Why don’t different organisms have nucleic acid genomes containing different bases and sugar? All organisms contain genetic material. Be it DNA or RNA, both of them have a fixed pentose group (deoxyribose and ribose). Also they contain the same types of nitrogenous bases, Adenine, Thymine(or Uracil), Guanine, Cytosine.
What makes ribose and these notrogenous bases so good that among all the molecules in our pre-historic chemical pool, these selective compounds made our genetic material.

Why don't different organisms have different bases/sugars? I understand that we all have a common evolutionary ancestor so the the genetic material will be similar. But mutation is possible, so why is that there are no nucleic acids found naturally that are made of different bases or sugars? Just for example, if we had a hexose like glucose for the sugar instead of pentose..

It sounds like you are confused about how Darwinian evolution "works".  For example, as we survey the current life forms in this biosphere there is absolutely no evidence that these species (or their molecules, which you refer to) are optimized in any way, shape, or form.  All we can state with any certainty is that at some time in the past, during one, or more, selective events, all the species that used ribose, deoxyribose, and the five common bases (A, C, G, T, and U) for their genetic material, survived to reproduce, and contribute progeny to the next generation.

If that putative selective event was different, then perhaps all the pentose-based species would have died off, and we would all have hexose-based genetic material.

We don't know how many different genetic material recipes were tried out before this one "won".

Evolution can only work on, or select, or select against, the current batch of organisms.  It is not an optimization algorithm, it is a filter that lets variants through.

It may well be that our genetic material, for example, replicates faster than the other candidates. That could be a selective advantage, but it doesn't have to be.

So what are you really asking here (since your original question contains incorrect assumptions)?


Plasmid gene knockout How do delete a single gene encoded in an operon on a plasmid using E. coli? Could you use the same principle as when knocking out a gene from the bacterial chromosome which is e.g. suicide vector-derived allelic replacement through homologous recombination?

Thanks for your response.

Well the simplest way is to cut the gene at the both ends from operon by means of proper restriction enzymes but in case that you get more than one recognition site then you can use microRNA or proper oligo to make a hairpin loop and break that part
If you only want to silence the operon then you just need to cut it nearly at middle of the gene and ligate it with a nonsense sequence, then it will loose it's functionality.


Why do gram-negative bacteria attack the digestive system more than gram-positive ones? I was researching for a biology project on the subject of contagious infections of the digestive system (mainly the intestines) and almost all of the bacteria that came up (E.coli, Shigella, Cholera, etc.) were gram-negative. Is there is reason that that type effects the digestive system so often or is it coincidental?

Gastrointestinal infections can be caused by Gram positive and negative bacteria:

Gram-positive:

Staphylococcus aureus
Clostridium difficile, botulinum and perfringens
Listeria monocytogenes
Bacillus cereus

Gram-negative:

Salmonella enteritidis and typhi
Campylobacter jejuni
Shigella
Escherichia coli
Vibrio cholerae and parahaemolyticus
Helicobacter pylori
Yersinia enterocolitica

Any part of the GIT can be infected by G+ or G- bacteria:

Stomach: S. aureus (G+), H. pylori (G-)
Small intestine: Bacillus cereus (G+), Salmonella enteritidis (G-)
Colon: Clostridium difficile (G+), Shigella (G-)

Certain bacteria typically affect only certain parts of GIT: H. pylori and S. aureus affect mainly the stomach; C. difficile affects mainly the colon.

Anyway, infections of the gastrointestinal tract are much more commonly caused by Gram negative than positive bacteria (Stat Pearls, 2019).

From the pathogenicity viewpoint, the main difference between Gram-positive and negative bacteria is that G+ bacteria produce exotoxins (which are proteins that bacteria secrete into their environment), while G- bacteria produce endotoxins (which are lipopolysaccharides as parts of bacterial walls). The differences between endo- and exotoxins (microbiologyinfo.com):

Endotoxins are heat stable, so they are not destroyed by cooking, they don't need specific receptors, they don't trigger antibodies and there are no vaccines against them.
Exotoxins are heat unstable, they trigger antibody response and have specific receptors in the GIT.

More than 80% of skin infections is caused by Gram positive bacteria, such as Staphylococci and Streptococci (Clinical Infectious Diseases).

75-95% of uncomplicated urinary infections (Microbiology Spectrum) and most sexually transmitted infections (Clinical Laboratory Science) are caused by Gram-negative bacteria.

Respiratory infections are caused by both Gram-positive and negative bacteria (Lumenlearning).

So, the only pattern I see is that in dry/air-exposed areas (skin, respiratory tract), most infections are caused by Gram-positive bacteria, and in wet areas (gastrointestinal and genitourinary tract) by Gram-negative bacteria. This doesn't mean that there is any actual biological mechanism behind this pattern, though.


Do plants have preference for the form of nitrogen as nutrient? In the nitrogen cycle (ecology), it is usually described that plants can use nitrogen in the form of ammonium (NH4+) and nitrate (NO3-). Do plants prefer one form of nitrogen over the other?

Quoting verbatim from this site. The reference is not really a scientific article but you can check the references it cites. Some were not in English so I did not check. However these points are fairly logical

  Nitrates are the preferred nitrogen source:

  Non-volatile: unlike ammonium, nitrate is non-volatile, so there is    no need to incorporate it in the soil when applied by top- or side dressing, which makes it a convenient source for application.
  Mobile in the soil - direct uptake by the plant, highest efficiency.
  Nitrates synergistically promote the uptake of cations, such as K, Ca    and Mg, while ammonium competes for the uptake with these cations.
  Nitrates can be readily absorbed by the plant and do not need to    undergo any further conversion, as is the case with urea and ammonium, before plant uptake.
  No acidification of the soil if all the nitrogen is applied as    nitrate-nitrogen.
  Nitrates limit the uptake of harmful elements, such as chloride, into    large quantities.
  The conversion of nitrates to amino acids occurs in the leaf. This    process is fuelled by solar energy, which makes it an energy-efficient process. Ammonium has to be converted into organic N compounds in the roots. This process is fuelled by carbohydrates, which are at the expense of other plant life processes, such as plant
  growth and fruit fill.

Many plants can carry out nitrification but this is not universal. From this article:

  Nitrification is sometimes considered so universal and rapid that
  applications of NH4-N are considered equivalent to
  NO3-N. This is not true in many forest, orchard, and
  grassland soils.

However, nitrate being more soluble is susceptible to leaching and wash off, care has to be taken when using nitrate based fertilizers. From the previously mentioned paper:

  Unlike the positively charged ammonium ion, which is relatively
  stationary because of its adsorption to organic matter or clay
  particles, the negatively charged nitrate ion is freely mobile in the
  soil solution (166). Thus, leaching and denitrification primarily
  involve a loss of NO3-N (171). Inhibition or retardation of
  nitrification of applied NH4-N can reduce nitrogen losses,
  increase efficiency of applied N, and establish a predominantly
  ammoniacal form of nitrogen available for plant uptake (105, 171,222,
  232).


How do I compare the variance of a distribution of species in one area versus another? It's possible that this question is better suited for stack overflow, but I think the ecologists on this site might be better equipped to answer it.

I'm trying to study two geographically-isolated populations of the same species. Inspecting the distributions, I see that both are bimodal (there's some seasonality to their occurrence), but the peaks in one population are much higher and much narrower (i.e., the variance of the local peaks is smaller).

What sort of statistical test would be appropriate to determine whether these differences are significant?

These are just some preliminary ideas...

I think you should look at the seasonal distributions separately, since the bimodal distribution is the outcome of two fairly separate processes. The two distributions might also be controlled by different mechanisms, so that e.g. winter distributions might be more sensitive to yearly climate. If you want to look at population differences and reasons for these I think it is therefore more useful to study seasonal distributions separately. An exploratory analysis could be to compare distribution percentiles (north/south and east/west coordinates) to look at range edges, or to use a fixed number of edge observations to establish borders. The weighted centre-point of population distributions can be used to look for differences in overall position. If you have grid occurences, percentage overlap between species/populations could maybe also be useful.

If you haven't already, you look also look at Maxent, which is a widely used software for modelling species distributions and habitats. Look at Elith et al. (2011) for an overview. If you want to look at changes over time (even if this doesn't seem to be your main point) you should also check out dynamic occupancy models that use occurrence records to model species distribution while taking detectability into account, e.g. MacKenzie et al. (2009).

As for a simple test for differences in variance (basically a test of homoscedasticity), there is Levine's test, which is used to compare variances of distributions between groups. Bartlett's test is an alternative, but Levene's test is supposed to be more robust to non-normality. In R the Levene's and Bartlett's tests are found in library(car). However, these are only suitable for unimodal distributions so, again, you should look at seasons independently.


Does malaria have a reservoir host? Can warm blooded vertebrates other than humans act as reservoir hosts for malaria parasites? I'm mainly interested in Plasmodium vivax and possible reservoir hosts in the wider area of Europe/ Eurasia.

There are 5 species of Malaria the can infect humans, and Chimpanzees and gorillas have also been found with 5 species, including vivax and falciparum.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4089193/

The parasite can go dormant in the liver for days to years, causing no symptoms and remaining undetectable in blood tests. They form what are called hypnozoites (the name derives from "sleeping organisms"), a small form that nestles inside an individual liver cell. The hypnozoites allow the parasite to survive in more temperate zones, where mosquitoes bite only part of the year.

Cows are known to carry falciparum protozoa, which has at least four reservoir species. (cows, chimps, gorillas, humans) Human with sickle cells also act as a reservoir in a different way, perhaps more or less invisible or innocuous, i haven't studied recent research, and sickle cell may also have some effect in cows and chimps and gorillas.


Evolution and different number of chromosoms? (a non-biologist) I understand that a species becomes a different one slowly and in a continuous way. However, the different number of chromosomes is bugging me. Chimpanzees, for example, have 48 chromosomes whereas humans have 46.

