ID this insect please. SE Brazil Oct 2017 A number of these large flies were praying on smaller stuff / mid day / in the low altitude rainforest sections of SE Brazilian Rainforest

This is, for sure, a robber fly (Diptera, Asilidae). My guess is that this one belongs to the Genus Promachus.

Here is a photo of Promachus rufipes (from North America) for comparison:

Coincidentally, even the prey (a wasp) is in the same position of the one in your photo!

This Genus has 9 species. If this is in fact Promachus, you'll have to find out which are found in South America.


Why is Capsaicin injection not used instead of nerve surgeries for pain? High concentration capsaicin kills c & a-delta nerve fibers permanently or at least long term.
This has been known for 30 years.

But capsaicin is only used in creams and patches, and not for injecting direcly into nerves, and people resort to nerve surgeries like nerve blocks, razor-damaging nerves, or rhizotomy to cut the nerve partially or fully. All of these options affect not just pain functions, but overall sensory functions.

On the other hand, capsaicin destroying c & a-delta fibers just affects pain.
So why is no one interested in capsaicin injection as an option before cutting nerves?

There is a simple answer to your question: it might cause a massive inflammation-like response and it might also hurt really, really badly.

Capsaicin activates heat receptors which are not only involved in heat reception (that would cause the pain as TRPV1, the receptor, is strongly activated at temperatures higher than 43 degree Celsius - accordingly, it will feel like burning from inside) but also in sensing inflammations within the body. That means that your body will think it has to take strong and immediate action if capsaicin enters tissues directly, flush out a bunch of neuropeptides and actually might start destroying the affected tissues.


Animals with substantial five-fold symmetry besides starfish? Any land animals? Animals with four, six and eight legs are widespread while the concept of seven legs (fictitious Heptapods) are the makings of amazing scifi short stories and blockbuster movies.

Are starfish the only types of animals currently (or ever) with five mostly equal sized appendages and substantial five-fold symmetry? Are there theories why five is unusual on land but common in the sea?

update: There is an interesting subtlety here. This answer points out that a sea star's legs are the little things under the five appendages, so I've adjusted the question to address instead five-fold symmetry and five appendages.

below: "Ophiopetra lithographica from the Lower Hienheim Beds (Lower Tithonian,Upper Jurassic) near Regensburg, Germany" from here.

below: "A green brittle star - Ophiarachna incrassata" from here.

below: "Une ophiure superbe (Ophiolepis superba) à la Réunion." from here.

Many (if not most) of the Echinoderms (to which starfish belong as well) have five-fold symmetry, such as many sea liliy (Crinoidea) and sea urchin (Echinodea) species.

Five-fold symmetrical sea lilly:

Sand dollar (type of sea urchin):


Mutating a protein without mutating the gene? Is it possible to mutate a region of a protein (says about 300 amino acids long) without actually mutating the gene?

One possible way that I can think of is to use RNAi and specifically block that region of the mRNA which codes for the 300 amino acids in the protein?

But then wouldn't it cause a problem in the translation of the remaining region of the protein?

Are there any methods out there to mutate a region of a protein without mutating the DNA?

I assume that you mean changing the amino acid sequence in a single protein in an organism to one that no longer reflects the sequence predicted from the DNA sequence.  In that case, I would suggest using ADAR (Double-stranded RNA-specific adenosine deaminase) or similar enzymes.  ADAR deaminates adenosine to inosine, which is read by the ribosome as a guanine.  I know that it's activity is regulated, but I'm not sure how you could redirect it (perhaps with an antisense RNA that yields a double-stranded binding stretch in the target RNA.


Why is 70% ethanol preferred for aseptic techniques? Are other concentrations (say 80%) less effective,or is this just for convenient manufacturing? Is the concentration chosen only because it is less volatile than 100 percent ethanol and hence safer?

70% ethanol is the minimum concentration when used in a lab setting for aseptic technique. You don't want to go lower, because it will not kill the microorganisms you are trying to kill.

However the solution requires water to be effective at doing its job. The 30% water is necessary to provide sufficient polarity to the solution.

EDIT

  A rough indication of a solvent's polarity is a quantity called the dielectric constant. The dielectric constant is a measure of the solvent's ability to insulate opposite charges (or separate ions) from each other...

  Water is the most effective solvent for promoting ionization, but most organic compounds do not dissolve appreciably in water. They usually dissolve, however, in alcohols, and quite often mixed solvents are used. Methanol - water and ethanol - water are common mixed solvents for nucleophilic substitution reactions.

Dielectric Constants

Water - 80
Methanol - 33
Ethanol - 24

-Organic Chemistry 11E T.W. Graham Solomons et.al.

Note

Dexter's answer provides experimental evidence for why 70% ethanol is used. My answer is based on my experience and understanding and the concentration that I have used in the lab. I would add that 70% was likely chosen as a balance between cost and effectiveness. If you are a little off on mixing the solution from 95% Ethanol stock, then you are still at a bactericidal level, where as if you err at 60% concentration, you could start to let a few bacteria survive.

70% ethanol is still flammable and should be handled with care. The issue with ethanol greater than 98% pure is that the only way to distill the last 2% of water out is to add benzene, and benzene is a known carcinogen. There will always be trace amounts of benzene in 100% reagent grade ethanol.


Is there a good explanation for this swarming pattern? A film clip would be helpful here. A few days ago I noticed a swarm of newly hatched flying bugs about 20 feet away from me with the sun behind them so the shape of swarming (such as it was) was easy to make out. Several times, after creating various spiral shapes or chaotic masses they returned to a sort of 'holding pattern' which I either never noticed or never saw before. To a pretty good approximation the bugs arranged themselves in what seemed like an "oscillating drum head" pattern that is well approximated by a rotated sinc function. The peak at zero is a little exaggerated here but the bugs were more or less dispersed on a shape like:

subject to a light breeze and continuous adjustment. I know that people have studied swarming behavior and made models but are there any that account for this one? It has a lot of significance in ODEs and engineering but I never associated it with swarming behavior.

Thanks!

I watched some youtube videos but couldn't find any swarming that looked like rotated sinc function.

The following is nothing but the guesses of someone who doesn't know much about swarming!

One pattern that is often found (through computer simulation and empirical observation) in swarming is a simple 2D rotation.

Let's first consider only the static form of the shape you observed. This shape might be the consequences of multiple rotating layers. Do you remember what kind of dynamic had the individuals within your sinc function?

Oscillation is a pattern that is also sometimes observed in swarming. The oscillating behavior might be the result of inertia. Just like a pendulum, individuals that are far away from the group accelerate continuously in the same direction up to the point they reach the middle of the group. Then they undergo a inverse acceleration up to the point they reach a null speed and then start their cycle again. This inertia depend on the number of neighbors they align their movement on are low. For example, it has been shown in I don't remember which species of birds (I can't find the reference) that each individual align their movement according to only the 6th closest neighbors.

For more information about the 3 basic rules (separation, alignment, cohesion) that allow swarming behavior, have a look to the wiki page

In short, I hypothesize that thanks to the underlying 3 basic rules of swarming, the patterns of rotations and inertia together allow to explain your observations.


Why is polyploidy much more common in plants than in animals? There are very few animals with polyploidy like salamanders. Why is it that polyploidy is so uncommon in animals? On the other hand there are numerous examples of polyploid plants. If ut something to do with the gene dosage, how does it not affect plants?

Polyploidy is common in plants than in animals because in animals sex determination mechanism involves number and type sex chromosomes. Polyploidy will interfere with this mechanism and hence it is seen rarely in animals. I believe its probably because an animal progeny with multiple sex chromosomes won't be able to reproduce more of its kind unless it can also reproduce asexually (which is seen in plants as mentioned below).

Plants, on the other hand do not have any such sex determination (based on number or type of chromosomes) and majority of them can also reproduce vegetatively. This vegetative propagation enables multiplication of polyploid plants. Sexual reproduction will result in loss of desired polyploidy as per the principle of segregation. However, if a polyploid plant can produce a viable progeny sexually, it might have a different ploidy than its polyploid parent which won't happen if the parent reproduces asexually. Hence, polyploid plants can be classified as sterile and fertile polyploids (the reference will give a detailed account on this mechanism).

Refer the section of Polyploidy (page 115, Chapter 6) of this book (Principles of Genetics, Snustad and Simons, 6th edition)

When it comes to gene dosage, animals do show gene compensation of X-linked genes by various methods. Example- formation of Barr Body in human females (Note that this has nothing to do with polyploidy, but happens since females have one X chromosome more than males). Whereas gene dosage in polyploid palnts has been exploited for improved agricultural yields as they have shown better productivity than their diploid couterparts.


What is delayed compliance in blood vessels? What I understand is it is a permanent stretch of the vessel wall. Is this true or does it mean something else?

First let's consider what compliance means:

C = compliance
ΔV = change in volume
ΔP =  change in pressure

Delayed compliance
The response of a blood vessel to a sudden change in pressure. When the volume and so the pressure highers in the blood vessel the vascualar wall will stretch. As the wall of the vessel stretches the pressure inside the vessel will fall. So an increase of compliance is the result(look at the formula ΔV will get higher because the wall stretching will make the vessel larger at so the volume bigger and the pressure less). this change in compliance is what they call delayed compliance.

I don't really think you can speak about permanent because it's a dynamic process.


Biological meaning of Lotka-Volterra Jacobian matrices In a book about community ecology, I learned about Lotka-Volterra models and dynamic food web models (I am not an ecologist in the first place).

In one of the chapters, a Jacobian matrix of partial derivatives of the Lotka-Volterra model at equilibrium densities is given:
\begin{bmatrix}-&-&0&0\\+&0&-&0\\0&+&0&-\\0&0&+&0\end{bmatrix}
where + and – represent positive or negative values.

This matrix is later interpreted in terms of direction of trophic links in a food web, but the reasoning allowing to jump form one to the other is not detailed.
So what is the biological meaning of these values?

The Jacobian tells how the system changes along different state variables (which can be, for instance, the concentrations of the predator and the prey).

