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small cocooned caterpillar found on bathroom door - what is this creature?

This larvae / moth has what seems to be a smooth gray cocoon which looks like a piece of cement. It can carry this cocoon with it as it crawls, and it can come out from both ends of this cocoon.
Would really be interested of knowing what this creature is and how it ended up in my bathroom.
Cheers!
As asked my location is Israel (Mediterranean climate)

You need to provide your location for species-identification questions

Possible duplicate of Identify this smooth-cocoon worm from Southern India

I live in South Aftica and suddenly have hundreds of these in my house. They seem to be nocturnal Would love to know what they are


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Why do we like music?
Music is, of course, just a sequence of sounds. Sounds are vibrations in the air, which our ears detect. So why do we find certain sequences of sounds to be appealing? What makes us want to hear these sounds (turn on a radio, for example), or make these sounds on our own (sing/play an instrument)?
Heck, why do we even move our body strangely when we hear certain music (dancing)?

Just a side info on the evolution of music appreciation: The field of evolutionary musicology is a field in the junction between evolutionary psychology and biomusicology. In evolutionary musicology (and in evolutionary psychology) empirical testing is very complicated and therefore, today we can only think and make hypotheses but we can't test them. So always take with a grain of salt what you read in those fields.

I assume our enjoyment of rhythm originates with the sounds we hear all around us (stop and listen some time!). I would also assume that lyrics originated as a useful way to pass on information and continue to be an effective form of communication. Enjoyment of harmonies and melodies must be much more complicated since they seem to be less consistent (perhaps these, too, are related to the sounds heard in varying natural environments?). Most curiously, though, is music's effect on our emotions (e.g., see Salimpoor et al. 2011).

Just a note, to say humans interpret sound in a similar way to animals, and they process music using the language and voice processing networks of the brain, and for that reason humans hear music far differently from animals.

DISCLAIMER: Usually I do research before I write. But the factual basis on this topic are pretty... meh.. So this time it was the other way around. So take note that the arguments here are just ideas. If you find references to empirical studies that support/deny these claims please leave a comment!
Turns out that I wrote a whole frickin' article in a short time. But I think this topic deserves it.
Short Answer:

Music is a primitive form of language. Both are sound patterns meant to convey information. Humans are drawn to music just as they are drawn to language.
When compared to visuals, noises are harder to localize and can't be back-checked. It's essential for survival to get the most information out of very little sound. That maybe explains why humans are so easily fascinated/obsessed with even slightest details in melodies and rhythms.
Mothers share their emotional state with their baby via endorphins, stress hormones etc., and that baby may associate these emotions with her heartbeat in the womb, learning a sense of rhythm.

Long Answer:

What came First? Talking or Singing?
What is singing? Singing is like talking, but with a melody. And when singing, we don't really care that much what words are used. That makes singing an easy way of conveying emotions between each other, much like a "primitive" form of language. Look at the asian language: Words shift their meaning when changing pitch.
So I had this idea that our complex language must have evolved after we began to sing. And it turns out that I am not the first (this article).

Even Charles Darwin "talked about our ancestors singing love songs to each other before we could speak articulate language," Patel says.

I think this makes it clear that our love for music is deeply rooted in our love for language.
This article also claims music is deeply rooted in evolution:

Music making seems to occur, in some form or another, in all human societies. Although musical behaviour varies in sophistication, music itself seems to be universal across all human cultures and plays a key part in rituals of all varieties, and the origins of these practices seem very ancient.

Detecting Sound-Patterns Is Like Learning a Language
Human hearing however, is unique among to animals. We have evolved to learn and speak a ridiculously complex language. And toddlers do not seem to have any issues by learning that language all by themselves. When mommy's lips move, sounds come out. And at some point they recognize a patterns of speeds, noises, repetitions, etc. They all represent and define things that we see around us. And learning these definitions is fun, because it helps them getting exactly that thing that they want right now.
My point is: Music is basically noises arranged in a complex pattern. But other than language, these patterns have no specific meaning. Still, that does not stop our inner child from trying to learn those patterns. After all, those patterns might tell us something.
Small Sounds Must Elicit Big Emotions
Hearing is essential to survival. Hearing must elicit an emotional response in the right situation in order to regulate our behavior. A hissing sound in a bush means "don't stick your hand in there". Screaming means problems. Yawning means sleep. Whispers mean secrets. Laughing means happiness.
But the problem with sound is, sounds can not be perceived a second time if we want it. If we see eyes looking at us from between the trees, reality allows us to look again and check. Noises however are harder to localize, so they are often singular events. And they can easily be missed or ignored. And that can have dramatic consequences. That’s why I think that the control of hearing over our emotional state must be so strong, so that even small sounds are allowed to override our current emotional state. It’s essential to survival, being able to instantly switch from e.g. relaxing at the campfire to standing up and checking in on the sound of branches breaking.
And I think that this idea goes even deeper. It’s not just branches breaking that should freak us out, but all those sounds that humans make. After all, the only dangerous „predator“ left to humans are humans. And humans can be hard to read. What did he say? How did he say it? Is he lying..? Did I say something wrong? Does he/she love me? And to read a human successfully, we must be able to discern even the slightest shifts of volume, pitch, tone, speed, etc.
My point is: We love hearing details, since it has always helped us to survive. And Music is full of details that are just waiting to be over-interpreted.
An Unborn Child may Associate Heartbeats with Emotions
But how do we learn to enjoy music in the way that we do? Why do minor chords sound sad, and major chords happy? I don't know the answer, but I might explain why we are able to associate different rhythms with emotions.
The first sound we ever hear is the heartbeat of our mother. It can be fast or slow. And that has a meaning. When mommy's heart is beating fast, she's also getting warmer. Also, the levels of hormones (Stress hormones, endorphins) in her blood change. In other words: A mother shares her emotional state with her baby. In fact, a mother's stress can change fetal heartrate, too (Monk et al. 2000).
And I presume that the child is able to associate different heartbeat frequencies to stress/happyness in the womb already. That might be the reason why we perceive slow rhythms are calming and faster rhythms as exciting.

As a musician, I find it difficult to explain this empirically. However, there are certain mathematical avenues one can take to analyze why exactly certain combinations of notes sound consonant- Andrew Huang has an excellent introduction video to this concept. If you're interested on why certain intervals, like the diminished 5th, sound grating, while octaves or perfect fifths are more pleasing to the ear, read a bit about natural harmonics. This, however does not serve to explain why music is so enjoyable to us.
I personally hold the belief that it is a largely cultural thing. There are many Muslims who are repulsed by music of all forms- their religion forbids it. while I may tap my hands in rhythm to a song played on the radio, someone from a muslim background may attempt to turn the music off. Our enjoyment and understanding of music is based entirely off of our expiriences, culture, and beliefs.
To expand on this, there are different systems of music, as well! Eastern music theory is far different from Western theory. While Western music often uses a 12 tone scale, (12 notes per scale), Eastern music, particularly Arabic music, utilizes microtonal scales that may sound displeasing to a western-trained ear. In my mind, this cements the concept that the expirience of music is a largely cultural thing. For more information on this, you can read about the Oud, an arabic microtonal instrument. there are plenty of youtube videos that exlpain this in an easy to digest manner.

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How can I tell if a protein has been denatured?
So i recently done an experiment using egg albumin, and we had 5 test tubes. the goal was to see if they have been denatured.
1- heat
2-acid (HNO3)
3-base (NaOH)
4- Alchol (ethanol)
5- heavy metal ions (AgNO3)
So some of the test tubes became cloudy/milky and some clear. Is it the clear ones that has been denatured? I don't know how to tell.
Thanks in advance :)

What is your starting state? If it was clear before you added the factor of change and the protein was in its normal conformation, then what does that say if solution stays clear or becomes cloudy?

untreated egg albumen is, contradictory to the colloquial term 'egg white', a clear mass. That is its native state.

In my experience, when protein denatures, it typically aggregates and precipitates from solution. I would expect a denatured protein to create a cloudy solution, or actual precipitates in the form of little globs or fine wisps. A solution where protein is correctly formed and solubilized in the solution should be clear.

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How "old" is a specific snake venom?
This is a World Building question, but it's biology specific (I think).
I'm looking for an approximate answer on how long, evolutionary, a specific venom has been roughly the same.  Is it pretty much species based (although I know that's a problematic term), so it would be the same as the "age" of the snake's evolutionary tree since it last branched?  Or is it based on something else?
Specifically looking for information on the Eastern Diamondback.  I am ok with extremely approximate/vague answers, or even just a hypothesis/educated guess.
If it helps, a possible rephrase of this question would be:
How far back in time could you time travel before a modern anti-venom starts to lose effectiveness?

definitely on topic!

This is a really interesting question. The best statement I could quickly find was in this paper. Snake venom glands evolved a single time, at the base of the colubroid radiation, 60-80 million years ago, with extensive subsequent “evolutionary tinkering”. ... I work some with peptide venoms from Naja cobras, so there's some personal interest. It should be simply a matter of sequence divergence. I'll keep looking :)

This article is interesting and contains some sources.

https://www.oist.jp/news-center/news/2013/12/9/biting-snake-venom-mysteries This story may be of help?

According to the following sources, venom resistance has evolved in both snake prey and predators. Also, resistance can be just regional/confined to a certain population. That suggests that arms races occur, where the composition of the venom of a certain species is constantly changing, and so are the defenses of the prey and/or predators who get bitten. In that case, a snake venom is not the same in chemical composition for very long, and might not be the same across populations of the same species of snake. But those differences might be on a smaller scale than you are looking for. I don't know anything about how this affects effectiveness of antivenom. However long it is until the antivenom loses effectiveness, it might be much shorter than the divergence time since that snake species branched off from the evolutionary tree.
Ground squirrels and rattlesnakes:
"Snakes win: Coevolution of venom function and prey resistance in a rattlesnake-squirrel arms race;
"Coevolution of venom function and
venom resistance in a rattlesnake predator
and its squirrel prey"
"How is rattlesnake venom like fine wine? Both have regional varieties"
(I wanted to make this a comment but don't have the rep for that).