I have few guesses which haven't satisfied me at all:

The species are not that different, despite of their different
number of chromosomes, and capable of breeding. The offspring is
somehow healthy and is also capable of breeding. But doesn't that
make the offspring sterile?
The other possibility is, at some point multiple offspring in a
    population formed with, say, 46 chromosomes and the breeding took
    place among them. Even though it doesn't sound impossible to me, what are odds really?

Can someone provide an insight to a non-biologist?

Speciation doesn't happen from one generation to another, it is a slow and continuous process, and for each changing that is kept by natural selection, there are millions of changes that resulted in less functional phenotypes and were negatively selected, and another million of changes that were lethal hence soon aborted (e.g. a mutation that causes an embryo to die even before a fruit or animal can get any development). So it might be possible that many chromosome number changes are taking plane in many organisms, but they  never will estabilsh in their populations. On the other hand, some numerical changes (and all the genetic processes that follow any change) may result in a good fit, and the individuals survive, establish and reproduce. But keep in mind that it is a slow and continuous process.

Theoretically, if among Chimpanzees, multiple offsprings outcome with 46 instead of 48 chromosomes:

In a theoretical scenario: They could be able to reproduce only among themselves (the 46-chromosomed-individuals) and, with time, accumulate some differences in relation to the 48-chromosomed-Chimpanzees, and them they would be named as another species.
In a theoretical scenario: In some conditions, they might be able even to reproduce with 48-chromosomed-Chimpanzees (e.g. if this numeric change resulted from fission of one chromosome, and when the two gametes meet, the two half chromosomes of one parental pair with the whole chromosome of the other one... That is not probable for animals, but happens a lot in plants)
If you are asking if they 46-chromosome chimps would crossbreed with humans... well, I believe they have accumulated too much differences in their genotypes and thus would no be compatible even if they have the same chromosome number. It happens that having the same number is not the most important factor allowing or preventing species to crossbreed. There are many barriers to hybridization, e.g. the lack of biochemical recognition between egg and sperm resulting in no embryo formation... in cases that embryo is formed, it may not develop, it may develop poorly, or it may develop but the offspring comes out compromised and live shortly. Another example that chromosome number does not prevent crosbreed is the mule, which is the offspring of a female horse (64 chromosomes) with a male donkey (62 chromosomes). That's because even having different chromosome numbers, they are still quite simmilar in a genetic perspective.

All that sayd, the odds that Chimps would loose two chromosomes, stablish in the population and reproduce with humans are really really really low... I would say that's impossible. But simmilar phenomena are possible and even quite common in plants (just so you know that it exists)

If you want to learn more about chromosome number changes, I recommend this link: https://www.ncbi.nlm.nih.gov/books/NBK21229/

(Modern Genetic Analysis. Griffiths AJF, Gelbart WM, Miller JH, et al. New York: W. H. Freeman; 1999.)


Were there lifeforms before LUCA? This question got me thinking about something. LUCA is the last universal common ancestor of all current living organisms, which is a very different definition from the first-ever living organism. Is there any evidence that LUCA had evolved and diverged from a now-extinct, more primitive lifeform?

To rephrase, is there any evidence to suggest that at some point, the first-ever living organism(s) had diverged into two phylogenetic groups, one being now-extinct and the other describing all current life?

Well, what you seem to be suggesting is "Did life evolve twice on Earth?"

Your original question has an answer: Probably yes. It's not unlikely to think that the original cell evolved into two different paths and then one went extinct. However, that doesn't address LUCA. If we found fossil evidence of what we thought was LUCA, and then fossil evidence that LUCA had a genetic cousin - all that would do is push the application of the term "LUCA" on more evolutionary step backwards until both shared a common ancestor which would then be called LUCA. You can do this indefinitely until all life originates from a single cell, with countless offshoots which have gone extinct.

If you mean was there a whole other type of life - one that did not originate from LUCA and existed - then the best answer we have right now is "No." All life we know of, no matter how different and old, is still based on RNA/DNA and proteins. Fossil evidence supports this premise until about 3.5 BYA.

If there was an 'alternate' construction of life, we have not found the fossil evidence for it, and might not know what it was if we did. If the alternate form didn't utilize cells, we might not be aware we had it. If it did, but utilized different metabolisms or structures for proteins and storage - that evidence would be long gone by now.

Our best bet for answering if life can evolve differently than what we have today is out among the stars.


Which strange fruit is this? Yesterday, my brother brought a strange fruit resembling Lychee (but much bigger in size). Here is a pic of it:

When cut it, it had smell like banana and fibers were like of the chicken meat, though taste was more or less like banana (sorry have no pic of that).

Can someone kindly help me identify it?

This appears to be a jackfruit. Jackfruit are a large, tropical fruit, commonly reported as smelling similar to banana.


Is there a way to know how many sodium channels are active (conducting) at a given time in the brain? I was doing some reading about anti-epileptic sodium channel blockers, then wondered how many sodium channels are actually conducting (actively passing ions) at any given time, that is, in an "average, awake" brain?

Unfortunately, there is no way to know how many sodium channels are active (or even present) in one person's brain due to the extremely high variability of channel and neuron density in a population and the lack of methodology around quantifying total number of healthy active synapses (1). Diseases like epilepsy can occur due various points of the sodium signaling process going wrong. It could be sodium channels are deformed and not accepting the proper signal, it could a low density of channel proteins, or it could be damage to the neuron themselves (2-4). No one has examined the "normal/healthy range" of sodium channels in the brain. When categorizing sodium channel deficiency scientists will often compare the number of sodium channels in a healthy brain vs. a disease brain using bioluminescence imaging or some other visualization technique. Bioluminescence specially quantifies the number of active sodium channels by binding causing healthy sodium channels light up and then quantifies density by the brightness of the synapse. This is not a direct quantification of the number of proteins, but I can not think of any technique that allows you to count the number of proteins on a cell without damaging the cell. I'm sorry this isn't technically an answer to your question, but hopefully it provides some helpful references to understand molecular brain protein imaging.

Principles of Neuroscience
Low Sodium Channel Density and    Epilepsy
Sodium Channel Mutations and Epilepsy/ Other Nervous    System Disorders
Neuropathy and Sodium Channel Related    Diseases


Assumptions of the models for haploid and diploid selection For a bi-allelic locus, the model for haploid Natural Selection is:

$$\frac{dp}{dt} =  \frac{pW_A}{pW_A + (1-p)W_B}$$

, where $p$ is the frequency of the allele $A$, which relative fitness is $W_A$. $W_B$ is the fitness of the allele $B$, which frequency is $1-p$. $\frac{dp}{dt}$ is the change in allele frequency through time.

The same model for diploid selection is:

$$\frac{dp}{dt} = \frac{p^2W_{AA} + p(1-p)W_{AB}}{p^2W_{AA} + 2p(1-p)W_{AB} + (1-p)^2W_{BB}}$$

, where $W_{AB}$ is the fitness of the diploid genotype carrying the allele $X$ on one chromosome and the allele $Y$ on the other chromosome. We define $W_{AB} = W_{BA}$ and therefore we use only the symbol $W_{AB}$ in the above calculations. Note: This equation assumes Hardy-Weinberg equilibrium.

Those equations can be found in any introductory courses in population genetics. For example, here is a source where you can find this same equation for diploid selection. They just express $q$ instead of $1-p$.

My questions are:

Do these models assume constant population size? Why?
Do these models assume threshold selection? Why?

Thank you!

Unless I am missing something the equations you have posted are incorrect. The second equation should be:

$$p' = \frac{p^2 W_{AA} + p(1-p)W_{AB}}{p^2W_{AA}+ 2p(1-p)W_{AB}+(1-p)W_{BB}} $$

$p'$ is not interpreted as $\frac{dp}{dt}.$

$p'$ is the frequency of allele A in the next generation. If zygotic frequencies via random mating are

$p^2(AA) + 2pq(Aa)+q^2(aa) = 1$

then all of AA individuals and 1/2 the Aa gametes bear the A allele. So we can find $p$ in the next generation as

$p^2+pq = p^2+p(1-p) = p^2+p-p^2 = p$ which shows that in a Hardy-Weinberg population the frequencies are stable.

The assumptions here are those underlying the HW model, which includes infinite population size (hence constant).


What happens to glucose taken up by the liver in type 1 diabetes? Type 1 diabetes is caused by insufficient insulin production.

Unlike in muscle and adipose tissue (GLUT4), glucose uptake by the liver is by GLUT2 and thus insulin-independent. Consequently, under very high blood glucose concentrations, glucose will move by facilitated diffusion into the liver.

However, insulin is not available to stimulate glycogenesis, or lipogenesis; glucagon will be secreted due to high blood glucose concentration, doing the opposite. What happens to this glucose? Does it simply diffuse back out (GLUT2 is bidirectional)? Presumably glucokinase produces glucose-6-phosphate, but the highly controlled points of glycolysis (e.g. PFK-1) will lack stimulation due to loss of insulin. Does a lack of glucagon (due to glucose still reaching pancreatic islet cells, also via GLUT2) have a positive effect?

1) Hepatic glucose intake may not be much greater in hyerglycemia than in normoglycemia:

Regulation of Hepatic Glucose Uptake and Storage In Vivo (Advances in Nutrition, 2012):

  ...neither hyperinsulinemia nor hyperglycemia can independently induce
  much net hepatic glucose uptake.

2) Glucose can be used for de novo lipogenesis in the liver despite the lack of insulin:

De Novo Lipogenesis and Cholesterol Synthesis in Humans with Long-Standing Type 1 Diabetes Are Comparable to Non-Diabetic Individuals (PLoS One, 2013):

  Fasting total hepatic lipogenesis (3.91±0.90% vs. 5.30±1.22%;
  P = 0.41) was not significantly different between diabetic and control
  groups...


How do you test soil for the nutrients present in it? I recently noticed that my rose garden has been in a very terrible state. The roses keep dying. I tested the soil for its pH and that was fine.
Now I'm wondering how would I carry out a test to see what specific nutrients I should use to get my soil better.