The Jacobian matrix by itself doesn't give you a lot of intuitive information. However, the eigenvalues of the Jacobian matrix at the equilibrium point tell you the nature of the steady state. For example if all the eigenvalues are negative then the system is stable at that point and the equilibrium point is called a stable node. If some of them are positive and some are negative then the system is metastable at that point and the point is called a saddle point. If all eigenvalues are positive then the point is unstable. If the eigenvalues have an imaginary part then the system exhibits oscillations. All these properties are local i.e. they just tell you the behaviour of the system near the equilibrium point.

I hope I am clear. This is not in a strict sense, a biological question. If you want to know more then read a book on nonlinear dynamics. Non-linear dynamics and Chaos by Steven Strogatz is a good place to start.

EDIT

When the system is locally linear (linearized at a given point) then the system dynamics at that point can be described as
$$\frac{dx}{dt}=J.x$$

Where $x$ is the state vector (a vector of the variables in the system) and $J$ is the Jacobian matrix. In this situation, the signs will denote the effect of a variable on the other variable. However, I am not sure (I feel it is highly unlikely) if this can be used to make any inferences about the food web.


hummingbird feeders - is sugar water healthy for them? The top results on google for DIY hummingbird feeder suggest a white-sugar solution for the feed.  In humans we make a big deal about processed sugar vs. the sugar you get from, say, eating a piece of fruit.  Does this matter for hummingbirds?  Their metabolisms so high, it makes me wonder if this is relevant.  Maybe it is not!  But I would like to know.

Hummingbirds absolutely eat insects, and HONEY and BROWN SUGAR are a huge NO NO.
  The following is a statement from: http://wildbirdsonline.com/index.html

  Every year, as more studies are completed, we learn more about
  hummingbird life and diets. However, we find that some people think
  that hummers can survive on nectar alone. Nectar provides quick energy
  to sustain their extremely high metabolic rate and little else. This
  is important enough that the shape of the bills of hummers have
  evolved in partnership with the flower shapes that they frequent.
  Consequentially, there is a wide variety of hummingbird bill lengths
  and shapes among the more than 300 species that exist.

  There is another critical food source for the hummers. Essential
  vitamins, minerals, amino acids, proteins, oils and fats, fiber, etc.
  all come from the insects they eagerly consume, not the nectar. Their
  preferred insects include, but are not limited to: small beetles, true
  bugs, weevils, flies, gnats, mosquitoes, aphids, mites, leafhoppers,
  flying ants, and parasitic wasps. Their favorite insect food source is
  the spider and harvestmen (daddy long legs). Some ornithologists
  estimate that spiders are between 60% and 80% of their diet.

But there are lots of other resources for you to find accurate information about feeding hummingbirds.


Clonal and subclonal mutations in cancer Likely this will sound as a silly question, but I don't know whom to ask. Ok, here it goes.

McGranahan et al link found that tumors with high clonal antigen load are more likely to respond to the immune checkpoint blockage.

Bozic et al link (at the same time) proposed a probabilistic model to determine the number of clonal and subclonal mutations. They found that fast growing cancer types (where growth is cell division over cell death) are more likely to generate a higher number of subclonal mutations.

Knowing that melanoma and NSCLC are fast growing cancer types, these results seem to contradict each other. We know that they are fast and we know that both melanoma and NSCLC are cancer types where immunotherapy is most effective.

Plus, probabilistically how likely it is for a certain cancer lesions to have lots of shared mutations? A totally genetically homogeneous lesion with no branches with a very high number of mutations.

Or (much more likely) I'm missing something.

They don't really contradict each other; the clonality of neoantigens adds an extra layer over the overall mutational load ; but overall mutational load (and consequently overall neoantigen burden, because mutations in a fixed sequence context generate neoantigens at a certain rate) by themselves are also predictive.

Tumours with a high neoantigen burden tend to generally respond better anyway (See Snyder et al, NEJM , Rizvi et al, Science and Van Allen et al, Science) and also the fact that mismatch repair deficient cancers generally tend to respond.

So if you take high neoantigen tumours already (both lung and melanomas have extremely high mutation burdens), and then stratify them based on neoantigen clonality , you tend to further stratify patients by response associating with checkpoint blockade.

The whole point of McGranahan et al was to point out that it is possible to raise immune responses that target all the cells in a tumour, and that the ability to do this may dictate survival in general and checkpoint blockade response in particular, but only when antigen presentation and immune infiltration are intact. McGranahan et al note that clonal neoantigens do nothing in Lung squamous cancers because of depleted CD8 infiltration and MHC class I expression and there is other work (See http://www.pnas.org/content/113/48/E7759.abstract )

As for this bit

  Plus, probabilistically how likely it is for a certain cancer lesions
  to have lots of shared mutations? A totally genetically homogeneous
  lesion with no branches with a very high number of mutations.

That is quite complicated to answer; but as a general rule it is worth remembering that,  as the number of divisions and the number of mutations (and ergo prospective subclones) increases, for tumours to stay clonal it requires extremely strong selective sweeps so that at any given time a very small number of clones tends to predominate, and at least in untreated/pre-treatment tumours, there is the tendency for a lot of them to show effectively neutral patterns of evolution ( http://www.nature.com/ng/journal/v48/n3/abs/ng.3489.html )


Do lunar rhythms have really impact on plant growth? It is commonly known that lunar rhythms have influence on plant growth, and there are even lunar calendars to know when planting, pruning, transplanting, harvesting, etc.

I know that the lunar cycles affect the tidal patterns, and this consequently can affect the life of sea organisms like reef corals, fishes, etc., but I am very skeptical that this can affect the growth dynamics or plant physiology.
 I would like to know how it works from a scientific perspective, E.g. the temperature and precipitation are the main limiting factors on plant growth, but I'm curious if the moon light or its magnetic field can also be a limiting factor on plant growth.

Then my question is simple, the lunar rhythms really influence the growth of plants, if so, how?

Great question! The way I will do this is by explaining a bit about what moon planting is, then I will go through the articles I have found one at a time, to provide the different persepctives on moon planting, as it is called.

What is moon planting?

Moon planting is a methodology of planting, in which the lunar cycles are used as guides to know when to plant.

How might it work?

The first article is a great article about a gardener who tried to do moon planting, but it did not work for her, until she realized she did it wrong. Then, she found out the logic behind why lunae planting works. It really doesn't have to do with lunar cycles. Here is her explanation:

  Let’s look at a possible scenario. Gardener I is a moon planter; Gardener II isn’t. Both gardeners wait till spring to plant their beans. (No sensible cool climate gardener will plant beans in winter. It’s too cold for them to germinate, and many seeds will rot or be taken by ants.) But come the first warm spell Gardener II succumbs to one of the great spring urges and plants the beans at the first hint that spring has arrived. Gardener I, on the other hand, waits till the next good moon planting time before planting the seeds. Early warm spells are usually followed by another cold one… and again seed planted too early may rot. Even if it doesn’t, plants that suffer any set-back when they are young usually don’t do as well as plants that have flourished right from the start. (The set-back can be from cold, boggy soil, snail or scale attack — the effect is the same). So counterintuitively, beans that are planted later in spring will probably do better than beans planted too early.

The opposite works too when planting in autumn. By the lunar planting schedule, it is better to grow earlier, and since the soil is warmer, the plants will grow better.

In the second article, the author reviews the research done on the effect of lunar cycles on reproduction, germination, and more. However, only the work of a researcher, L. Kolisko, shows evidence for the benefits of lunar planting. Therefore, the conclusion was lunar planting are not significant to affect crop yield.

However, in another article, it shows that there are many cycles in plants that are affected by the lunar cycles and that for some organisms, the lunar cycles do affect reproduction, germination, and production of different metabolites. Therefore, lunar planting might have an effect in that way as well.

Conclusion

The conclusion is that lunar planting may actually work, but many scientists are debating about it. So in reality, we aren't 100% percent sure about it, because there is evidence supporting it, and evidence contradicting it.

References

http://danfingerman.com/skeptic/Moon_planting.pdf
http://www.howplantswork.com/wp-content/uploads/2009/07/beeson_1946.pdf
http://www.howplantswork.com/wp-content/uploads/2009/07/schad.pdf


Why did the indigenous peoples of northern Asia and America not evolve the same physical characteristics as people of Nordic ancestry? I was watching DW's documentary on the Arctic the other day, and I was struck by how the indigenous peoples of the far north seemed - visually speaking - to fit into two categories. On the one hand, there are the peoples of northern Europe, with their pale skin and their preponderance of blue-eyed and blond-haired individuals. On the other hand, there are the Yakuts, Inuit, Aleuts and many more, whose physical similarities - they all seem to share an East Asian-looking bone structure, as well as black hair, deep brown eyes and a skin tone akin to white coffee - belie vast differences in language, culture and belief. Why did northern Europeans evolve these distinctive physical traits while other northern peoples did not? It's probably worth noting that the physical and temporal separation between, say, the Finns and the Nenets is much less than that between the Yakuts and Inuit.
It might be helpful to approach this by splitting up the different characteristics:

Pale skin: Of all the physical characteristics, pale skin seems to confer the most obvious advantage: better absorption of sunlight, and the various benefits connected therewith. Although I've not carried out any kind of systematic analysis, non-Nordic northern peoples do not seem to have a lighter skin tone than their southern neighbours (i.e. the Chinese, Japanese, Native American, etc peoples).
Blond hair and blue eyes: These are the most striking physical differences between Nordic and non-Nordic northern peoples, however it's not clear - at least to me! - what advantage they confer in high latitudes. Is it just blind chance that these characteristics evolved in northern Europe, and not in, say, Central America? If it's not blind chance, why did these characteristics evolve in northern Europe, but not in other northern regions?
Other characteristics: I have read that there are other characteristics, e.g. greater height, associated with high latitudes. Do Nordic and non-Nordic northern peoples have any of these characteristics in common? If there is divergence here, how might it be explained?