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Chemoautotrophic eukaryotic cells?
There are heterotrophic prokaryotes, and there are autotrophic prokaryotes. In the autotrophic prokaryotes category, there are photoautotrophic prokaryotes and chemotrophic prokaryotes.
Are there chemotrophic eukaryotes?

There are two ways of classification of Prokaryotes(on the basis of mode of nutrition) that you will generally come across:
Way 1

Way 2

The First classification is very much based on a complete segregation between respiration and photosynthesis. In the first classification, anything that needs another animal to get food is a 'Heterotroph'. (Here, chemotroph and chemoautotroph are the same things)
But Generally the 2nd Classification is preferred, because prokaryotes have some very unique nutritional habits that cannot be explained on the basis of 'Eating/Not Eating'
In a way synthesis is the creation of a carbon compound by use of some energy.
So we need to classify based on energy and carbon source. Here organic carbon source means it is a 'hetero'troph and inorganic means it is an 'auto'troph. Similarly if Light energy is the direct energy required, it is a 'Photo'troph and if a chemical compound is required it is a 'Chemo'troph
By the First Classification, there are no 'Chemotrophic/Chemoautotrophic eukaryotes' meaning no eukaryote can produce food from inorganic material using chemical energy.
But by the 2nd Classification, essentially all eukaryotes that do not photosynthesize, instead use organic compounds as a food source, all animals, fungi etc. are 'Chemoheterotrophs'*However no Eukaryote is a 'Chemoautotroph'


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What is the function of the human eye white?
If you have a look at the eyes of most animals, you never see the white part unless the eyes are averted. In contrast, humans always have the whites visible because the iris is quite small. The only explanation I found so far is that the evolution made it this way because we are very social animals and we express a lot by eyes movements. I wonder if there is any other explanation?

Short answer
The relative large surface area of the white sclera in humans has been linked to an enhanced ability to detect eye gaze.
Background
The white of the eye is caused by the sclera. Human eyes indeed have the highest relative amount of visibly exposed white sclera. The amount of visible sclera provides information about the orientation of the eyeball. Specifically, the iris-to-sclera ratio is an important cue for eye gaze perception (Schulze et al., 2013).
Eye gaze is important. Most mammals generally interpret direct gaze as threatening, or as a sign of dominance. Humans, in contrast, tend to associate mutual gaze with positive interest, love and attraction. A preference for direct gaze seems to be present at a very early age. Infants as young as 2 days old prefer to look at faces that gazed directly at them, than to faces with averted gaze. Yet, humans sometimes find eye contact uncomfortable, for example if a stranger keeps staring at them (Schulze et al., 2013).
The ability to detect gaze has been established in many primate species, other than humans. Gaze detection may have evolved because direct gaze can signal that a predator is attending, making its detection an important tool for survival. Many animal species respond to the presence of staring eyes with displays of fear and submission, indicating that such stimuli act as warning signal. In humans, prolonged eye contact can also be perceived as an aggressive approach signal, as it leads to increases in galvanic skin response (Frischen et al., 2007).
The cooperative eye hypothesis assumes that the large scleral surface in humans developed especially for gaze detection (Tomasello et al., 2007). The authors base this conclusion on the fact that human infants mainly followed gaze, while several species of great apes (including gorillas and bonobos, but not macaques) mainly followed head movements.
However, from my humble opinion, concluding that humans developed a large relative surface of white sclera for communication purposes is kind of far-stretched. For one thing, macaques also have quite a large white scleral surface (Fig. 1.) and macaques share a dedicated neural circuit with humans that involves the superior temporal sulcus (STS). The STS is thought to process biological motion, including gaze. The STS projects to the amygdala, a structure of the limbic system that implicated in the processing of the emotional content of stimuli, including facial expressions and gaze detection. It links this information to emotional responses in the observer. There are also connections between STS and the intraparietal sulcus, an area that is associated with spatial processing and shifts of attention. Via these connections, information about eye-gaze direction could project to spatial attention systems to initiate orienting of attention in the corresponding direction, as in joint attention. Indeed, passive viewing of a face with averted gaze elicits a stronger response in the IPS than viewing a face with direct gaze (Frischen et al., 2007).

Fig. 1. Macaque. Source: Fine Art America
Personally, from these data I think the brain in humans and primates like the macaques adapted to process the information available from the eyes. It can be true, however, that brain circuits and eye structures developed/evolved in parallel to ultimately result in a large white scleral surface and a dedicated neural circuit to process its information.
References
- Frischen et al., Psychol Bull (2007); 133(4): 694–724
- Schulze et al., Front Hum Neurosci (2013); 7: 872
- Tomasello et al., J Human Evol (2007); 52 314-20
Further reading
- Frans de Waal

Wow! Thank you so much! It is indeed a very detailed and informative answer.  Im very grateful!

For further reading I've added a link to Frans de Waal's FB page. I have searched through online material but couldn't find a better source than that :) He's awesome and I own a book from him, but currently it's heading back home across the Pacific. When I get my hands on it again I can add a reference. That may take a few months - it's sent by sea mail :-)

Oh, you are so kind! I will follow all the links you gave. I find it very interesting :)

Awesome answer. I have to agree with you that it is less likely that the brain function driving the physiology and more the physiology driving brain function, given that there is much more plasticity in neural networks... I was wondering if the enlarged brain case "pushing" the orbital bones further forward causes more of the Human sclera to show.


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Is the Basic Reproduction Number in epidemiology dependent on population size?
I am assuming that the basic reproduction number $R_0$ of a disease depends on the population size (or the number of susceptible individuals). When $R_0$ is reported it seems to be without such information. Is there a standard population size for reporting $R_0$?

I'd think there'd be a required sample size to get your data within the necessary margin of error, but agencies like WHO actually provide standard population data I believe. Someone let me know if i'm mistaken!

Actually, population density and structure is far more important than population size.

OK, so $R_0$ depends on the environment. For example, different countries experience different $R_0$ for the same pathogen. So the commonly reported values correspond with what environmental conditions?

From what I understand (as an ecologist/population modeller), $R_0$ in epidemiology is not dependent on host population size per se, at least not in its basic form. It is also not dependent on the number of susceptible individuals, since it is defined as the number of secondary infections in a fully susceptible population, see e.g. this section in Farrington et al (2001):

The basic reproduction number of an infectious agent in a given population is the average number of secondary infections which one typical infected individual would generate if the population were completely susceptible.

This is also consistent with the Wikipedia description ("...in an otherwise uninfected population"). $R_0$ is however dependent on the environment (dispersal routes, host-host interactions etc), which also why it is used to evaluate and compare the effect of control measures. Host-host interactions is also dependent on population density, so $R_0$ is indirectly influenced by host population density, and this is partially why estimated $R_0$ values for the same disease will differ between countries and populations.
Fundamentally and conceptually, $R_0$ is the same thing as the Net reproductive rate (often also labelled $R_0$) in demography and population modelling, and it was originally borrowed from demography to epidemiology. As such, the net reproductive rate is often used in for instance pest control to evaluate the potential impact of pest species on agricultural crops, in direct analog to the basic reproduction number in epidemiology (see Emiljanowicz et al, 2014 for a randomly picked, recent example). Most commonly, $R_0$ (both in population dynamics and epidemiology) is calculated from static demographic rates, but nothing prevents you from considering stochastic effects, density dependence or e.g. ways that demographic rates are functions of host density or population size. This could lead to formulations where $R_0$ is an explicit function of host population  density, but that is not the standard use of $R_0$.
To me, it seems like you are asking for the effective reproduction number ($R(t)$), which can be defined by:

...the average number of secondary cases that result from an infectious case in a particular population (Box 1). R depends on the level of susceptibility in the population, in contrast to the basic reproduction number (R0), which is the average number of secondary cases arising from one infectious case in a totally susceptible population."

This section is from a WHO paper on meases (Chiew et al, 2013). So basically, $R(t)$ is the average number of secondary cases per primary case at time $t$ (including the effects of immunity and/or control measures). As you can see, $R(t)$ is a function of time, and it can e.g. be used to describe the temporal dynamics of SIR-type models.

But a well established result in epidemiology models (e.g., the standard SIR model) is that a disease will die out before infecting all susceptible individuals in the population. Also an epidemic will not even take place if the population size is small. This is because $R_0$ itself is a dynamic quantity.

@quibble That diseases will die out is not a function of the $R_0$, but of the buildup of immunity described by the dynamics of SIR models. $R_0$ is not supposed to describe this, and bringing it into discussion is just confusing things.The dynamics in small populations is also another thing (related to e.g. low host density or stochasticity). Remember that $R_0$ is mainly a measure of maximum growth, similar to e.g. $r_max$ in population models, which is describing exponential growth under "ideal" conditions (e.g. a completely susceptible population).

@quibble What you seem to be after is the effective reproduction number ($R_t$), which can be described as "...the average number of secondary cases that result from an infectious case in a particular population (Box 1). R depends on the level of susceptibility in the population, in contrast to the basic reproduction number (R0), which is the average number of secondary cases arising from one infectious case in a totally susceptible population." (Chiew et al, 2013)

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What does high CD4 level means?
I was going through this webpage and I found the following lines:

We hypothesised that despite unimodal distribution of CD4 co-receptor on naïve CD4 T cells they are not homogenous in their function.By testing naïve CD4 population from mice and humans expressing highest and lowest (~10%) levels of CD4 in a variety of functional assays we find that indeed naïve CD4 cells with high CD4 levels respond much better to activation and survive more easily post-activation.