Send soil samples to a soil lab (e.g., here).
They will likely use the Mehlich III extractant   method to extract and quantify the nutrients (most importantly the bases such as  Ca, Mg, K, and Na). Will cost less than $25.


Viral susceptiility of Nose and eyes I read that opening in our face like nose and eyes are one which get us infected with numerous communicable diseases like  cold , flu ebola etc.
Both these organs have preventive mechanism like nose hairs, eye lash , etc.
Which one of eye and nose does protect human better from airborne virus and bacteria?

Between the eyes and nose, which offers better immune protection

Neither. Both are mucous membranes lined by epithelial cells. Each is their own niche (and the nose has a number of sub-niches), with particular receptors, environmental factors, and immune factors that interact with pathogen factors. The interaction between the two produces the tissue tropism of a particular pathogen. Each is colonized with many commensal microbes, with some overlap (see Murray Medical Microbiology Ch 7 and this study of the eye). As far as "airborne" transmission, vs. inoculation by physical contact, the nose and nasopharynx are important structures in respiration. The eye is not.


Species Identification: Waterborne larvae, Texas USA Can you help identify this worm?

It was found in a cup of water at a restaurant (unpleasant, yes), likely came through the water system. (Location: Texas)
Found these images of it online (in which they were also found in water systems - dog bowl, sink), but none of the sites identified it.

Significant features: black head, black pointed tail, clear body with grayish intestines visible, tiny (2-3 mm)

Similar larvae that don't match:
-Mosquito larvae
-Midge larvae

Any insight is appreciated, including if you are familiar with similar looking larvae. Thank you.

The larvae are moth flies (Psychoda sp.)

The black head, black pointed tail, clear body with grayish intestines visible and also their small size 2-3 mm can be seen on both pictures.

Where they can be found in nature:

  In nature, moth fly larvae, Psychoda sp. (Diptera: Psychodidae) normally occur in aquatic habitats that experience intermittent submersion or flooding. The larvae develop in polluted, shallow water or highly moist organic solids where they feed on decaying organic material in mud, moss or water.

Where they can be found in households:

  In homes, the adult flies, which resemble tiny moths, are most likely found on the walls of bathrooms, kitchens, basements and other locations where sewer drains and plumbing fixtures are located. The flies are poor fliers and usually are found close to the drain or area from which they came. Moth fly larvae are known to live in drain traps, garbage disposals, toilet tanks, sides of drain pipes and overflow pipes in homes, wet areas around leaky pipes, sewer lines, and septic tanks where they feed on stuff that might accumulate in such areas. The moth flies that live in Michigan do not bite and are not known to transmit disease of any sort.

What to do against them:

  The best way to control moth flies is to eliminate or reduce the larval food sources by thoroughly cleaning drain lines and plumbing fixtures. Pouring boiling water down the drain where larvae are suspected to be may help to reduce their numbers. Adults can be controlled with the application of a household aerosol insecticide (like Raid) or a good flyswatter. Be sure to read and follow all instructions and safety precautions found on the label before.

There are various other methods which are far more precise, listing how to eliminate moth flies from drains.


Chemistry of phosphodiester bond formation by DNA polymerase As I'm teaching General Biology to my college students, I realized that I don't fully understand how a 3-P nucleotide like ATP is broken down to be incorporated into DNA during replication. How does this work??

In other words, what is the actual mechanism/reaction pathway for the following:

What I know:

I understand that ATP is typically hydrolyzed to become dephosphorylated in other contexts. I also understand that a phosphate of one nucleotide is bonded to a deoxyribose of an adjacent nucleotide via dehydration synthesis from the joining of their hydroxyl groups to form DNA.

However, I cannot seem to find a good resource (online or in any of my [admittedly simple] general bio textbooks) that demonstrate how exactly both of these reactions take place during replication...

I'm assuming that DNA polymerase is taking advantage of the released phosphates from ATP (and the appropriate forms of GTP, CTP, TTP) to become activated?

Overall, what does this whole process look like on a chemical/molecular level?

I'd love a visual (especially a video) if you could provide such a resource in addition to a thorough explanation of what's going on here.

I found this paper, which goes very deep into the molecular details of the individual steps of this reaction and also discusses how this is coupled to nucleotide selectivity.

The 'basic' details about the reaction (quoted from this section, which also has a nice figure):

  The polymerization reaction proceeds by a simple nucleophilic attack
  of the 3'OH of the primer on the α-phosphate of the incoming dNTP
  followed by the elimination of pyrophosphate [...] The reaction uses a
  "two metal ion" mechanism in which metal ion A activates the 3'OH as a
  metal hydroxide while both metals A and B stabilizes the developing
  negative charge on the α-phosphate in the transition state.

The metal ions are Magnesium (Mg$^{2+}$) and are properly positioned by the enzyme structure and some additional amino acid side chains also help with the activation of the reaction.


Why all trees have cylindrical stems? Why a huge number of  trees/plants have cylindrical stems? I have been told that this question's answer lies in Physics but I don't know where to find. Can any one help?

1)
You know most bridges have vertical cylindrical pillars.

This is probably because cylinder is among the strongest 3D structures to support anything.
So, cylindrical trunk provide best support for tree crown.

2) Most accurate
It is natural for any cell to grow equally in all directions. This, leads cells to expand in all directions equally in a circular girth.

3)
Resistance
Cylindrical girth provides least resistance to air. So, tree naturally takes this shape to prevent damage by air strikes.

4) Read
 https://m.reddit.com/r/askscience/comments/1973mh/

for more info.

5) http://www.stevespanglerscience.com/lab/experiments/balancing-act-cylinder-strength/

for strength of Cylinders.


What is the evolutionary explanation for bat's echolocation The bat's ability for echolocation is amazing (so are other the abilities of other animals). I was wondering how all of it came to be.

The main reason for bats to "develop" their echolocation system was the avalability of an almost empty niche: Hunting insects at night. Birds are not able to hunt without light and here is where the bats come in. They are able to hunt at night and also to live and orientate in environments where they are protected over the day: Caves. Bats at night are also protected from predatory birds.

There is are a few interesting sources if you want to dive deeper into the stuff:

The evolution of flight and echolocation in bats: another leap in
the dark
Echolocation in bats
Evolutionary aspects of bat echolocation


What happens to plants if they are exposed to "sunlight" 24h a day? I just wondered if one could grow plants faster, if they were exposed to sunlight-like light all the time.

In a similar question which is not the same, I could confirm that plants have different processes going on at day and at light. However, it didn't answer the question about the consequences of permanent exposal to sunlight.

However, I don't understand what would happen if there was light all the time. What would happen to different plants if they are exposed to "sunlight" 24/7?

(Similarly: What is the "optimal" amount of sunlight time different plants have? Is it basically what is common in the environments they typically grow in?)

This review (from 2011)1 states that it depends on the plant species and cultivar.

  Some continuous light (CL)-grown photosynthetic organisms show
  increased productivity. However, CL also induces negative effects in
  several plant species. The most visible CL-induced negative effects
  are leaf chlorosis and necrosis. CL also lowers photosynthetic
  parameters ... The CL-sensitive species include eggplant, geranium,
  some onion species (Allium fistulosum), peanut, some cultivars of
  potato, tomato, and even lichens (Xanthoria parietina) and mosses
  (Pleurozium schreberi and Ceratodon purpureous).

Among the plants that have better yields under continuous light are lettuce, roses, some potato cultivars, some algae.

The reasons why some plants can be damaged under continuous light aren't completely clear (at least they weren't in 2011). One of the problems is carbon imbalance. Leaves produce too much sucrose and other organs such as roots are not able to process it fast enough. This leads to high sugar concentrations and can cause leaf senescence. Continuous photosynthesis also results in more photo-oxidative damage and plants that better detoxify reactive oxygen species have less negative effects from continuous light.

So look for research on the particular species you want to grow or just experiment with different light conditions.

 1. Velez-Ramirez, A.I., van Ieperen, W., Vreugdenhil, D. and Millenaar, F.F. 2011. Plants under continuous light. Trends in plant science, 16(6):310-318.


Meaning of letter "c" in description of mutation: "Homozygous c.195C>G; (p.Cys65Trp)" In a table in a paper titled Cerebral folate deficiency: Analytical tests and differential diagnosis, there's the following description of a mutation in a patient:

  Homozygous c.195C>G; (p.Cys65Trp)

I wonder what the letter c means here.

I typed "c dna mutation" in Google and this article was the first hit:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1867422/

The "c" denotes coding DNA, which given the context of the amino acid mutation having the letter "p", this makes sense.


How to identify active protein in a complex mixture? I am trying to figure out how to identify which protein in a complex mixture is producing a certain effect.

There is an assay for the effect, so anything (a fraction of the mixture) can be tested on microplate.   The part of the mixture producing the effect is pretty definitely a protein (or has a protein component).

Unfortunately, the mixture is serum... which contains >10,000 proteins and peptides, some in tiny amounts and some in huge amounts.

There is not enough information to go the other way, ie guess what is producing the effect and test that by itself (or remove it from serum and test the depleted serum as a confirmation).

There is also no possibility to use affinity (use a receptor as bait, etc) because many components of serum stick to the cells in the assay (or, practically to any cells).

I need a way to narrow this down from "serum" to one specific protein (or a handful), but how?

This is a classical protein purification problem - you have to find ways to fractionate your mixture so that each fraction can be assayed for the activity you are interested in. When you find the active fraction you then subject that to a different type of fractionation.

Salting out

The solubility of proteins is affected by the ionic strength of the buffer. If the ionic strength is raised above a critical value (which is a characteristic of an individual protein) the protein  will precpitate, usually without being denatured. By doing a series of such precipitations at increasing ionic strengths a protein mixture can be fractionated according to this property. The salt used is ammonium sulphate, because of its very high solubility. You can find more details at this Wikipedia page (ammonium sulphate precipitation).

