How do harsh conditions cause an increase in the male birth ratio?

Issues with the post

Sexual selection is a mode of natural selection where members of one biological sex choose mates of the other sex to mate with (intersexual selection), and compete with members of the same sex for access to members of the opposite sex (intrasexual selection). This question has nothing to do with sexual selection.

What do you mean by random gene combination? More globally I don't understand the last sentence.

As a consequence, I don't understand the question. IMO, the post should be closed as unclear. However, I can imagine a question that I would consider interesting. I am answering to the question Is it possible that selection yield to a sex-ratio that deviates from 1:1 at equilibrium? How does it relate to environmental conditions?.

Fisherian scenario

Evolution of sex-ratio under a standard Fisherian scneario is often refered to as Fisher's Principle.

Basics

In the vast majority of strictly sexual species, every individual has exactly one mother and one father. It means that at equal sex-ratio the average relatedness of all offspring and all males in the previous generation is equal to the average relatedness of all offsprings and all females int he previous generation. When the sex-ratio is biased toward more females (for example), males have on average a higher reproductive success than females. As a consequence individuals that produce more males will increase their fitness and will increase in fecundity. As a consequence, the adult sex-ratio will always go back to 1:1 (fifty-fifty).

Adult vs baby sex-ratio

Now, it is important to understand that the adult sex-ratio is not necessarily the same as the babies sex-ratio. If typically, there is higher mortality in males than in females (could happen depending on the species and the environment), then selection would favour a bias sex-ratio toward males in babies. The adult sex-ratio will in any case be 1:1

Kin/group selection (non-fisherian scenario)

See for example the case of social spider Aviles (1993).

What is good for the population?

Thinking about the same problem but thinking about what is good for the population (rather than for the individual). For the population, the limiting factor in the number of babies produced are often the females. As a consequence, it would be good for the population if the sex-ratio were biased toward females.

When can alleles that are beneficial for the population overweight what is beneficial for the individuals

Under a standard fisherian scenario this cannot happen though selection will increase the frequency of alleles that spread the best and not the ones that are good for the population. However, typically when the relatedness within the population is high enough (you should read about group selection and kin selection) such trait that are good for the population may evolve.

Recommendation

I recommend that you take some time an introductory class to evolutionary biology such as Understanding Evolution for example. It is fast and you will learn more and faster than what you can learn here with your question. I think I already gave you this suggestion a number of times.


This is basically a trick question and a bit of a cheap shot. All of the reasons cited boil down to "bats huddle to conserve heat", they are basically the same, single, reason.

In order for bats to feed, they need to move, fly out of their cave or wherever they happen to sleep and go forth and look for food. Therefore, they will not be able to huddle while feeding because they will be flying around trying to find fruit or donkeys or whatever each species feeds on. Unless they can figure out a way to huddle while flying, they will not be able to huddle while feeding and so number 5 is wrong.


Programs/software to graph biological data

There is no standard software, programming language, or library used for computing and graphing biological data. The R language is commonly used for statistical work, but Python (in conjunction with the SciPy stack) and C++ also gets used a lot.

Before going further, I should point out you are asking two questions. One about computation and the other about presentation.

Computation:

You mentioned R. That is a programming language (with specialized software built around it). When it comes to programming language choice, the three most important factors are personal preference, available libraries, and the language already in use if you are joining a project with a pre-existing code-base. You might notice performance is not on this short list. The reason for this is that modern languages on modern hardware are efficient enough to, very often, make language choice irrelevant from a performance perspective. Most computational tasks suitable for R are also suitable for languages like Python and Julia.

R's strength is in its focus for statistical work. Whereas Python's standard library comes with many bells and whistles intended to ease the design of small to moderate sized pieces of software across many situations, R comes with many features focused specifically on easing the task of writing code for complicated statistical calculations. Due to it being so common in academia, R one language you are very likely to encounter in academic, computational work. That makes knowing it a helpful skill (whether you regularly use it or not). R, having such a strong suite of tools and large userbase, is also the basis for many third-party tools. One interesting example is Bioconductor

That being said, there are also advantages to using (or at least knowing) Python. It is one of the most common languages in programming in general. That means it has a diverse assortment of libraries designed for it by members of the community. When it comes to nonstatistical libraries, few languages have as many options. When it comes to statistical work, Python does not have as many options as R, but it does still have a lot. The SciPy stack, which includes the NumPy and Pandas libraries, is a big part of that. Another benefit that comes from Python's popularity in the programming world is that you will have an easier time finding programmers to help you on a large project if you decide to look for help outside of your field. (For example, far more computer science majors will know Python than R ...multiple times over.)