Now what does "CD4 level" means? How is the CD4 receptors distribution obtained? With repect to the value of which feature is it obtained?(If you are not able to understand the last question, let me know, I will try to explain more in details)

In this case, I would email the corresponding author of the article and request that they provide you with a definition of what High means. A scientific text should not use vague qualitative descriptions like that. They should provide you with at the very least a range of what they classify as high, low, and normal expression of CD4 receptors.

and what does just CD4 level mean??

The number of CD4 co receptors on a CD4 T-Cell... when the T-Cell Receptor binds to MHC II the interaction is stabilized by the CD4 coreceptor. It binds to the side of the MHC II receptor on the Antigen Presenting Cell and greatly increases the efficiency of binding. I thought with the second question that you understood that CD4 refers to plasma membrane receptors on the surface of helper T-Cells.

okay okay, it is my fault actually, i was not able to frame it properly

@AMR it looks like the answer is in the question - "high" and "low" were defined as the 10% on either side of the curve...

@MattDMo The problem is that they do not defining what that 10% refers to. Are they talking about the top and bottom ten percent of cells that have been FACS sorted for CD4 receptor levels or is it like you suggested +/- 10% range above and below the mean that differs the highest number of receptors on a T-cell surface to the lowest numbers. I initially thought that Rishika understood what they meant by CD4 levels and suggested the author contact to clarify, but I think that their question was more basic, that CD4 was referring to the corecptor in the plasma membrane.


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Can immortality of the Turritopsis dohrnii be learned or adapted by other species?
I have heard that Turritopsis dohrnii is a species of jelly fish which is immortal, as it can grow old and then back to growing young.
So, how is it possible?   Can other species (marine and/or land) species adapt or  evolve into such a system?

Possible duplicate of Why is the Hydra Biologically Immortal?

@AliceD I had a look at that question, and I don't think this is a duplicate of it.  This asks whether some other species can adapt or evolve itself to have such features which helped Turritopsis dohrnii with the immortality characteristics

The answers of linked question answers the 'how' part and the theory whether other species could evolve such a system is opinion based and open-ended. Knowing how it works (stem cells, telomerase activity) can be extrapolated to other species, in theory and in theory only.


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How do I run each individual record in a multi-fasta file against a database using PSI-Blast?
I'm new to standalone blast+ and the linux terminal.
I set the bash-profile to load the PATH and BLASTDB for my blast already, but I don't know how to use psi-blast yet.
How can I do the search against db with one query sequence? The file has >400 FASTA sequences. I need to checkout every sequence alone against database. Is it possible to run this job automatic in blast+?  (one run in loop for every seq?)

BLAST takes a fasta file with many sequences as a query. Have a look at the BLAST manual. The running in loop question is off-topic since it is about shell scripting.

I agree with @WYSIWYG that the manual should be your first port of call, however it is rather crap. If you're comfortable with ruby, perl or python, consider learning about the respective bio module. They all have great BLAST integration.


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Homeopathy is placebo, but isn't placebo good?
I never considered homeopathy as a serious and scientific medicine, and now we have plenty of evidence supporting this (http://www.theguardian.com/commentisfree/2015/mar/12/no-scientific-case-homeopathy-remedies-pharmacists-placebos).
But placebo effect is also a thing that works, strange as it may be. The placebo effect deals with the importance of the brain's role and perception in physical health. So, in my understanding, placebo is better than nothing.
But now I can't treat myself with homeopathy, because I don't believe on it. Other people believe, and are happy with it (benefiting from the placebo effect).
So, my question is, wouldn't be benefitial to illude someone (or yourself) in order to achieve the placebo effect?

I would consider making somebody else believe in something that does not work morally wrong. If there is another treatment option that works, it might keep them from using it (or if they try both at the same time, might interfere in the worst case). If there is no other option, you give them a false hope of healing. For yourself, feel free to try. I have trained my mind on homeopathic tablets to believe they make me more focused. I know it is just sugar, my subconscious is tricked into focusing.  It might be a Pavlov's response to the taste of those tablets. As it works, I don't care.

Welcome to Biology.SE. This question appears off-topic. It is not about biology but about sociology and ethics. I suppose it might be on-topic on philosophy.SE

It's maybe off topic (it's medicine / medical ethics I guess) but I do think it's a good question. There is actually a serious debate among healthcare professionals about whether placebo treatments should be used when no other options are available, because it does bring about a positive response. You can make an argument that it would be unethical to withhold any option that improves the life of the patient, even if we know the effect is merely psychosomatic. The answer is not obvious.

This is not about ethics or sociology but the mechanism behind the placebo effect. Great question.

@GoodGravy that ethical component comes from you, not the question.

@AliceD I think given the history of homeopathy, it is difficult to answer this question without ethical consideration. However, a similar question could be asked: "Is a placebo better than no treatment" is more objective. There is no need to mention homeopathy here, and doing so is distracting.

The point of a double-blind trial is that treatments are compared to placebo effect. Therefore, conventional treatments that "pass" double-blind trials are better than placebo.  If homeopathy is equal to placebo, that means that homeopathy is worse than conventional treatment.  Therefore, people who treat with homeopathy are giving worse than standard care.

But still better than nothing, right?

That's only relevant if the only option is "nothing", and in the developed world that is not true.  It's worse than the realistic options, so comparing it to "nothing" is deceptive.

Of course a proven uneffective treatment is unethical if there is a proven effective one. But there are many disorders in healthcare for which there is no effective treatment, even in the developed world. What then?

You are moving the goalposts, continually concocting new, less and less plausible, scenarios in an attempt to force the answer you want to hear.  If your only interest is squeezing out a positive answer for a wildly unlikely situation, and then claiming victory, you're in the wrong place.

@Roland there are many things that can't be cured, but there aren't all that many where no treatment at all, like pain relief or lessening of the worst symptoms, is possible

Placebos are good to use in case-control studies. Suppose you have a cohort with depression and a cohort without depression. If you gave the cohort with depression a homeopathic cure and their mood changes for the better, you can't take that as positive results yet. You first have to use a placebo on the cohort without depression to see if their mood remains stable.

But placebo effect is also a thing that works, strange as it may be.
  The placebo effect deals with the importance of the brain's role and
  perception in physical health. So, in my understanding, placebo is
  better than nothing.

If you think, say, that your lung function is improving, but it's actually not, that's not a good thing.  It would be better for you accurately know that you are not healthy, then to wrongly believe you are better.

you think, say, that your lung function is improving, but it's actually not - If you think this is the placebo effect, you have misunderstood it.


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What is the role of gills in terrestrial Crustaceans?
Why do Crustaceans that live on land have maintained their gills? In aquatic species, the gills play a pivotal role in respiration, but terrestrial crustaceans have tracheal lungs. So why do they have gills?

Short answer
Gills in terrestrial crabs serve a role in water storage and ion homeostasis.
Background
Crustaceans are a huge group of species within the phylum of arthropods, including crabs, lobsters, crayfish, shrimp, krill and barnacles. Because of the huge variety of species within the crustaceans, I'll focus this answer on terrestrial crabs.
Air-breathing crabs have universally retained gills, but have also developed accessory breathing organs, usually lungs formed from the inner lining of the gill chamber. Aquatic crabs generally have large gills with very thin closely packed lamellae. Land crabs feature lungs that are well vascularized, have short blood-gas diffusion distances and often have adaptations to increase surface area, all of which greatly increase the diffusing capacity of the respiratory
system (Farreley & Greenaway, 1994).
In contrast, the gills in land crabs  are reduced in size and in surface area. The epithelium is usually modified for ion transport as indicated by the presence of densely packed mitochondria and relatively long blood/gas diffusion distances. Hence, the gills in land crabs are thought to primarily serve an osmoregulatory role, rather than a gas-exchange function (Farreley & Greenaway, 1994). The gills are thought to be involved in salt and water uptake. Their spongy structure is thought to aid in their function as water storage areas in periods of molting (Edney, 1977).  However, the gills in many species are still capable of gas exchange, although less efficiently than the lungs (Farreley & Greenaway, 1994).
References
- Edney, Water Balance in Land Arthropods, Zoophys & Ecology, Springer, New York (1977); 9
- Farreley & Greenaway, J Exp Biol (1994); 187: 113–30


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Why did humans evolve the ability to feel such a high level of heat pain?
It's probably because our ancestors were frequently around 300°C metal which badly damages flesh in a fraction of a second because they made fires to cook. I don't see why that would cause natural selection to make that pain so extreme instead of only slight. It's so rare for somebody to die from getting a nasty burn from touching such a hot metal. Is it because those who didn't feel heat pain were frequently holding very hot metal objects and although each one touching made them only a tiny bit less likely to survive, the damage added up and eventually they would have held such hot metal objects so many times that they had a very high probability of dying?

You are thinking way to close in evolutionary history. 1) Early life likely arose in thermal springs or around volcanic vents in the oceans. It would be beneficial even for single celled organisms to have proteins that helped them detect or repair damage from heat. Those evolve a different function in multicellular organisms and is how you can detect heat. 2) We evolved in forests and brush land. During dry periods, lightning strikes set off forest fires. those that react and flee reproduce another day, those that don't, don't, but you could likely go back to the very first mammals for that.

Without antibiotics it absolutely is not rare to die from an infected burn wound.

Do we have burn specific receptors or does it just hurt because it damages the tissues as a physical damage could do? Are other apes less sensitive to burn pain? I think these questions should be answered first (and maybe you guys know the answer).