Ion exchange chromatography

Proteins have different intrinsic charges, and the net charge on a protein will vary with pH. This property is exploited in ion-exchange chromatography. In this technique the protein mixture interacts with a solid matrix carrying fixed charges. Under the correct conditions your protein plus others will bind to the matrix, while lots of other proteins won't. That's already a purification step, but you can then treat the matrix with buffers of increasing ionic strength. Weakly-bound proteins will be eluted from the matrix first, and as the ionic strength of the elution buffer increases proteins will elute in order of strength of interaction. By performing this procedure with the matrix in the form of a chromatography column and collecting eluate fractions you can achieve another step in the purification of your protein.

Size exclusion chromatography (gel filtration)

This technique is used to fractionate a mixture of molecules according to size. In this case the solid matrix that is used is charaterised by pores of a specific size. Proteins that are too large to enter the pores will pass through quickly;  small proteins will spend a lot of time moving in and out of the pores and so will pass through slowly; and proteins of intermediate size will spend some time in the pores. Essentially the average time spent passing through the matrix will depend upon size. Read more here.

These are just three of the possible fractionation procedures - others, including  hydrophobic interaction chromatography are described here). The key point to grasp is that using any one of these techniques will give you your protein in a fraction which also contains other proteins, but if you apply them sequentially you will progressively remove contaminants because each approach is based on a different physical property of proteins, and your target will have a unique combination of these properties.

At each step you will be assaying fractions to locate the protein of interest, and also running fractions on  SDS-PAGE to get a feeling for the number of proteins left. If you have an assay that lends itself to measuring some kind of unit of activity (as you would with an enzyme), then by also measuring the protein content of the active fraction you can express the purity as a specific activity (units of activity per mg protein). At each step in your purification this specific activity should increase because you recover most of the activity, but discard a lot of the proteins that were present in the previous material. The increase in specific activity can be used to assign
a purification factor to each step. A useful purification step will give a reasonable yield in combination with sigificant purification.

Finally, what order to do these steps in? I've listed them in a logical order - salt precipitation is a low-tech method that can give a quick first step and which has the advantage that it concentrates the target protein (since the precipitate is redissolved in fresh buffer). Size-exclusion chromatography doesn't deal well with large amounts of protein so is best left until later. However, protein purification is a craft, and an expert will use the available techniques according to the exact nature of the project.

UPDATE

From the tone of your original question I had inferred that you were a beginner, but from your comments, apparently not, since you are thinking in terms of mass spec as an endpoint.  A starting concentration of pg/mL is quite a challenge, and clearly you are never going to have enough material to see your molecule on standard gels.

Here are a couple of thoughts on aspects of your problem.

It seems that  in trying to purify minor components of serum a good starting point is to deplete the serum of its major proteins. This is a link to an imunodepletion product, and here is a related product from Biorad (no connection with either company and no recommendation implied).

I also found these papers which may be of interest. (Incidentally I think you'll find that each of the techniques I described is still used, perhaps just with modern instrumentation.)

Li,J et al. (2012) Purification, identification and profiling of serum amyloid A proteins  from sera of advanced-stage cancer patients. JOURNAL OF CHROMATOGRAPHY B-ANALYTICAL TECHNOLOGIES IN THE BIOMEDICAL AND LIFE SCIENCES 889: 3-9

Fertin, M et al. (2011) Strategy for purification and mass spectrometry identification of SELDI peaks corresponding to low-abundance plasma and serum proteins. JOURNAL OF PROTEOMICS 74: 420-430

Finally, a quick look at the Wikipedia page on plasma reveals that brain natriuretic peptide seems to be present at the levels that you are considering  perhaps you should look for papers describing its purification.

Other than that I think you have to hope that a proteomics expert will come by and give you an expert answer.


Why are the genomes of Humans 99.5% the same? Human's DNA sequence is said to be roughly 99.5% equal. As far as I understand, this means that if I walked up to you and compared our DNA, the sequence of base pairs would be 99.5% the same.

My question is: Why is there only 0.5% variation in our DNA? I can think of two reasons:

For some reason, the other 99.5% (roughly) is locked in place. These sections, if changed, either result in us not being 'human', or simply get some sort of genetic disease and so aren't very good mutations.
There hasn't been enough time. I remember hearing that all humans have a common ancestor some long time ago. If that's the case, perhaps over time only about 0.5% of our DNA has had time to randomly mutate, and if we wait a really really really long time, more and more of our DNA will mutate, and we will become 'less like each other'.

Or am I completely misunderstanding the situation? I didn't take biology in high school so answers should be simple please.

In a genome that is 3 billion base pairs, a difference of 0.5% works out to a difference of 15 million bases. When a single base change can change the amino acid sequence of a protein, that can add up to a huge amount of diversity, which is what we see over the nearly 8 billion humans on the planet, and the 99.5% sameness is why we are linked together so closely as a species.

How can the lack of diversity be explained?

  Nothing in Biology Makes Sense Except in the Light of Evolution.

The above quote was made by the evolutionary biologist Theodosius Dobzhansky. What this basically means is that you need to take a look at your question from the perspective of evolution and natural selection.

The first thing you need to note is that there is evidence to suggest that modern humans went through a population bottleneck. What that means is that at a certain point in our history, there were very few individual members of our species alive and this can account for the "lack" of diversity that we see in our genome. The number that is quoted is as low as 10,000 individuals left alive after the supereruption of the Toba volcano about 75 thousand years ago.

That means that there were very few mating pairs left, and that significantly reduced the genetic diversity of our species. This is known as Founder Effect.

  Founder effects

  A founder effect occurs when a new colony is started by a few members of the original population. This small population size means that the colony may have:

  reduced genetic variation from the original population.
  a non-random sample of the genes in the original population.

So if we use an average of 20 to 25 years per human generation, we are only looking at about 3,000 to 4,000 generations since there were maybe only a few thousand breeding pairs of humans. Contrast that with bacteria which can go through three to four thousand generations in less than a week, and you can begin to get a feel for why there is so much sequence homology (sameness) in the human genome. See Bottlenecks and founder effects at UC Berkley's Understanding Evolution site for more information.

You also should understand that any changes that are deleterious will be under strong selective pressure. This may not mean that the organism may not survive to reproduce, in may just mean that on average, they may be less successful; fewer offspring that have fewer offspring in comparison to the rest of the population. At some point that lineage may go extinct, either because the change makes it very difficult to survive, or the offspring make less desirable mates and eventually don't get the opportunity to reproduce.

Any changes that disrupt a vital gene will likely be fatal and will lead to spontaneous abortion or if the mutation was sustained in a sperm, then the inability of that sperm to survive to fertilize an egg, so the sperm that was heavily mutated may just never make it to the egg. The average number of sperm in a single human ejaculation is about 250 million. And yet only a single sperm makes it to fertilize the egg, and that is assuming that a fertilization event takes place. There is an incredible amount of selection that goes on in the act of procreation, even before we get to development.

Why the 99.5% to 0.5% figure might be misrepresentative of the population as a whole.

Another thing that you will want to think about is how the 0.5% to 99.5% number was arrived at. The referenced in the question links to a Wikipedia article Human Genetic Variation. The reference provided for this was from a New York Times article about J. Craig Venter, In the Genome Race, the Sequel Is Personal - Wade, Nicholas. September 4, 2007. The quote that is references in Wikipedia is:

  Biologists had estimated that two individuals would be identical in 99.9 percent of their DNA, but the true figure now emerges as much less, around 99.5 percent, Dr. Scherer said.

The 0.5% figure is provided as a quote from Stephen W. Scherer, who was a coauthor of this paper, The Diploid Genome Sequence of an Individual Human, Levy, et.al. PLoS Biology; September 4, 2007. DOI: 10.1371/journal.pbio.0050254. From that paper the following quote is found:

  Inclusion of insertion and deletion genetic variation into our estimates of interchromosomal difference reveals that only 99.5% similarity exists between the two chromosomal copies of an individual and that genetic variation between two individuals is as much as five times higher than previously estimated.
  - The Diploid Genome Sequence of an Individual Human, Levy, et.al. PLoS Biology; September 4, 2007.DOI: 10.1371/journal.pbio.0050254

So at the very least, the statement was made in a peer reviewed article. However there are some problems with this.

The first is the method of the paper. It looks at a single human genome, that of Dr. Venter, and is used to draw the conclusion of 0.5% difference between any two individuals. And the comparison is made based on the analysis of differences between Dr. Venter's maternal chromosomes and paternal chromosomes. Let's look at what the problems might be here:

It is a huge leap of statistical faith to assume that a single genome is representative of the nearly 8 billion genomes out there.
Dr. Venter's genealogy is English on both parental lineages. We have to remember that there was another population bottleneck in middle ages Europe caused by outbreaks of cholera and the Black Death. This fact may imply that Dr. Venter's lineages are genetically close and that if his lineage were more diverse, say Indigenous Oceanian and English, they may have found a much higher percent difference between maternal and paternal chromosomes.

  The donor's three-generation pedigree is shown in Figure 1A. The donor has three siblings and one biological son, his father died at age 59 of sudden cardiac arrest. There are documented cases of family members with chronic disease including hypertension and ovarian and skin cancer. According to the genealogical record, the donor's ancestors can be traced back to 1821 (paternal) and the 1700s (maternal) in England. Genotyping and cluster analysis of 750 unique SNP loci discovered through this project support that the donor is indeed 99.5% similar to individuals of European descent (Figure 1B), consistent with self-reporting.
  - The Diploid Genome Sequence of an Individual Human, Levy, et.al. PLoS Biology; September 4, 2007.DOI: 10.1371/journal.pbio.0050254

Dr. Venter is male. The Y-chromosome was problematic to sequence, and you cannot really do a comparison between it and the X-chromosome. How would the genome of a woman compare?