If you look at the Wikipedia image from their lovely article on human migration, you'll notice that after arriving from Africa, some humans went west and others went east.  The ones who went east went on to most of the arctic regions, except in Western Europe.  The physical differences between these groups probably can be explained as random variation, though we may never know what social and environmental factors (such as the behavior of predators or prey) might have driven adaptive changes.
Previously some might have suggested different levels of Neanderthal ancestry could be involved, but this seems even harder to credit in light of recent evidence that all humans have a small but significant degree of Neanderthal heritage.


tools to reconstruct the transcriptional regulatory circuits? What are commonly used tools to reconstruct the transcriptional regulatory circuits that govern diverse cellular responses and what input data sets do they accept?

Inferring transcriptional / regulatory networks from empirical data is an active area of research, and to my knowledge there aren't many mature tools for this type of analysis. I see mostly mathematicians, statisticians, and engineers working on this problem, probably because of the intense quantitative theory involved. Even if mature tools do exist, I doubt they're tailored for the typical biologist--more likely, they are geared toward scientists with a more quantitative background.

That being said, I am aware of 2 or 3 pieces of software that may provide a starting point for the curious or the adventurous: AIRnet (described here), iBioSim (described by Barker's PhD thesis, currently the second hit on this Google search), and maybe Ingenuity Pathways Analysis (which requires a paid license). The only one of these tools I've even tried to use is iBioSim, and at the time (2 or so years ago) it was a very kludgy process.


is there a limit to how much humans can taste? kind of a weird question, sorry, but i was wondering--is there a threshold at which our taste buds become overwhelmed? if i, say, put some supersweet compound in my mouth, would there be a point at which adding more compound would not increase the level of sweetness i perceive? i'm sure that if i experienced too much sourness or spiciness, my tongue would probably go numb, but what about sweetness and bitterness? and what is that amount? does it vary from person to person, or are people's opinions on different sorts of food just preferences, and the threshold at which they become unable to process more of a specific taste the same for everyone?
thank you. i hope this makes sense.

Yes, there is a threshold of taste.
According to this article

The taste system encodes information about the quantity as well as the identity of stimuli. In general, the higher the stimulus concentration, the greater the perceived intensity of taste. Threshold concentrations for most ingested tastants are quite high, however. For example, the threshold concentration for citric acid is about 2 mM; for salt (NaCl), 10 mM; and for sucrose, 20 mM. Since the body requires substantial concentrations of salts and carbohydrates, taste cells may respond only to relatively high concentrations of these essential substances to promote an adequate intake. Clearly, it is advantageous for the taste system to detect potentially dangerous substances (e.g., bitter-tasting plant compounds) at much lower concentrations. Thus, the threshold concentration for quinine is 0.008 mM, and for strychnine 0.0001 mM. As in olfaction, gustatory sensitivity declines with age. Adults tend to add more salt and spices to food than children. The decreased sensitivity to salt can be problematic for older people with electrolyte and/or fluid balance problems.

Interestingly,

In fact, all of these tastes can be detected over the full surface the tongue. However, different regions of the tongue do have different thresholds. Because the tip of the tongue is most responsive to sweet-tasting compounds, and because these compounds produce pleasurable sensations, information from this region activates feeding behaviors such as mouth movements, salivary secretion, insulin release, and swallowing. In contrast, responses to bitter compounds are indeed greatest on the back of the tongue. Activation of this region by bitter-tasting substances elicits protrusion of the tongue and other protective reactions that prevent ingestion

And in most of the individuals, this threshold is same for both right and lefts parts of the tongue.
Reference
Now as stated by the first article, taste threshold depends on the age of the individual.
More interestingly, it also depends on the individual's state of mind, i.e. whether depressed or anxious.

Circumstances in which serotonin (5-HT) and noradrenaline (NA) are altered, such as in anxiety or depression, are associated with taste disturbances, indicating the importance of these transmitters in the determination of taste thresholds in health and disease.

Measurement of taste function in healthy humans before and after a 5-HT reuptake inhibitor, NA reuptake inhibitor, or placebo showed that enhancing 5-HT significantly reduced the sucrose taste threshold by 27% and the quinine taste threshold by 53%. In contrast, enhancing NA significantly reduced bitter taste threshold by 39% and sour threshold by 22%.
Reference

Hence threshold value varies from substance to substance as well as from individual to individual.
Here is a good article giving threshold values of different chemicals in various food items.
Hope all your questions are solved :)


Difference between water and tea My friend heard that tea is worse for drinking than water because "cells have a special membrane and tea has special supplements and membrane doesn't let tea pass and this is why skin is dry even when you hydrate with tea a lot", something about "lipid bilayer".

Is there is some nice scientific article on water andd tea difference to human organism?

Your question is very awkward.

Let's define Tea as boiling leaves in water. At the end, you remove the leaves and drink the flavoured water.

At this point, the "tea" is still very much water - as in tea is water with dissolved chemicals from the leaves. Note, the word chemicals is not to be interpreted in a negative way because everything (including water) is a chemical.

So, the difference between tea and water are the chemicals that dissolve. What are these chemicals? The answer to that depends very much on the tea. Another difference is the temperature - tea is typically hot.

You can look at this article about chemicals in green tea and their associated health benefits. You can do further searches for other tea types and for each of those chemicals.

In short, no you do not get dehydrated because of tea vs. water. Dry skin can be caused by a lot of different reasons. Oh and no, caffeine doesn't cause any significant amount of dehydration as far as I know.


Neuro-simulation tools I know, this question is opinion-based, but where else should I ask it (or how could I ask it here without being flagged "opinon-based!")?

Which neuronal simulators - in the line of NEURON and GENESIS - are the "best", "mostly used", "mostly influential" today, not only in supercomputing, but also for small scale (personal) use?

The one I found best - even though designed for large scale applications - for my small scale (personal) requirements was nest, an explicit successor of NEURON. I have the impression, that nest is "better" for me than NEURON, in terms of usability, visualization, data exploration, ... but I don't know if there aren't even better neuro-simulation tools.

Would anyone mind giving his/her opinion?

I have only used NEURON and the DIY approach for small scale simulations.

You can have a look at this comparative table:

  https://grey.colorado.edu/emergent/index.php/Comparison_of_Neural_Network_Simulators

which was last updated in 2014.
Except NEURON, GENESIS, and NEST, I have also heard positive comments about Brian.


What is the identity of this fruit/tree found near Berkeley, California, USA? Please help identify this fruit/tree found near Berkeley, California.

The tree had no leaves. The fruit looked like a pear from far. It has no flesh. When the outer skin is peeled, the seed looks like a large avocado seed. Very little smell from the fruit/seed not a bad smell and not an appetizing smell as well.

Could this be a Yellow Buckeye?

Given that it's in central California, it's almost certainly California buckeye (Aesculus californica).  The tree is common in the Coast range and Sierra foothills of California.  It has adapted to the Mediterranean climate of the region by growing during the wet winter and spring and then dropping its leaves during the hot, dry summer.  The large seed is toxic if consumed.


Autosomal genes expression occurs from both alleles simultaneously Based on my understanding of Knobil and Neill's Physiology of Reproduction.
For the vast majority of autosomal genes, expression occurs from both alleles simultaneously. In mammals, however, a small proportion (<1%) of genes are imprinted, meaning that gene expression occurs from only one allele (some recent studies have questioned this assertion, claiming that the number of regions of parent-of-origin methylation in, for example, the human genome, is much larger than previously thought).

I'm confused, why would expression occur from both alleles simultaneously? Ex. if it was "Rr" - the expression would only occur from "R", as opposed to both alleles simultaneously?

Definition of dominance and recessivity

By definition, an allele is dominant over another allele if the phenotype of the homozygotes for the dominant allele and the phenotype of the heterozygote are the same but not the ones of the homozygotes for the recessive allele. In other words, let $p_{ab}$, be the phenotype of an individual with alleles a and b, then

$p_{rr} = P_1$
$p_{rR} = P_2$
$p_{RR} = P_2$

, where $P_1$ and $P_2$ are two phenotypic describer.

Note btw, that very very few traits have their variance explained only by the genetic variance, even fewer are explained only by variance at a single locus and yet even fewer have a locus that show a simple dominance / recessivity pattern.

Expression

If needed, please check gene expression.

The fact that an allele is dominant over another does not mean that the other allele is not being expressed. In fact, it does not say anything about the molecular mechanism by which this dominance pattern is achieved. It is possible that in some cases, if the recessive allele was not expressed at all, then the resulting phenotype would be $P_3$. It just so happen that most of the time, both alleles are being expressed.

Imagine for example a case of a locus coding for a black pigment. Let's consider haplotypes that where the gene is missing (copy number variation). Let's refer to such haplotype with 0. 00 are white. 0r individuals are light grey. rr individuals are grey. The allele R causes the expression of a lot of pigments so that both rR and RR individual are indistinguishably black. The allele r is still being expressed in heterozygotes rR even the phenotypes of rR and RR individuals are the same.


The Uniqueness of DNA Paradox How can everyone have unique iris and fingerprints? After a certain amount of human beings have lived on earth, wouldn't it be possible to exhaust all possible combinations?

The same principle applies to DNA. Lets say counting all the nucleotides on a strand of DNA we find that there are a total of $N$. We know there are 4 types of nucleotides, thus the total number of possible DNA sequences equals $4^N$. This is exponential, and since $N$ is immensely huge, $4^N$ will be unthinkably huge as well. However, since $4^N$ is a finite number, how can DNA be guaranteed to be unique? Doesn't that contradict the pigeon hole principle?

The uniqueness of irises and fingerprints are, as you said, limited to the number of possible permutations of irises and fingerprints.

A similar problem exists in computer science, and is known as a hash collision. Given sufficient samples, there will always be a collision for a hash of finite size. However, the sample space is sufficiently large for iris and fingerprint analysis for this to not be a problem.

A typical iris analysis system produces 2048 bits of entropy, while a typical fingerprint analysis system produces about 82 bits. Even accounting for the birthday problem, the information space is large enough that the chance of a given false positive is sufficiently low to prevent a random person from passing fingerprint/iris authentication.

For comparison, the current world human population is 7.2 billion, or slightly under 33 bits. The risk of a hash collision occurring is small enough to be negligible.

Of course, side-channel attacks against such biometric systems are relatively simple, but that's another issue altogether.