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Why both sexes of the species don't show equal level of Competition?
In most species, it is seen that either males or females have evolved to be aggressive towards approaching members of the same species of the same sex and maintaining strict territorial boundaries. The logical explanation is that such behavior is advantageous in the evolutionary context. If you increase competition, then the chance of genes suited to the environment getting passed on increases. Obviously, if one male wards of another male from his territory then the genes possessed by him are positively selected for.
In such a scenario, why haven't both the sexes developed a similar level of aggressive competition (Wouldn't this also increase the chance of genes that are suited to the environment getting passed on?)

Well if women are competitive, doesn't that mean that they risk dying if this competitive is physical? And if a women dies, she cant pass on her child, and therefore her genes to the next generation right?

There are so many species that contradict what you're trying to ask I'm afraid. If you have a specific species in mind then the question would be more answerable.

But what about maternal gene selection? There must have been some way natural selection got around the problem of aggressive competition right? If they competed in a non-aggressive manner, then it would still be an evolutionary advantage, right?

@ChitinousExoskeleton It sounds like you have an example in mind. What species are you talking about?

Three-Spined Sticklebacks from Tinbergen's Experiment...

@ChitinousExoskeleton After making a nest a male wants a female to lay eggs there for him to fertilise and pass on his genes. Why would a male fight a willing female in that situation? And of course the male doesn't want another male to take his hard made nest from him.

@GoodGravy I'm sorry for the edit saying 'members of the same species of the opposite sex' . I want to know that if males fight each other to promote their genes to be selected, then what is the mechanism for females for the same process. Because, they don't seem to have any...

@ChitinousExoskeleton So you're looking for examples of competitive female bahaviour in the context of mate selection? https://en.wikipedia.org/wiki/Naked_mole-rat#Queen_and_gestation is a pretty brutal example.

@RoSiv That exact same sentence could be used to explain why males would be non-competitive.

Why Can't both be competitive? That's all I'm asking. If the males are competitive and its helping them in a way, and females are also competitive in the same population wouldn't it have an evolutionary advantage? (Or vice versa, if females are competitive, shouldn't males also be competitive?)

@ChitinousExoskeleton This article explains the stereotype that I am trying to explain. It is a popular misconception that males are competetive and females passive. This article furthermore shows female armoury and a few have competitive male counterparts too. All the scenarios you mentioned exist in the natural world, and unfortunately the question remains if not unclear, now broad.

The reason for this discrepancy is mainly a consequence of Bateman's principle. Citing wikipedia:

Bateman's principle suggests that in most species, variability in reproductive success, or "reproductive variance," is greater in males than in females. This is ultimately a consequent of anisogamy. Females, especially mammalian females, almost always invest more energy into producing offspring than males invest. Bateman's principle anticipated and is consistent with Robert Trivers's theory of Parental investment—in most species females are a limiting factor over which males will compete. This competition results in some males being more successful than others, leading to greater reproductive variance among males than females

Variation in competition abilities for access to a mate is called sexual selection. As a consequence of Bateman's principle, sexual selection is more common in males than in females. You can split sexual selection into intra-sexual selection and inter-sexual selection. These terms are poorly chosen IMO. They mean:

Inter-sexual selection: One gender try to look sexy and the other gender chooses the mate. Fighting to impress females is one type of behaviour that can evolve under inter-sexual selection
Intra-sexual selection: Individuals of one gender fight for the access to an individual of the other gender. This individual cannot chose who to mate with.

In both case, fighting can be involved. As a consequence, you will see among-males fighting is more common than among-females fighting.

Thank You, I suppose the question was really unclear, but this is essentially what i wanted to know. Whether its necessary for one of the species to always be less competitive (or as you put it 'to have less reproductive variance) than the other!


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Are missing limbs hereditary?
So with my basic understanding of biology, DNA can change over time.
Does this mean that if one (or both) parents have something major missing (like a limb), the kid will come out without a limb?  Does it matter if the parents had limbs amputated or were born like that?  If someone got melanoma from laying in the sun a lot, would their kid have a higher risk of getting it?

Sun lights do not play a role in transmission of risk of melanoma development from parents to their children because melanocytes are not a germ line.

Human genetic makeup doesn't change just because the parents are missing a limb. The kid will be fine

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

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

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

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

DNA can change over time

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

So you can't a(e?)ffect your offspring by what choices you make (to a degree)?

@CodyJHeiser most choices won't have an effect, no. At least not genetically.

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

If the parents are born without a limb, it could have a genetic reason or from external factors such as medicines and radiation. If the baby was born with gene mutations, he may come out without a limb.
So if mutations have taken place in the parents, they may have the chance to be passed on to following generations. And the condition you have presented may be caused by mutations.
This is also suitable for you second question.

I think, that for this answer, you really need to provide references for your claims. They can be case control studies, but I don't think that you just infer this by stating what you think is the case.

DNA can change over time

This is a terribly misleading thing to say. You don't have "your DNA", you have a few billion copies of your DNA, one for each cell 1. Within an individual, there are events (called mutagenic) which can change the DNA in an individual cell. The change is practically random. It is like having a pile of DVDs and tossing them around, so some of them get scratched a bit. If one event hits many cells at once (for example a strong dose of ionising radiation), the cells will likely get different mutations each. There is no event during adulthood which will lead to having the same mutation across all DNA copies of an adult organism. 2
A second point: most events which change something in our body don't change a single copy of our DNA. Amputation of a limb is such an event. All (remaining) cells of an amputee have the same DNA as  before.
Having cleared up that, the implications for your question are simple, YviDe already mentioned them.

If two humans experience a non-mutagenic event in their adulthood, their DNA will be the same as before, and the consequences of the event will not be inherited. Thus the child of two people with amputations will be born with all limbs present.
If two humans experience a mutagenic event in their adulthood, it will change the DNA in a very small part of their cells. If they get a melanoma due to UV damage, it's only the DNA in the tumor cells that's different (and probably the DNA in other skin cells which got changed, but not enough to turn them into tumor cells). The DNA copies in the rest of their body, including the DNA of their egg cells and sperm cells, stays the same. Therefore, their child is born without a melanoma.
If two people were born with the same mutation which causes a visible symptom like a missing limb, their child will be born with it too, and will also be limbless. In this case, parents and child have the exact same mutation in all cells throughout their bodies. This is however not due to an event which "changed their DNA over time". Also note that not all birth defects are genetic.

1 This is not exactly true, but true enough for this explanation.

2 I shortly pondered whether a retrovirus can do it across the body, but all the ones I know of only work on certain cell types.


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Is this "Sympathetic fight response" axis accurate?
Peripheral sensory cell > Preganglionic cell > Dorsal root ganglia cell in the ''Sympathetic chain'' > Ventral root ganglia cell in the ''sympathetic chain'' > Post-ganglionic cell that activates an organ such as the pancreas (or a muscle).

The typical axis of the fight response is depicted in Fig. 1.

Fig. 1. HPA axis. Source: Social Psychology principles
This axis is the hypthalamus-pituitary-adrenal axis, or HPA axis. It mediates not only the fight response and is typically referred to as the fight-flight-fright response. It is the central stress response system that prepares the body in a fraction of a second for survival, basically under the influence of adrenalin and cortisol produced by the adrenal glands.
The circuit you are describing, by the looks of it, is more typical for a reflex arc (Fig. 2.).

Fig. 2. Reflex arc. Source: Sweetibnotes
A typical example of a reflex arcs is the pain-withdrawal reflex. Although the sensory stimulus triggering the reflex arc may also trigger the HPA axis, the basic circuitry of a reflex arc does not include the HPA axis. The pain-withdrawal reflex, for example, is basically designed to jerk a limb away as fast as possible in the presence of acute pain as a protective mechanism.


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Are erythrocytes lysed during alpha hemolysis?
Wikipedia says:

When alpha hemolysis (α-hemolysis) is present, the agar under the colony is dark and greenish. Streptococcus pneumoniae and a group of oral streptococci (Streptococcus viridans or viridans streptococci) display alpha hemolysis. This is sometimes called green hemolysis because of the color change in the agar. Other synonymous terms are incomplete hemolysis and partial hemolysis. Alpha hemolysis is caused by hydrogen peroxide produced by the bacterium, oxidizing hemoglobin to green methemoglobin.

From this it seems that in alpha hemolysis , it's not the lysis that's the defining event rather the chemical change of the hemoglobin molecule.
Wikipedia states:

Beta hemolysis (β-hemolysis), sometimes called complete hemolysis, is a complete lysis of red cells in the media around and under the colonies: the area appears lightened (yellow) and transparent.

I am unsure of the reason for color change (blood agar plate) in beta hemolysis, my guess it's due to diffusion as I have found no mention of chemical change in hemoglobin molecule anywhere (yet).
So far my position is chemical change in hemoglobin without lysis is alpha hemolysis and lysis followed by diffusion of the hemoglobin molecule is beta hemolysis. Problem is my support is shaky at best.

Alphahemolysis simply oxidizes hemoglobin to methemoglobin and causes a color change on blood-agar. The RBC membrane is left in tact as far as I know. If you look at a picture of the 3 types of hemolysis, you will see that there is no zone of clearing in the alphahemolysis plate. Compare that to the obvious zone of clearance observed on the betahemolysis plate, in which complete lysis occurs. Here is a nice picture

Anaerobic condition and CO production

Hemolytic and nonhemolytic bacteria were incubated aerobically and anaerobically with the following substrates: erythrocytes, hemoglobin, myoglobin, cytochrome c, hematin, iron hematoporphyrin, copper hematoporphyrin, protoporphyrin, and bilirubin. After 18 hr at 37 C the evolved CO was measured by gas chromatography. None of the bacteria formed CO anaerobically.

