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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.

So both genes are being expressed  as in "Rr", but because "R" is dominant, only, "R" is demonstrated via the phenotype.

Yes, by definition of R begin dominant, the phenotype of Rr is the same of RR but r might be expressed (or not). See added example at the end of the post.

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. WHAT DOES THIS MEAN?

What part of this sentence is unclear to you? You should maybe check the word 'locus'. You probably should need to have a look at the post Why is a heritability coefficient not an index of how “genetic” something is? that offers an intro to quantitative genetics to get a sense of why I am talking about variance.

thanks asked a new question with my interpretation of the terms.

why would expression occur from both alleles simultaneously?

Why wouldn't it?  What mechanism do you propose and have evidence for that would cause one allele to not be transcribed, based only on the phenotypic outcome of its expression?


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

What does genetic variance mean in (A)? does it imply that environmental factors are at play
So does (B) mean that mutliple genes affect traits?
Does (C) mean that multiple alleles are at work as opposed to simply 2 alleles?

by the way, i'm not a science student, so explaining it in simple terms would be appreciated. thanks.

I understood your question because I wrote the answer from which you took the quotes and I saw you having misunderstanding but no one else will understand your question. I am sorry if I am being too pedantic with you today. Can you please 1) use > symbol at the beginning of a quote to highlight it is a quote and 2) indicates where your quote is from.

FYI, when you think an answer answered your question, you can click on the checkmark next to the answer.

What does genetic variance mean in (A)? does it imply that environmental factors are at play

Yes and other things. For more information, have a look at Why is a heritability coefficient not an index of how “genetic” something is?

So does (B) mean that mutliple genes affect traits?

Yes, often many loci are involved in explaining the phenotypic variance.

Does (C) mean that multiple alleles are at work as opposed to simply 2 alleles?

multiple alleles or some other relationship between the two alleles than recessivity/dominance (such as additive, underdominance or overdominance, incomplete dominance). There might be epistasis among loci too.

Thanks Remi, I appreciate the answers and will follow the posting protocol in a better way. I read the above captioned post and it went over my head. In a nutshell apart from genetic and environment factors, do you have a list of other factors at play in affecting traits?

The "What is heritability coefficient not an index of how 'genetic something is?" post  expounded on the concept of genetic variance. In essence, the two factors that affect trait phenotype is environment and genetics.

Genetic variance, environmental variance and other things as explained in the section Other sources of phenotypic variance

source: Stack Exchange

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Help identify this small spiney praying mantis?
Trying to identify this praying mantis for a short film. It's found on the wild cosmos flower. It's found when the flower is in bloom at this time of year (February) in Harare, Zimbabwe.

This appears to be a species of Sub-Saharan flower mantis in the genus Pseudocreobotra.
Specifically, it resembles the spiny flower mantis Pseudocreobotra wahlbergi.

 © 2013-2018 carlarush
The species gets its name from the spiny structures on its abdomen. According to Wikipedia, the color is variable:

being typically greenish, but it can equally be yellowish, pinkish or reddish

According to here, you can determine the sex of your specimen by counting the "abdominal appendages" (i.e., spikes):

females have just 5 abdominal-appendages on the underside, however males have 6

 © 2004 Steffi Schuttauf
This might also be P. ocellata, which would be able to be distinguished from P. wahlbergi based on its smaller adult size [source].

That's fantastic, thank you so much for the identification. I will be sure to send you the short clip when completed. Many thanks from Zimbabwe

No problem @WildZimbo. Don't forget to click the checkmark to indicate  the answer as "accepted" if you're satisfied. Thanks!

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Succulent Plant identification
Can anyone identify this succulent plant?
Location: Tamil Nadu,India

This looks possibly like a species of Sansevieria, also known as Snake Plant. Perhaps Sansevieria parva or Sansevieria dooneri. Parva is usually much darker in colour than dooneri, but it's difficult to tell in the photo. Both are perennials that can be found in India.


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Genetic modifications in humans to prevent disease
I was reading an article about "designer babies", which was about how before birth the DNA can be modified so to achieve certain features. Can a technique such as this also be used to prevent diseases, such as down syndrome or some others, before the birth of a child? How far into the future are we to achieving something like this?

Regardless of the ethical and philosophical concerns involved, it is theoretically possible to modify a child's DNA to prevent various diseases, with a few caveats.
First of all, many diseases have multiple potential causes, and there is rarely a single method which would work for every case.
Second, the actual modification is not a trivial task in eukaryotes. The more controversial method would be for a mother to be implanted with "petri dish" embryos, who have undergone gene transplantation early enough for all of the embryo's cells to be transformed. The other method involves repeated gene therapy treatments later in the child's development (and even into adulthood) which would not necessarily prevent the disease, but would minimize it's effects.
Technically it could be done right now, but to the best of my knowledge neither procedures are approved for use as of yet. Given the controversy regarding modifying a child's DNA before birth, it may never be approved, but several gene therapies are undergoing clinical trials.


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If women need more dietary iron than men, then do blood donors also?
My understanding that women's dietary iron requirements are slightly higher because I've heard the only way of losing iron from your body is by losing blood, and this happens in menstruation. This got me thinking if someone donates blood does their dietary requirement increase also?
Also, related to this, when a person gives blood we're told that our body remakes the blood we've lost, does this replenish the iron in the blood also, or is this "newly created blood" absent of the iron normally present in our blood?

This can indeed be an issue.  Frequent blood donors are known to get low on iron, which begins to result in fatigue, even before it starts resulting in low hemoglobin and anemia.
The cause is simple: like you pointed out, the loss of blood results in the loss of iron, and it takes the body a certain amount of time to rebuild the iron store.
As for your second question, the "newly created blood" will be low on iron until the body can absorb enough iron to replace that which has been donated.  Even on iron supplements, it can take up to half a year to rebuild the iron stores of the body to where they ought to be.

Sources:

Frequent blood donors risk iron deficiency, Miriam Shuchman, MD
Iron Deficiency & Anemia Treatment, Webmd.com


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Polyploidy, or why plants of different species can produce fertile offspring hybrids more frequently than animals?
This site says:

Plants hybridize much more frequently and successfully than animals do. [...] Chromosomal doubling (polyploidy) occurs more frequently in plants and facilitates the fertility of the hybrid offspring.

Outcomes of the successful hybridization of different species of plants (i.e. yelding fertile offspring) can be easily observed in agriculture - for instance, Triticum aestivum is 6n, while Triticum durum is 4n. The latter comes from the hybridization of two plants from different genera (!). So it seems to me that not only can plants hybridize more easily, but also that the evolutionary distance between the parents can be greater than in animals.
As far as I know, the preferred animal strategy to have fertile hybrids is to go partheno/androgenic (for example in Phasmida).
My question is:
Why can plants produce fertile hybrids more often than animals? What constraints are present in animals and absent in plants?
To my knowledge, polyploidization is the main mechanism by which this is achieved. If this is true, then my previous question can be rephrased as why does animal polyploidization occur more rarely?
I'm not entirely sure about my assumptions, so feel free to correct me, of course with references.

While I do not know if there is a definitive answer to this question, I suspect that at least part of the answer can be found in the fact that animals typically have much more complex and delicate mechanical interactions in their bodies than plants.
From a mechanical perspective, plants are pretty simple. They move, but generally quite slowly and via very simple mechanical principles, and the interconnection between different tissues and organs is mostly via chemical and fluid flow.  Many plants are also highly flexible in their size and also change their size by orders of magnitude even after sexually mature.
Animals, by contrast, are often ferociously complex and intricate systems of joints and complex and highly differentiated organs. They also tend to have a well-defined typical size of mature individuals, which doesn't vary all that much compared to plants.
When you have a change in ploidy, a major effect is to multiply or divid the levels of gene expression, based on the change in number of copies.  Where that interacts with the processes of morphogenesis, it will thus often have radical effects on the size or growth patterns of the effected tissues or organs.
With a more intricately connected and scale-sensitive system like an animal, it seems then unsurprising that such changes might be much more difficult to survive.

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What does "optimal balance of biological control" mean in nematodes?
I have been reading several articles on nematode life-history for my insects class. Several articles say that Entomopathogenic nematodes(EPNs) are the only nematodes possessing an "optimal balance of biological control attributes". What does this mean?

It is a long-winded way of saying that these are the only nematode genera that are useful for biological control. In particular the article is referring to Steinernema and Heterorhabditis, both of which genera are used for control of some pest insects.


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Are humans Gnathostomates?
Gnathostomates are vertebrates having jaws. But when I search on the internet for Gnathostomates, I always find out that they are sharks and fish-like organisms.
But are humans not also Gnathostomates? Don't we have jaws?

Humans are fish-like organisms.

Absolutely, humans belong to the superclass Gnathostomata. It's simply the class of jawed vertebrates, and includes 99% of vertebrates.  It also includes the class Mammalia, which includes humans.

For basic and fairly light reading, check out Wikipedia on Gnathostomata and Mammalia.

What's a stem group and a crown group?

TIL: Snakes are Tetrapoda.

@user28434 Absolutely. Pythons and boa constrictors, for instance, still have vestigial hind leg bones hidden within their muscles. They also have tiny buds sticking out where their hind legs used to be. See, for instance, the first paragraph and image here.

Nitpick: It's mammalia, from Latin mamma, old greek μάμμη for breast or (baby-talk) mother.