  The Y chromosome is 59% covered by the one-to-one mapping due to difficulties when producing comparison between repeat rich chromosomes. In addition, the Y chromosome is more poorly covered because of the difficulties in assembling complex regions with sequencing depth of coverage only half that of the autosomal portion of the genome. The X chromosome coverage with HuRef scaffolds is at 95.2%, which is typical of the coverage level of autosomes (mean 98.3% using runs). However it is clear that the X chromosome has more gaps, as evidenced by the coverage with matches (89.4%) compared with the mean coverage of autosomes using matches (97.1%). The overall effects of lower sequence coverage on chromosomes X and Y are clearly evident as a sharp increase in number of gaps per unit length and shorter scaffolds compared to the autosomes (Figure 3). Similarity between the sex chromosomes is another source of assembly and mapping difficulties. For example, there is a 1.5-Mb scaffold that maps equally well to identical regions of the X and Y chromosomes and therefore cannot be uniquely mapped to either (see Materials and Methods and Figure 3). From our one-to-one mapping data, we are also able to detect the enrichment of large segmental duplications 10 on Chromosomes 9, 16, and 22, resulting in reduced coverage based on difficulties in assembly and mapping (Table S3).
  - The Diploid Genome Sequence of an Individual Human, Levy, et.al. PLoS Biology; September 4, 2007.DOI: 10.1371/journal.pbio.0050254

There is another thing that you need to remember and that is the history of the Human Genome Project. Dr. Venter developed a new method of sequencing and became a commercial competitor to the International Human Genome Sequencing Consortium project. While the International Human Genome Sequencing Consortium project beat out Dr. Venter's enterprise(8), it's approach, to use an amalgamation of the DNA of many donors, some of whom had their DNA included and some who did not, to preserve anonymity, Dr. Venter circumvented this by performing the sequencing on his own DNA. When his team was beat out by the International Human Genome Sequencing Consortium, he doubled-down, invested more time and effort and came up with the sequence put forth in this paper, which had a higher degree of resolution than previous efforts. The paper is making an argument for the value of their technique over the techniques being used by the International Human Genome Sequencing Consortium and is trying to make a claim of the superiority of their method. The data being presented is likely factual, but because of this history you have to look at the paper, the methods, and the motives behind it.

It is only 15.5 years since we had a full draft of a Human Genome Project produced by the International Human Genome Sequencing Consortium. In order to sequence that genome samples were taken from a few hundred individuals. Small stretches of the DNA were sequenced and then all of those pieces were put together in computer. That means that there was a lot of averaging that happened. So by default, the most prevalent base in the population of volunteers at every position was chosen. That means that that should be representative for the rest of the population as well.

When we make statements about comparisons in datasets as large as the human genome, more often than not we are looking at known, small subsets of the genome, and we are extrapolating by statistical methods based on that fact. One thing you learn as you read science papers, and not just science news articles, is that you always need to look at their materials and methods to determine how they arrived at their data and headline numbers. It is often quoted that we have only a 1.5% difference between Humans and Chimpanzees, however when you look at those papers the comparisons were done only on areas of the genomes that lined up well. That isn't to say that there isn't a remarkable degree of similarity between us and our nearest living evolutionary relative, it is just that there is more to the story than the headline.

Also, we don't have that many full genomes sequenced to compare to one another, as a percentage of the 8 billion people alive today. While we have representations from most a vast majority of the ethnic groups identified, we may be missing families with novel lineages.

Another thing that you need to think about is that many of the areas in the human genome are repeats and structural elements that do not encode for genes of affect gene expression. Things like telomeres, which protect the ends of chromosomes, and centromeres which are the attachment points on chromosomes that make sure that the are distributed properly into newly divided cells. These elements tend to stay the same because the proteins that bind to them require that sequence specificity in order to function properly, so those are regions were almost every ones DNA will be the same, and not just between humans. These elements often are very similar in most vertebrates.

We also need to consider structural RNAs. These molecules have functions within the cell that require that there sequences be highly conserved (unchanged). Ribosomal RNAs, Transfer RNAs, Small Nuclear RNAs all rely on their specific sequence to fold properly in order to perform their task in the cell. A single base change can change the folding of these elements and as a result they will loose their function, which means those cells won't be able to produce proteins properly which means that the cells will die. If this is happening in germline cells, then they are not going to be involved in fertilization so any mutations there will be passed on.

I could go on and on, but the take away is that it isn't surprising that there is very little sequence diversity on a percentage bases within the human species, but there are many caveats to that fact as well.

Edit: Significant edits to add relevant, referenced information to back up answer.


Are missing limbs hereditary? So with my basic understanding of biology, DNA can change over time.

Does this mean that if one (or both) parents have something major missing (like a limb), the kid will come out without a limb?  Does it matter if the parents had limbs amputated or were born like that?  If someone got melanoma from laying in the sun a lot, would their kid have a higher risk of getting it?

Does this mean that if one (or both) parents have something major missing (like a limb), the kid will come out without a limb?

Unless there is a genetic basis to the missing limb, no. Even for people born with missing limbs, this is usually not caused by genetics, but by a problem during limb formation in the womb (for example, through medication taken by the mother). A genetic condition associated with missing limbs is tetra-amelia, which is indeed heritable; however, it is very rare, a recessive trait and people actually showing it rarely have children.

  If someone got melanoma from laying in the sun A LOT, would their kid have a higher risk of getting it?

No, at least not in the way you seem to think from the way you phrased this. There are people who are more susceptible to melanoma due to genetics. For these people, their offspring can also be more susceptible to skin cancer. However, this is passed to the next generation whether or not the parent has melanoma.

  DNA can change over time

Yes, it can. DNA even in adults can change over time, but either this is your germline cells, so it will be passed to the next generation, but won't bother you, or it's in the rest of your cells and may or may not have an effect on you, but won't be passed to the next generation.


How long can Vibrio cholerae live in its ambiental optimal context? How long can the Vibrio cholerae live in its ambiental optimal context?

Thank you in advance. My problem is that i can't find this information. I did some research on google, but nothing was retrieved, I even used other search engines. Thank you very much for your help.

I Found It!!!!    SURVIVAL OUTSIDE HOST: Cholera can survive in well water for 7.5 ± 1.9 days and the El Tor biotype can survive 19.3 ± 5.1 days(Footnote 21). The bacterium can survive in a wide variety of foods and drinks for 1-14 days at room temperature and 1-35 days in an ice box(Footnote 21). It has also been found on fomites at room temperature for 1-7 days(Footnote 21).

Source>>http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/vibrio-cholerae-eng.php


How can I determine the mRNA sequence from a given template DNA strand? Can I determine the sequence of nucleotides of the mRNA strand transcribed from a template DNA strand that goes from (5' to 3')?
I know that RNA-Polymerase enzyme cannot work but on the (3' to 5') direction of the template DNA strand. So, for instance, if the question was to:
Determine sequence of nucleotides in the transcribed mRNA from the DNA strand
5'...A-T-T-C-G-T-T-A-C....3'
Which direction should I start with?

I'm assuming you are working with a small sequence, but for larger sequences, or if you want to double check your answer, you can use tools like this one: http://www.attotron.com/cybertory/analysis/trans.htm


Identification of a lifeform There's a video I found on Facebook and I'm unable to figure out what the creature featured happens to be.
Adding images that have been taken from the video itself, apologies in advance since they're not high qualify images.

Can anybody shed any light on what it is?
The video was shot near Ratan Babu Ghat which is situated along the bank of Hooghly river, Kolkata, West Bengal, India. Here to be precise.

This is a polyclad flatworm.

Here is a video of notoplana vitrea moving similarly to the one in the video that you linked:
https://www.asturnatura.com/especie/notoplana-vitrea.html
Here is a gallery of polyclad flatworms observed in India:
https://inaturalist.ca/observations?place_id=6681&subview=grid&taxon_id=52318
A number of the images in this gallery look similar to the one in your video, but very few of them are identified beyond this order taxon of polyclad flatworm.


Do any amphibians start their lives on land? Most amphibians - at least, all the ones I know of - start their lives in the water (at least, after they hatch). They then spend time maturing before venturing onto land, where they can breed. The cycle than begins again.

Are there any cases where the reverse is true, i.e. a young amphibian starts life on land before venturing into the water as an adult?

Wikipedia hints that this may be the case, but fails to provide examples:

  Amphibians typically start out as larvae living in water, but some
  species have developed behavioural adaptations to bypass this.

From wiki:

  Most amphibians lay their eggs in water and have aquatic larvae that undergo metamorphosis to become terrestrial adults

This suggests clearly that not all of them do so.

Here are a few interesting cases I could think of:

The common midwife toad carry the eggs on their back. The eggs are not necessarily submerged by water then.
To my knowledge, the Seepage salamander have terrestrial larvae but they don't feed before they reach the adult age.
The lungless salamanders has a larval stage that is within the egg. When the egg hatches, the individual that comes out is already an adult.


What is the fastest way to build an alanine scanning library? For interfacial studies, I would like to build an alanine scanning library for one of my proteins examining 20 sites. I will ultimately express the gene using E.coli cell-free protein synthesis. I already have the template gene which was originally built using PCR assembly. Now, what's the best way to build a scanning library?

The fastest will change as time passes and better technologies are developed.

I think the fastest method existing at the moment is Shotgun Mutagenesis (provided by Integral Molecular Inc).

This does not employ any new method of doing that. They just provide a set of plasmids, that has all the possible mutations. The set itself is generated by automated DNA synthesis.

So if you don't have a DNA synthesizer with you then simply order the kit from the company.


What is meant by "genes involved in the stress response"? I would like to know about the term stress response. For example "some genes of a species under study is involved in stress response". What does that mean? I got this as a part of my assignment question.

The comment by @fileunderwater is apt: stress-response-related genes are genes that are activated during stress, such as exposure to heat. In bacteria, for example, there are heat-shock proteins that are involved in keeping the tertiary structure of proteins (folding/3D shape) intact during periods of heat exposure. Genes encoding these heat shock proteins are then called to be upregulated, and you would find them back in a typical micro array experiment. Hope this helps.