CO and alpha hemolysis

Because our two strains of S. mitis differed with regard to H202 production and hemolysis, we also compared an H20 2-producing strain of Streptococcus faecalis with a peroxide-negative mutant, kindly supplied by Beulah Gray Holmes. In both cases the H20 2-producing organisms generated alpha hemolysis and formed CO from heme compounds, whereas the peroxide-negative bacteria did not demonstrate alpha hemolysis or CO formation. If, in alpha hemolysis, hemoglobin is converted into a green pigment without lysis of the red cell membrane, then the failure of this pigment to diffuse away from the colony would be explained.

Color change in beta-hemolysis can be explained with diffusion of content from lysed erythrocyte.

All six strains of bacteria that formed hemolytic zones on blood agar plates also produced CO from erythrocytes, and conversely the four strains that were nonhemolytic did not make CO. Despite this concordance, it appears that the formation of beta-hemolytic zones around colonies grown on blood agar plates does not depend on hemoglobin catabolism. Thus, prominent beta-hemolytic zones were formed under anaerobic conditions that prevented CO formation. Also, hemolysis but not CO formation was produced by sterile filtrates of the extracellular products from beta-hemolytic bacteria.
Clear zones resembling beta hemolysis can
  be produced by simply freeze-thawing a spot
  on a blood agar plate and then waiting a day
  for hemoglobin to diffuse away from the lysed
  cells. Although hemolytic B. cereus grown on
  aerobic hemoglobin agar plates gradually produced
  diffuse color changes, the discrete zones
  observed on plates with sheep erythrocytes
  were absent.

http://jb.asm.org/content/112/3/1310.full.pdf+html


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Alternatives to PCR
PCR uses cycles of heating and cooling to denature the strands, calling for special thermostable DNA polymerases. In a cell, during replication, Helicase unwinds the DNA without the requirement of heat. Can Helicase be used instead of the heat cycling to achieve single stranded dna? Would that eliminate the need for heat cycling, and hence special thermostable polymerases?

The temperature is cycled because we want to control the reaction. We control the reaction to multiply the DNA to the levels required. Thirty to forty cycles are usually good enough. You can't control helicase in the same way. So, no, helicase cannot be used instead.

Edited after clarifications in question,
Let's start with normal functions of both enzymes. Helicases separates DNA strands while polymerase synthesize DNA strands as shown in the following figure. (Image Source: Wikimedia Commons)

Watch this animation, it will clear your doubts about function. However, RNA polymerase does have both activities.
In cells, helicase action is required to separate DNA strands. After that only polymerase can act. During PCR, separation of strands is done by increasing the temperature. This process is called DNA melting. This temperature is generally very high, around $90^oC$ to $100^oC$ depending on your sequence. At this temperature many proteins will not function, hence you need thermostable polymarase. About 40 years ago, such an enzyme was discovered from extremophiles (Chien et al 1976). Now it is commercially available as Taq polymerase. These enzymes are recombinant proteins with a few mutations which have also increased its yield and stability (Villbrandt et al 1997).
Now coming to your main question (Which I think I understood correctly this time).
The concept you are asking about has already been successfully tested in RNA detection. Researchers have used "Isothermal reverse transcription thermophilic helicase-dependent amplification"(Goldmeyer et al 2007). They used not only helicase but also reverse transcriptase (because they were detecting RNA). The following image (taken from the paper) shows the main steps in this process. Circles indicate DNA polymerase, squares indicate reverse transcriptase, and triangles indicate helicase.

Quoting from the paper (bullet points are mine),

Arrows indicate specific primers, circles indicate DNA polymerase, squares indicate reverse transcriptase, and triangles indicate helicase. The first-strand cDNA is first synthesized by a reverse transcriptase

(steps 1 and 2). The RNA-DNA hybrids from the reverse transcription are then separated by UvrD helicases generating single stranded (ss)
  RNA and DNA templates
(steps 3 and 4). The ssRNA enters next round of RT reaction
(step 5-a) generating more first strand cDNA. The ssDNA was converted into double-stranded DNA by the DNA polymerase
(step 5-b) and amplified concurrently in the tHDA reaction
(steps 6 through 9). This process repeats itself to achieve exponential amplification of the RNA target sequence.

I think you misunderstood the question: it wasn’t asking whether a helicase could substitute a polymerase in the PCR, but whether it could substitute the heat cycling.

Thank you for the answer, but Konrad Rudolph is right.I meant to ask if the heat cycles could be avoided altogether.

Ah, ok. I will edit answer accordingly. Now wording is better and with more clarity.

CubeMaker, @KonradRudolph, check now. I have edited answer. I guess this is what you are looking for.

Isothermal DNA amplification technologies have been developed. You do not need thermal cycling to amplify DNA fragments by this method.
http://www.ncbi.nlm.nih.gov/pubmed/17720718


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percentage of animal diseases caused by bacteria?
I know this is a long shot, but what is the approximate percentage out of all the animal diseases that are caused by bacteria? One of the Q&A websites answer it as 90, but is there any conclusive scientific evidence?


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How to annotate a .broadpeak file with 9 columns?
I have this peak file I retrieved from an ENCODE chip-seq matrix. Its .broadpeak file looks like this:
chr22   16096195    16096367    .   517 .   8.245591    1.4 -1
chr22   16191942    16192481    .   374 .   4.452878    1.7 -1
chr22   16192350    16192560    .   480 .   7.273034    1.3 -1
chr22   16848326    16848437    .   687 .   12.776952   3.4 -1
chr22   16849900    16851299    .   374 .   4.444921    12.8    -1
chr22   16851301    16851828    .   394 .   4.968297    3.2 -1
chr22   16852259    16852459    .   514 .   8.182164    2.4 -1
chr22   16853163    16855156    .   328 .   3.229621    7.6 -1
chr22   16856415    16857273    .   374 .   4.450283    5.9 -1
chr22   16857361    16857946    .   375 .   4.475713    2.4 -1
chr22   16857760    16857903    .   637 .   11.443585   4.2 -1
chr22   16858449    16858683    .   645 .   11.655504   11.1    -1
chr22   16860284    16860823    .   382 .   4.655282    2.4 -1
chr22   16861104    16862410    .   370 .   4.343772    10.8    -1
chr22   16928019    16928525    .   385 .   4.743283    2.2 -1
chr22   16928388    16928554    .   602 .   10.515230   4.4 -1
chr22   17066663    17067190    .   487 .   7.452445    12.6    -1
chr22   17076317    17076417    .   699 .   13.091462   2.8 -1
chr22   17079512    17087549    .   1000    .   29.157293   13.6    -1
chr22   17105156    17105287    .   582 .   9.993482    1.6 -1
chr22   17162805    17163461    .   763 .   14.801068   100.0   -1
chr22   17198501    17199415    .   615 .   10.861807   15.1    -1
chr22   17228872    17229131    .   713 .   13.478983   15.7    -1
chr22   17229147    17229434    .   621 .   11.023589   13.2    -1

I want to make the annotation and have the entrez ids for the nearest genes. I'm new to this I keep trying some tools but nothing seems to work. I used peakanalyzer a lot but it keeps saying that this file is missing columns it needs to be 12 column file but I don't know how to do it. If I add more columns would that change the annotation.

Have a look at the GTF/GFF3 format which are standard formats for genome annotation. You can find proximal genes by mapping these peak locations to the genome GTF file. If you are specifically interested in using peakfinder then I would suggest that you read the manual carefully for what the input format is supposed to be like.

i have read the manual of peakanalyzer i need a bed file with 12 columns although thw first 3 are needed for the annotation. I cant find a way to convert the file i have in another format so i can use it .

This is what the columns of broadPeak format mean (from UCSC):

chrom - Name of the chromosome (or contig, scaffold, etc.).
chromStart - The starting position of the feature in the chromosome    or scaffold. The first base in a chromosome is numbered 0.
chromEnd - The ending position of the feature in the chromosome or   scaffold. The chromEnd base is not included in the display of the    feature. For example, the first 100 bases of a chromosome are defined
  as chromStart=0, chromEnd=100, and span the bases numbered 0-99. If
  all scores were '0' when the data were submitted to the DCC, the DCC
  assigned scores 1-1000 based on signal value. Ideally the average  signalValue per base spread is between 100-1000.
name - Name given to a region (preferably unique). Use '.' if no name is assigned.
score - Indicates how dark the peak will be displayed in the browser (0-1000).
strand - +/- to denote strand or orientation (whenever applicable).    Use '.' if no orientation is assigned.
signalValue - Measurement of overall (usually, average) enrichment for the region.
pValue - Measurement of statistical significance (-log10). Use -1 if    no pValue is assigned.
qValue - Measurement of statistical significance using false    discovery rate (-log10). Use -1 if no qValue is assigned.

And this is how the BED format looks like (from UCSC):

chrom - The name of the chromosome (e.g. chr3, chrY, chr2_random) or    scaffold (e.g. scaffold10671)
chromStart - The starting position of the feature in the chromosome    or scaffold. The first base in a chromosome is numbered 0.
chromEnd - The ending position of the feature in the chromosome or    scaffold. The chromEnd base is not included in the display of the feature. For example, the first 100 bases of a chromosome are defined
  as chromStart=0, chromEnd=100, and span the bases numbered 0-99.
name - Defines the name of the BED line. This label is displayed to    the left of the BED line in the Genome Browser window when the track is open to full display mode or directly to the left of the item in pack mode.
score - A score between 0 and 1000. If the track line useScore attribute is set to 1 for this annotation data set, the score value will determine the level of gray in which this feature is displayed (higher numbers = darker gray).
strand - Defines the strand - either '+' or '-'.
thickStart - The starting position at which the feature is drawn    thickly (for example, the start codon in gene displays). When there is no thick part, thickStart and thickEnd are usually set to the chromStart position.
thickEnd - The ending position at which the feature is drawn thickly    (for example, the stop codon in gene displays).
itemRgb - An RGB value of the form R,G,B (e.g. 255,0,0). If the track    line itemRgb attribute is set to "On", this RBG value will
  determine    the display color of the data contained in this BED line.
  NOTE: It is    recommended that a simple color scheme (eight colors or
  less) be used    with this attribute to avoid overwhelming the color
  resources of the    Genome Browser and your Internet browser.
blockCount - The number of blocks (exons) in the BED line.
blockSizes - A comma-separated list of the block sizes. The number of items in this list should correspond to blockCount.
blockStarts - A comma-separated list of block starts. All of the blockStart positions should be calculated relative to chromStart. The number of items in this list should correspond to blockCount.