Where can I find pdb files for macromolecules like receptors? I have tried going to the RCSB website and quite frankly it was useless since when I looked up receptors like say the metabotropic glutamate receptor 2 (mGluR2) I got no helpful results.

As pointed out in the comments, if you look for PDB files and you don't find them in the PDB, there is no solved structure. However, you can look in databases that contain models of proteins. Especially for the receptors the coverage has been increasing in recent years and so you may be lucky.

A good starting place to look for protein information is UniProt, where you find links to the Protein Model Portal and SwissModel. They contain models based on the PDB structure for Metabotropic glutamate receptor 3.


How to understand Aposematism and Batesian mimicry EDIT I want to understand the reason for intense animal colors. I.e. I don't want to understand the variety of the colors, just the intensity.

The Wikipedia page for Cethosia biblis says, the intense colors are a "warning" to enemies, which means the enemy is warned by the colors that eating that butterfly may result in death.

  [...], while the intense color of the dorsal sides of the wings is a warning
  to predators that the Red Lacewing has a bad taste, deriving from the
  poisonous host plants of the caterpillars.

In general it would make sense to me, that animals have learned something like "intense colors means danger". Although, I don't know how good animals recognize colors, but that would be another question.

But poisonous animals don't have necessarily intense colors. E.g. Sydney funnel web spider is very poisonous, but doesn't have intense colors, while on the other side some very intense colored butterflies are not poisonous like explained here. As a result, the explanation given in the wikipedia article doesn't make sense to me. I estimate it very unlikely, that animals learned something like "intense colors means danger", because there are of course examples where this is not true.

Therefore, I don't think the "Golden poison frog" has survived because his enemies recognize his intense colors and conclude "eating this frog will result in death" are hence hesitated to eat him.

My question is: Why does wikipedia say then, the intense colors of Cethosia biblis are a warning for their enemies?

PS: I just found the correct terms for my thoughts ("aposematism" and "batesian mimicry" and are reading now the appropriate wikipedia article. I didn't knew them when I've asked this question.

PPS: to avoid confusion: @DavidBlomstrom answered this version of my question https://biology.stackexchange.com/revisions/42554/2

I could be misreading your question, but it doesn't sound very specific. Rather, it sounds like you're asking "How can I make sense of all the various color schemes employed by venomous species?" So I'll take a stab at it...

Animal coloration is a very complex phenomenon, with a number of overlapping physiological traits, evolutionary strategies, etc.

Consider the famous relationship between the monarch and viceroy butterflies, which bear a striking similarity. The viceroy was long regarded as a harmless insect that predators avoided because it resembled the monarch, which many predators find non-appetizing.

More recently, it was proposed that the viceroy is also unpalatable. Thus, the similar color patterns may simply reinforce each other. (Mutual Mimicry: Viceroy and Monarch)

But that's just one isolated example of a bewildering spectrum of color schemes. Some animals apparently use bright colors as a warning - "I'm toxic!" - while other venomous species may be dull colored for whatever reason. A dull-colored species may use its venom to capture prey, which it captures in ambush; thus, it has evolved camouflage, rather than conspicuous colors.

Coloration is also about more than warning. Coloration can serve as a means of communication. It can help a member of a species recognize fellow members. Bright colors are very popular in mating rituals.

So you have all these overlapping traits and countless unique evolutionary experiments interwoven into a can of worms.

One example that comes to mind is venomous snakes native to the United States. The rattlesnake and cottonmouth are pretty drab-colored and generally well camouflaged. Of course, rattlesnakes warn potential enemies with their famous rattles. I think the cottonmouth can be considered fairly drab colored as well.

However, the coral snake has a very vivid and distinctive color pattern. And there are snakes that bear a remarkably resemblance to coral snakes (see some examples).


Where can I find histograms and tables of prevalence of mutations in cancer? At some point in the past I found a cancer portal site which had aggregated data for the relationships between various mutations and their prevalence in cancer types and tumor data. The data was presented in various pleasantly coloured interactive histograms and you could search per-gene or per-disease.

However after spending a few hours, I cannot find the site again. Though I have found many sites with a great deal of data and nice visualizations.

The nearest looking site, was this one:
http://plugins.biogps.org/data_chart/data_chart.cgi?id=673

But that doesn't have the level of detail that I remember.

Perhaps you mean COSMIC? The EBI Gene Expression Atlas also has pretty charts, but now mutations.


What is in Mosquito bites? I was wondering what is in the mosquito bites, which causes the swelling of the skin at the bite and also the itching. I know that the mosquito injects some stuff, but what is it?

When female mosquitos bite to suck blood, they need to overcome the body reaction against it. So when they found a bood vessel, they inject their saliva into the wound. This saliva contains substances which affect blood clotting and platelet aggregation (so the blood will stay liquid which is essential for sucking) and a vasodilatory substance (which widens the blood vessel and prevents contraction of it). The exact composition depends on the exact mosquito species.

These "foreign" substances cause a local immune reaction which results in the release of histamine in the skin. The itching and also the red skin and the swelling are a result of the histamine release. See the Wikipedia article on mosquitos for more information.

If you are interested in a deeper look on the composition of the mosquito saliva have a look at these two articles and their references (if there is help needed in getting the articles, let me know):

Role of arthropod saliva in blood feeding: sialome and post-sialome
perspectives.
Toward a description of the sialome of the adult female mosquito
Aedes aegypti.

Since the substances affect the blood coagulation cascade, there is some research going on if and how this can be used clinically. See this article for an overview or have a look at the original publication here ("Unique thrombin
inhibition mechanism by anophelin, an anticoagulant from the malaria vector")


DNA Topology of two circular chromosomes I'm reading DNA Topology: Fundamentals from where I quote :

  Topological aspects of DNA structure arise primarily from the fact that the two DNA strands are repeatedly intertwined. Untangling these two strands, which occurs in all major genetic processes may prove rather difficult. In the simplest case of a linear DNA in solution, untangling is possible due to the free rotation of the ends of the DNA. However, for all natural DNAs, free end rotation is either restricted or forbidden altogether. Consequently, untangling the two DNA strands becomes topologically impossible.

And from Wikipedia:

  However, a circular chromosome can provide other challenges for cells. After replication, the two progeny circular chromosomes can sometimes remain interlinked or tangled, and they must be resolved so that each cell inherits one complete copy of the chromosome during cell division.

Is there any evidence that proves the idea represented in the figure?

Yes, there is an abundance of evidence. I think the following electron micrograph is pretty convincing.

This image is from a review:

Gil-Ramirez G, Leigh DA, Stephens AJ. 2015. Catenanes: Fifty Years of Molecular Links. Angew Chem Int Ed 54:6110-6150.

It was adapted from the first paper to observe naturally occurring catenated DNA molecules, which were isolated from HeLa mitochondria:

Hudson B, Vinograd J. 1967. Catenated Circular DNA Molecules in HeLa Cell Mitochondria. Nature 216:647-652.

You can see this answer for an explanation of why catenanes form during replication:

How do catenanes form when DNA replicates?


How many centrioles/basal bodies are there in multi-ciliated cells throughout the cell cycle? I thought there were only two centrioles per cell, that convert to the basal body at some point during the cell cycle. I also thought there's one basal body per cilium, so I'm not clear on where the other basal bodies are coming from. I'd like to know the distribution of basal bodies and centrioles throughout the cell cycle in multi-ciliated organisms/cells.

It seems that there is one basal body per cilium in multiciliated cells. Centriole duplication (as far as I understand, a basal body is just a different name for a centriole that is attached to a cilium) is tightly coupled to the cell-cycle. There is always one pair of centrioles that are at the base of the primary cilium (of which there is exactly one in most cells).

But not in multiciliated cells. These cells are differentiated and can no longer divide, and their centriole duplication process is decoupled from the cell cycle. In fact, they aren't, strictly speaking, "duplicating", since many procentriolar bodies may form around one cylinder. Indeed, each cilium has its own basal body; thus a cell with hundreds of cilia has hundreds of basal bodies.

Ishikawa 2011 is a review that examines the structure of primary and motile cilia, and ciliogenesis. It does not spell out how the basal body gets there.
Anderson 1971 describes the formation of new cilia in monkey oviduct. They first remove the ovaries of these monkeys to prevent cells from differentiating (this apparently requires estrogen), then administer estrogen and look at EM images of the cells over the following 6 days. They describe at length the processes of basal body formation.
Dirksen 1991 is another review focusing specifically on basal body formation during ciliogenesis. From their introduction:

  In order for the 200-300 cilia to form that the fully differentiated cell will need, production of that many centrioles is required first.
  The cell, after the last division, has usually retained a pair of
  centrioles. To what extent these mature centrioles are involved in the
  earlier stages of centriole formation, in which centriole precursor
  structures of varying sizes and shapes are generated and proceed to
  undergo transformational changes of great complexity, is largely
  unknown..

Sorokin 1968 is apparently a classic text which goes over EM images of ciliogenesis at various stages, and proposes a series of events describing what is happening. This is probably what you want, re: where are the other basal bodies coming from.
Bettencourt-Dias 2007 reviews the research on the formation of new basal bodies. This is another publication that answers your question very directly:

  Many ciliated cells, such as those in vertebrate respiratory and
  reproductive tracts, can have 200–300 cilia per cell. This requires
  the generation of multiple centrioles during ciliogenesis. Here,
  centrioles are generated by two pathways, a centriolar and an
  acentriolar mechanism. In the first one, a parent centriole usually
  produces one daughter at a time; however, in certain cases several
  centrioles have been observed to develop simultaneously around one
  parent centriole, with the daughter centrioles being released into the
  cytoplasm to mature. The acentriolar pathway is the major pathway for
  basal body production. In this pathway, fibrous granules 124 that are
  70–100 nm in diameter first appear in the cytoplasm and subse quently
  move to the apical cytoplasm. Deuterosomes appear within the area.
  (...) Multiple procentrioles can grow out from deuterosomes, and
  mature daughter centrioles travel towards the apical region where they
  form ciliary basal bodies.