Yes, all jawed vertebrates belong to the infraphylum Gnathostomata, including all mammals (and therefore all humans).
Here are 3 different taxanomic trees showing this:

 Source: Wikipedia

 Source: UCL

 Source: INTECH

Yes of course Humans are Gnathostomes. Under division Gnathostomata you have 2 Superclasses that include Pisces and Tetrapods. Under Tetrapoda are 3 classes- reptiles, Aves, mammals. So Humans are indeed Gnathostomes.

Taxonomically humans have been grouped as mammals placed under superclass Tetrapoda (Includes amphibians, reptiles, Aves and mammals) being different from  other superclass Pisces which includes sharks and bony fishes. All the animals placed under superclass Pisces and Tetrapod are have been grouped as gnathostomes characterised by the presence of jaws in their mouth. In contrast all animals which do not posses jaws like lampreys and hagfishes (primitive jawless fishes) have been grouped as agnathans.Both gnathostomes and agnathans have been grouped as vertebrata (sub phylum) and as Chordata (Phylum) groups.
Source : Vertebrates: Comparative anatomy, function & evolution  By Kenneth V Kardong


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Costa Rican Centipede Species
What species of centipede is this?
Found it 3 miles from San Ramón, Costa Rica

I appreciate the coin for the scale but honestly, I have no idea what the diameter of a 500 colones coin is :D


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Distance between species
Is there an on-line database that will enable one to find the genetic distance between two species?
I'm vaguely aware that there are various metrics used that may give different results, but I'm looking for a database that can be used to derive any of these metrics.

Unless someone has already done the work to determine genetic distance between the two species you're interested in, unfortunately the answer is "no, there is no such database".  If representative members of the two species have had their DNA fully sequenced, any of the relevant metrics (e.g., those described in Wikipedia https://en.wikipedia.org/wiki/Genetic_distance) can be used to calculate a value for the genetic distance.  But it's important to keep in mind that "genetic distance" is a pretty vague notion when talking about different species.  There are all sorts of epigenetic factors and gene rearrangements that can play important roles in determining the developmental and phenotypic differences between species; and those factors won't show up in most methods for calculating genetic distance.


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Isolating gene of interest from a large strand of DNA
I was always confused about this in class and never learned it fully.
So say you have 10,000 bp of DNA and you just want to isolate 100bp of specific region(gene of interest) using restriction enzyme.
How can you ensure that at the both ends of your gene of interests has the right sequences for certain restriction enzymes to cut.

What research have you tried to do on your own to answer this question? Please update the question with evidence of such research to avoid having the question closed. Thanks.

Assuming that you know exactly where in the full DNA strand the gene of interest is located, it is fairly easy to isolate the gene. There are several restriction enzymes you can use, it's just a matter of determining which one(s) are most appropriate for your gene of interest.
Remember that it is usually fine to have extra nucleotides on either end of the gene; the ribosomes will start and stop adding peptides based on start and stop codons, independent of how far the ribosome moves before reaching the start codon. Analyze your DNA strand and try to find a restriction enzyme that will slice the strand somewhere before the gene begins, and usually another that will slice it somewhere after it ends, although sometimes the same enzyme will work for both ends of the gene.
Edit: As @Untitpoi mentioned, if the restriction enzyme's slice sequence is found within the gene of interest, it will cut your gene in two (or more). It is very important to ensure that the enzyme(s)s you choose do not slice the gene of interest, otherwise the strand will be useless. It's possible to re-join the strands (which, thanks to sticky ends, isn't too difficult), but why take the extra effort when you don't have to?

won't it be a problem if the sequence is found again in the gene of intersest?

You have to know something about the sequence you want and the flanking sequence then you pick a restriction enzyme that will cut approximately where you want.  There are so many different enzymes with different cutting target sequences, it's usually possible to find a suitable one.


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what is the difference between gene and allele?
I want to know about gene and allele As we know allele is pair of genes they are ;present on only one chromosome or on homologous chromosomes? Or its like that;one chromosome has only one gene out of an allele and other homologous chromosome has another gene from the same allele?please clear this

An allele is a variant form of a gene.
You can obtain a more detailed explanation of alleles using Encyclopaedia Brittanica.


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Is there a standard way of measuring culture nutrient levels in real time?
I am working on optimizing growth rates for a culture, and one thing I'm trying to monitor is nutrient consumption rates to pinpoint any bottlenecks, i.e. the culture goes through all the calcium in a few hours and then stops growing.
Short of manually taking samples every few minutes and running individual tests for wide arrays of nutrients (minerals, amino acids, nitrogen compounds, etc.), is there a standard way of monitoring nutrient levels automatically in real-time? This is a personal research project, so unfortunately I don't have access to industrial bioreactors and the like.

I assume LCMS is out of the picture?

@canadianer Unless it can be conducted by a self-contained sensor that doesn't require my intervention for measurements, obviously a bit of a stretch

Enzyme-based sensors for taking real-time measurements of growth substrates do exist. In brief: an enzyme degrades the substrate and thus changes the local redox state which is detected electronically (example glucose sensor). There's no guarantee that the substrates that you want to measure can be measured using such sensors. Also I think those sensors are fairly expensive and are tailored to specific conditions (ie it's not as simple as dipping the sensor into your culture medium). Practically speaking I think systems using these sensors are limited to monitoring just a small number of substrates.
LCMS or GCMS is the standard method for measuring concentrations of substrates. LC or GC  (without the MS) may be possible, but probably not since there are are many components to culture media and so lots of overlapping peaks. Using this method is labor intensive (lots of samples), likely to be low resolution (temporally), and the equipment is pretty pricey, but if you have access to an LCMS and are willing to put the time in to become an LCMS expert then this is a good option.
Culture based methods using minimal media supplemented with substrates is an option, these experiments may achieve the same thing as real-time monitoring of substrate concentrations. If you have access to a plate reader this will be so much easier. The speed at which different substrates are consumed, and the order in which they are consumed can be inferred by measuring the growth rate of the bacteria and the final population size/dry weight of the culture.
I mention this culture-based method because, although it's not exactly what your question was about, it's much cheaper than the other options and much more established (and in my opinion more fun: you get a great feel for how the bacteria grow and what media they like, and the graphs look great).

The whole purpose of this is to identify bottlenecks in growth and factors which increase growth rates. If I only measured the bacteria themselves, I'd know the effects but not the causes. How is there not a real-time way of measuring this stuff considering the same factors can be used to optimize plant growth in the industry that feeds the world? Do realtime nutrient sensors not exist?

@TheEnvironmentalist As I said, they do exist, but they are expensive and not as convenient as say a temperature sensor. And about the culture based method: you can match effects to causes if you are causing the causes. So if you compare [M9 (minimal media) + glucose] to [M9 + glucose + acetate], any difference in growth will be due to the acetate.


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How can I verify my true genetic relationship with my close relatives with simple physical traits?
Question
I don't know if it is ethical to ask a question like that, but I would like to know every simple physical trait that I can observe on me, my parents and my siblings which are regulated by a single or really low number of genes.  I don't want any disease-related traits, just simple traits that could illustrate genetic relatedness.
Already done search
During my research I've found about:

Hair on the second phalanx which is controlled by a single gene and absence of hair being recessive. (Recessive means you need two copies of the allele to have the trait absence of hair!) So if both parents have the trait absence of hair (on second phalanx), every child must have it as well.
Merged ear lob is also a recessive trait.

These are some for which I am not sure of the underlying genetics.

Hair in V on the forehead
Presence of dimples
Able to make a U with tongue
Able to detect Phenylthiocarbamide (PTC)

Don't hesitate to answer with references
EDIT: This site is saying that both hair in second phalanx and merged ear lobs are not as simple as they seemed...
Question: What trait can I use to illustrate genetics?

What do you mean by "physical trait"? I assumed you meant something visible, but "Able to detect Phenylthiocarbamide" doesn't come under that. Put another way, what would a "non-physical" trait be?

Well, it would mean something easy to assess for a classroom (and no lab studies), To be honest I wasn't thinking about PTC when first writing the question. for example blood type is not easy to assess without a lab. I agree physical is not the best way to say that

Here are the answers for your four questions:

Widow's peak (hair in V): dominant: Dominant and recessive characteristics, blinn.edu; Dominant Inheritance, Genetics Generation
Dimples: irregular; tendancy toward dominant *: Mendelian Genetics, uni.edu; What Is the Genotype for Dimples?, seattlepi.com; Understanding Genetics, genetics.thetech.org
Curling tongue: complex; tendancy toward dominance: Myths of Human Genetics, udel.edu; Debunking the biggest genetic myth of the human tongue, Cathrine Woods
Phenylthiocarbamide detection: dominant: Phenylthiocarbamide tasting, Encyclopedia Britannica; Genetic study of phenylthiocarbamide (PTC) taste perception, Egyptian Journal of Medical Human Genetics, Volume 13, Issue 2; PTC The Genetics of Bitter Taste, genetics.utah.edu

Hope it helps!
*See comments

So i shouldn't use Curling tongue to illustrate genetic trait :-(.

@Untitpoi probably not.  There's even some discussion about the phenylthiocarbamide gene being more complex than a simple dominance.

I found that Dimples is irregular as it can change along the life (like curling tongue) http://learn.genetics.utah.edu/content/basics/observable/

Hmm, interesting, I wasn't aware of that one.  I'll edit to reflect that.

Well these was more complicated than i have expected, almost no trait are really controlled by one gene... the only one i have found with no doubt on it is dry earwax http://udel.edu/~mcdonald/mythearwax.html

"no trait" is a bit of a harsh judgement when so many single genes control so obvious traits like having a symmetrical body plan, two fore and two hindlimbs, five fingers... :) to find inter-individual differences within one species, you're looking at extremely high-level genetics.