How fast does the rotor in ATP synthase spin? I'm sure the exact frequency varies, but does anyone know roughly how many revolutions per minute / second the rotating center part makes?

According to "Resolution of distinct rotational substeps by submillisecond kinetic analysis of F1-ATPase" (Yasuda et al., Nature, 2001), ATPase rotates at 130 revolutions per second when saturated with ATP.


How can bats achieve good resolution with wide beams? I have been reading about the echolocation system in bats. papers state that bats tend to produce a sonar beam that has a beam angle (-3db) of about 30-40 degrees. This would be considered a wide beam given the fact the sonar sensors used by robots have beams 15-20 degrees or down to 10 degrees with multi-sonar.

As the beam width increases, the azimuth resolution decreases. Yet, bats have good navigational capabilities and good object discrimination in azimuth. How is that achieved? what is the technique used?

I searched hard but what I found is that they rely on the timing between two ears. however, given the complexity of the environment and the multiple echos that return, how is it possible to correlate which echo in the left ear belongs to which in the right ear?

I have been contemplating about this question for months and although I cannot provide you with a concise short answer, I do wish to share what I have so far.

First off, the acoustic beam that is sent is not really part of the echolocation resolution (the bat's echo-locating acuity). Consider the human field of view, which is nearly 180o wide in the horizontal plane. Covering your eyes and obscuring, say, half of the field will not substantially improve visual acuity, because it simply blocks half of the retinal surface from receiving light - it does not double the retinal surface devoted to the field of view.

Hence, I think it is not so much the bat's projected beam that matters, it is the incoming echo that matters. Note that objects such as a tree may scatter the sound that is reflected back, so the projected beam of 40o may be a dramatic underestimation of the chaotic signals bouncing back to the bat. What can they do to improve spatial detail in the received acoustic field of view?

Bats may increase the pulse repetition rate when they are approaching a target. Hence, they basically build a map by sampling the environment multiple times. Sampling frequencies may exceed 50 Hz (Grinnell and Griffin, 1985). For example, imagine you are blindfolded and allowed to scan an object with your fingers. Scanning it multiple times will definitely help you to mentally reconstruct the image. Indeed, bats can assemble information about echo delay changes over time, enabling them to temporally integrate information of the auditory scene. Moreover, they can change the spectral content of their calls that may help in echolocation (Moss & Surlykke, 2001).

Furthermore, to conclude with a personal thought - I think that bats must learn to decode complex echo profiles. For example, a chaotic huge blob of echo with low-echo efficiency (lots of sound is absorbed) that only changes when the bat moves is probably a tree. A big blob with a large echo-efficiency (a lot of sound comes back) with well-defined edges that only changes when the bat moves is likely a human structure or a rock. A pinpoint-echo that moves with respect to the bat is likely something tasty.

References
- Grinnell & Griffin, Biol Bull (1958): 10-22
- Moss & Surlykke, JASA; 110(4): 2207-26


Confusion regarding the Kir2.1 inward-rectifying potassium channel I was trying to find out more about gustation and the transduction of sourness when I came across the supposed inward-rectifying potassium channel $\ce{K+_{ir} 2.1}$. Here's the thing, despite being inward rectifying, all the articles I read about it involves it sending potassium ions out of the cell. I thought that maybe there is a special mechanism that makes it outward-rectifying, or just switches off its mechanism for inward rectification but to no avail.
So here's the context: On taste buds that detect $\ce{H+}$ ions, when intracellular pH rises due to intake of protons, potassium channels will be closed which causes accumulation of $\ce{K+}$ and thus depolarisation. The article pinpoints $\ce{K+_{ir} 2.1}$ as one of the potassium channels involved, saying that its inhibition will allow for depolarisation. This doesn't make sense to me, if this channel is supposed to prefer intake of potassium ions and almost entirely prohibit outward flow. If we want to accumulate potassium in the cell, shouldn't this channel be left open?
The only thing I can think of is that this channel remains open at membrane potentials near that of resting potential. So maybe then there is no selectivity over which direction the ions travel, so there is a net outward flow?
I'll link some of the articles I mentioned below:
The K+ channel KIR2.1 functions in tandem with proton influx to mediate sour taste transduction
Inhibition of Kir2.1 channel-induced depolarization promotes cell biological activity and differentiation by modulating autophagy in late endothelial progenitor cells.

Short answer
"Inward rectifying" doesn't mean "only allows inward current". Current through inward-rectifying channels can be (and often is) entirely outward in physiological settings.
Explanation
For a non-rectifying channel, there is a linear current-voltage relationship. If you plot current through the channel at various holding voltages, you get a straight line.
For inward-rectifying potassium channels, you get less current as you depolarize, like this:

(from Wikipedia)
At negative voltages, the channel is pretty linear and strongly inward (negative). However, at more positive voltages, the linear trend is attenuated.
However, this relationship does not upset the equilibrium potential for a given ion. For a potassium channel, if you have a cell with a potassium reversal potential that is more negative than the membrane potential, you'll still get an outward flow of potassium ions (in the figure, note all the lines above 0, representing voltages more positive than the potassium reversal potential; they're positive/outward even if they're small). What is different for the inward-rectifying channel is that as you depolarize the cell, the current does not increase the way you would expect it to increase for a non-rectifying channel.
For example, for a non-rectifying channel, you'd expect with a potassium reversal of -90mV, the current would be the same magnitude but opposite sign at -120 mV and -60 mV (30 mV above and below reversal). For a inward rectifying channel, you will still have the same change in sign, but the magnitude will be less at -60 mV than at -120 mV.

its inhibition will allow for depolarisation

Any channel permeable to some ion (or combination of ions) will tend to move the voltage towards the reversal potential for that ion/ions. So, as long as potassium reversal is more negative than threshold, all potassium-only conductances are inhibitory, whether they rectify or not.


Why is urea not converted to ammonia in the body? After the liver processes metabolites to produce urea and other by-products, these travel in the blood to the heart, then they are oxygenated, and some travel through the renal artery to the kidneys.

Urea in water can decompose into ammonia which is toxic, as mentioned in a textbook page no 170 (6), under production of ammonia.

Reactant and product are at equilibrium. Also a gaseous product, CO2, is present which could potentially escape during oxygenation of blood. Hence, according to Le Chatelier's principle, an equilibrium shift towards  the product is possible

NH2CONH2 + 2H2O → (NH4)2CO3 ⇌ 2NH3 + H2O + CO2

The chance of urea decomposing into ammonia is high while travelling in the blood (i.e taking long route) and in the bladder, but it still does not happen. Why not?

The answer to this question is quite simply this:

  The activation energy for the uncatalysed reaction is such that the
  amount of decomposition of urea in aqueous solution at blood temperature and
  pH is negligible in the time taken for the transfer of urea to the
  kidney.

The literature supporting this is very old, so I shall first cite a relatively recent (2004) and (I think) freely available paper by Robert P. Hausinger on urease in which he writes:

  The substrate [i.e. urea]  is highly resonance stabilized (30 to 40 kcal/mol), thus
  decreasing the reactivity of its carbonyl carbon so that spontaneous
  hydrolysis of urea has never been observed. Rather, urea decomposes
  in solution (with an estimated half-life of 3.6 years at 38°C) by
  the slow elimination of ammonia to form cyanic acid (17)

Reference [17] is a paper by Zerner in Bio-organic Chemistry from 1991 which requires a library subscription. In effect it quotes the same half-life:

  The urea molecule is very stable. Between pH 2 and pH 12, the
  nonenzymatic decomposition of urea in aqueous media is independent of
  pH and has a half-life of 3.6 years at 38°C (36-38).

References 36 is a book written in 1923, and references 37 and 38 date from 1942 and 1955, respectively. I have not checked the latter, but can if anyone demands it.

All of which is not surprising, as the purpose of the urea cycle in mammals (etc.) is to eliminate toxic ammonia, and, as @Fizz points out, the enzyme urease is needed by bacteria that utilize the compound.


Help me understand my membrane potential assignment Epithelial with the ability to transport NaCl is bathed in an isotonic salt solution with these values (in mM): 136 Na, 6 K, 140 Cl.
The intracellular concentrations are: 45 Na, 100 K, 13 Cl.

The cell's resting potential is -63 mV and the temperature is 37 Celcius.

Which ions will passively diffuse over the membrane?

My attempt: I calculate the nernst potential of each ion and taking the first ion (Na) as an example I get that it's equilibrium is at 29 mV. So as there are more of these cations outside the cell and the membrane potential is negative, the ions will want to "reach" 29 mV by flowing INSIDE the cell (to increase the membrane potential). I think they will do this by diffusing into the cell? I'm not sure if I am attacking the problem correctly or if it's rather lunging at my abilities in transporters. The NaK transporter is active transport so maybe the do not diffuse at all?? However there are Na channels that can open...Which is passive diffusion..

Calculate the cation permeability Pna/Pk

I have no idea how to do this. I still need more constants in the Goldman equation (Pcl for example) before I could isolate even one of these.

Thanks!

If there is passive transport for each ion, then every ion will diffuse over the membrane until the concentrations will be the same, and the membrane potential will be zero. So there is active transport in the cell, which maintains the resting potential which is -63mV.

So with the current concentrations the membrane potential will differ from this -63mV, and so the cell will change the ion levels to change the current potential to be equal to the resting potential.

I think you should try to simply summarize the Nernst potentials. It won't be so accurate as the Goldman equation, but you don't have the relative permeabilities of this cell type, so the questioner probably does not wait the Goldman equation from you.

I would solve it this way:

Em = RT/zF * ln(out/in)

R = 8,314 J/molK
T = 37 + 273 = 310K
F = 96485 J/molV

RT/F = 26,712mV

ENa = 26,712mV*ln(136/45) = +29,543mV
EK = 26,712mV*ln(6/100) = -75,152mV
ECl = -26,712mV*ln(140/13) = -63,486mV
Em = ENa + EK + ECl = -109,95mV

Emr = -63mV
Emr - Em = -63mV + 110mV = +47mV

So we have to increase the membrane potential. Decreasing intracellular K+, Cl- concentration and increasing intracellular Na+ concentration can do that.