Looking for university/graduate-level texts on RNA Although I was not a biology major in college, I took the biology introduction sequence, as well as organic chemistry and biochemistry.

I would like to learn more about RNA and ribozymes. What texts/textbooks are currently used? Perhaps it's best to begin with a genetics textbook.

The scope of the book should cover be at a undergraduate level or higher, and should cover the dynamics and purpose of ribozymes.

As suggested by others, you can start with some basics on molecular biology. Genes - Benjamin Lewin and  Molecular Biology of the Gene - James Watson et al. are good books for the basics.

I haven't seen any book dedicated to RNA-biology and most of my understanding has come from reviews.

You can start by studying RNA secondary (and higher order) structures which is essential for understanding how riboswitches function. I would suggest that you first begin with the wikipedia article on this (it is not that great). The above-mentioned books would also cover the basics. You may then have a look at this review which is about thermodynamic and kinetic aspects of RNA-hairpins:

       Structures, Kinetics, Thermodynamics, and Biological Functions of RNA Hairpins

For Riboswitches you can refer to these reviews, which are quite comprehensive:

Ribozymes, riboswitches and beyond: regulation of gene expression without proteins
Riboswitches: Emerging Themes in RNA Structure and function

This is another comprehensive review on ribozymes:

        Ribozyme Structures and Mechanisms

PS: Some of these articles may not be freely available. You can mail the corresponding author (email address would be mentioned in the article) requesting for a reprint.


What is the energy source for adipocytes? Since adipocytes export fatty acids and glycerol and don't use them as an energy source, what is the main source of energy for adipocytes?

Adipocytes use glucose as an energy source. They express the insulin-responsive glucose transporter GLUT4 just like muscle cells so that when blood glucose levels rise they are primed to take the glucose up for fatty acid biosynthesis, but they also use glucose as a fuel molecule.


Can two populations of the same species pollinate during different times? My question comes from the Barron's SAT Subject Test Practice Test #1 question 2
It states:

Two populations of rhododendron, R. ferrugineum, grow in the same region of Connecticut. Although rhododendrons are able to cross-pollinate, these two population never hybridize. Which of the following is the most likely reason for this phenomenon?
A) Genetic drift has caused one populatoin to be betteer adapted than the other.
B) Self pollination is more advantageous because it increases variation in the gene pool.
C) One population produces pollen in early June when the pistils of the other population are not ready to receive pollen.
D)The two populations demonstrate convergence of two separate species over time.
E) The two populations fill different niches

The Barron's book says that the correct answer is C. Why? If the it's the same species, shouldn't they produce pollen at the same time?

Yes, they can.  Consider an original population that produces pollen over a fairly long time, and then something happens to select earlier & later times for different populations.  This is actually quite common for domestic plants such as fruit trees, where different varieties are selected (by humans) to produce fruit at different times.

As far as the question itself goes, it's more a case of the other answers being either obviously wrong, or not supported by the information in the question.


Why there is no neurovascular drug-eluting stent? I'm researching on neurovascular stents and I'm wondering why there is not much about drug-eluting neurovascular flow diverters in the literature? I read in an article that it's because of complex shape of cerebral arteries in comparison to cardiovascular system. But it doesn't look satisfactory to me. Any suggestion or idea is appreciated.

Despite some superficial similarities, the design of coronary stents and neurovascular stents are quite different. Coronary stents are hard metal, made out of stainless steel. They are quite solid, and if you crush one, it will remain crushed. They are deployed by expanding a balloon at potentially very high pressures (10-20 atm). Coronary stents are relatively short, and are deployed in vessels that are relatively straight given the length of the stent.

Drug-eluting variants of coronary stents are additionally coated in a polymer (i.e., plastic) matrix that contains the active ingredient and releases ('elutes') it over time. The common commercially available drug-eluting stents release anti-proliferative agents to prevent neointimal growth.

The purpose is also somewhat different: you mention flow diverters, so you are likely thinking about the context of aneurysms, where they may be used alongside coils to seal off the aneurysm from the normal flow. They are not providing structural scaffolding to prevent vessel occlusion from atherosclerosis.

Neurovascular stents, including flow diverters, are often made of self-expanding metals like nitinol. They are more flexible, but try to keep their nominal shape. These stents are deployed by retracting a sheath and then they themselves pop out to their nominal diameter. Because of this different deployment strategy, they can also sometimes be retracted and repositioned. The way these stents deploy is a lot more gentle, and they are also typically longer than the coronary varieties. They also may be placed in vessels that can be accessed superficially, such as in the neck. A stainless steel stent in the neck would be a disaster: if you laid pressure on that part of the neck you could permanently collapse the stent. A self-expanding stent will bounce right back open.

Back to your actual question...

The actual purpose of coronary vs flow-diverting stents are different; the purpose of drug-eluting coronary stents, preventing neointimal hyperplasia, is not as relevant in the neurovascular context. Additionally, there are lots of good reasons to use self-expanding metals in the neurovasculature because of tortuous anatomy and superficial vessels in the case of the carotids. The hard plastics that are coated onto steel stents can't be easily placed onto self-expanding stents, so other techniques would need to be developed.

The article you read talking about the complex shape of cerebral arteries is in large part correct.


Can herbs absorb harmful substances leached in water supply I have small herb garden (parsley, coriander mint and basil) that is watered from below by a hydrophilic filter using capillary action from a reservoir. This filter allows water soluble nutrients to be fed to the herbs.

The manufacturer of the filter use a special propitiatory additive in the filter that allows for excellent water flow. I need to know the the harmful implications of the material as they have stated the unknown "additive in the filter is not FDA approved". They will not tell us what additive is to protect their intellectual property.

My question is that will the herbs absorb the additive regardless assuming the additive is leaching into the water. Say that 1 ppm (parts per million) of substance X is in the water. Will the herbs absorb that and propagate it to their leaves. If so how much of the substance? (very rough estimate will do)

TIA, Dave

You'd have to test it. Plant roots naturally pull poisons like heavy metals out of the soil through water. These are called metallophytes, and can even be classified into what're called hyperaccumulator plants. The use of plants to remove harmful substances from the soil, air or water is called phytoremediation.

The process of absorbing harmful substances, however, relies on the structure and size of the substances involved because the substances must enter cells. We know from elementary biology that cells only allow molecules of certain properties to pass their cell membranes. Since the filter additive in question is an unknown, it's hard to say if a plant would absorb it. It's also hard to say if it's harmful to you, or if it even gets into your water. Testing for a chemical of unknown behavior requires some analysis like mass spectrometry (fair example).


Do humans have enough biological differences to be grouped into races or subspecies? After my online research on the subject, I learnt that, biologically speaking, many scientists believe that there is no such thing as a race. Homo sapiens as a species is only 200,000 years old, which has not allowed for any significant genetic diversification yet, and our DNA is 99.99% similar. I've read statements that there can be more genetic variation inside a racial group than between different racial groups, meaning that, for example, two individuals from the same "race" can have less in common with each other than with an individual from another "race".

Wikipedia on Race (human classification) quote:

  Scientists consider biological essentialism obsolete, and generally discourage racial explanations for collective differentiation in both physical and behavioral traits

Q1: If Homo sapiens has no races (according to biologists), why are we so different morphologically? (hair/eyes/skin colour and even athletic performance seem to differ between human populations)

Q2: Is it common for other species too, when genetically close populations have very different morphological traits? Are there any other mammal or animal species that exhibit biological diversity comparable to human diversity, and how do taxonomists treat these species? (excluding intentionally bred domestic species to keep the comparison fair)

The question has been paraphrased to emphasize that it is the biological debate that is in question, not the sociopolitical. I.e., why is there no consensus in evidence and opinions of scientists?

Firstly, it's not true that you can't tell racial background from DNA. You most certainly can; it's quite possible to give fairly accurate phenotypic reconstruction of the features we choose as racial markers from DNA samples alone and also possible to identify real geographic ancestral populations from suitable markers.

The reason that human races aren't useful is that they're actually only looking at a couple of phenotypic markers and (a) these phenotypes don't map well to underlying genetics and (b) don't usefully model the underlying populations. The big thing that racial typing is based on is skin colour, but skin colour is controlled by only a small number of alleles. On the basis of skin colour you'd think the big division in human diversity is (and I simplify) between white Europeans and black Africans. However, there is vastly more genetic diversity within Africa than there is anywhere else. Two randomly chosen Africans will be, on average, more diverse from each other than two randomly chosen Europeans. What's more Europeans are no more genetically distinct overall from a randomly chosen African than two randomly chosen Africans are from each other.

This makes perfectly decent sense if you consider the deep roots of diversity within Africa (where humans originally evolved) to the more recent separation of Europeans from an African sub-population.

It's also worth noting that the phenotypic markers of race don't actually tell you much about underlying heredity; for example there's a famous photo of twin daughters one of whom is completely fair skinned, the other of whom is completely dark skinned; yet these two are sisters. This is, of course, an extreme example but it should tell you something about the usefulness of skin colour as a real genetic marker.


How do you merge SNP data with a reference genome? My Data

I have a 23andMe file listing SNPs in the form:

rsid       chromosome      position        genotype
rsXXXXX         1           PPPPPP          CT
rsXXXXX         1           PPPPPP          GG

Fields are TAB-separated and each line corresponds to a single SNP. For each SNP, four fields of data are supplied.

An identifier (an rsid or an internal id)
Its location on the reference genome.

The chromosome it is located on.
The position within the chromosome is is located on.

The genotype call oriented with respect to the plus strand on the human reference sequence.

The reference genome is the human assembly build 37 (also known as Annotation Release 104).

My Question

How do I merge the SNPs into the reference genome?

For example, take the first line in my SNP file:

rsXXXXX        1           PPPPPP          CT

Part 1

I can see that I need to replace the nucleotide at position PPPPPP on chomosome 1 of the reference genome with a nucleotide from the genotype field, but which nucleotide am I supposed to use? C or T? And why?