So, first six columns are basically the same. The 7th and 8th column of your new BED file should be same as 3rd and 4th columns respectively. Since columns 4-12 are actually optional for a BED file you need not actually fill the rest of the columns. In any case blockCount would be zero for your case. RGB value is also not necessary. However, if whatever software you are using is asking for a 12 column file then set these:

itemRGB (column 9) = 0,0,0 (black)
blockCount (column 10) = 0

You can use whitespace in rest of the two columns.
You can easily use any scripting language to do this. I am not going to explain how to do that because that is off-topic here.

How to find nearest genes without using Peakanalyzer?

Download the GENCODE annotation GTF file and decompress it.
Read the broadPeak file and store the locations of the peaks.
Define what the minimum level of proximity is (for e.g. 2kbp up/downstream)
Parse only those lines of the GTF where the third column="gene"
Subtract the downstream window to start and add the upstream window to stop position of the gene. Columns 4 and 5 respectively.
Gene information is stored in 9th column.
If the stored peak position falls within the modified start/stop positions then print the 9th column.

Again, this is has to be done programmatically. It is not very difficult. To explain how to do that is off-topic in this forum. I explained the algorithm which you can implement in your favourite scripting language.

Thanks a lot for your answer i have found a way to make the .broadPeak file(6+3 bed file) to a 6 bed file that was accepted by the peak analyzer with this command in cmd
cut –f-6 total_pooled.broadPeak > final.bed i dont know if the genes are correct i assumed that they are because i read somewhere that to annotate and find the nearest genes you need only the first three columns of my .broadpeak file? The second solution seems interesting i  will look it and try to implement it in R after i solve some other more important issues with the ENCODE API.

@XanthoulaAtsalaki awk is a very nice scripting language for these kind of jobs. For something like printing selected columns it is as easy as awk -F "<column separator>" '{print $i, $j, $k}' inputfile > outputfile (where i, j & k are column numbers).

thanksss a lot for the precious informations you are giving me really you are so helpful , i just started to study bioinformatics and R for a master. i want to find a subject for a doctoral i want to try in this field, im so confused i keep reading and reading and there are so many tools and software and papers in this field i feel constanlty like a first grade student  . I will look into this scripting language definitely. Thanks from my heart for your time and the information.


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How many nucleotides are there in the LMO1?
Dr Maris at CHOP has linked the cause of high-risk neuroblastoma to a common SNP in  LMO1. How many nucleotides are there in the LMO1 gene?

1274bp
http://www.ncbi.nlm.nih.gov/nuccore/NM_002315.1
If you need to know gene size and are confused w search results, search for gene name + "cDNA"

Technically, this is the mRNA, not the gene itself.

mRNA has u's not t, it's cDNA, but yes it represents the transcript.

right, that's what I meant :)


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How do human cells respond to mechanical pressure such as heel contact during walking?
Basically, I'd like to do a full accounting (inventory, assets, liabilities) of a human cell under mechanical pressure.
For example, if in steady-state, does the cell consume more or less energy under pressure?
Is membrane transport affected? For example are ion gradients or cell fluid levels changed in response to pressure. If there is a change, how does the cell sustain this over a period of time.
Conversely, if a gradient is disturbed by mechanical pressure, what are the energetic consequences? Does the system behave like a spring such that if the concentration gradients are perturbed out of balance, there is a restoring force (say passive) that will rebalance after the mechanical pressure is removed?
Any focused sources or references would be greatly appreciated.

What is the difference between a cell's inventory and a cell's assets in this context?


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What are the metabolic consequences of negative mechanical work in muscle contractions?
When a muscle contracts while it shortens (concentric), it consumes ATP I believe primarily due to cross-bridge shortening to remove the myosin head from it's attached state.
However, when a muscle contracts while it lengthens (eccentric), it must absorb negative mechanical energy. Is this negative mechanical energy absorbed used to disengage an attached cross bridge and thus doesn't require as much ATP?
If fatigue of concentric muscle contraction results from a shortage of ATP for contraction, is there a similar rule for eccentric contractions. Since it is known that eccentric contractions cost 5x less metabolically then concentric contractions, where do these savings come from?


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How to determine sensitivity in a dose-response curve?
In a dose-response curve the % inhibition can be plotted against concentration antagonist. In our case, the effect of the antagonist is tested in different genetic variants of a microbe.
When trying to determine the potency of a drug on the different variants, I compared the IC50 values. The lower the concentration required for 50% inhibition, the more potent the drug.
When comparing drug efficacy, I compare the concentrations required to reach Emax or the maximum inhibition that each drug can exert - which turns out to be 100% inhibition.
To compare sensitivity, how does one proceed?

Wouldn't it be a sensitivity assay like Kirby Bauer?

You could do percent viability of the microbe at MIC50 versus control over a time course. The lower the percent viability, the more sensitive the strain is to the compound. There are other factors you would need to test such as biofilm formation prevention, killing of sessile versus planktonic microbes, but % viability should tell you the sensitivity of the strain to the compound.

I think you are after the slope of the dose-response curve:

Dose-response curve. Souce: Merck
The slope indicates the change in response per unit dose, which translates to sensitivity.


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Mechanism of Octoxynol-10 as a preservative in vaccines
I noticed that the Fluarix Quad flu shot this season contains Octoxynol-10 rather than Thimerosal as a preservative. I am not expert in this area, so I did a Google search of "Octoxynol-10", and noticed that it has lysing properties and so speculated that this must be how it would kill any bacteria present and thus act as a preservative. Nonoxynol-9 is an active ingredient in anti-spermicides, I speculate for the same reason.
My question is: What does the Octoxynol-10 do when injected into my muscle tissue? I speculate that there may be some lysing of my cells. Perhaps only the cells with very thin membranes lyse? bacteria, sperm, nerve?


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Human Endogenous Retroviruses
I am reading this paper, which shows that a Human Endogenous Retrovirus (HERV) K provirus is present at the orthologous position of gorilla and chimpanzee genomes but absent in the human genome.
If it's not present in the human genome, why is it still called a HERV? Should it not just be an endogenous retrovirus?
(I am not a biology student, so I might not have understood the idea of a provirus/retrovirus entirely.)

First of all, the HERV-K virus is present in the human genome, in fact it is one of the most common endogenous retroviruses there (see references 1 and 2).
In a viral infection, these proviruses get integrated into the human genome and can be found later there. This is a useful tool when you want to find out details about the split of closely related species like the great apes and humans. If you find such a provirus in all analyzed species, the integration must have happened latest at the last common ancestor. If it is only found in a part of them, it happened after the species divided. The figure (from reference 3) shows this shematically:

The authors of "your" article did this and found the integration of the retrovirus in a specific locus in the genome of gorilla, chimpanzee and human and found it only in the first two. From this they conclude that the apes are closer related to each other than to the human.
So in summary it means that the HERV-K is not present at one specific site of the human genome, not in general.
References:

HERV-K: the biologically most active human endogenous retrovirus
family.
HERV-K(HML-2), the Best Preserved Family of HERVs: Endogenization,
Expression, and Implications in Health and Disease
Differences in HERV-K LTR insertions in orthologous loci of humans
and great apes.


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Are there animal species with sex of an offspring determined by sex of preceding offspring?
For instance, if an animal's first offspring is male, then all subsequent offsprings will be male too (the sex of first offspring could be determined randomly).
Does it happen in any species?

Are you interested in processes operating both pre- and post zygotic formation, and both pre- and post ovulation? In other words, are you asking only about primary sex (primary sex ratio) or offspring sex at birth. It is also possible to have a situation where parents adjust sex ratio of offspring at the egg stage (e.g. birds) or when offspring are very young (e.g. by adjusting feeding rates), and this could theoretically be influenced by the sex of previous offspring.

I mean sex ratio at birth.

fileunderwater, what you mention would be tertiary sex ratio. It's adjustment is also an interesting question, but I wonder if there are any physiological mechanisms that can adjust secondary sex ratio depending on the sex of preceding sibling. We don't know if such mechanisms exist in humans, but perhaps there are animals with a known effect...

I can think of one (perhaps trivial) case where this happens. In insects with haplodiploid sex determination (like Hymenoptera) then almost all of a male's offspring will be female, as they will be diploid.

Another case you might think about is female-only, clonal animals, e.g. https://www.nytimes.com/2018/02/05/science/mutant-crayfish-clones-europe.html

Why 'almost' all?

Also I'm not sure this answers the question, as the sex of offspring 2...n doesn't depend at all on the sex of offspring 1.

Regarding "almost all," in bees, for example, sex detemination occurs at a single genetic locus. The usual rule is hemi- or homo-zygous for the sex determination locus, you're male, heterozygous, you're female. So in inbred populations diploid males are somewhat common, in outbred populations they're very rare.

And I agree, neither of these cases is as weird as the OP asks about, where the sex of first offspring might not be predetermined, but has a large effect on the sex of subsequent offspring. I am sure if you look long enough you'll find a story that matches it; I thought it might be helpful to share some more common stories that might be food for thought.