Concentrations: extracellular 136 Na, 6 K, 140 Cl, intracellular 45 Na, 100 K, 13 Cl. So possible passive transports are increase Na+, decrease K+, increase Cl-.

Conclusion the passive transports will be increasing Na+, decreasing K+ the active transport will be decreasing Cl-.

Note that I haven't used these terms for 5 years, so if you can consult with somebody else about this, then ask him/her whether this is correct.


What specific sensory nerves act as receptors for "pins and needles" (neuropathy)? According to this excellent answer, the difference between "pain" and "pins and needles" (neuropathy) is that different receptors (sensory nerves) trigger in reaction to different stimuli.

Different types of pain receptors (hot/cold, pressure, etc.) send pain signals to the brain.

Different receptors are responsible for sending neuropathy signals to the brain. These receptors are usually triggered when the nerve receives a shortage of blood flow.

According to the Wikipedia Article on Sensory Receptors, there don't appear to be any nerves that produce pins-and-needles sensations to the brain...

So I ask: What are the specific types of nerves/receptors that send "pins and needles" signals to the brain? What are they called?

I would imagine that it either has to be a specific, specialized receptor that (perhaps) starts firing if its senses "something is wrong" (such as decreased bloodflow to the area, etc.), or it's that all sensory receptors are capable of firing "pins and needles" signals under special circumstances.

Pins-and-needles (PAN) sensation and pain stem from the same nerves. The pathophysiologic process is different, though. PAN is characteristic of nerve lesion, and is therefore a pathologic reaction. Pain is a physiologic reaction to a stimulus perceived as ominous.
Pathophysiologically speaking, the PAN sensation is a distortion in somatosensory stimulus processing due to injury to peripheral nerves.
Of course, the PAN sensation will stem from somatosensory nerves. Pure motor nerves will not cause such a sensation.


Identifying flying insect from northern Poland / Baltic Sea area Found during this year vacations at Baltic Sea (northern parts of Poland):

I don't have a picture containing other object, for size verification, but I'd say, that it was 3-4 cm long.

There were two interesting characteristics of this insect, that I haven't found in case of any other:

it was not flying / running away, when when being chased / waived by a hand; you actually had to snap it with a finger and sent it airborn, to make it fly away,
once touched by finger or upon falling from certain height it was pretending dead, but when you tried to remove "dead body" it turned out in most cases that it is alive and it was flying over.

This is all I can tell about this insect. Can someone help me with identifying, what species is it?

It is possibly a vine weevil (Otiorhynchus sulcatus)

Others of the family:


What is the disadvantage of having no anticoagulation after pulmonary embolism? Is chronic anticoagulation always given after pulmonary embolism?

What are the risks or disadvantages

if anticoagulation is not given?
if terminated early?

Not always, however typically it is given for at least a few months. Lack of anticoagulation therapy would greatly heighten the risk of having another PE or related cardiovascular events. At the worst side this could cause death or permanent disability, and PE related deaths are quite common. However this depends on the nature of the PE and risk factors. For example, obesity, cancer and the pill are all risk factors and if these were reduced then it is likely the person wouldn't have another PE despite not being on long term anticoagulation therapy. However, if there is an underlying cause even despite anticoagulation therapy a person may suffer a PE.

The problem with anticoagulation therapy is of course it stops your blood clotting. Thus haemorrhages are more common and also more severe. However in an individual receiving anticoagulation therapy, they typically have increased clotting so this may be balanced out by therapy.

Finally anticoagulation therapy is typically warfarin in the long term. Warfarin interacts with so many drugs including even antibiotics, it is teratogenic and quite sensitive to diet (any changes in Vitamin K will directly affect the effectivity of warfarin) thus frequent monitoring is required. This is annoying for the patient as they have to report for frequent blood tests as well as watch their diet etc.


Cell dye in red fluorescence spectrum There are some cell dyes available for stianing cells intracellularly / membrane. I am aware of other channels (CFSE \ PKH26). But I want to stain cells for flow cytometry with a 'red' dye.
I have looked at a few options from Thermo but did not find sufficient data on either.

Specifically I am planning to stain a single cell population with two different dyes, treat each stained population somewhat different in between, and then culture them together and distinguish read-outs later. Antibody-staining for a surface marker would be possible with Fab fragments (the antibodies itself may interfere with cell activation during culturing). Therefore I would rather use a red-spectrum dye like CFSE or PKH26 as this may be cheaper and possible for secondary use with other cell lines.

I have multiple cytometers available and the specific emittance doesn't matter as we can pick what is generally possible (LSR/Fortessa).

Thus, I am looking for a dye with emittance in the red fluorescence spectrum which has staining protocols available that can be adapted for my purposes.

Is anybody willing to share their experiences?

Edit

Clarified that I needed a 'no-antibody-staining'
Clarified question with regard to biological question and FACS

I've used the ThermoFisher brand of CellTrace dyes. Specifically, I co-cultured two populations of cells, one with CellTrace Far Red in the APC channel and another with CellTrace Yellow in the PE channel. My choice was in part guided by a product review by another lab touting the relatively low cytotoxicity of these products.

The protocol is quite straight forward. It's also available in CFSE and Violet, though I haven't tested those. These dyes are also optimized for lymphocytes, and so I'd recommend titrating if you're staining anything else.

The dyes are quite bright, and so there were issues with costaining APC-Cy7, for example. I ended up leaving my CellTrace dyes as the only markers on their respective lasers and stacking my phenotyping on the 355nm and 405nm lasers.

For compensation, you might just stick with cells, but in the product manual for CellTrace, however, it says:

"The CellTrace™ reagents readily diffuse into cells and bind covalently
to intracellular amines, resulting in stable, well-retained fluorescent staining that can
be fixed with aldehyde fixatives."

So if you use the ArC amine-reactive comp beads for LIVE/DEAD kits, you might be able to just make comp beads with those. I'll verify this when I'm back at work if need be, as I haven't done it myself, but it's a nice thought!


Gene Sequencing and Plasmapper Is there anything similar to this in Java (especially the circular map sequencing along with hover effect)?
For information I would like to convey that I am using Plasmapper and BioJava for achieving this, but, as the output is in image format, so I am not able to achieve the above said requirement.
Thanks...

Check these out. They provide the functionality that you want:

ApE
SnapGene viewer


Is there any measure by which the Germans today could be called a genetically superior race? The Nazi eugenics programs are well known. Despite their controversy, I cannot find any indication on their effectiveness. Were there ever and studies done on the (arguably subjective definition of) superiority of German genetics due to (or possibly in spite of) these programs?

Do we even have a way to objectively measure genetic superiority or fitness? In the case of a lack of such a measurement, the idea could be qualified for purposes of this question as:

Lower instances of genetic disease.
Lower instances of mental retardation, criminal tendencies, and mental illness.
Higher general academic achievement.
Healthier, longer lived population.

Note of course that I am not promoting or condoning eugenics in any way. I am only interested in knowing if the results were effective (i.e. achieved their goals), without comparing the programs' possible benefit against its obvious drawbacks. All contemporary discussion of the programs concentrate only on the drawbacks, unfortunately.

EDIT: Before anyone accuses me of bigotry or crimes against humanity, I will mention that my grandfather lost all seven of his siblings, his parents, and all the rest of his entire family to this same regime. My grandmother lost five of eight siblings, both parents, and all the rest of her entire family to this same regime. What these people did to Jews, Gypsies, and the feeble was terrible and I do not excuse it. This question is intended only to concentrate on the scientific issue of forced, deliberate genetic improvement, a form of "breeding" if you will.

I am leaving the word 'superior' aside (it's ill-defined and strongly valuing).
In any way - unlikely. If any ethnic group is 'superior' (at least, intellectually) - then, ironically, Nazi main victims - Ashkenazi Jews. But while there is some genetic component, it is impossible to disentangle it from societal and historical factors. Here are some links, is you are interested.
When it comes to Germans, as far as I remember, they are not a group genetically distinct from, say Poles. Yet Slavs were considered by Nazi also an inferior race, to be enslaved or eradicated.
In any case, culture and socioeconomic factors seem to be much stronger than (relatively small). In particular, for Germany itself, there was a huge difference between West and East Germany, prior to the fall of Berlin Wall. It can be hardly explained by 'genetical superiority' of West Germans. An excerpt from Race, IQ, and Wealth by Ron Unz:

Consider, for example, the results from Germany obtained prior to its 1991 reunification. Lynn and Vanhanen present four separate IQ studies from the former West Germany, all quite sizable, which indicate mean IQs in the range 99–107, with the oldest 1970 sample providing the low end of that range. Meanwhile, a 1967 sample of East German children produced a score of just 90, while two later East German studies in 1978 and 1984 came in at 97–99, much closer to the West German numbers.
These results seem anomalous from the perspective of strong genetic determinism for IQ. To a very good approximation, East Germans and West Germans are genetically indistinguishable, and an IQ gap as wide as 17 points between the two groups seems inexplicable, while the recorded rise in East German scores of 7–9 points in just half a generation seems even more difficult to explain.

See also The East Asian Exception to Socio-Economic IQ Influences and The Myth of American Meritocracy (on how ethnicity can affect admission) by the same author.


Why is sedimentation rate significant for a ribsome When we take a look at biology textbooks (Campbell,  Pearson etc), they will only mention the difference between eukaryotic and prokaryotic ribosome sedimentation rates. Why is sedimentation rate numerically important for ribosomes and not for other organelles like the mitochondria or the nucleus?