The other side of this is that you're unlikely to find common genetic traits that are shared by close relatives, yet not fairly common in the generatl population.


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Effect of light spectrum on photosynthesis
It is said that the blue and red fraction of VIBGYOR is mainly used for photosynthesis. Can somebody explain why this is so?

The there are two main types of chlorophyll involved in photosynthesis, chlorophyll a and chlorophyll b. Each one is effective at absorbing energy in the form of light at a different frequency - one absorbs red light best, the other absorbs blue light best. The two are also used in two different photosystems, I and II, which have different functions, but the end result for both is that the chlorophyll gains energy for the plant to use.
The rest of the spectrum isn't used because plants haven't evolved proteins that utilize the rest of the spectrum; what they have is apparently sufficient for their needs.
This is a good resource to get a better understanding of the details of photosynthesis, and honestly Wikipedia doesn't do a bad job of explaining it.


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Inexperienced divers damage coral, but parrot fish eating coral doesn't do damage?
I've been learning about life on coral reefs. Recently I've become aware of the damage to coral reefs caused by tourism and inexperienced divers:
1) Corals have a thin membrane which keeps them healthy. Touching them could break this membrane, causing infection which can lead to death.
2) Stepping on, leaning on, and sitting on coral could smash their polyps.
I am not against being responsible as a diver, respecting nature, arriving and leaving without a trace. I'm just curious what the difference is between human and animal contact. Parrot fish eat coral, taking bites out of it, leaving exposed areas and this damages the coral. I've seen footage of sharks having feeding frenzies on reefs, where they smash into the reef during the commotion and while trying to catch their prey. Fish rub up against coral and peck at them to get algae, and crustaceans walk on the coral with legs that seems like it would break the thin protective membrane on the coral.
Obviously, as humans we technically do not belong in their world, so I'm sure there are reasons for damage with that alone; but why does marine life causing damage not cause actual damage? Or does it, and it just repairs differently or faster somehow?

If I am not mistaken, most parrot fish species eat algea that live on corals, not corals themselves.

I'm voting to close this question as off-topic because, however well-meaning it is, it is not a question about biology in the terms of SE Biology. It is merely an exhortation for social responsibility in relation to the environment.

@Remi.b some species of parrotfish do eat the coral and the algae that live within coral.

Yes, some. That's why I said "most" and not "all"

@David I disagree, the core of the question is what is the ecological role of parrotfish and how does it not pose a threat to the ecosystem.

Why do you assume that this doesn't cause actual damage or pose a threat to the ecosystem? Perhaps it does; ecosystems may change (and get destroyed) by natural causes as well.

You are absolutely correct in regards that marine life does cause damage to corals. In particular, parrotfish have been found to play an important role in regulating the biodiversity of coral reefs through their feeding behavior. Certain species of parrotfish feed on certain species of coral, typically faster growing species that branch out into easier access bits of corals that the fish can consume. This has the effect of allowing slower growing species that may also be harder corals to consume (in terms of hardness, shape accessibility, or other factors) to grow and compete in the coral reef and prevent the reef from being overgrown with the faster species. A similar process is seen on the land with grazing herbivores which help propagate biodiversity by consuming certain plant species thereby giving increased chances for other species to grow. These ecosystems and the relationships between corals and species like parrotfish have had an extremely long time to come to shape through evolutionary pressures on both sides of the organisms, consumer and producer.
The problem with divers who cause damage to corals is that it is an introduction of artificial stress and arbitrary damage to the coral reef in a short time without much time to adapt, placing additional stress on the environment which is already stressed. Unlike the parrotfish, divers may not discriminate on what corals they damage. Additionally, areas where inexperienced divers damage coral generally will see more inexperience divers often at the same diving site, so from the standpoint of protecting the coral reef, minimizing the damage caused by divers becomes an important priority to the stewards of those areas and the diving shops which bring divers to those areas.

The core answer is great and ultimately applicable to all environmental stress caused by man: the problem is not the interaction itself, but is its intensity coupled with its suddenness. The environment can adapt to a variety of stresses, but it needs its time.

OTOH, it is indeed true that a coral reef can be overgrazed by animals. An example that readily comes to mind is the infestation of the Great Barrier Reef by the crown-of-thorns, Acanthaster planci:

Normally, these starfish help the ecosystem by feeding off fast-growing coral species, thus promoting diversity. However, every so often, there is a boom in the population of these animals, and overgrazing thus occurs.

Do things like this ever happen naturally, or do they occur directly/inadvertently because of man? Like the lionfish invasion of Altlantic waters that was due to captive fish getting into the ocean; or jellyfish blooms due to several manmade causes.

I can't point to a specific example offhand, but it would be quite strange to assume that population blooms are always caused by man.

I think an essential part of this is the fact that there really is nothing particularly special about humans. We are as much a part of the environment as any other animal and produce our own evolutionary pressures (See proliferation of household/farm animal populations vs. almost a total annihilation of large predators).
The problem usually is that we (i.e. humans as a race, but mostly the developed world) don't like the results. We both like the idea of the great cats (albeit from a distance or behind glass/bars) and are afraid that the evolutionary pressures we generate are too large.
From what I understand it is very unlikely that we are able to destroy nature/life on earth, but it is very likely we are able to cause enough devastation that it won't be able to sustain the human race at the very least short term (couple hundred thousand years). This is bad for us and as such we should be mindful about not causing too much evolutionary pressure too fast to keep the planet in the state where it is capable to support us and possible also look really nice.


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What molecules does amylase enzyme work on?
I know that in the human body cellulose cannot be broken down by enzymes; however, I am confused as to which molecules amylase enzymes during fermentation.
I also looked at https://en.wikipedia.org/wiki/Amylase where it says that "All amylases are glycoside hydrolases and act on α-1,4-glycosidic bonds." so now I am confused.
Does amylase work to break down starch into glucose exclusively?
If not...
Does amylase enzyme break down corn cob extract which contains xylans, cellulose, lignin and some sugar for fermentation?
Does amylase enzyme break down corn stem which contains cellulose, hemicellulose and lignin for fermentation?

Your incomprehension is due to the fact that both starch and cellulose are polysaccharides.
As it is said in the wiki page. Amylase is active only on alpha linkage like starch or glycogen. If you want to break beta linkage like in cellulose you need a cellulase enzyme, which humans do not have.


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

I don't know the species, but it's from the superfamily Pentatomoidea, probably family Pentatomidae.

I agree. Not a beetle, but a true bug.

That is Catacanthus incarnatus (Pentatomidae). http://cyy4993.blogspot.com/2012/11/stink-bug-pentatomidae-catacanthus_17.html
http://eol.org/pages/3685880/overview

aka Man-faced Stink Bug


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What kind of ants are these? Are these venomous?
I found these ants on a small mango tree in front of my home. Could someone identify them for me.
Length: 2-3 cm
Location : North India(Chandigarh)
Temperature: 21-24 degree celsius
More info: They built a home out of leaves of the tree.

Found it from google images. Its weaver ants. Its not venomous but they can inflict painful bites along with formic acid spray.

These ants are called weaver ants, they are in the genus Oecophylla.
'Helcium is attached relatively high on abdominal segment III only in Oecophylla'
http://www.antwiki.org/wiki/Formicinae
They use the silk produced by their larvae to bind leaves together to make chambers for their brood. As any ants in the Formicinae subfamily, they do not have a stinger. They can however bite and drop formic acid on your skin, which can cause irritation. They are used in orchard as biological control agents against pests.

You seem to be answering a lot of questions about ants recently. That's fine, but please try to add a reference or citation to your answers if possible,

This is a very broad question about ants, there won't be any useful citation for this because the question is too broad. With the name of the genus, Sumeet will be able to find all the information needed.

I think there is a real issue on this forum, wrong answers get accepted with no reference while I get in trouble for rightful identification. Forcing me to add references is irrelevant because none of them provide support for identifications based on the habitus.


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double PCR with tailed primer
I would like to make a double PCR with universal tailed primer. The first PCR would make a tailed amplicon. The second PCR would generate fragment labeled with fluorescent dye. Here is my protcole. Could you tell me if I am wrong ?

is my second PCR forward primer well designed to fit with the tail ?
What would be the ratio of primer to use if I want to merge the two PCR into one ?

Fist PCR ( works )
In bold, you have the tail M13(-20)
Forward : 5'-GTAAAACGACGGCCAGTTCTGCAGTTGTACTGAGTGAA-3'
Reverse : 5'-AAAGCGTGCAGCTGATATTT-3'
Mix for 1 sample

Water              = 15.8µL
MgCl2 (25mM)       = 18µL
Buffer (5x)        = 6µL
dNTP (4mM)         = 1.5µL
Forward(20pmol/µL) = 1µL
Reverse(20pmol/µL) = 1µL
GoTaq (5U/µL)      = 0.15 µL
DNA (50ng/µL)      = 1 µL

Second PCR ( not working = no fragment signal )
Forward : 5'-[FAM]-GTAAAACGACGGCCAGT-3'
Reverse : 5'-AAAGCGTGCAGCTGATATTT-3'
Mix for 1 sample

Water              = 15.8µL
MgCl2 (25mM)       = 18µL
Buffer (5x)        = 6µL
dNTP (4mM)         = 1.5µL
Forward(20pmol/µL) = 1µL
Reverse(20pmol/µL) = 1µL
GoTaq (5U/µL)      = 0.15 µL
DNA (50ng/µL)      = 1µL from my previous amplicon

Are you forced to use the reverse like this? I've been taught to avoid A/T ends and stretches of more than 3 consecutive C/Gs or A/Ts; your reverse has both. Besides that, did you try a gradient for the anneaing temperature?