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Why Can't the passage of acquired behavior be considered acquired inheritance?
While reading about a cross-fostering experiment conducted on Male California mice and Peromyscus californicus, I came across the fact that the behavior acquired by a generation of mice due to foster-parents is transferred to the next generation as the next generation also gets the same amount of parental-care and attention as the first.
As we can say that behavior is also a character in a way (and is influenced by genes as well as environment), wouldn't the transfer of such behavior over time (if the mice bred by foster parents were positively selected for) be considered 'inheritance of acquired characters?'

Yes, a behaviour is definitely a phenotypic trait.
Some acquired trait (typically behavioural traits but not only) can indeed be transmitted to a few future generations. But make sure to understand the mechanism. I can think of 3 different mechanisms:

epigenetics
covariance between parent fitness and offspring fitness (within one genotype and one environment) typically due to to parental care.
Transmission of tradition (in the broad sense). A tradition is also sometimes called a meme.

One will need a link to the specific paper you are reading to know what mechanism is in play in the study you are reading.


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What is this dried animal for sale?
I found this image on the Internet, which features an African youngster holding up an animal for sale to a potential customer sitting inside a car. It appears to be some sort of dried and disemboweled animal.

What is the identity of the animal?

Looks like bat !

I'd guess it's a primate, or a big rodent.

@Dexter Definitely not a bat. It may be cane rat but I am not sure.

The boy is holding a couple of smoked/barbecued cane rats, also known as "grasscutters".  These are commonly hunted as bushmeat in West and Central Africa and have recently been farmed as well.
You can see some similar photos here:

http://members.virtualtourist.com/m/p/m/178963/
http://westafricaadventure.blogspot.com/2011_04_03_archive.html
http://www.fionaleonard.net/2012/04/rodents-of-unusual-size.html
http://2summers.net/2015/01/23/pop-up-travel-cane-rats-in-ghana/


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How sterile is working next to a bunsen burner?
When I was still doing lab work, many people would just wear gloves and work next to a bunsen burner because the clean benches were all in use.
This was mostly for plating bacteria like Bacillus subtilis. The equipment had been autoclaved, of course, but is just having the bunsen burner next to you without working in a clean bench really enough to avoid contaminating your plates?

Nice question. Although the upward flow of air does likely reduce the chance of falling something on your plate, I always wondered if it doesn't equally increase the chance of sucking something into it from below :/

For doing bacterial work on an open bench, this is standard "Sterile Technique." The updraft from the heat generated by the Bunsen Burner should create a relatively sterile field with which to work, so long as you aren't breathing directly on your plates.
Also part of sterile technique is to "flame" all of your pipets, agar plates, and the openings of bottles to remove any contaminants from those areas, and also to protect them from getting into sterile mediums. Every time you uncap or cap a media bottle or test tube you are suppose to quickly pass it over the flame. Obviously these days, plastic equipment makes that a little less practical, but it still can be done if you pass quickly and aren't too close to the flame.
Disposable serological pipettes should remain covered until just before use and then the "banana peel" method of removing the wrapper should be used. If the tip touches anything it should be discarded.
The true test of your sterile technique is whether or not you are getting contamination. Some labs that work with recombinant bacteria don't even bother with sterile technique for bacteria work as they are using antibiotic selection, and contamination becomes much less of a concern. That being said, an ounce of prevention is worth a pound of cure, so if you keep your work space clean, and there isn't a risk of fire, i.e. you don't have organic solvents in the area or the stack of lab reports you are supposed to grade spilling over onto your bench, then it doesn't hurt to light up a burner even if you are using selection.
You are also supposed to have cleaned your work space prior to lighting the burner with 70% ethanol, which will rather quickly kill most bacteria on the surface. Wearing gloves and proper glove technique also helps keep contamination to a minimum. Keeping hair tied back and wearing a clean lab coat can also help, though lab coats are usually more for your protection and for the protection of others (not transmitting hazardous materials on your personal clothing) than to prevent contamination.
Most people get the false impression about BSL-2 Laminar flow cabinets or glove boxes are suppose to be sterile and prevent contamination. Their real purpose is to keep things in, not really to keep things out. Laminar flow hoods will keep aerosolized particles within them from getting to you, so long as you keep the hood area fairly clear and do not block vents, but as you pass your hands through the flow, you are bring whatever is on you and has tagged along for the ride into to work field. Glove boxes can maintain a sterile field, so long as it, and everything going into it, other than your samples have been sterilized, and your sample hasn't already been contaminated.

you must work near a lit Bunsen burner when culturing microorganisms because it helps stop your results from getting contaminated because heat sterilises (kills bacteria). Also, the upward flow of air reduces the chance of anything falling onto your plate and contaminating it. this is the best way to get true results if you don't have lots of fancy equipment.


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Why are compost worms sensitive to light?
I read that compost worms dislike light. But I'd say they don't have eyes and I couldn't imagine their skin is sensitive to light in general, is it? And if so, then why?

Making a quick guess I would say that Sunlight would dry them out fairly quickly as they do not have the dead layer of keratinized cells on their surface that protects them as mammals do. Also UV light will damage their DNA pretty rapidly, again for similar reasons, so keeping in the dark and having a photosensitive response to sunlight would likely have been an evolutionarily advantageous strategy for the niche they inhabit.

And yes, cells, even unicellular organism, can be sensitive to light and can move as a result of those sensations. Aquatic Microorganisms will often adjust the depth they are at in water as a result of the presence or absence of light. Remember that a photon will impart its energy on electrons in the cell and excited electrons can cause chemical reactions to take place and these reactions can stimulate the organism to move.

It will sounds counter-intuitive you but earthworms do sense light with their skin. They don't have eyes but they have specialized nerve ending equipped with photoreceptor cells. They are all over skin but concentrated towards first segment of worm. Prostomiun are main light sensing organ in worms. Following image shows their position in first segment of earthworm. (Image source: cronodon.com).

Closer look of above image taken from same website,

Structure of photoreceptors
Earthworm have microvillar photoreceptors like insects (Rohlich et al 1970). Detailed structure is discovered long back.

There is not much information about phototrasnduction in worms but it is well characterized in it's close relative C. elegans (Ward et al 2007).
Now coming to why part, you might wonder if they are spending most of time buried why do they need photoreceptors ? @AMR has guessed it correctly. They use this as protective system. Photoreceptors helps them providing information about how near they are to surface because UV radiation will harm them or probably kill. If there is higher light sensing, they go back to darker regions. You can find similar information from UMICH press release.


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Calculating pairwise Fst from allele frequencies
I am trying to refresh my memory on population genetics for a project, and I'm having some trouble.
Assume I have genetic data on 3 populations with 5 individuals in each of a given species, with the following number of genotypes:
      0101 0102 0202 0103 0203 0303 0204
Pop1   2    3    0    0    0    0    0
Pop2   1    1    1    1    0    1    0
Pop3   1    0    3    0    0    0    1

I have named alleles 01-03. So 0101 is a homozygote individual for allele 01, 0102 is a hetorozygote individual etc.
Is it possible to do this, from the following formulae:

If I input the information above into Genepop to calculate pairwise Fst using the following dataset:
Test Genepop
TestLocus
pop
Pop1, 0101
Pop1, 0101
Pop1, 0102
Pop1, 0102
Pop1, 0102
pop
Pop2, 0102
Pop2, 0103
Pop2, 0303
Pop2, 0101
Pop2, 0202
pop
Pop3, 0101
Pop3, 0202
Pop3, 0202
Pop3, 0202
Pop3, 0204

it produces the following result:
Pop    1       2
2    0.0278
3    0.2308   0.0669

However, how can this result be reproduced and calculated by hand?

The original Wright's formulation
$$Fst=\frac{var(p)}{\bar p}$$
, where $\bar p = \frac{1}{J} \sum_{j=1}^J p_{j}$ and $var(p) = \frac{1}{J}\sum_{j=0}^J (p-\bar p)^2$ is the variance in frequencies among populations.
This original formulation is valid only for a bi-allelic locus. Nei (1973) generalizes this definition to loci that have more than two alleles.
Nei (1973) general formulation
I recommend to have a look a the paper (Nei 1973), it is a really nice paper.
Nei shows that defining that within Subpopulation gene diversity (a.k.a. expected heterozygosity) $H_S$ and the Total gene diversity (a.k.a. expected heterozygosity) $H_T$ as
$$H_S = \frac{1}{J}\sum_{j=1}^J \frac{1}{I}\sum_{i=1}^I p_{ij}^2$$
$$H_T = \frac{1}{I}\sum_{i=1}^I \left(\frac{1}{J} \sum_{j=1}^J p_{ij}\right)^2$$
, where $I$ is the number of alleles and $J$ is the number of populations. Then Wright's definition of $F_{ST}$
$$F_{ST} = \frac{var(p)}{p(1-p)}$$
generalizes (for cases with more than one allele) into
$$Fst = \frac{H_T-H_S}{H_T}$$
Have a look at Nei 1973 to understand why they are equivalent.
Weir and Cockerham (1984) formulation for several loci
Averaging $Fst$ over several loci is more complicated than one would expect at first place. The solution is given in Weir and Cockerham 1984.
The formulation is a little cumbersome so I just invite you to have a look at the paper.

Thank you for your reply, Remi.b. I am aware of both papers, but I will read through them again.
In this case, I was mostly interested in the practical approach of solving a calculation as the one above.
Would you say, that it is not possible from the formulars I have listed?

I am not sure I understand what you mean. You have two formulas, one defining $H$ and one defining $Fst$ from $H_T$ and $H_S$ (but not $H$). How would it be possible to calculate $Fst$ from the frequencies in each population $j$ ($p_j$)?


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What's the difference between tumor cells and host cells?
When you talk about cancer, is there a difference between tumor cells and host cells ? What is the role of immune cells ? in a nutshell ?