As far as the Julia language goes, it is still new. It is being developed as a competitor to R and Python, but it is not mature enough to be a serious contender just yet. However, since your question is about what people use, I would be remiss to ignore it. It may become a serious contender, but for right now, it is still trying to grow and prove its worth.

If performance becomes a serious issue, you would probably be forced to dump R, Python, or whatever very high level language you are using in favor of C or C++. Both are far more efficient than the so-called "batteries included" languages. C and C++ are system programming languages. They are often used in operating systems, databases, video games, and other large pieces of software which you would not want slowed down due to features being included which you did not explicitly program in. (C and C++ are also used in small projects, but I digress.) However, taking advantage of this efficiency requires some insight into how computers actually work. This is not a difficult task, and any good tutorial or book will cover such topics. Using C or C++ without this basic understanding will likely be counter productive, as doing so can lead to you inadvertently creating a program far slower than it needs to be, which could be an issue if performance is becoming a serious concern.

A non-performance benefit of C is the large library selection. As I mentioned above, few languages can compare to Python's library selection. C is definitely one of those few. Actually, C is essentially the lingua franca of libraries (due to its age, its dominant position, and aforementioned efficiency). This means you might find yourself needing to use some highly specialized library with no bindings to languages like Python or R. I have come across a few.

Presentation:

R is also a nice language for graphing data. It comes with a package known as ggplot2, which is responsible for this functionality. This is a common source of data visualizations. However, this does not mean you must use R if you want to create graphs that follow the norms of academia. First off, many people use other pieces of software for plotting. Secondly, there is the library for Python called matplotlib. It is fully featured and is capable imitating the visual appearance of ggplot. One of its built-in style sheets was included just for this purpose. Not surprisingly, matplotlib is the graphing library used in SciPy.

There are many other graphing/plotting libraries, and many of them are fairly language agnostic. Presentation is not often a deciding factor in what language to use for computation. However, if you found yourself needing to use a specific language for its presentation options, doing computations in one language and then feeding the results into another for presentation is not unheard of.

Software:

I include this as a third category because this is more complicated than deciding on programming language A or B or choosing a plotting utility. Non-computer scientists often confuse software with languages. You have to use software when writing a program in a given language, but all the work is done by the program you write. Large software suites, on the other hand, do work for you in many ways. They often come with some sort of quasi-programming language included, but that is only one part of a larger whole. While R comes with a number of software tools, Matlab and Mathematica are better example of this. Free, open source alternatives to these proprietary suites would be Octave and Scilab, although such open source software traditionally has not very competitive with the likes of Matlab. SciPy is a recent example of open source software closing the feature gap (which is a very good thing in terms of avoiding vendor lock).

Beyond that, it is hard to say what you would encounter or what is common. Most large software tools are proprietary. Different companies, universities, and individual projects will use different software, and you will not know what to expect until you you are recruited by a team.

This is why projects sticking to programming languages over large software is preferable in terms of ease of recruitment. Also, programming code can be published with papers a lot easier than describing how you used a piece of software (which is big if open data is important to you). That being said, it can not always be avoided. Many machines in biology require specialized software and many kinds of data are most easily manipulated with proprietary software. Do not worry about such situations. It, obviously, will not affect your current work from being presented in a standard way.

EDIT:

Sorry for the wall of text. The question was broad and this is a complicated issue. It was hard to summarize.


How to build a trimeric protein structure from monomeric PDB file?

There are no MTRIX cards for that molecule. This seems like the easiest path:

http://www.rcsb.org/pdb/explore.do?structureId=4G3Y

Download Files -> Biological Assembly 1

i.e.:

http://www.rcsb.org/pdb/files/4G3Y.pdb1.gz

And read that file into Coot (should you wish)


What are housekeeping and constitutive genes?

I think the best answer is both: they are continually transcribed at a rate that maintains the synthesized products at a (roughly) constant level. These terms are really just descriptive terms, there is no true biological dichotomy, it's just that some genes are expressed pretty much all the time and others are only produced when needed, for example genes for proteins needed at a particular stage of the cell cycle.

As @canadianer mentions in a comment, there are also other forms of post-transcriptional regulation, such that constitutive transcription doesn't necessarily mean constant production of protein at an equal rate.

