amount of carbon dioxide in the atmosphere.


texts: Where to put the gene after eukaryotic promoter for best expression levels?

texts:
As far as I know there is an optimum distance between a promoter and the gene for the best expression levels. What is that distance for common promoters like CMV, SV40? If you have a first hand experience about this (e.g. if you have cloned the gene way downstream of the promoter and didn't/did see expression) and share it I will be grateful.

If you have comprehensive knowledge for other promoters please feel free to add them in the list too; they don't need to be common. I just want to hear people's experience on the subject.


texts:
(a) At the moment of fertilization a female egg is about 100μm in diameter. Assuming that each lipid molecule in the plasma membrane has a surface area of 10-14 cm2 , how many lipid molecules are there in the egg plasma membrane if 25% of the surface is protein?

(b) Each fertilized egg cell (zygote) divides 30 times to produce all the eggs that a female child will need in her lifetime. One of these eggs will be fertilized giving rise to a new generation. If lipid molecules are never degraded, how many lipid molecules have you inherited that were synthesized in your grandmother? Assume for calculation purposes that the lipid molecules synthesized by your grandmother is equally divided between the daughter cells at each cell division.

My answer:
 (a)  Given, a female egg is about 100μm in diameter.  Radius = 50μm
           Each lipid molecule in the plasma membrane has a surface area of 10-14 cm2.
           25% of the egg surface is protein and 75% of the surface is lipids.
           Therefore, Surface area of egg is = 4π(radius)2
                                                                                =  4*3.14*2500*10-12
                                                                      =  3.14*10-8 m2
                                Area for the presence of lipid molecules = 3.14*10-8 *3 / 4
                                                                                = 2.355*10-8 m2 = 2.355*10-8 * 104 cm2
        Number of lipid molecules in egg plasma membrane = 2.355*10-4/10-14 = 2.355*1010 molecules

(b) Each fertilized egg cell divides 30 times into 2,4,8……230 cells. Assuming that the lipid molecules     synthesized by our grandmother is equally divided between daughter cells at each cell division.
•   After 30 divisions we have 230  cells synthesized in grandmother
                      Initially the zygote has 2.355*1010 lipid molecules from above calculations.
                      Therefore, each cell has 2.355*1010/230 = 21.93 molecules.
•   After mother takes birth, she inherits lipid molecules present in zygote, that is a single cell

Number of lipid molecules that is inherited from grandmother by mother is 21.93 molecules.

This zygote undergoes division for 30 times.
Thus, each cell inherits = 21.93/230
                                          = 2.0424*10-8 lipid molecules from zygote

•   Finally, a single cell in mother undergoes the zygote formation that leads to our birth.

Hence, we have 2.0424*10-8  lipid molecules inherited from our grandmother.

Can anyone please confirm it?


texts:
In this link, it is suggested to use high-pressure cryonics to freeze living cells, tissues or small organism as opposed to various and potentially toxic anti-freeze agent. The core idea is that over a certain pressure, ice is anamorphic and will not form ice crystals. Thus, organic manner will not be destroyed by said crystals.

Detailed information about the proposal can be found at this link:

https://www.benbest.com/cryonics/pressure.html

I have considering self-financing the experiment. Could anyone chip in with some advice? Do you see any red flags, design tips, etc.?


texts: Why do buffalos not leave the lion alone?

texts:
In the Buffalo Kill Lion - The Stronger is The Winner video the buffalos seem to be attacking an incapacitated lion.

Why would they do that?

They seem to risk injury for no gain (they don't eat lions).


texts: What makes certain obligate anaerobes viable in fermentation starter cultures?

texts: If Propionibacterium are obligate anaerobes (to wit, poisoned by oxygen), what makes 'Dairy' or classical propionibacteria (e.g. P. shermanii, P. jensenii, P. acidicpropionici, et al) viable in Fermentation starter cultures?


texts: Using RNA-seq to compare gene expression across patients instead of between Control and Experimental conditions

texts:
I am working with RNA-seq data from the Cancer Genome Atlas TCGA and I have been reading about how people have compared gene expression levels measured by RNA-seq. Many of the papers I have read talk about "differential expression" for comparing each gene's expression levels in the Experimental and Control conditions.