No, I can change the primer ! Thanks for your advice.

I'm not sure to understand your query. I can say that in my lab we are also using fluorescent dye (for SSR detection). But we are doing it with a one step approach:
Our forward primers are like yours preceded by the fluo sequence (M13-forward primer). But instead of making a second PCR, we add directly the fluo primer (let's called it M13-FAM) in the first PCR. It is REALLY important to put your M13-forward primer in lower quantity than the reverse one (factor 10 for me). To achieve that I use 0.1mM primer solutions and I mix my primers before
For 96 wells (20µL/well)
Primer Mix

1.25 µL of M13-F primer
12.5 µL of R primer
240 µL of water

PCR Mix

200 µL of Primer Mix
20 µL of M13-FAM
Master Mix 1mL
Water 1mL

Thanks ! You answer to my question perfectly ! I was doing 2 PCRs to check my primers first . But my final goal is what you did .
Could you give me your primers ? To check if I am not wrong ? I m not sure if M13-tail primer and M13-FAM have to be in same orientation 5'-3'


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How might IV-saline cause kidney damage that seems to be less likely with "balanced fluids" IVs instead?
The ABC News article What's in the IV bag? Studies show safer option than saline includes:

Saline — salt dissolved in water — has been the most widely used fluid in the U.S. for more than a century even as evidence has emerged that it can harm kidneys, especially when used a lot.
Other IV solutions called balanced fluids include saline but also contain potassium and other things that make them more like plasma, the clear part of blood. They're widely used in Europe and Australia.
The studies involved 28,000 patients at Vanderbilt University who were given IVs of saline or a balanced fluid. For every 100 people on balanced fluids, there was one fewer death or severe kidney problem.

and refers to research "...which were discussed Tuesday at a critical care conference in San Antonio and published by the New England Journal of Medicine."
Presumably the traditional saline solution does not contain a "wrong" or dangerous concentration of salt, but it seems that it's now conclusive that a balanced combination of ingredients beyond NaCl is safer.
Is there any understanding of the particular mechanism by which saline alone lead to issues with kidneys that seems to be alleviated by the addition of other natural constituents of blood plasma?
At first I thought the issue may be connected to "...especially when used a lot." by itself, but (also presumably) the study would have accounted for this.

I've won a Tumbleweed badge with this question, a dubious honor. Any ideas how the question might be improved? https://i.stack.imgur.com/NwioR.png

Short answer
There is not likely to be a single mechanism involved, but the study authors suggest that high chloride is the main issue; they refer to previous work showing a whole variety of issues that can be caused by higher-than-normal chloride levels.
Although saline contains roughly the same sodium content as blood plasma, it contains a lot more chloride than usual, because blood plasma contains several other anions such as bicarbonate.
However, please see the rest of my answer: this study shows a fairly modest effect and is certainly worth some more investigation but might not be as definitive as the news makes it seem.
The study in question
I assume the news article you reference refers to this recent paper:

Semler, M. W., Self, W. H., Wanderer, J. P., Ehrenfeld, J. M., Wang, L., Byrne, D. W., ... & Guillamondegui, O. D. (2018). Balanced crystalloids versus saline in critically ill adults. New England Journal of Medicine, 378(9), 829-839.

I am constantly befuddled by why journalism considers it appropriate to refer to a study with no citation at all of the original article, only barely noting one of the original authors and only after mentioning an interview with someone completely different. Even their link to "New England Journal of Medicine" is not a link to the journal but to other articles written by that news organization that also refer to NEJM.
Careful interpretation of the study results
First, note that this study is talking about a fairly small difference. It isn't like saline is causing people to just drop dead, and you recognize this in your question, writing:

Presumably the traditional saline solution does not contain a "wrong" or dangerous concentration of salt

Rather, the study showed that 1139/7924 (14.3%) with "balanced fluids" had an adverse kidney event versus 1211/7860 (15.4%) with saline.
They also reference two previous papers, one from the same authors:

Young P, Bailey M, Beasley R, et al. Effect of a buffered crystalloid solution vs saline on acute kidney injury among patients in the intensive care unit: the SPLIT randomized clinical trial. JAMA 2015;314:1701-1710.
Semler MW, Wanderer JP, Ehrenfeld JM, et al. Balanced crystalloids versus saline in the intensive care unit: the SALT randomized trial. Am J Respir Crit Care Med 2017;195:1362-1372.

each of which showed no difference between "balanced fluids" and saline.
Therefore, I think concluding

"...that it's now conclusive that a balanced combination of ingredients beyond NaCl is safer."

is not necessarily true. In Young, et al., 102/1067 (9.6%) versus 94/1025 (9.2%) of patients showed signs of acute kidney injury for the "balanced" versus saline groups - a difference that was not significant (i.e., there are not enough subjects in the study to know that an effect this size is unlikely due to chance), but numerically the "balanced" group was worse. In Semler, et a. 2017, major adverse kidney events were 128/520 (24.6%) "balanced" versus 112/454 (24.7%) saline - literally as close to "no difference" as possible with this number of subjects (i.e., 111/454=24.4%).
Therefore, although this latest work shows a significant result with a larger population size, if you consider the previous work in this area the results are definitely mixed. The more recent Semler et al. 2018 paper's result is based on a p-value of 0.04, which is just below a commonly used threshold of 0.05 for deciding whether a result is significant. That doesn't mean the result is wrong, but it means that it should be considered in the context of other work being done in the area.
This study is also focused specifically on kidney issues, and although they have some other general secondary measures like deaths, the study is not designed or able to tell whether certain patients may actually be harmed by use of 'balanced' IV rather than saline IV.
To your actual question,
How might IV-saline cause kidney damage that seems to be less likely with “balanced fluids” IVs instead?:
The authors refer to other work showing that high chloride levels lead to a variety of issues; saline has a higher chloride level than normal blood plasma levels, so they suggest that if there is an issue with saline, the chloride levels are a likely cause, but this study has no ability to test those mechanisms.
Relevant quotes from the article, with emphasis mine:

In preclinical models, the high chloride content of saline has been reported to cause hyperchloremia, acidosis, inflammation, renal vasoconstriction, acute kidney injury, hypotension, and death. Studies involving healthy volunteers suggest saline may decrease renal perfusion through chloride-mediated renal vasoconstriction.

Thank you for taking the time to write such an in-depth analysis of the paper's statements, analysis, and it's citations, and locating the relevant xkcd to go with it as well.

You might want to re-unite "...that it seems..." with the block-quote snippet from my question, and include the "..." to indicate that words are still missing.

@uhoh I added the ellipsis - I prefer leaving out the "that it seems" - in the context, you wrote both "it seems" and "conclusive" which are sort of contradictory. I've been trying to remove "it seems" from my own writing in that context, because it sort of hedges something that isn't meant to be hedged. If it didn't seem, you wouldn't be saying it in the first place, so it's sort of redundant.

I chose "...seems...conclusive..." to allow an opportunity for the answer to be instructive and cautionary about concluding too much from one paper or one study, which you did quite nicely! I may combine those words again in the future if something seems conclusive to me, but I am not certain that it is, and I'm asking a question about it. Thanks!


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Cutting of DNA strand
Would EcoRI cut the following sequence??
5'CTCGAGTTCGAG3'
3'GAGCTCAAGCTC5'
What is the logic of cutting? Please explain how restriction enzymes work.

No, it will not cut it, because EcoRI recognizes the following palindromic sequence: GAATTC, and only if the whole sequence is present it will cut it at particular site. You can find these information for all restriction enzymes at sites of the providers, for example at New England Biolabs site https://www.neb.com , just enter the name of the enzyme you are interested in.


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Can disease resistance from vaccination be inherited?
If a person has taken a vaccine against a particular disease and is resistant to that disease, will his/her children will be resistant to that disease??

No. See
Passing virus/diseases immunity to newborn

Note that the question in your title and the question in your body are different; immunization with vaccines is only one of many mechanisms for disease resistance, and many types of resistance to disease are indeed hereditary.

I have changed the title from "Is disease resistance hereditary?" to reflect what appears from the body to be the specific question.

Not usually. I say usually because there's a fairly new (~15 years old) branch of genetics known as epigentics which has been shown to allow for inheritance of acquired traits. So it's possible that if the way in which a vaccine worked was altering your epigenome or genome, that it could be passed down to your children. However, that's just a hypothetical since none of the vaccines that I know of currently work in that way, but maybe something in the future will.
As of now, vaccines generally give you immunity by introducing some portion of the virus you're vaccinating against and "sensitizing" your immune system against it. This could be the viral envelope, it could be viral DNA/RNA, could be a viral protein, etc. However, in all of these cases, your immune cells are carrying out a fairly complex process in which they make antibodies with an almost random pattern constantly, and when one is produced that binds to this virus, it tells the B cell that produced that antibody to start making more. In this way, it "confirms" that this B cell is onto something.
Having said that, the B cells themselves are not passed on from parent to child, so a child would not be permanently immune to a virus even if the parent was. BUT, some antibodies can be passed from mother to child through the umbilical cord. These antibodies have a finite life and since they're not cells, they don't replicate and device. So the child would be immune to whatever a given antibody works against as long as that antibody remains in their system (usually on the order of weeks to months). Once the antibody is degraded, they no longer have any immunity, just as their parents did not have immunity before being vaccinated.


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Why do we value species that are on the brink of extinction?
As I understand, biodiversity has two benefits:

Species might be a functional part of the ecosystem, e.g. balancing other species' numbers or beeing part of the foodchain.
Species with diverse abilities make sure that "life as a whole" can adapt to changing environments.