Wikipedia has quite a list of different "housekeeping genes" and you will see the list is quite extensive. It certainly isn't true that all of these genes are expressed at exactly the same levels all the time, it is simply that their expression is consistent enough to be used as an approximate standard when comparing expression levels.

If I could produce a definition that reflects reality better than the ones you found, I would amend the Oxford definition to something like:

  Constitutive Genes are genes that are expressed following interaction between a promoter and RNA polymerase at a level that doesn't seem to vary much across cells of the same type, doesn't require a very special transcription factor, and so far biologists haven't found an experimental condition that greatly impacts the expression level.


Recommendation for book about soil and their food webs

A very good resource can be found here:

http://esdac.jrc.ec.europa.eu/content/global-soil-biodiversity-atlas

If you focus on soil analysis this resource could be helpful:

http://www.geokniga.org/bookfiles/geokniga-handbook-soil-analysis.pdf

I could also recommend the book
http://www.springer.com/gp/book/9783642309410
with which I worked extensively. It covers the soil chemistry very well.


Why is PCR possible to amplify DNA template before Sanger Sequencing for unknown DNA sequences?

PCR is used to amplify a sequence included inside two known regions. So, if you're able to clone (for example with recombination) two sequence forward and backward to your sequence, by using PCR you'll amplify also the sequence included.

This image in example will clarify my statement.


Can a miRNA be upregulated and downregulated in the same disease

Since diseases are frequently complex, it is not surprising to find specific genes (both miRNA coding genes or protein coding genes) being deferentially regulated when different studies of similar-sounding-diseases are compared. In other words, things like glioblastoma or Pacreatic Cancer should be treated as labels describing grossly similar disease states (i.e. excessive proliferation of glia and pancreatic cells, respectively), rather than as labels of specific cellular state associated with a particular gene expression pattern.


How do download a list of the gene length of all genes?

Some basic information like length can be obtained in the GTF file (you can get the latest ENCODE GTF from the UCSC genome browser).
Other information are also available and obtainable from the UCSC genome browser → table browser. Select the group and tracks that you want from the corresponding dropdown boxes. You can export the data as a text file or forward it to the galaxy interface for analysis.

If you are familiar with some programming then you can pull out the lengths (it is not explicitly given in the output or in the GTF). Also, the gene length may be different from the mRNA length because of the presence of introns in the former. The third field in the GTF file denotes the feature (gene, transcript, exon, etc); you can parse the GTF for picking up only desired features, lets say the mRNAs.
The fourth and fifth fields denote start and end positions respectively; all you have to do is end - start to obtain the length.

A small scriptlet such as this would work in linux/cygwin terminal (I wont go in detail because this is not the scope of this forum):

awk -F "\t" '$3=="transcript"{print $9, $5-$4}' file.gtf > output.txt

The $9 refers to the ninth field which holds information about that feature including the gene name, gene id etc.

The first link that I mentioned also shows some basic methods of extracting information from GTF.


Brood Parasitism - Parasitism/Ammensalism/Commensalism?

The cuckoo chick hatches earlier and instinctively pushes the host eggs out of the nest. If you view this from the genetic perspective of the crow, it becomes the foster parent of offspring that does not carry its genes. The harm, therefore, is to the host's passing on of genes, rather than to the immediate health or well-being of the individual.

For more information see:

Brood parasite (Wikipedia)
The Ecology of Avian Brood Parasitism (Nature)


It seems like they're both springtail species, as suggested by Arthur's comment.
The white one appears to be a type of folsomia, which is easy enough to guess from the appearance (mine don't jump though, I guess ruling out folsomia candida?).
You can compare it to this image of one, from Wikipedia:

I purchased a cheap USB microscope to inspect the second one further. Indeed, as Arthur suggested, it only has three sets of legs:

Additionally, I turned it around and got a look at the underside. I can only guess this is the furcula (though, interestingly, this one doesn't jump either!)?

I'm not sure what the genus is. Could be folsomia, or perhaps hypogastruridae? Either way, they're both springtails! Great news!


Clarification regarding a statement in "The Selfish Gene" by Richard Dawkins

"Impact on the world" is just his writing style.  Dawkins means "evolutionary significance".  For example, all the intermediate forms leading up to the modern horse have been evolutionarily significant because they contributed to survival of the lines of descent that are still present.  Any tiny evolutionary branch that dies out would have little significance or impact.