In TCGA data, I typically have a patient cohort who have had the mRNA in their tumors sequenced just once so there is no Experimental-vs-Control dynamic. I am interested in finding which patients' tumors show gene-expression that is significantly higher than the rest of the cohort but I have not had any luck finding literature describing this kind of comparison. I'm thinking maybe I can apply existing differential expression techniques to my situation but that seems cumbersome and not-necessarily appropriate so thought I'd ask the community here if there's a better way of finding which members of a cohort are outliers for specific genes.

Also: all of my RNA-seq data has already been RPKM normalized for me. I have been advised that using RSEM instead would be better for comparing gene expression across multiple samples but, for logistic reasons, I'm probably stuck with my RPKM-normalized expression levels.

Fundamentally, I'm looking for the best way to compare gene expression across samples to determine which samples have outlying high/low gene expression. Intuitively, I figure I could just compute median z-scores for each gene's expression levels within my cohort and consider anyone with a |z-score| greater than 2 to be an "outlier" but I haven't found any literature to support this kind of approach either.

Any suggestions, papers, or advice will be greatly appreciated.


texts: Is it possible for a prion to have a short incubation period ie 1 week or 1 month?

texts: I know that all prions so far have long incubation periods but is there a possibility for one to have a short incubation period, is there any evidence that suggests this is possible. Thank you


texts: Why does 4-thiouracil labelling to map RNA-binding proteins cause a T-C change?

texts:
I am now reading a paper about the purification and identification of mRNAs and its RNA binding proteins by using UV crosslinking and immunoprecipitation. I came upon this sentence which puzzled me

  Up to 28% of all uridines present in 3' UTRs showed diagnostic T-C
  changes in the protein occupancy profiling sequence reads. This number
  is reasonably high, considering observations that typically only one
  of a few uridines in RNA binding sites when substituted by 4SU,
  crosslinks to proteins.

What I do not understand is why does 4-thiouracil (4SU) labelling in the cell show T-C changes. Would the uracil-adenine base pairing not be affected?

How does the 4SU labelling really work?


texts:
After I googled 'sigma TF' I stumbled upon two papers(only).
From a paper:

Sigma factors (sigmas) are bacterial transcription factors that bind core RNA polymerase (RNAP) and direct transcription initiation at cognate promoter sites.

and another paper had the title -

Specific binding of the transcription factor sigma-54 to promoter DNA.

However this contradicts with my book- Principle of Genetics Snustard and Simmons:

Unlike their prokaryotic counterparts, eukaryotic RNAPs cannot initiate transcription by themselves .... require the assistance of protein transcription factors to start synthesis.

Is it a TF?
Note: From what TFs are, sigma factor seems to be a TF to me.


texts: What information can Uniprot give me about phosphorylated forms of proteins?

texts:
I have a list of proteins formatted like this:

Protein Name        Gene Name
4E-BPI              EIF4EBP1
4E-BPI_pS65         EIF4EBP1
4E-BPI_PT37_T46     EIF4EBP1
53BP1               TP53BP1

Its my job to pull the following from Uniprot:

Subcellular Location information (this is easy)
Information about phosphorylated forms

The first thing I did was compile a list of Uniprot IDs for each gene's human form that I could plug into the Upload List function.

Next, I used Uniprot's "Customize Results Table" page, to add the "Subcellular Location" column to the output. Do you know columns will provide information about the phosphorylated forms of these proteins? I added columns PTM > PhosSite and PTM > PhosphoSite but they return the Uniprot ID or nothing at all.

Is there somewhere else in Uniprot that I can look for information about phosphorylated forms of proteins?


texts:
Which is the strongest muscle of human body ?