Part 2

Where am I supposed to start counting from on the reference genome? Looking at chromosome 1 of the human assembly build 37, the first ~10,000 characters (excluding the first line description) are N. Is the first N number 1? eg. If PPPPPP was 100,000 would I replace the 100,000th character in the reference genome with the correct nucleotide from Part 1 of this question? Or should I start counting from the first non-N character in the fasta file?

First, you need to know which genome sequence does the SNP file refer to. They must have mentioned the reference sequence that they used.

As others mentioned the case of CT is heterozygosity. If you just want to mark the changes then discard the residue that is already present in the reference genome and use the other allele. However, you want to keep a track of the haplotype then you have make sure that a set of SNPs come from the same chromatid. This is difficult- you might still be able to know it for SNPs that are close enough to be mapped by a single read but it is almost impossible for SNPs that are separated well enough.

As Endre said, you have to start from the first nucleotide. However, it seems dubious that you are getting $\ (NNNN)_n$ in the beginning of chromosome 1. Complete assembled chromosomes do not have such stretches. Below are the first 10 lines of the chromosome 1 fasta file. See for yourself.

>gi|568815364|ref|NT_077402.3| Homo sapiens chromosome 1 genomic scaffold, GRCh38 Primary Assembly HSCHR1_CTG1
TAACCCTAACCCTAACCCTAACCCTAACCCTAACCCTAACCCTAACCCTAACCCTAACCCTAACCCTAAC
CCTAACCCTAACCCTAACCCTAACCCTAACCCTAACCCAACCCTAACCCTAACCCTAACCCTAACCCTAA
CCCTAACCCCTAACCCTAACCCTAACCCTAACCCTAACCTAACCCTAACCCTAACCCTAACCCTAACCCT
AACCCTAACCCTAACCCTAACCCCTAACCCTAACCCTAAACCCTAAACCCTAACCCTAACCCTAACCCTA
ACCCTAACCCCAACCCCAACCCCAACCCCAACCCCAACCCCAACCCTAACCCCTAACCCTAACCCTAACC
CTACCCTAACCCTAACCCTAACCCTAACCCTAACCCTAACCCCTAACCCCTAACCCTAACCCTAACCCTA
ACCCTAACCCTAACCCTAACCCCTAACCCTAACCCTAACCCTAACCCTCGCGGTACCCTCAGCCGGCCCG
CCCGCCCGGGTCTGACCTGAGGAGAACTGTGCTCCGCCTTCAGAGTACCACCGAAATCTGTGCAGAGGAC
AACGCAGCTCCGCCCTCGCGGTGCTCTCCGGGTCTGTGCTGAGGAGAACGCAACTCCGCCGTTGCAAAGG

How to replace $N^{th}$ residue is quite a straightforward task. But that is a programming question and not the scope of this forum. Assuming that you have solved the part 1 problem and have a tab separated sorted file like this:

chromosome  position    residue
 1           79989           G
 1           100232          T
 3           341342          A

This script may not be the best but would work in a linux/*nix/Cygwin terminal, to replace the residues (ensure that you have gawk version >=4.0):

gawk -F "\t" '(FNR==1){x++} (x==1){a[$1][$2]=$3;next} (x==2){if($0~/>/){h=$0;sub(/^.*chromosome /,"",h);sub(/ .*/,"",h)} else{seq[h]=seq[h]$0}} END{for(i in a){s=0; for(j in a[i]){m=m substr(seq[i],s,j-1) a[i][j];s=j+1} m=m substr(seq[i],s); print ">Chr"i"\n"m}}' SNP_file Genome.fa | fold -w 60


Question regarding when it's a homoplasy in a phylogenetic tree If you have 2 organisms that both come directly from the same common ancestor on a phylogenetic tree, and that common ancestor does not have trait "x", is it possible for both of its direct descendants to develop that trait "x" independently, and would that be an example of a homoplasy?

Phylogenetic tree vs first generation offspring

Please note that on a phylogenetic tree, the time scale is big enough so that the generation time is completely undistinguishable. Hence, questions of first generation offspring won't rise. Also, in practice when reconstructing a phylogenetic tree, our level of accuracy does not allow us to distinguish exactly at what generation did specific mutation occur.

Rephrasing your question

The term homoplasy is typically used in the context of phylogenetics. Also, most of the time the term homoplasy refer to phenotypic trait and not to genetic sequence but I will not go into these specific complications here. The term is also mainly used in intro textbook and not so much in the peer-reviewed literature. In all cases, one can define the concept of homoplasy as a shared trait that is caused by a mutation that is not identical by descent. In other words, if in two lineages/individuals that share the same trait, the trait is caused by the same mutation(s) (same, not only by its state but by descent), then the shared trait does not represent a homoplasy.

With this, I can rephrase your question as

  If two siblings share a (heritable) trait that the direct parent does not have, are the traits identical by descent?

If two siblings share a (heritable) trait that the direct parent does not have, are the traits identical by descent?

Well.. it depends as to whether the mutations happened happened twice independently in the two different gametes or if the mutation happened once in the (germ line) lineage that gave rise to these gametes in the parent body.

The second is much more likely. Because, it is very unlikely for the same mutation to happen twice independently in two different gametes for the same individual and much more likely that the mutation happened once in a cell that gave rise to the two gametes, it is very much more likely that the shared trait among the two offsprings is caused by a mutation that is identical by descent. Hence, not a homoplasy.


Flow cytometric counting of apoptotic adhering cells I have been trying to measure rates of apoptosis in epithelial cells by marking apoptotic cells with annexin V conjugated with phycoerythrin (PE) and sorting using flow cytometry. Unfortunately, the cells are adherent, and have been cultured in a collagen coated plate. Thus, to suspend them for flow cytometry, I have been using a trypsin treatment. Unfortunately, my results have been quite poor. I believe that there are several problems. First, the trypsin treatment is likely to induce the disruption of integral membrane proteins, potentially causing the externalization of phosphatidylserine (PS) (to which the annexin binds) on the outer plasma membrane of cells. Since the cells were incubated with the annexin V following suspension with trypsin, this could have led to a substantial increase in apparent rates of apoptosis, and masked real differences between rates of apoptosis in WT and KO cells. Furthermore, I was informed that epithelial cells, in order to maintain their structural integrity, have a relatively large ratio of cytoplasm to nucleus, and a prominent cytoskeleton resulting in increased background noise (greenish in color). In order to solve these problems I was considering several alternatives, such as changing the fluorescent marker that annexin V is conjugated with to reduce autofluorescent interference, using a different marker of apoptosis (in the place of annexin V), or, if I were to continue using annexin V, I think that incubating with annexin V followed by washing off of excess annexin, followed only then by trypsin treatment could potentially solve one of my various problems (or then again, it might not). Please help me find a suitable protocol for flow cytometric analysis of apoptotic markers in adherent epithelial cells. Additionally, if you know of any studies which utilize such methods, please direct me to them. Thanks in advance.

Here some resources,

Cell harvesting effects on Annexin V staining.
Protocol for apoptotic analysis using Annexin V.
Quite a long discussion about this issue.
Another protocol.

Cheers,

Pedro


Programming Languages for Bioinformatics Good day everyone,

I am very much interested in math, biology, and programming; ideally I would like to study bioinformatics and, as such, was wondering what languages are typically used by bioinformaticians? Particularly for fields of bioinformatics relevant to biochemistry, virology, and immunology, what are the most useful programming languages to know, as well as their strengths and limitations? (i.e. in what setting would it be better to program in C++ than Python, is R good to know and if so why, etc.)

Thank you in advance.

The languages currently popular for bioinformatics work are Python, Java, R, Perl, and BASH, though the use of Perl is gradually declining. Note that Python has become the most popular language in a general context, so it's natural that it's the most popular in bioinformatics too. Of course 'most popular' doesn't mean 'best'. Pick a computer language and I'll point you to some publication that uses that language in a bioinformatics context (perhaps excepting COBOL, and RPG).

Some bioinformaticists spend most of their time performing analyses using existing software, perhaps using a scripting language like Python or BASH to 'glue' together existing programs or to control the submission of jobs to a computational cluster. Scripts and packages using the R language are often used in these analysis pipelines to perform sophisticated statistical analysis and visualizations.

Other bioinformaticists are developing new algorthims. In these cases computational speed can be very important, so languages like C, C++, or Java are often used. However, newer languages like Go, Julia, and Rust are also used, according to the taste of the researcher. New machine learning tools are often prototyped using MATLAB.

If your interest is primarily biology (biochemistry, virology, and immunology) then you'll want to focus on learning the biology, and supplement it with Python, BASH, and R. If your interest is primarily in developing new algorithms, then focus on statistics, and computer science. You'll still want to learn Python, BASH, and R, but you'll also want to add something like C++ or Java. The good news is that once you've learned 2 or 3 computer languages, you can pick up additional languages much more easily.


Why are sea dwelling mammals less aggressive than land dwelling mammals? Many mammals on land seem to be quite dangerous to humans: e.g., tigers, lions, elephants, hypos etc. However, their sea-dwelling counterparts (e.g., orcas, dolphins, sea lions, whales etc.) are relatively friendly to humans (and in contrast to say sharks). Is there a simple reason for this?

More encounters on land

There are more land animals that meet humans walking around than there are sea animals that meet humans swimming around. If fewer attacks happen on humans in the sea environment, it might just be because there are fewer encounters with marine mammals than with land mammals.

Greater species diversity on land

In your list used as example, you cherry-picked a few aggressive(-ish) land mammals but the vast majority of land mammals are not aggressive toward humans. The fact that there are no marine mammal that are aggressive toward humans might just be because there are too few fewer marine mammal species.

Pseudoreplication and phylogenetic signal

I would argue that your sample size is not as large as you might think. There are only four lineages of mammals that evolve to live in the seas. There is therefore a phylogenetic signal and ignoring it would be a problem of pseudo replication.

For example, I could very well think of territorial behaviour (which is where a lot of aggressive behaviour comes from) as having a strong phylogenetic signal.

Why considering only humans?

Your post title talks about aggressiveness in general and the content of your post talks about attacks against humans. It sounds that considering only attacks against humans to be very unfair. Orcas, typically, are fierce and violent predators although no orcas have ever attacked a human in the wild.