In the first part of your second question, the answer is again Dawkins' writing style plus the fact that he's writing for popular consumption.  And, his own thoughts have a way of evolving just as they should; so we shouldn't expect perfect consistency between what is said between sequentially written books.  The Blind Watchmaker was written to convince people that evolution can produce complex organisms without any pre-existing goal to do so, using a relatively simple process.  The Selfish Gene was written to promote his idea that the unit of evolution is the gene. (Note that his idea is not necessarily correct.)

In the second part of your second question you ask:Why must there be many copies of entities that are being selected for evolution to be possible?.  The answer to this is that it is NOT necessary.  It's simply a much more easily implemented - and generally better- evolutionary strategy.  If there is only one organism, and selection means killing it if it is unable to adapt to a given environmental change, then failure to adapt puts an end to it and all its possibilities.  If, on the other hand, that one organism produces a series of single copies (offspring) and each of them has some random genetic variation that's subjected to selection, there's a chance that some will make it past the selection process.  That's equivalent to the one organism producing a lot of offspring at the same time, each with its own genetic differences.

This is a slightly SiFi perspective on the above, but: In general, it's a lot safer to test a disposable copy of oneself against a new danger, than to test oneself directly.  If the copy passes the test, it's safe to face the danger directly.  If the copy fails, then you can test a slightly modified version of yourself against the danger.  If that modified copy passes, then if you're able to do so, you could make the same modifications to yourself and go face the danger.  However, there are now two identical new modified copies of you.  One of you is superfluous, so you flip a coin to decide which survives.

In the SiFi scenario, we have one organism evolving safely up one possible branch of an evolutionary tree.  But if that organism reaches a dead end from which there is no escape, its branch dies.  On the other hand if all the other branches are allowed to continue (that is, if you let both copies survive and evolve independently), there's a far better chance at least one branch will still be growing and branching far in the future.

I personally think Dawkins "Selfish Gene" idea fails when we try to fit it into that picture.


What determines the physical location of differentiated cells in an organism?

Cool question. As the other answer mentions, the process is very complex, and we are still learning the relevant mechanisms in organisms other than the fruit fly. But it is considerably well described in the fruit fly which merits a brief summary.

Since a lot of asymmetric (A-P axis, for our purposes) development occurs pretty early in embryonic growth, whatever drives this pole-specific differentiation must act early. As it happens, it begins as early as maternal ovum (Bicoid mRNA). Using cellular machinery (microtubules, motor proteins), these are concentrated towards one end of the egg and subsequently of the early embryo. Once such an asymmetry in the concentration is achieved, further development genes can take advantage of this patterning by being influenced by downstream signalling. Hence there is a cascade of gene activation downstream, which involve Gap genes, Pair-rule genes and several homeotic genes (see Hox genes) which are also differentially expressed along the A-P axis. They directly control patterns of the organs formed from there. Using a gradient of these genes, further patterning of organs can be similarly achieved (the retina gene would be activated only at a concentration of these genes which is found only at the top and so on).


Suspensory ligaments: why are they ligaments?

"...The suspensory ligaments connect the ciliary muscle to the lens..."

You must be referring to the Zonule of Zinn (Such a great name).
You are absolutely correct, the definition of Ligament varies across texts which can create confusion.
For example:
Merriam-webster:
A tough fibrous band of tissue connecting the articular extremities of bones or supporting an organ in place.
Wikipedia:
A ligament is the fibrous connective tissue that connects bones to other bones.


I might be wrong, but aren't numbers $n$ and $m$ are connected as $n=m+1$?

Answer seems to be combinatorial: how many combinations of $n$ objects can be assembled under certain restrictions? Namely, how many isoforms certain gene can have.

Restrictions include: how many exon-intron junctions on codon (or precisely between codons), how many exons are actually contain protein-coding sequence of mRNA (some exons are coding untranslated region, 3'- or 5'-UTR, for example), how certain gene processes alternative splicing.

So, as you can see, answer will highly depend on sequence of given gene. As far as I know, maximum number of isoforms is limited by 5, even though there are genes with hundreds of exons.


How do you call the species that gives its name to a upper-level clade?

I guess you are looking for the type species.
Although it is defined to be a "name giver" for the genus or subgenus level you could potentially extend this to higher up levels.

EDIT: After looking this up and actually reading the full article myself, yes, at least in zoology you can extend it to higher levels by for example using the type genus.


how many copies of tp53 (p53) gene do we have?

Humans have one copy of the p53 gene per set of chromosomes along with most other mammals (a notable exception being elephants with 20)[1]. Since it is located on an autosome (chromosome 17), each parent gives one copy of the gene[2]. Meaning two copies per human cell (and 40 per elephant cell).