I think this is way too broad to be able to answer. There are many different type of tumor and "host" (normal body) cells, and they differ in a variety of ways. It sounds like you're pretty much asking to sum up all of cancer biology ...

In the comments of FrankyG's answer I posted a review of the hallmarks of cancer. For that reviews purpose, cancerous hallmarks can be subdivided 6 major ways. Consequently, you can subdivide either of those six hallmarks into multiple specific pathways, each of which could merit their own graduate-level course exploring. For SE's purpose, the scope of your question is very broad! Here's my recommendation: (1) Search the site, there are good answers buried somewhere, and (2) read up before you ask your question so it has some specificity!

This is far too broad. Asking "what is the role of immune cells?" in cancer is the subject of literally thousands of research papers every year.

This question is a bit broad but I'll try to narrow it to be specific in the terms of "tumor" vs "normal" cells.
 (Source)
Basically a tumor contains cells which have a part of the cell cycle regulation broken (very broad way of saying this). There are literally thousands of things that can cause this. Broad groups of things that cause this could be knockdown of a protein (of which many are involved in replication), mutation of a gene (most likely), etc etc. Basically any type of DNA damage can lead to cancer.
 (Source)
So what creates damaged DNA? Well here is a small list:

UV light (Can cause DSBs)
Carcinogenic chemicals (eg: Ethidium Bromide)
Replication proteins getting stuck or loosing function

 (Source)
Well how does that compare to a "normal" cell. Normal cells have a proper cell cycle with all the "checkpoints" working normally to essentially throw away any cells that detract from the cycle in any way. They also have mechanisms to fix DNA that has been damaged before it gets replicated. If none of that works they have mechanisms to basically commit suicide so they never replicated. When all of that fails you get cancer.
In summary, a cell becomes cancerous when the following things happen:

DNA is damaged by one of the above methods
The DNA damage repair mechanisms fail to fix the damage, or cause further problems by attempting to repair (NHEJ is a repair mechanism for DSBs that is implicated in causing cancer)
The DNA damage causes abnormalities in the cell cycle (replication)
The body fails to recognize the particular cell with abnormalities in order to kill it
The abnormal cell is allowed to replicate without hindrance from the body's checkpoint mechanism
You now have cancer

As for the role of immune cells that question is too broad as there are many different types of immune cells. Their "general" role is to clean the body of foreign agents but there are differences even in that role. There are many different types of them.
 (Source)
While I love teaching this stuff I do feel like you could find A LOT of this by doing google searches. Please try that next time.
EDIT: Updated with plenty of sources.

Nice answer. However it would have been way better if you could have added references to your points and images.

True but to be fair a lot of this is found with simple google searches which is what I told him to do next time at the bottom.

I agree. But you should try to give scientific references if possible. And definitely image source.

For these types of questions I feel Hallmarks of Cancer: The Next Generation is an informative survey of the differences between cancerous and healthy cells (It's also open access!). I suppose it also requires a little background in what constitutes "healthy," however.

@FrankyG just because something shows up on a Google Image Search doesn't mean it can be reproduced, especially without a citation. This is a science site, and scientists expect citations. Unsourced material may be challenged and removed.

@MattDMo I'm well aware of what scientists expect (am one myself). This was an oversight of mine, I apologize for that. Dexter already made me aware. As you can see I changed it.


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Can a hairpin (stem loop) within a transcript stall a eukaryotic ribosome?
Is their evidence of RNA secondary structure causing a stall in translation within a eukaryotic cell?

Hi @LeeAnn, and welcome to biology.SE. Someone has voted to close your question because you haven't shown an attempt at the answer. What prompted the question and how have you tried to solve it before coming here?

Can a hairpin (stem loop) within a transcript stall a eukaryotic ribosome?

It seems that could happen.
C9orf72 translation is one of the examples. In this gene, GGGGCC repeats exist in 5' UTR of the mRNA (upstream of the first ATG). The repeats expand in subsets of neurodegenerative disorder such as ALS. The repeats can form a stem loop structure and stem loops of expanded repeats are more stable.
mRNAs having expanded repeats seems producing poly-GlyAla, poly-GlyPro, and poly-GlyArg peptides which codons are GGG-GCC, GGG-CCG, and GGC-CGG from different frames from GGGCC repeat.
This means the translation starts somewhere in or upstream of the repeat without ATG. To explain this, there is speculation that ribosomes stall because of the tight structure of the stem loop by expanded GGGGCC repeats, mistakenly take tRNAs and start translation. It is called "Repeat-associated non-ATG translation".
You might want to refer to:
Repeat-associated non-AUG translation and its impact in neurodegenerative disease.
https://sites.tufts.edu/als/the-answer/c9orf72/
RAN translation and frameshifting as translational challenges at simple repeats of human neurodegenerative disorders


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difference between "Petri dishes" and "Petri plates"?
In microbiology, we often hear "we use Petri dishes to prepare our cultural media".
Which is correct — "Petri dishes" or "Petri plates"?

Typically you'll hear either "petri dishes" or "plates", not usually "petri plates". Either way though people will understand what you're talking about.

I tried growing bacteria on paper plates once because the protocol just said plates.

@user137 That'll get you every time. Just leave some leftover food on the plate and it should grow just fine

@user137 lol. Seriously ?

@Dexter No not seriously, but it's generally a good idea to be as specific as you can in your methods section. You can say plates, but be sure to list size, material, manufacturer, etc. In the rest of the paper you can just say plates, but the reader needs to be able to look up how you did the procedure, and sometimes details about plates matter.

In my experience, a "Petri dish" or a "dish" refers to something like this:

From Wikimedia
i.e., a single-well container, made of either glass or, more commonly nowadays, plastic.
On the other hand, a "plate" (I've never heard the term "Petri plate" before) typically refers to a multi-well container, having anywhere from 6 to 1536 individual wells:

From pipette.com
Disclaimer: I work almost exclusively in the eukaryotic/mammalian world, so there may be different nomenclature among bacteriologists.


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General transcription factors vs. DNA Binding transcription factors
I know that DNA binding transcription factors are trans-acting, but what about general transcription factors?
Are they cis or trans acting?

Hi there and welcome to biology.se. For this site users are expected to do a little background reading before asking a question. What sources have you looked at that lead to this question?

From Wikipedia: A defining feature of transcription factors is that they contain one or more DNA-binding domains (DBDs), which attach to specific sequences of DNA adjacent to the genes that they regulate. So, there's no differentiation between "DNA-binding transcription factors" and "general transcription factors". In order to be classified as a TF, a protein must be capable of directly binding DNA.

When we say trans we mean that a diffusible factor, or agent is involved. So a molecule synthesized at one location, that can have a regulatory role in another location in the cell is said to be a "trans-acting" factor.
When we say cis we mean physically linked to, in such a way that the biological regulation only affects other molecules that are attached (in other words, something that is "cis-acting" cannot be freely diffusible).
So prokaryotic operators or promoters, and eukaryotic enhancers and promoters would be examples of cis-acting sequences, or elements.  All protein transcription factors, or even DNA-binding proteins, are therefore trans-acting.

General transcriptional factor complexes bind to DNA at promoters of genes via DNA binding proteins such as TATA-binding protein.
It is quite clear that it is trans-acting.

I agree, all transcription factors are trans-acting. I just am not sure that I agree with you first sentence completely. Some of the proteins bind to other proteins and don't themselves have a DNA binding domain. I might be wrong in the sense that these proteins may not be canonically considered TFs, but they do exist.


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Parametric Bootstrap Capture Recapture
I am using the (one sample) capture recapture for estimating hidden human population. One sample method uses purely frequencies of capture to estimate population. One of my colleague suggested parametric bootstrapping method to assess the variability of the population size estimate. I tried to research online a little about this parametric bootstrap method but I just still don't understand how it is performed. I know bootstrapping is basically resampling data with replacement and then calculating the variance of it. However how do I perform parametric bootstrapping (I assume the frequencies of capture follows Poisson Distribution) on capture recapture data? Do we treat the frequencies as datas, i.e. so if f(1)=100 and f(2)=9, our data has 100x 1 and 9x 2 and then resampling this? Is probability of daily capture the parameter $\lambda$ in Poisson distribution?
I guess what I am trying to ask is, how do you perform the sampling bit of a parametric bootstrap [in capture recapture]?

I'm a little confused when you say "[your method] uses purely frequencies of capture". Is there any 'recapturing' going on?

@CactusWoman So unlike the normal capture recapture where they have discrete timings and capture history, my capture recapture is a continuous model (since only 1 individual can be captured at a time) and only frequencies of encountering individuals are noted. So the only data I have f(1), frequency of capturing individual once, f(2), ... Does this make sense?

I did a little research and I think it works like that:

Collect a dataset of $n$ observations.
Fit a parametric model to your data. If you want to model the recaptures, I would suggest a Poisson-GLM. You can also estimate the parameter directly from your data and simply parametrize a Poisson distribution. However, this approach would not model the random variation in your data.
Use the fitted model to draw a sample of size $n$
Calculate your desired metric based on the sample. I guess in your case this would be human population size (calculated as ${N} = \frac{nM}{m}$?)
Repeat steps 3 and 4 many times (1000+)
There you go! Now you can easily assess the variability in population size based on the estimates from your bootstrap samples.

Im confused with step 2, I thought for estimating parameter from the bootstrap sample we use the same method we use for the original data?

I was referring to the parameter $\lambda$ of a Poisson distribution. You can estimate lambda based on your data using maximum likelihood. Some function to do this should be included in every serious statistical package. So what 2 says: Build a model from your data (a glm or a parametrized Poisson distribution) and use this model in steps 3 and 4 to for bootstrapping.