These hold true for most species currently alive. For species that have only a few thousand or even a few dozen exemplars left, neither function seems to be achievable. Yet there is a wide consens in protecting such species - what's the reasoning?

The concept of benefit depends upon what we ethically judge to be good. In those terms, biodiversity has other benefits (and, arguably, drawbacks) that are very unrelated to biology such as an appreciation for richness and pretty landscape for example. A sense of guilt and melancholy toward extinct species plays a big role in what species we decide to protect as a society. Hence, the reasons for protecting a species go way beyond biology and those reasons cannot be discussed on a biology website only.

I'm voting to close as off-topic because the question asks for justification of political decision that go beyond the field of biology.

Consider that to protect a single species, we must protect its essential habitat. In protecting its habitat, we afford protection not only to the target species, but all species that utilize that habitat. One reason for putting emphasis on species that have suffered drastic declines is that they are often associated with concomitant reduction in their  habitat, which endangers many other species, and even entire ecosystems.

This seems like a question for philosophy or political policy, not biology

I agree with all the comments above, but also think it is a valid question. Besides the value of biodiversity for both ecosystem function and aesthetics, the use of species as indicators of whole ecosystems, and the moral values we impose upon ourselves, it can also be said that we can never know if a species may hold some property that we will need for our own survival.


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Do "real" human samples tend to return fewer protein identifications in Proteomics experiments?
I'm working with bottom-up (shotgun) mass spectrometry-based proteomics and have encountered an issue. If I do a run with a HeLa digest standard, the resulting data returns many protein IDs. When I do the same experiment with cultured human cells (TCells specifically), the number of IDs drops dramatically.
We've been racking our brains trying to determine why, and it doesn't seem to be an issue with the data itself. It's as if the database search can't find sequences that fit the data.
My boss also encountered a similar issue when dealing with a previous project; the system worked well on murine samples, but there was a huge drop off in IDs when looking at human cells (with a human database, not murine of course!)
Is there some kind of known issue when looking at human cells from patients/in vitro samples? Is there a high proportion of point mutations/non-canonical sequences that upset database searches?

What is the actual difference in protein IDs? 10%, 20%, 70%?  Assuming the same starting material amount was used on the same column on a clean instrument, there could be a number of reasons from alkylation/digestion differences to protein abundance differences (e.g. presence of high abundance ECM proteins) to the database used (e.g. Uniprot with or without isoforms).


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Is it safe to use an egg incubator to grow bacterial cultures?
I've been using a small egg incubator to grow environmental bacteria in petri dishes. I always wear gloves and glasses when I handle the plates and do Gram staining. How likely is it that bacteria grown on dish could become airborne when I open the incubator or the dishes themselves?

the type of egg incubator would be important that is a vast variety which produce very different risks.

A good practice to minimize the contamination of a Petri dish and of the external environment is by never completely removing the lid of the Petri dish: to access the content of the Petri dish with an inoculation loop, lift the lid on one side, slowly: just high enough for the inoculation loop to get in, get some of the content, and get out.

if you keep the petri dishes covered there will be little or no contamination and there will be negligible e coli aerosol when you open the incubator. as mentioned by @MartinKivana don't open the plates, esp near the incubator.  In a sterile environment is better...
if you don't keep the petri dishes covered your experiment will be ruined.
you can wipe it down with bleach once in a while...
so that about covers it.


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What spider is this? Found in Hawaii
I found this spider at the edge of a park in Hawaii. ~1cm in length. The area I found it was very dry and had thick tall grasses just a few feet away.

Looks to be an araneid (orb weaver spider).

You have a Spotted Orbweaver (genus Neoscona). Likely either a Western Spotted Orbweaver (N. oaxacensis) or Red-femured Spotted Orbweaver (N. domiciliorum)


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How do (commensal and mutualist) microorganisms colonize the seminal vesicles?
Human's seminal fluid has it's own microbiome (Javurek et al. 2016). How do species of this microbiome (bacteria and eukaryotes) colonize the seminal vesicles?
It is possible that different species would colonize the seminal fluid through different means. What are the possible ways by which such colonization could happen?


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Why do left and right eyes can require different power of lenses?
Both the eyes almost see the same things throughout our life. It is not like we use one eye more than other that it should become weaker. What causes requirement for different power of lenses for both eyes? Shouldn’t they be same?

Because we have two hands, two feet, two ears, etc., we are tempted to think that we are perfectly symmetrical.  But if you compare the details of your two hands, for example, you will find that the blood vessels are in somewhat different positions, the lines in your palms are different, and the fingerprints of corresponding fingers are different.  The same is true of your eyes: they differ from each other.  These kinds of differences are due to the fact that genetic instructions relating to symmetry during embryo development are not exact; they are approximate.
Probably if you measure the size of the biceps on each arm, or the size of the forearm muscles, you'll find that they are slightly different.  This is partially due to the fact that you use one arm and hand differently from the other: you are right-handed or left-handed.  Similarly, people tend to be left-eyed or right-eyed, using the two eyes differently.  And, people tend to sleep more on one side than the other.  These are differences that emerge due to experiences and habits.
Those factors make it unlikely that the two eyes will ever be identical, and make it likely that eventually they will need different eyeglass prescriptions.


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Does incomplete dominance follow or not follow the law of segregation?
The law of segregation says that in hetrozygotes, dominant and recessive alleles remain together without mixing into one another. In incomplete dominance, two alleles blend with each other, and the hetrozygote is a new individual with blend of both. So can it mean that incomplete dominance does not follow the law of segregation and also the law of dominance? What about law of segregation? Does it follows it?

Hello @Rabik  Why do you mean by "mixing into one another"? Do you mean phenotypes are not mixing? Alleles are versions of a gene, so they don't really "blend" or anything, what could happen is dominance of one over the other making the phenotype look like the expression of the dominant allele.

I mean each allele, either dominant or recessive. Maintain its individuality one is dominant over other but they donot blend ;according to law of dominance ,and incomplete dominance disobeys this,so I just wanted to know that does incomplete dominance obeys law of segregation?

I think you are mixing different notions, you need to be clear on what you are talking and then your answer will appear as evident to you. I invite you to check this site to get the definitions. Firstly
What is law of segregation also called first law of Mendel?

It is the hypothesis that during the formation of reproductive cells (gametes), pairs of hereditary factors (alleles of genes) for a specific trait separate so that offspring receive one allele from each parent.

Note that there is nothing here about expression (which is what is visible), it's all about genes and alleles.
What is law of dominance also called third law of Mendel?

It states that one of the allele for a pair of inherited allele will be dominant and the other recessive.

This one is about expression, you know you can have two different alleles but this law says one will always be dominant over the other (which means the allele will be expressed whether the other one will be silenced or not visible).
And what about incomplete dominance?
Well Mendel during his studies encounter more complicated case than simple dominance, sometimes the two alleles will express equally (co-dominance)  giving a third observable phenotype (like blood-type AB for example). In reality, most of time the observable phenotype is nearer of one phenotype given by the domniant allele.
To conclude: incomplete dominance doesn't break the first law of mendel (segregation) as alleles will be equally transmitted to offspring but it breaks the law of dominance because the phenotype is not exactly one given by a unique  allele but rather a mix between both.
Remember: Segregation law is not about expression or phenotype

What a perfectly phrased answer +1

Thanks untitpoi!I will make my basics more strong. There is one more thing that bothers me a lot that;one allele is a pair of genes on homologous chromosomes. I wanted to  know that in a pair of homologous chromosomes there are two alleles on" each" chromosome ? Or there is only one allele on "both" ?Or it's like that out of a pair of genes in allele one gene is on one chromosome and other gene is on another homologous chromosome?

For one given gene, there could be multiple version of that gene in a population like allèle A B and O for blood type. But one individual only has two alleles one coming from mom and one from dad. What could have make you think there is four allèle per individual is the bad double chromosome visualisation(In X form you know). But that happens only during meiosis and is NOT the normal state of DNA


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Why can polar molecules like water pass aquaporin better than unpolar like H2 or CO2
We learned in our lecutre, that aquaporin lets Water pass, but blocks Ions like H+ and unpolar molecules like CO2 and H2. The reasons for the Ion blocking are comprehensible, but I dont get, why less-than-water-polar molecules are blocked. Our professor said, it has something to do with the water molecules are orient in the aquaporin towards the positively charged n-terminus of the alpha helix, but why is that an advantage compared to non polar not charged molecules?

Electrostatics.


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Is synesthesia caused by crossing the circuitry of different sensory inputs?
I have a question about human perception. After reading the book "Sensory Perceptual Issues in Autism and Asperger Syndrome" and knowing about synesthesia (https://en.wikipedia.org/wiki/Synesthesia) something occurred to me.
If unique circuits of neurons are responsible for each of our senses, and the circuits can cross with each other (synesthesia), and given that autistic people can switch off a sense or may have problems filtering inputs, and all impulses are of one kind, how can the brain know where these inputs are coming from? For example if input is coming only from the eye, can a person think that it is coming from the ear? Can we see with our ears, or hear with our eyes, through some sort of circuit-crossing?

Thank you i highly aprreciate all feedbacks, because english is not my mother language and i am glad to learn more about it to improve my skills.

You can write a thesis about that topic. You should rephrase it a bit, perhaps: At what stage in the circuits of neurons can sense perceptions of synesthesiacs become confused? What prevents ordinary people from seeing sounds and hearing what we see, if the circuits are eventually merged? Because subconcious perception is very fascinating that's an awesome topic to learn from, I donno if i will find a resonable response though, you need a pscyhologist/neurologist experience.