Confusion b/w Masseter muscle (Muscle of Jaw) and Tongue and Muscle of Heart and Muscle of Uterus.


texts: What happens when too much sodium flows in the cell due to a faulty voltage-gated sensor? What about too little?

texts:
The activation gate opens, signaling depolarization. Eventually, the inactivation gate closes, ending depolarization and beginning repolarization.

What is the physiological impact of the inactivation gate remaining open too long, letting in too much sodium into the cell than a normal action potential? This would raise the magnitude of the action potential.

What would be the impact if it remained open for too short a time?


texts: Is there an advantage to having cellulite

texts: There are many ads nowadays advertising cellulite removal, and it causes me to wonder if there is an advantage to having cellulite or if it is just a result of too much fat unevenly spread?  Is it structurally more efficient at storing energy or providing insulation?


texts: Biomedical consensus on human aging and lifespan

texts:
Medical technology is improving quickly. Unless there is a global disaster and human progress is set back significantly, e.g. by an asteroid or a global nuclear war, there will come a day when humans can live indefinitely. This does not mean infinitely- people will still die in vehicle accidents, get murdered, etc. Also, at least at first, access will be prohibitive due to costs and possibly outright selection/rejection of patients.

Based on trends in the progress of biomedical research, what is the consensus in the biomedical research community for approximately what year will the average person vs. a very elite person be able to get treatment to live indefinitely?


texts: Proteomics data Vs Transcriptomics data?

texts:
I want to use either of Proteomics or Transcriptomics data for integrating it into my kinetic model. Before proceeding, I want to know what are the advantages of using either of them so that I could make an informed decision on it!

Many studies have shown that the best we can do is integrating both transcriptomics and proteomics data with our kinetic model, but I've some time constraints and have to proceed with only one of those.

My effort and findings: I've found from discussions with researchers that gathering transcriptomics data has an amplification step which increases the chance of finding a particular one whereas gathering proteomics data has no such step but has fragmentation and then rejoining which creates many problems(such as splice variants etc) and thus leads to a loss of data. But a PostDoc told me that even after the loss of that data, I'll get more information from Proteomics data.

I want to know such type of points and want to know if these are valid or not!


texts: Vitamin and mineral contents of common fruits

texts:
I'm looking for nutritional data, mostly vitamin and mineral contents of common fruits, such as apples, bananas, oranges, kiwis etc.

Are there scientific (published and peer-reviewed) sources that list or compare those? I spent an hour on Google Scholar but most of the sources there discuss only a small aspect (e.g. vitamin C content) or compare different states of fruits (frozen, fresh, canned). I'm not well educated in human nutritional aspects so I may overlook this one keyword to search for.

I'm aware of tables on the Internet discussing these aspects but I need a solid scientific basis.


texts: Characters do not make the genus, but the genus gives the characters?

texts:
In his Origin of species, in the chapter entitled 'Mutual Affinities of Organic Beings: Morphology: Embryology: Rudimentary Organs', Darwin, speaking of the nature of classification systems of living organisms, writes:

  Such expressions as that famous one of Linnaeus, and which we often meet with in a more or less concealed form, that the characters do not make the genus, but that the genus gives the characters, seem to imply that something more is included in our classification, than mere resemblance. I believe that something more is included; and that propinquity of descent, the only known cause of the similarity of organic beings, is the bond, hidden as it is by various degrees of modification, which is partially revealed to us by our classifications.

What does he mean by  "that the characters do not make the genus, but that the genus gives the characters"?


texts: How can I pare down a PDB file in Python to only include specific residues?

texts:
I'm trying to make a script that will take a MTZ file (reflections), convert it into a CCP4 map, then pare that map down to only encompass a desired area to cut down on the size of my PyMol session files so they're email-able (a.k.a. not 200 MB) and ease the burden on my POS computer.

I currently have a Python script that can fft (CCP4) to create the map and mapmask to fix unit cell tiling issues.  What I want to add now is something that can take a PDB file and strip out most of it except, for example, residues within 10 Å of #123.

I've been looking at ProDy, but not quite sure where to start.  I would also be open to using something in the CCP4 toolkit.