Are they really that friendly to humans?

There has been a number of attacks in captivity (well known cases with orcas). Also, there have been a number of whales attacks against boats (according to this BBC article).

In short...

In short, I think your comparison is unfair. I think you are looking for an explanation for a pattern that does not really exist.


Detrimental effects of fructose in fruit on the liver? Fructose is mostly broken down by the liver. During this breakdown, the liver also creates fats (by the process of lipogenesis) which over time can get accumulated in the liver and give rise to nonalcoholic fatty liver disease.

Now, fruits contain fructose. So, here is my question: "Will eating lots of fruit lead to fatty liver disease?" If yes, how much fruit consumption is too much? If no, why not? What about lipogenesis, then?

I got the above information from this article by Harvard Medical School.

There is insufficient evidence to claim that high consumption of fructose, when part of isocaloric diet (no weight gain), is a risk factor for non-alcoholic fatty liver disease (NAFLD).

Fructose Consumption, Lipogenesis, and Non-Alcoholic Fatty Liver Disease (PubMed, 2017):

  ...the available evidence from human epidemiological and
  interventional studies does not support the hypothesis that
  fructose, when consumed in isocaloric amounts, causes more liver fat
  accumulation than other energy-dense nutrients. The observed
  prosteatotic effect of fructose in hypercaloric trials is likely
  confounded by associated weight gain...

Effect of fructose on markers of non-alcoholic fatty liver disease (NAFLD): a systematic review and meta-analysis of controlled feeding trials (PubMed, 2014):

  Isocaloric exchange of fructose for other carbohydrates does not
  induce NAFLD changes in healthy participants.

Consumption of fruits, if part of isocaloric diet, is also not likely associated with NAFLD.

No association between fruits or vegetables and non-alcoholic fatty liver disease in middle-aged men and women (PubMed, 2019):

  No obesity-independent association was found between fruit or
  vegetable intake and NAFLD.

The main source of dietary fructose are probably soft drinks, not fruits, anyway:

Popular soft drinks can contain 60-70 g fructose per liter (ScienceDirect, Fig. 2).
Four apples (150 g each) contain 36 g fructose, which is more than in most other fruits (USDA.gov).

And finally, even if there is abundant evidence that fructose stimulates lipogenesis in the liver, this does not automatically mean that it stimulates the development of NAFLD (according to the first source above).


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

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


Protein Biology Cheat Sheet I'm looking find a cheat sheet for protein biology to stick on my desk to remind of some of the key principles of protein biology. I seem to remember the specific and complex principles in protein biology but at the expense of the basics.

Can anyone point me to a protein biology cheat sheet or formulate some suggestions to go on one?

EDIT

What I am looking for:

Amount of amino acids in a helix turn
Amino acids typically found in Beta sheets and Helices
The types of protein interactions (i.e. ionic, hydrophobic) and the  amino acids usually involved.
Definition of Globular and fibrous form
Types of post-translational modifications
Any other useful characteristics

For 95% of the work I do with protein, I find this chart very helpful, showing common post-translational modifications, for each amino acid, with molecular weights, associated codons, pKa values, 1- and 3-letter amino acid codes, chemical structure and chemical properties (polar, non-polar, aromatic, acidic, basic).


Difference between viral and human genetic material I have heard that there is a difference between viral and human genetic material. What is that difference?

If I take my cells and take DNA out of them and insert only a small part of it having a sequence, say, AGTTC, and viral DNA with the same sequence, can my body distinguish between the two? If so, how?

To sum up: If we are not talking about chromosome organization, nucleotide sequences and overall genome architecture (which are incomparably different in eukaryotes and [even their] viruses) the differences in the genetic material are as follows:

viruses are much more diverse in their choice of genetic material, which is in the cornerstone of viral higher systematics. It can be DNA or RNA, single- or double-stranded, circular or linear. Animals, in turn, possess only double stranded DNA as their genetic material: linear dsDNA for the nuclear genome and [usually] circular dsDNA for the their mitochondrial genomes.
DNA termini pose a special problem for the maintenance of the molecule and show very unusual organization in terms of DNA sequence and structure. Repetitive terminal sequences of eukaryotic chromosomes have 3'-overhangs, which form a special quadruplex form of DNA. Termini of viruses are naturally much more diverse and are (nearly?) never of the same structure as in Eukaryotes. [Circularization/decicrularization is one of the mechanisms recruited by viruses]. (Deng et al 2012)
DNA methylation is normally present in varying degrees in animals and in vertebrates most of the cytosines in CpG dinucleotides are methylated. Viruses differ considerably from one another in this respect, but it seems that smaller viral genomes are generally under-methylated and larger genomes do not show under-methylation, although it depends on the stage. This conclusion is based partly on indirect evidence that CpG motifs are considerably much less frequent in smaller viruses. Integrated "genetic parasites" like retroviruses are normally rich in CpG and are highly methylated. (Hoelzer et al 2008)
although I couldn't find relevant literature, I'd hypothesize that the highly packed genetic material in viral particles may potentially exist in more compact forms of the DNA helix (in dsDNA viruses). Most of the dsDNA in cells is present in a so-called B-form, but there are more compact A-form and less compact left-turned Z-form (there are other forms, most of which are biologically not relevant). (cf. Wikipedia for an introduction)


What species of spider is this? Could anyone help This image was taken in assam, India. The size was around 1cm. Could anyone help identify?

This is a male Carrhotus sannio (the females are brown/grey). The white dorsal stripe on the cephalothorax is right beneath the outside eye; the upside-down v-marks on the back of the abdomen point to two white lines (sometimes broken) which run parallel to the length.
Gallery of males:
https://inaturalist.ca/taxa/334660-Carrhotus-sannio/browse_photos?quality_grade=any&term_id=9&term_value_id=11


Determine the chances of blood group type and rhesus factor of unknown parent? First of all, I'm not a biologist so my jargon might not exactly be common on this site. I'm a programmer and as a hobby project I try to make an algorithm that does two things:

Determine the possible blood group and rhesus factor of a child based on the blood groups and rhesus factors of both parents.
Determine the possible blood group and rhesus factor of an "unknown parent" based on the blood group and rhesus factors of the child and the known parent.

I found two great examples online, the "Child Blood Type Calculator" and the "Parent Blood Type Calculator" calculator on endmemo.com.

The first calculator shows some percentages of the chances. But the second calculator does only show a static answer when it comes to the blood group type and rhesus factor. According to the calculator that indicates that the rhesus factor of the "unknown parent" can only be negative when both the child and the known parent have a negative rhesus factor too.

In case the known parent and child have both RH+ the calculator shows that the unknown parent must have had RH+ as well. But isn't the statistical chance  6.25% that the unknown parent still have had RH- instead?

Secondly, how can I calculate the likelihood/chance that the unknown parent has a certain rhesus factor or blood group type? Now the calculator shows 'A/B/O' and 'RH+' when the child has 'O+' and the known parent has 'O+' but what are the chances the unknown parent has A, B or O or RH- anyway?

Side-note: I'm not related to endmemo.com.

Simple explanation: that "Blood Type Calculator" is wrong.

Inspecting the source code of that page we can find the if statement that chooses the outcome for the unknown parent, regarding the Rh factor. And it has a problem. Whoever knows JavaScript will understand the problem, but even people that don't know programming languages can follow this, it's not complicated. Let me explain it.

When you choose the Rh blood type in the dropdown menu, the Rh+ blood is associated to the value p and the Rh- blood is associated to the value n. Those are just strings, the programmer can chose any value he/she wants, that's not important, as you know. The variables that hold those values are msel2 for the known parent and csel2 for the child.

Now comes the if statement:

var frh = "+";
if (csel2 == "n" && msel2 == "n") frh = "-";

Let's break it down:

The default value that will be printed on the result, called frh, is + (positive), as you can see before the if statement. As already said, msel holds the value for the known parent, and csel holds the value for the child.

In the if statement, only if the user chooses the known parent type as Rh- (msel2 == "n") AND the child as Rh- as well (csel2 == "n"), the value of frh will be changed to - (the double && represents the AND). Any other combination will not change frh, which will remain +.

And that's plain wrong!

There is no need for me to explain you the genetics of Rh factor, there are plenty of resources online and answers here at Bio SE as well, but here is a summary:

Given that Rh+ individuals can be either DD or Dd, it's easy to show that the unknown parent can be Rh- in case that the known parent and the child have both Rh+:

(Known parent)     (Unknown parent)
    D_ --------------- dd
              |
              |
             Dd
           (Child)

The lesson to learn here: don't trust everything you find online.

Correct algorithm:

For your second task ("Determine the possible blood group and rhesus factor of an "unknown parent" based on the blood group and rhesus factors of the child and the known parent."), let's see all possible cases:

Known parent Rh+ and child Rh+: the unknown parent can be either Rh+ or Rh-.
Known parent Rh+ and child Rh-: the unknown parent can be either Rh+ or Rh-.
Known parent Rh- and child Rh-: the unknown parent can be either Rh+ or Rh-.
Known parent Rh- and child Rh+: the unknown parent has to be Rh+.

As you can see, in only one case the unknown parent cannot be either Rh+ or Rh-. That being said, this is a possible solution:

var frh = "+/-";
if (csel2 == "p" && msel2 == "n") frh = "+";

What this snippet does is this:

It assigns the default value for the unknown parent (frh) as +/- (meaning that he/she can be Rh+ or Rh-, we can't know) for all possible combinations. However, if the mother is Rh- AND the child is Rh+, that value is changed for + (because, in that situation, the unknown parent has to be Rh+).


Is cannibalism part of mainstream food-chain? There are some species who sometimes eat their own kinds. Is this cannibalism considered their regular food? Do the link in food-chain for those animals make a loop on themselves?

Can this statement: "Food chains are found within the population of a species." be held true?

Disclosure: The above statement was part of a question that asked to identify the correct among statements. I tried to find relevant content in books and internet but couldn't find any. I'm not trying to get my assignment solved, but I want opinion on cannibalism and it's impact on food chains.