I think you are confused about what is happening we can all filter out information (Sensory gating), we take in vastly more information than we pay attention to, autism reduces or removes the ability to filter out incoming signals. https://en.wikipedia.org/wiki/Sensory_gating

Good question; I tried to rewrite your title to be more of a question format rather than a topic heading - feel free to edit it if this wasn't quite the question you meant to ask.

i think you didnt change the meaning. I even love that format !! :D thank you very much

Short Answer
Synesthesia happens at a point during processing where we are not dealing with "raw visual input" or "raw auditory input" anymore, but already with more abstract constructs such as "colors" or "sounds".
Full Answer
Your question seems to consider sensory perception as a matter of "inputs" and the brain detecting those inputs, such that for example the only difference, from the brain's point of view, between visual inputs and auditory inputs is that one comes from the ear and the other from the eye.
A more accurate way of seeing it is that our sensory perceptions are really the brain constructing a coherent reality from the information it got from our senses. And I do mean "information" in the most abstract, computer-sciency sense possible. It's not like our eye is a photographic plate that contains "what we see", and the brain just has to reconstruct that. The processing of visual information, by which I mean picking out various features from the light received and deriving meaning from them, starts right in the retina. Some examples from the "14.5 Visual Processing in the Retina" section in this page:
http://nba.uth.tmc.edu/neuroscience/s2/chapter14.html
On bipolar cells:

The two bipolar cell types have different functional properties.

The off bipolar cells function to detect dark objects in a lighter background.

The on bipolar cells function to detect light objects in a darker background.

On horizontal cells:

The surround effect, produced by the horizontal cells, enhances brightness contrasts to produce sharper images, to make an object appear brighter or darker depending on the background and to maintain these contrasts under different illumination levels.

On the retinal ganglion cells:

The retinal ganglion cells provide information important for detecting the shape and movement of objects.
Type P retinal ganglion cells are color-sensitive object detectors.
Type M retinal ganglion cells are color-insensitive motion detectors.

On amacrine cells:

There are 20 or more types of amacrine cells based on their morphology and neurochemistry. The roles of three types have been identified. One type

is responsible for producing the movement sensitive (rapidly adapting) response of the Type M ganglion cells.

enhances the center-surround effect in ganglion cell receptive fields.

connects rod bipolar cells to cone bipolar cells, thus allowing ganglion cells to respond to the entire range of light levels, from scotopic to photopic.

Similarly in our ears, the cilia cells that vibrate in response to sound are frequency-dependent, and it is information about those frequencies that gets transmitted to the rest of the brain for processing. In other words the very organ that detects sound also performs a kind of Fourier transform on the sound waves it detects before anything else.
See for example:
https://psychology.stackexchange.com/questions/15274/how-does-the-inner-ear-encode-sound-intensity
This parsing, combining and interpreting of information continues throughout the perceptual circuits of the brain, and not in a straightforward way either - it is hypothesized that there are two independent or semi-independent processing streams for visual information, the ventral and dorsal streams, one which is for identifying objects and the other for guiding actions:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4678292/
There is also information flowing the other way, where more "advanced" brain regions draw conclusions about what's actually there and feed those conclusions back into the more "basic perception" parts to ensure that that's what we see. I.e. perception has both "feedforward" and "feedback" processes, or "bottom-up" and "top-down".
All of this is to say, there is absolutely no way for the brain to confuse information from the retina and information from the ear; the early processing in both of those is too tightly linked to the organ itself, and perception as a whole is inextricably linked to cognition. It's not like a mouse and keyboard that you can plug into different sockets; the retina technically is part of the brain in the first place!
This is not to say visual and auditory senses cannot be confused, obviously synesthesia happens, but it likely happens at a point in the processing where we're not dealing with "raw visual input" or "raw auditory input" anymore, but already more abstract constructs such as "colors" or "sounds".
For example this paper (gotten from the Wikipedia page https://en.wikipedia.org/wiki/Neural_basis_of_synesthesia) :
https://web.archive.org/web/20060527085838/http://psy.ucsd.edu/~edhubbard/papers/JCS.pdf
Hypothesizes that the synaesthetic association of letters with colors is caused by cross-wiring between the area of the visual cortex that processes letters and the one that processes colors.
This paper from the same source:
https://academic.oup.com/brain/article-abstract/118/3/661/321747?redirectedFrom=fulltext
Finds that color-word synaesthetes had, when told words the associated with colors, activation in the language and "advanced" visual processing areas but not in more basic visual processing areas.
Similarly for autism, given that sensory perception happens at every level in the brain, including conscious thought, those perceptions can be blocked or filtered (or not) by the brain at any stage. No need to assume it is at the "raw input" stage.

Nice answer, I hope you don't mind my edit to bring the punchline up to the top.


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Microinjection intestinal organoids
I am attempting to microinject small intestinal organoids, using the Eppendorf FemtoJet 4i microinjector and Femtotip capillaries, and have come across several issues. This is a new set up in our lab, and I am first to attempt it so I apologise for the basic questions.
When attempting to fill the Femtotip capillaries using a needle or Western blot tip the liquid backs up and does not fill the capillary, leaving a large air bubble. Is this a common issue with the Femtotip capillaries? Are there other methods for filling (that do not require specialised microloader)?
When I attempted to use a tip where I had let the liquid be pulled to bottom by gravity, I had issues with leakage out of the tip bottom. Just to be absolutely clear, is it necessary for the entire tip to be filled with liquid prior to injection (no air bubbles)?
Finally I would be grateful for any advice on injection pressure and time used for organoids.
Thank you

Hi, initially I too had the same problem. Then I figured out that just gently tapping the injection needle would remove the air bubbles from the needle. Give a try

@MosquitoMan delighted to see this answered so quickly, less delighted to see it as a comment. Can you possibly post it as an answer? :)

I found that using the Femtotip loaders gives a continuous block of liquid, which can then be moved to the end of the tip by injecting several times. It is fine to have a air above the liquid at the tip.


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Why is easy to clone cats but it's hard to clone dogs?
According to this article, Here is why we're not cloning humans
there are species who are easy to clone and other who are hard to clone. Cats and mices would be in the easy to clone set , and dogs and humans would be in the hard/very hard to clone set. Why is this so? Why is easy to clone cats but it's hard to clone dogs?

If you have enough money, you can have your dog cloned.

Out of date. Primates have now been cloned.

But there it doesnt say they havent been cloned. They say it's hard. I have to assume this is confidential information and nobody knows why


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What insect could this be?

There is a bush in my garden that I love to observe, as it often has large rain spiders building nests in its leaves, but I occasionally notice large groups of an orange-headed insect on the leaves, and I can only assume that they are the primary prey item of the spiders, but I can't seem to identify them, and I only managed to get a picture of one this morning, as they usually run and hide if I get close enough for a picture.
It has a very similar morphology to a cockroach, in my opinion, but after looking over common species in the area, I still have no matches, it is around 2 - 2.5 cm. I have never seen them anywhere but this bush. I live in Johannesburg, South Africa.
I would really appreciate any help in identifying the species.

please add your location and approximate size of the specimen. Thanks

@theforestecologist Thanks for the feedback, I have added the requested information.

They usually come out during a large rain to prevent drowning

It looks like two insects there, with the one in the background (top) impossible to see. But the one in the front, with its head down looks very much like the American cockroach, Periplaneta americana (Blattodea, Blattidae)

Thanks for the answer, I have considered that, but it looks too dark in my opinion? Although I suppose it could be their diet or some other factor...

The exoskeletal plates on the legs don't really match that cockroach. But yes, looks like something related to that...

The darkness of the American cockroach is affected by its habitat and when it last molted. For example American cockroach found in the forest grasses is usually solid black, where as the pictures you find online are of indoor cockroaches which are more light brown. You can have variations of darkness when they interbreed. The cockroach in this image is hands down an American variety.


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Effect of the Marcus Theory on Photosynthesis
As far as I know, the Marcus Theory explains the rates of electron transfers in reactions as a function of differences in free energy between the product/reactant's potential well.
Furthermore, there is the so called inverted region which is often said to be important to explain effects as the photosynthesis. Sadly, I do not see the connection here. The inverted region seems to reduce the transfer rate in the backwards reaction but not in the forwards reaction which creates a net reaction flux. But how can this be explained by the Marcus Theory? I tried to read several sources which claimed to talk about this online, but apparently missed the crucial point.

Please provide a reference link to the Marcus Theory. I have never heard of it myself, and suspect that very few on this site will have.

@David I am tlaking about this theory: https://en.wikipedia.org/wiki/Marcus_theory Do you think I should rather ask this question at the chemistry stackexchange?

Not sure. I'd wait a little to see if anyone answers.


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What does enzymatic equilibrium in % represent?
I am studying an enzyme which can catalyse a chemical reaction in both directions. The paper I am looking at is mentioning a thermodynamic equilibrium of 1% in the synthase direction.
What does that mean more intuitively? I am mostly confused by the percent unit as I expected a constant rate without unit...
My guess would be that under these specific concentrations of substrates/products, the enzyme is catalising 1 synthase reaction and 99 inverse reactions for each 100 reactions it is catalising. In other words, the equilibrium constant K of the synthase reaction under these conditions would be 0.01.
Is that correct?

Please provide an exact quotation in your question with a link to the paper so that anyone interested can check the context.  My guess would be the same as yours, if you are reporting verbatime, but the terminology seems most non-standard to me.