Summary

Ultracentrifugation was necessary to identify and ribosomes, and characterize them on the basis of their size. The method does not allow an absolute measurement of molecular mass, but uses a relative quantitation as sedimentation coefficient, expressed in Svedberg Units (S).
Nuclei and mitochondria were characterized by light microscopy and, being much larger than ribosomes, sediment at speeds which do not require an ultracentrifuge and would not be resolved in an ultracentrifuge.
Nuclei and mitochondria vary in size, so their size is not a defining property for them. Ribosomes from one source all have the same size, which may differ from that of ribosomes from other sources in a definitive manner.
Ribosomes are composed of smaller subunits, which are assembled from precursor particles of a different size. They occur in larger complexes on mRNA (polysomes). These forms of different but specific size can be separated and characterized by on the basis of size in the ultracentrifuge — i.e. by their sedimentation coefficient.

Amplification and examples

Prokaryotic monoribosomes (e.g. E. coli) have a sedimentation value
of 70S, the cytoplasmic monoribosomes of eukaryotes (e.g. rat) 80S,
and those of mammalian mitochondria between 50 and 60S. The values may differ for different eukaryotes and prokaryotes, but are constant for one species, reflecting the constant ribonucleoprotein composition of the particles.
All ribosomes have two subunits — a large subunit (50S and 60S for the prokaryotes and eukaryotes mentioned, respectively) and a small subunit (30S and 40S). The subunits are identified by ultracentrifugation, which is also used to separate them preparatively. Hence it is natural that their S values should be used to name them.
The formation of ribosomal subunits from RNA and protein involves sequential addition of proteins. The different sized intermediates at different stages can be differentiated by their sedimentation, and it is natural to refer to them by their S values.
Ultracentrifugation is also used to separate and characterize the ribosomal RNAs in a similar manner.

Bibliography

The Wikipedia entry on ribosomes corroborates some of the factual data I have presented.


What happens when we know that there is something that we forgot but we can't remember what it was? I think it happens for everyone that sometimes we go to a room and forget why we went there. Is there any research or article on this?

It is a phenomenon known as room amnesia, some research has shown that your brain may use physical barriers like the room and doorways as a way to compartmentalize thoughts.
One article summarizes it here:

  The researchers say that when you pass through a doorway, your mind
  compartmentalizes your actions into separate episodes. Having moved
  into a new episode, the brain archives the previous one, making it
  less available for access. It’s as if you slam a mental door between
  what you knew and…what was I saying?

This is the research.


Why African species are larger in size compared to other parts of world? Why are African species larger in size compared to other parts of world?

Best Example: African elephants are very famous for Giant ears.

So many African Animals listed in Guinness World of Records. (Source)

When it comes to mammals this cannot really be evaluated without taking the Megafaunal mass extinction into account. This mainly refers to the extinction of large mammals from the Pleistocene Megafauna, which affected different parts of the world differently. More species were extinct in the Americas, Australia and northern Eurasia, and fewer species in Africa and southern Asia. One of the reasons for the differential extinction is thought to be the shorter evolutionary history together with humans in the areas that were more affected (since over-hunting is though to be one of the main explanations, see e.g Sandom er al. 2014).

If you only look at currently extant animals, you ignore the Wooly mammoth, the Woolly rhinoceros, Ground sloths and many other large species inhabiting higher latitudes, and this will give a very biased picture when searching for evolutionary reasons for the differences in body size between continents.


Sugars which are Carbohydrates and vice-versa? Is it right that are all sugars are carbohydrates but not all carbohydrates are sugars?

If so, which carbohydrates are sugars and which aren't and why all sugars are carbohydrates?

If I had to answer I'd say there are carbohydrates of three kinds: sugars, starch, fiber and from which we can deduce that "not all carbohydrates are sugars".

You need to make a distinction between polymers and monomers (or dimers).

Typically, sugars are monomers like glucose, maltose, or fructose. Sucrose (table sugar) is a dimer. These are all carbohydrates (made up of carbon, oxygen, and hydrogen).

Polymers of these sugars are also carbohydrates. For example, starch, glycogen, and cellulose.

Cellulose, which you called fibre, tends to be structural, and is only found in plants (think celery, or wood, or paper). Starch, is also synthesized by plants, and could be used for energy storage (as I recall). In animals, monomeric glucose is stored as glycogen in skeletal muscle, where it becomes available as energy for short bursts of energy.


How does natural selection explain sexual display? As I understand it, animals sometimes grow more vibrant colors, bigger feathers, elaborate dances, build shiny nests, all to impress the other sex. However, these are all superfluous to survival -- any nutrition or energy spent developing these attributes or conducting these rituals are no longer usable for hunting or child rearing, for example. Given the same animal who does one of these wasteful practices versus the same animal who doesn't, in theory the latter should have the advantage in its chances of passing its genes down.

Why is it then, that sexual preference grows towards these wasteful growths and habits, rather than ignoring these sexual displays for sheer survival efficiency?

Short answer
Survival does not get your genes into the gene pool, reproduction does.
thus reproduction based selective pressures can be stronger than survival based ones. there are plenty of organisms that die during or right after mating because of this.
Consider an example In species A finding a mate is fairly rare, it may only happen a few times in an organisms life. if individual X is guaranteed to mate and reproduce when they find a mate but will die after mating, and individual Y will not die after mating but only has a low chance to mate then the genes from X will spread much faster than the genes for Y, because mating is already a rare event, but X genes spread every time while Y genes will also only spread once or often not at all, and will also take much longer.
Or to put it another way, a chicken is just an eggs way of making another egg, the survival of the chicken is only useful as much as it facilitates reproduction.
Any mutation  that happens to make you better at attracting a mate will spread, how it does so is basically irrelevant as long as it works, loud noises, bright colors, eye spots anything that draws the females attention works. studies on several bird species have shown even the colored bands used to identify birds for study effect their mating chance is they are right colors. Animals often already have a variety of biases for their attention hijacking them is an easy way to improve your chances of mating.  Of course once a way evolves that reliably improves mating chances preference for that becomes favorable as well which can lead to a run away selection feedback loops AKA Fisherian runaway
https://link.springer.com/article/10.1007/BF00172135


positive and negative feedback I want to know more about positive feedback in gene regulation and to know the similarity and differences between positive and negative feedbacks.

A feedback loop is a network structure in which the gene is able to regulate itself via a single path.

$A\rightarrow B\rightarrow C\rightarrow A$

Interactions can be called positive or negative depending on their effect on the downstream gene. If a gene A represses another gene B, then it is a negative interaction; when it activates then the interaction is positive.

If you multiply the signs of all the interactions in the path from gene-A back to itself you will get the sign of the loop.

So a positive FBL will result (in the above example) if :

A activates (+) B; B activates (+) C; C activates (+) A
A represses (-) B; B activates (+) C; C represses (-) A
A activates (+) B; B represses (-) C; C represses (-) A
A represses (-) B; B represses (-) C; C activates (+) A

Any other combination of interaction will result in a negative feedback loop.

Differences are based on their properties. I'll mention two main unique properties of each.

PFBL

Switching circuits
Hysteresis

NFBL

Expression control (feedback control)
Oscillations

Similarity: well, nothing more that they both are called feedback loops and the topology is similar (just the nature of interaction is different).


why dead mouse doesn't bleed when we cut their skin? When we are pricked by a needle, we bleed nevertheless it's so small wound.
But when we do mouse anatomy, it doesn't bleed even if we cut their whole abdominal skin.
Other student asked about that, professor didn't know exactly but just guessed that mouse skin has no blood vessel. But I think it's wrong. that makes no sense.
As my guessing it's because mouse is dead when we do anatomy so there is no enough blood pressure.
Mouse have to bleed like ourselve. is this wrong?

From personal experience, extracting organs/tissues of over 1000 mice I can give some hints:
Mice blood coagulates quite fast after death. If you need to extract blood, you are under time-pressure and many scientists extract the blood directly after death from the heart using a syringe. If you are not fast, you miss the chance of drawing blood as this can't be done after coagulation. Others cut up the thorax (post mortem) and then directly draw blood with a syringe. I personally never tried this technique but I spectated that mice bleed a bit, directly after death, when opening the thorax, however it's not much.
After drawing all blood from the heart, mice don't bleed, no matter where you cut, potentially because of low blood content remaining. (Un-?) Fortunately, I never had to cut mice that were alive.. so I cannot tell you what would happen if they were alive.
Edit: Also, in theory, the smaller an animal is, the higher becomes the diffusion/volume ratio and surface-tension/volume ratio. This means smaller animals need less active blood circulation and and their blood vessels might have a small diameter, so that most blood would be kept inside by surface tension if these vessels were cut.
Edit due to comment:
The extractable blood from mice is around 1.5 ml, and I have seen opening of the thorax within seconds post mortem with minor bleeding. Afterwards, the majority of blood (1.5 ml) was extracted directly from heart with a syringe. As this was post motrem, I cannot exclude the possibility that coagulation of blood in small peripheral vesicles already affected the observation or how heart beating would affect it. I cannot say what would happen in live mice and I am happy that I don't have this knowledge.


Adaptive radiation vs divergent evolution What is the difference between divergent evolution and adaptive radiation? People have Said different things
Divergent evolution is when species from a common ancestor evolve differences by adapting to different environmental conditions
Adaptive radiation - species evolve differences due to the different environments
Are they essentially the same thing also I’m confused with the terminology niche
Could someone please tell me the similarities and differences between the two

They are similar, but distinct, concepts.
In divergent evolution, selective pressure causes differences within a single species to accumulate, eventually leading to speciation. Speciation can be caused by a variety of factors, such as geographical, reproductive, behavioral, or temporal isolation, etc.
In adaptive radiation, typically several niches are present in an ecosystem, leading to several species evolving from a single common ancestor. A niche is essentially an opportunity for a species in an ecosystem to evolve, to where there is little to no competition. Darwin's finches tend to be the prime example for adaptive radiation. Since there was little competition when the finches first arrived at the Galapagos islands, they speciated into multiple distinct species to specialize in consumption of seeds, fruits, insects, etc. Eventually, each species evolved to have distinct traits, such as in their behaviour and reproduction, making mating between species close to nill.