Cannibalism can be found across most animal groups. For some groups of organisms (e.g., spiders, fishes) cannibalism can be common within a single generation. Sometimes it will be between siblings, but more often with other members of their species.

As @heracho pointed out, from a network/food web/flow-diagram perspective, yes, cannibalism is repressed as a negative feedback loop on itself.

Evaluating the statement: "Food chains are found within the population of a species," I interpret is as, within species, there are subgroups that consume subgroups, that consume subgroups. You'd need at least 3 levels for it to be considered a chain (i.e., you don't have a chain with two species/a single link). Cannibalism would be a single link/two species, and not considered a chain. As to whether or not chains exist within a species, I suspect it is not common if it exists at all. If it did, I would guess it'd be found in a group like fishes where prey are often size dependent.


Why do stomata close in salt water? Why do the guard cells of the stomata close when they come in contact with salt water?

I recognize it has something to do with osmosis and the fact that osmosis makes the water drain in some sort, following this distilled water has the opposite effect.. why?

INTRODUCTION:

The basic process by which opening of stomata takes place is by endosmosis.Endosmosis causes an increase in turgidity in the guard cells thereby causing its opening.

The closing of stomata is achieved by exosmosis which makes the guard cells flaccid.

HOW DO THE REGULATION TAKES PLACE IN PLANTS:

If you read the theory proposed by Levitt from the given [link]
,in which the theory is explained in simple steps with diagrams, you will understand that $K^+$-$H^+$ pumps is the main driving force which regulates whether endosmosis or exosmosis would take place.

When the concentration of $K^+$ increases in the guard cells there is osmotic influx of water from the surrounding epidermal cells  and thus 'endosmosis' occurs causing opening of stomata.

Similarly when concentration of $K^+$ decreases there is osmotic loss of water from the guard cells to cause 'exosmosis' and thus closing of stomata.

WHY THE STOMATA CLOSE IN SALT WATER:

When the guard cells of the stomata are open it means they are turgid due to endosmosis.However when such a turgid plant cell is placed is  in salt water(hypertonic solution) the latter having a higher concentration of salt ions than the guard cells causes the loss of water from the guard cells.

Thus the salt water is inducing exosmosis to take place in the guard cells due to which they become flaccid and close.

REFERENCE:
[link]


Is there a gold standard for syphilis? When you say the Venereal Disease Research Laboratory test (VDRL) has a specificity of x% and sensitivity of y%, what are you comparing to? What is considered as the truth?

Because, Wikipedia says, even a gold standard needn't be perfect. It is just the best test available(?). It too has its specificity and sensitivity (<100%)

So, my question is, when we say that the VDRL has a 75% sensitivity, what are we comparing it to? Is it the clinical diagnosis of syphilis according it the case definition? Wouldn't it be much less accurate?

Specificity and sensitivity are terms used in the pharmaceutical and in vitro diagnostics (IVD) industries that have specific meanings relating to how the particular assay in question was validated. Generally the values are being compared to spiked standards in matrix using recombinant protein or purified virus or whatever the antigen is (depending on how the test operates) where the analyte concentrations are known. With a certain number of titrations and assay repeats, along with a bunch of statistical calculations, you can then compute your expected and actual recovery, as well as values like the LLOQ (lower limit of quantitation) which gives you your sensitivity (we can reliably detect 1e4 viral particles per ml, for example).

Specificity is calculated using related antigens, such as proteins from other types of bacteria that are of varying degrees of relation to syphilis, or perhaps of different serotypes that aren't claimed to be detected by the test, or whatever. Again, you spike known amounts of these materials into your testing matrix (blood, sputum, urine, semen, whatever) and see what your test returns. So, say I have a virus with 2 serotypes (A and B) that I claim recognizes A specifically. I spike in perhaps equal amounts (for example, 100 units) of A and B, then run the A-specific quantitation assay. The readout might then say the sample only had 75 units of A, meaning 75% specificity of the reagents.

For more reading, search for "clinical assay validation" or something similar. There are a ton of papers out there giving guidance for particular types of assays, as well as regulatory agencies' interpretations of the relevant laws covering the tests. There are also many books, reviews, etc. if you're just looking for an overview. It's a huge field, and I've just given a very basic description to avoid writing pages and pages.


Is this a grackle with an unusually long decurved bill (Phoenix AZ, USA) Can someone help me identify this bird (sorry only had the iphone)? It looks like a grackle, but the bill is much longer than any I have seen. The bill looks like a Le Conte's thrasher, but it was all black. It looked pretty ratty because he was molting. It was definitely black, and in an area with lots of grackles.

The pictures don't do it justice, it was a really long bill. The pictures were taken in Phoenix, Arizona, US on Greenway bike path near Thomas Rd on 7 Sept 2014.

The picture is not that clear, but it definitely was not something that the bird was holding in his beak. That was my first thought when I saw him, but I watched him awhile, it was very clearly his beak that was long and decurved. Sure wish I had my real camera at the time.

It could be a crow, a blackbird or a raven for all we know because deformed bills on birds has been a matter of debate (reference) and there is a group on flickr (reference) where you can post such pictures. I have actually noticed few pictures of birds with beaks that resemble the one in your photo.

A crow with a deformed bill (reference)


How does the immune system distinguish own and foreign antibodies? Therapeutic antibodies, for example Rituximab which recognises CD20 on B lymphoma cells, can cause adverse effects (e.g. http://www.ncbi.nlm.nih.gov/pubmed/19399690)

One reason behind these adverse effects could of course be an over-response of immune cells stimulated by the Fc region of antibodies attached to lymphona cells.

However, it could also be thinkable that the immune system launches a response against the antibody itself, recognising it as foreign. Does this occur? If so, what part of the injected antibody acts as the epitope recognised by immune cells as foreign?

The short answer is that antibodies are proteins like any other, and if an antibody from a foreign source is injected it can result in an immune response. This is, of course, exploited in the production of secondary antibodies for use in research (e.g. goat anti-rabbit IgG is a goat  antibody that recognises rabbit IgG).

Because of this, therapeutic antibodies are "humanised" and this is the case with Rituximab which is derived from a mouse monoclonal IgG:

  Rituxan is a genetically engineered chimeric murine/human monoclonal antibody directed against the CD20 antigen found on the surface of normal and malignant B lymphocytes. The antibody is an IgG1 kappa immunoglobulin containing murine light- and heavy-chain variable region sequences and human constant region sequences. Rituximab is composed of two heavy chains of 451 amino acids and two light chains of 213 amino acids

Presumably it would be possible for the remaining mouse-derived variable regions to be recognised as foreign by the human immune system, and this possibility is hinted at in the abstract of an early paper on rituximab (McLaughlin et al. (1998) Rituximab chimeric anti-CD20 monoclonal antibody therapy for relapsed indolent lymphoma: half of patients respond to a four-dose treatment program. J Clin Oncol.16:2825-33.) My emphasis...

  A chimeric monoclonal antibody more effectively mediates host effector functions and is itself less immunogenic than are murine antibodies.

However, I'm not aware of any evidence that simple immune responses to Rituximab actually occur.


Is there a name for the use of sunlight in metabolic processes? "Photosynthesis" is what is used to describe how plants use sunlight to synthesize sugars, but, I also heard some animals like humans use sunlight in the process of creating vitamin D. Is there a comparable name for when sunlight is used by animals in a metabolic process?

Photometabolism or photocatalysis would be apt terms and the former would specifically refer to biochemical reactions.

Photometabolism is also used in the context of the light dependent conversion of 7-dehydrocholesterol to Vitamin-D.

A google scholar search with photometabolism returns many peer-reviewed articles that have used this term. Some examples:

Photometabolism of 7-dehydrocholesterol to previtamin D3 in skin.
The photometabolism of glucose by an hydrogen-adapted alga
Photometabolism of Heterocyclic Aromatic Compounds by Rhodopseudomonas palustris OU 11.


Comparion between machine vision & human vision I hope this is the correct Stackexchange to ask this question.

I am trying to know : What is the current status of knowledge regarding human vision and pattern recognition.

More specifically,

How does the human eye read signals from  the cone cells? Is it row
by row, column by column like a computer? or or there other things
happening ?
When detecting, say, an edge, or a connected component - does the human eye continue searching row by row? or does it jumpimmediately to the next neighbor? Are human cone cells arranged in arectangular gird with 8 neighbors per cone besides for the edges?(my guess is no). Then how are the neighbors addressed? Does somerace condition occur?

As you can see, I am not a biologist, I am a physicist working with computer vision. I have moderate knowledge of anatomy, but I am willing to learn.

Thank you

This is a potentially very very broad question, but I'll try to provide a simple answer that addresses the biggest misconceptions.

First of all, animal vision (and brains more generally) is massively parallel. There may be some serial processing steps, but these are also massively parallel. Computers need to digest information into stereotyped operations that can be executed on a CPU. The brain has separate dedicated machinery to each point in space for early vision, so there is no need to process individual "lines" or points in sequence: it all happens at once.

Photoreceptor inputs are converted into center-surround receptive fields in retinal ganglion cells, where light in the center excites and light in the surround suppresses (ON-center cells), or vice versa (OFF-center cells). These receptive fields are then transmitted to thalamus (the lateral geniculate nucleus), and from there to V1, primary visual cortex.

You can then combine many of these circular receptive fields to detect straight edges, like this:

From https://grey.colorado.edu/CompCogNeuro/index.php/CCNBook/Perception

The cells in V1 that respond to these "edges" are called "simple cells"; there are also "complex cells" that have more complicated receptive fields, and other sensitivity like to motion and color. Some computer vision strategies end up producing receptive fields that look a lot like the ones found in early visual areas, the earliest ones built out of Gaussian-filtered sin waves.

From V1, there are higher order visual areas that respond to things like shapes, motion, optic flow, etc.

Basic neuroscience textbooks tend to contain a lot of information on the early visual system, Purves Neuroscience is a good example, any edition is fine:

Purves, D., Augustine, G. J., Fitzpatrick, D., Hall, W. C., LaMantia, A. S., McNamara, J. O., & White, L. E. (2014). Neuroscience, 2008. De Boeck, Sinauer, Sunderland, Mass.