You are correct in stating the relative rates of the two reactions.  What may have you confused is the percent sign in the statement.  The percent sign is not a unit in the sense that you are taking it.
What you have in a simple reaction like you are examining are two opposing rates of reaction.  The rate of a catalytic reaction, like others, usually depends on the concentrations of at least some of the reactants in the direction under consideration.
At equilibrium, by definition, the concentration of every material involved in the reaction is unvarying.  Otherwise, the reaction would not have reached equilibrium yet.  What that also means is that the rates of the forward & inverse reactions are equal at equilibrium.  So what does the statement signify?   It means that thermodynamically, the synthase reaction is the more unfavorable direction.  That is, at equilibrium, the product concentration of the synthase direction will be in the minority.
The statement involving the percent sign is just giving the ratio between the [arbitrary] forward direction, here stated as the synthase direction, and the inverse reaction.  The percent sign is just a mathematically short way of stating that the number stated is parts per hundred.
The equilibrium constant K is exactly the same ratio, stated as a decimal value rather than a integer per hundred.


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PCR not working
I am trying to check the integration of DNA into a very specific region of the E. coli genome, and for that I'm comparing via 2.5% agarose gel electrophoresis the length of whole cell PCR products (I'm expecting 120 and 242 bp bands).
Unfortunately, the last 3 PCRs were very unsuccessful, or should I say not interpretable, as only the non-consumed primers were visible (+ gDNA) and no 120 bp amplicons.

Those bands are 120 bp amplicons - Q5.

I wouldn't trust those fainted bands - Taq.
The ladder I used is 2-Log 0.1-10 kb.
Here's also the recipe for one 25 ul reaction:
- 5 ul polymerase buffer 5X
- 0.5 dNTPs 10 mM
- 0.25 ul of each primer 50 uM
- 0.25 ul polymerase (I tried Q5, Taq and Phusion)
- 1 ul template (bacteria)
- 17.75 ul H20
What could have possibly gone wrong? Am I misinterpreting the results? Am I adding too much template DNA? Is it possible for the primers to degrade after several freezings? Are there too many inhibitors inside bacteria?

First you should check that your annealing temperature is appropriate for the melting temperature of your primers. (and that the other PCR parameters such as extension temperature are appropriate for your polymerase)
Secondly, although most people will tell you it's not necessary, I've found that it can helpful to clean up the template DNA just a little. For bacteria, I would boil in water (put a colony into 20-30 uL) for 5-10 minutes, spin down the cell debris, and take 0.5uL of the supernatant.
Do you have a positive control? (try to amplify some other region of the genome that you haven't modified)
Of your other suggestions, I would say that primer degradation is incredibly unlikely.

No one can tell you exactly what went wrong, I'd check to see that your primers are the right sequence.  You can reorder them again, or reorder slightly different ones; primers are cheap, and come fast.

MgCl2 can also be the reason.i have tried titers of MgCl2 1.5 ,2,2.5,3 with all other conditions same and it worked


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Where does DNA fit on the Chomsky hierarchy?
Since adenine pairs with thymine and guanine pairs with cytosine, this seems to imply that there's a trivial Regular Expression for DNA (i.e. it's trivially a Regular Language, which is Type 3 on the Chomsky hierarchy). With that said, is there a "less trivial" Regular Expression for DNA? Or, even better, is there a "deeper" grammatical structure for DNA, such as a Context-Free Grammar?

I'm voting to close this question as off-topic because it is about language hierarchies, and not biology per se.

@fileunderwater How is this not about biology? I'm asking a specific question about the overall structure of DNA - in particular, if we can find a structure of DNA on the Chomsky hierarchy.

Well, as a start, the theoretical background to your own question, and the only reference/link in it, goes to a wiki page on "formal languages of computer science and linguistics". Sure, you need knowlegde on DNA to answer it, but the question is dealing with language classes. That is my opinion though; others may disagree.

@fileunderwater The question's fundamentally about DNA.

In truth DNA doesn't fit in the Chomsky hierarchy at all. DNA isn't a language, it is a complex molecule in a complex chemical environment. The fact that in many situations we can usefully abstract the structure of DNA as a string of four symbols should not obscure the underlying complexity. There is a simple code that describes the aminos acids encoded by triples of nucleotides, and some elements of a "grammar" in the structure of genes if you squint (start codons, stop codons, introns, and exons). But much of the function of DNA is stochastic and driven by the biophysics of the binding of RNA and protein molecules to DNA.


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What are the enzymes with the lowest concentrations in a cell?
Or are there any enzymes which are only translated one time per cell?

Please include your question in the body of the question. A title is not part of the question. You can't start a question with "or". You mention a cell. Clarify. Eukaryotic or porkaryotic. If eukaryotic, multicellular or unicellular? There are often low concentrations of enzymes in non-specialised cells, when these are hugely expressed in other differentiated cells. Really only enzymes or any proteins?


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Which cancers are routinely treated with anti-angiogenic therapy?
I have been asked to discuss 2 of these cancers and how the therapy is used. I understand angiogenesis and its role in tumour progression, but need some help in explaining how the therapy is used.

Welcome to Biology.SE. You might want to consider giving more work on your future post. For example, spelling correctly the very concept you are interested in would be the least you should do! Make sure to always read at least the wikipedia page when there is one and make sure to let us know what you found, what you understand and what you don't understand.

Assuming you meant "Angiogenesis" instead of "Antiogenesis"...
From wikipedia > angiogenesis inhibitor

Angiogenesis inhibitors were once thought to have potential as a "silver bullet" treatment applicable to many types of cancer, but the limitations of anti-angiogenic therapy have been shown in practice.2 Nonetheless, inhibitors are used to effectively treat cancer, macular degeneration in the eye, and other diseases that involve a proliferation of blood vessels

You should definitely have a look at this webpage form the National Cancer Institute.

Angiogenesis plays a critical role in the growth and spread of cancer. A blood supply is necessary for tumors to grow beyond a few millimeters in size. Tumors can cause this blood supply to form by giving off chemical signals that stimulate angiogenesis. Tumors can also stimulate nearby normal cells to produce angiogenesis signaling molecules. The resulting new blood vessels “feed” growing tumors with oxygen and nutrients, allowing the cancer cells to invade nearby tissue, to move throughout the body, and to form new colonies of cancer cells, called metastases.
The U.S. Food and Drug Administration (FDA) has approved bevacizumab [a angiogenesis inhibitor] to be used alone for glioblastoma that has not improved with other treatments and to be used in combination with other drugs to treat metastatic colorectal cancer, some non-small cell lung cancers, and metastatic renal cell cancer


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What is the structural difference between beta and gamma globin chains of Hb?
Hemoglobins are tetramers composed of pairs of two different polypeptide subunits. The subunit composition of the principal hemoglobins are α2β2 (HbA; normal adult hemoglobin), α2γ2 (HbF; fetal hemoglobin) and α2δ2 (HbA2; a minor adult hemoglobin)
The total number of amino acids in beta chain and gamma chain is the same-146. The higher affinity of HbF to oxygen is due to presence of serine(in gamma chain) in place of histidine(in beta chain), which inhibits its binding with 2,3-bisphosphoglyceric acid.
Is this the only difference, or are there more such differences in the amino acid sequence?

Here's a pairwise sequence alignment of the human hemoglobin beta (HBB) and gamma (HBG1) chains:
HBB_HUMAN          1 VHLTPEEKSAVTALWGKVNVDEVGGEALGRLLVVYPWTQRFFESFGDLST     50
                     .|.|.|:|:.:|:|||||||::.|||.|||||||||||||||:|||:||:
HBG1_HUMAN         1 GHFTEEDKATITSLWGKVNVEDAGGETLGRLLVVYPWTQRFFDSFGNLSS     50

HBB_HUMAN         51 PDAVMGNPKVKAHGKKVLGAFSDGLAHLDNLKGTFATLSELHCDKLHVDP    100
                     ..|:||||||||||||||.:..|.:.|||:||||||.|||||||||||||
HBG1_HUMAN        51 ASAIMGNPKVKAHGKKVLTSLGDAIKHLDDLKGTFAQLSELHCDKLHVDP    100

HBB_HUMAN        101 ENFRLLGNVLVCVLAHHFGKEFTPPVQAAYQKVVAGVANALAHKYH    146
                     |||:|||||||.|||.||||||||.|||::||:|..||:||:.:||
HBG1_HUMAN       101 ENFKLLGNVLVTVLAIHFGKEFTPEVQASWQKMVTAVASALSSRYH    146

You can see the H143S (or S143H?) substitution, as well as many more.


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Processing of speech/non-speech sounds in the human brain
I have a ""which came first: the chicken or the egg?"-kind of question regarding the processing and understanding of speech / non-speech sounds in the human brain.
I'm wondering whether speech and generic non-speech sound processing in the human brain are somehow related and whether one of the two is used as a "basis" mathematically speaking or a reference to understand the other.
Most people use "His voice/It sounds like .." to describe sounds/human voices, besides, we are able to tune out and block any non-speech acoustic activity surrounding us if we are not in a conversation which suggests that we have a special sensibility for hearing speech (or maybe our language or just our names if someone is calling us).
I've read an article which states that :

Knowledge of our mother tongue acts as a sort of auditory "template" that influences the way we perceive the sounds of other languages (scientists call this "native listening").

Hearing other languages differently than its native speakers is easy to grasp but is there any research that studies the difference in brain activity when speech / other sounds are heard and whether there is something special about hearing speech in particular.

"I'm wondering whether speech and generic non-speech sound processing in the human brain are somehow related and whether one of the two is used as a "basis" mathematically speaking or a reference to understand the other."
They both have in common acoustic energy - whose rate of change is information in itself. The mathematical basis of choice to compare each against the other, I think, is in how each relate that energy to the brain response - aka the forward model of the stimulus-response relationship.
In auditory studies you often get the (spectro)temporal response function (S/TRF) to estimate an approximate "summary" of this relationship. Note that traditionally, this is done independently, that is, either energy from speech or from other types of sound are separately investigated.
"is there any research that studies the difference in brain activity when speech / other sounds are heard"
There is a history of work contrasting the differential encoding of natural versus artificial sound classes (check out foundational work by Theunissen and colleagues). At these scales (neurons or neuron groups), the differences can be rather stark and happen in birds and mammals alike.
If you are more interested in these coding rules regarding "brain activity" at a larger scale, there are local-field-potential studies (e.g. Gaucher et al. 2012 J Physiol-Paris) that also relate mathematically to the S/TRF. However they are most likely invasive animal studies. Also I don't recall if they contrast speech S/TRFs versus other sound's. If you want something closer to human cognition, probably you might want to look at EEG or MEG studies also.
It turns out that finding similarities can be a bit harder than finding out the differences, maybe because the sounds are so different themselves. The mathematical relationship cannot escape this fact, and may then give distinct S/TRF patterns in return.
In a pre-print that seeks out similarities across stimulus types it is reported that certain information about the acoustic energy changes, in particular temporal onset edges, can be coded by the human auditory cortex, be it from speech, or music, or something else, in a more or less generalizable format across classes, at least qualitatively.  https://www.biorxiv.org/content/early/2017/07/27/168997


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Help me identify the following insect
This is my first post in this forum. I found the following insect at my kitchen in my apartment in Kolkata, India. Could you please help me identify the insect.
Thank you.
Best regards,
Saugata

Might be a red palm weevil
Rhynchophorus ferrugineus
https://en.m.wikipedia.org/wiki/Rhynchophorus


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How is the effect of proof-reading on error frequency during DNA replication determined?
An article in Nature Scitable on DNA Replication and the causes of Mutation states that:

When an incorrect nucleotide is added to the growing strand, replication is stalled by the fact that the nucleotide's exposed 3′-OH group is in the "wrong" position… During proofreading, DNA polymerase enzymes recognize this and replace the incorrectly inserted nucleotide so that replication can continue. Proofreading fixes about 99% of these types of errors

I am interested to know how this value of 99% was determined, and this is not explained in the article.

hi @Johny, maybe you can be more expansive in your question. What is proofreading for example, you didn't even mention DNA replication. You have to make the distinction between Translation/ transcription and Replication...

Very sorry, I was unaware of the standards of asking questions on stackexchange. I have updated the question and if anymore information is needed please feel free to give me feedback.

I have edited your question in form that answers my criticism. Please note that the article and hence your question is about DNA replication — not transcription or translation. Consult a standard text book or Wikipedia if this is not clear to you. I have now recinded my negative vote and close vote as the question is reasonable and the answer not easy to find by an internet search.

It would be nice if Nature Scitable actually used citations. The most used technique in molecular biology to determine the function of something is actually to prevent it from functioning and observing the effects. I would venture a guess that, simply, replication error rates were determined with and without the proofreading activity. I’ll try and find some of the original papers that studied this, but they may be hard to dig up.


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How fast animals habituate to wearing shoes
You probably have seen hilarious videos of dogs wearing shoes for the first time. Animals usually very uncomfortable and try to "shake it off", as they seem to consider shoes be some sort of sticky dirt.
I could only find short clips of dogs wearing shoes for the first time, but I would like to know, how fast dogs, or other animals, will learn that shoes are an integral part of their feet and continue with normal stride?

From AllDogBoots, it seems that teaching dog to walk in shoes will take up to 4 days and a lot of treats.

It probably is the same as making you wear socks full of dry peas and walking, added with dog reasoning whereby they don't know if they will be able to get the socks off. If you put some floppy socks on a yanomami/ a forest tribesperson, so they can walk in the forst with socks, they would take 4 days to get used to it too.


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What is the mechanism behind sympathic effusion of serous cavities due to nearby abscess?
Patient with left perinephric abcess which does not ruptured have reduced breath sound that is mostly due to plural effusion revealed by CT scan which was sterile. I found this called sympathetic effusion , Why it named as this and what is the mechanism behind it ?

The left perinephric space is adjacent to the left subpleural space so inflammation can spread from the former to the latter.
Diaphragmatic inflammation then results in a left exudative sterile pleural effusion. It's called sympathetic since it's not infective.
https://radiopaedia.org/articles/perirenal-space
https://emedicine.medscape.com/article/1979032-clinical#b4


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What's the lowest possible reaction time for the human brain?
I could not find an answer for this question out there so I thought it would be proper to ask it here.
Since our reaction time can be increased or decreased by ingesting certain drugs, I could not help but wonder: What would be limit for speed reaction and why is there such limit?
Furthermore, have we been able to quantify the delay between an event "actually" happening and our eyes seeing it and sending the corresponding signal to the brain?

It can probably be measured as eye perception to finger response speed, in tests... the lowest sober values are arond 70ms for very fast humans (computer games) top sportspeopke etc. and about 250ms average, you can certainly go beyond 1 second for very drunk, and those who are approaching an unconscious state, it may take several seconds.

That is not easy to answer because it can be difficult to agree on what is meant by "reaction time" of the brain.  If you're thinking of the time between receiving a stimulus (e.g. a flash of light) and a major physical response (e.g., stepping on the brakes), the time really depends on the length of the signal chain from the retina of your eye to the activation of your leg muscles. That tends to be around 0.275 second.
To quote from Sourakov (2009):

The fastest tactile reflex time belongs to the star-nosed mole, Condylura cristata L., which uses 22 nasal appendages to navigate through soil and can react in just 120 ms, when one of these appendages comes in contact with food (Catania & Remple 2004). Here, I would like to report the startle reflex time in skipper butterflies, which is among the fastest recorded for the animal kingdom and which is at least twice as fast as startle eye-blink reflex of humans.
Startle reflexes have evolved as fast defensive (usually escape) responses in animals, engaging subcortical reflex mechanism that bypasses cerebral processing and voluntary movement. Because circuits involved are shorter, the latencies of the startle reactions are much shorter than those of voluntary reactions. In terms of electromyographic responses recorded in vitro, acoustic startle reflexes tend to be very short. In rats, for example, electromyographic responses can be as fast as 5–10 ms, and in humans as fast as 14 ms (Yeomans & Frankland 1995).

So the method of measuring reaction time has a strong influence on results, because it can amount to measuring reaction at different points in the signal chain.
Finally, it has been shown that task complexity, level of mental arousal, and conditioning can all affect reaction times. One hypothesis is that those influences can change the effective length of the signal chain going from stimulus to response. Drugs can affect any of several factors that contribute to the length of the signal path and the speed at which a signal propagates along the signal path.

Can you provide a source for That tends to be around 0.275 second.?

@vkehayas, Sure: [www.humanbenchmark.com] is a good source.  Different sources vary from about 215 ms to 285 ms.

S.McGrew you probably meant to tag @problemofficer


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Is this a real dinosaur species?
I recently got  and would like to know if this is a real species. It doesn’t look quite like a Styracosaurus, but is close. Can someone identify?

I'm pretty sure that's an Achelousaurus.
Two curved horns on top, plus hump on nose:
Front view:

Side view: (for nose)


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Cell cycle arrest and apoptosis
Is cell cycle arrest needed for apoptosis to occur? I note that some of the factors that mediate cell cycle arrest induction (e.g. DNA damage) happen to be responsible for initiating apoptosis as well. However can apoptosis occur without first arresting the cell cycle?

As I remember, apoptosis is generally triggered by mitochondrial membrane being destroyed. I don't think cell cycle arrest is necessary to trigger this process.

@RoniSaiba not necessarily... that would generally be the pathway for the intrinsic pathway of apoptosis (release of cytochrome C from mitochondrial IM space), but it doesn't necessarily apply for the extrinsic pathway.

For context, realize that a large proportion of cells in complex multicellular organisms (for which apoptosis is relevant) are in G0 for most of their life. Cell cycle arrest is the norm.

Apoptosis can occur without cell cycle already being arrested.  For instance, in the case of extrinsic apoptosis, which could be induced by T lymphocytes, for example, a trimeric receptor such as TNF-R or TRAIL-R's containing a DD can be bound at any time by the death ligand secreted by (TNF, TRAIL) or bound to the immune cell membrane (FasL, TRAIL).
The DD (death domain), independent of where cell cycle is, recruits adaptor proteins with DED domains (ie., FADD), which in turn recruit procaspase 8.  Procaspase 8 is cross-activated (becoming caspase 8) when two of them are recruited, then released.  It then begins activating procaspases 3, which begins the actual work of killing the cell (cutting cytoskeleton => blebbing, etc.), activating CAD.
It bears mentioning, however, that once it's kicked in, cell cycle will inevitably stop, since CAD will start fragmenting the DNA...  It also bears mentioning that caspase 8 also activates the intrinsic pathway via Bid => tBid => Bax => Bak => mitochondrial leakage, cytochrome C activating caspase 9...

Sources:

Sayers, Thomas J. 2011. Targeting the extrinsic apoptosis signaling pathway for cancer therapy. Cancer Immunology, Immunotherapy 60 (8): 1173-80.

Eimon, P. M., E. Kratz, E. Varfolomeev, S. G. Hymowitz, H. Stern, J. Zha, and A. Ashkenazi. 2006. Delineation of the cell-extrinsic apoptosis pathway in the zebrafish. Cell Death and Differentiation 13 (10): 1619-30.