A little extra information on p53 and the effects of only having 2 copies:

Since humans only have two copies per cell and p53 forms a homo-tetramer, it only takes one mutated copy to lose functionality.[3] This is because p53 needs to tetramerize to function, meaning only 1 out of 16 p53 proteins are effective if one copy is mutated (24 possibilities and only 1 combination has 0 mutated copies, ~6% are functional). This makes p53 a rare human tumor-suppressor gene with dominant negative mutations.

But with elephants, the more copies they have, the less and less one mutation affects the amount of functional p53. ($\bigl( \frac {39}{40}\bigr)$4 probability of having a functional tetramer = 90% functional, which is very high)


Does food lose some of its mass in form of energy during metabolism?

Physics answer that is a bit silly

If you want to be real technical about physics, mass and energy are the same thing, so any chemical bond that has some energy and is broken results in a change of mass (mgkrebb's estimated in a comment the final mass would be 999.999999814 g, if you started with 1 kg of protein, also known to a very precise biologist as 1.000 kg).

This is sort of a "technically correct" answer that is totally silly from the standpoint of biology, but if your opponent wants to stand by it as "technically correct" based on physics, so be it. We are talking about changes in mass that are not measurable by modern science to sufficient precision, these are only theoretical ideas based on relationships between mass and energy that can be measured on a much larger scale.

Biology answer

Since this is Biology.SE, the biology answer is that mass is conserved in chemical reactions. If you greatly simplify the metabolism of, say, glucose, to the equation:

C6H12O6 + 6 O2 --> 6 CO2 + 6 H2O

you find that the net result is that the hydrogen and oxygen atoms become water, and the carbon atoms become part of carbon dioxide (yes I am simplifying where the actual atoms end up in the biochemical reactions, just talking in terms of net changes here). Other food molecules are processed similarly, and will produce some combination of water/carbon dioxide/nitrogenous wastes. If your cat eats 1 kg of food, that 1 kg of food will become 1 kg of something else out to many many decimal places: waste solids (including anything not digested at all) and liquids, exhaled carbon dioxide, lost skin/hair, etc.

Physics answer if you just want to win the argument

If you want to still win the argument with the physics-based answer that relies on mass-energy equivalence and ignores the fact that from the perspective of biology they are best understood as different concepts, then it's just as fair to go the other way and treat the lost energy as mass, in which case you'd consider the heat lost by the cat's metabolism as mass and include that tiny tiny tiny fraction in the 1 kg and call it a day.


The lower leg is anatomically called the crus1 and you can refer to the area above the knee as the thigh.

Sural refers to the calf region of the crus, while Peroneal refers to the side of the leg2.
The front (anterior) side of the crus is called the shin.

Patellar and Popliteal refer to areas associated with the front and back of the knee, respectively2.

You can see a summary of regional leg and other body terms here. (Below is a chart from the site):

Alternatively, you can refer to the regions of the leg using relative anatomical directional terms:

 Sources:
 1. Wikipedia;
 2. Rutgers


Is the squid giant axon the fastest conducting unmyelinated axon known?

The conductance velocity in the unmyelinated axon has been calculated and measured to be proportional to the square root of the axon diameter (see for example: Rushton, 1951). Since the giant axon is, well, giant, it conducts much faster than others. AFAIK, all other large neurons studied are myelinated. Maybe try to find bigger squids! ;)


Rosetta - What score does RosettaDock use for I_sc?

Unless you (a) ran some absolutely ancient version of Rosetta or (b) explicitly specified a different score function, your protocol should have used the current default ref2015. This will be the default until a few years when the next major update is released.
You can verify this by checking your log file, which should have a line like
core.scoring.ScoreFunctionFactory:  SCOREFUNCTION: ref2015


Edward George Gray went by the first name of George, which isn't evident from his initials (he was born Edward George), but I happened to stumble upon the Wikipedia article below.  From there, I found his obituary.

From his obituary:

  GEORGE GRAY was a pioneer in the study of brain ultrastructure. He was Professor of Cytology in the anatomy department at University College London from 1967 to 1977 and then headed the Laboratory of Biological Ultrastructure at the National Institute for Medical Research.

From the Wikipedia article for synaptosome:

  In a collaborative study with the electron microscopist George Gray from University College London, Victor P. Whittaker eventually showed that the acetylcholine-rich particles derived from guinea-pig cerebral cortex were synaptic vesicle-rich pinched-off nerve terminals.  Whittaker coined the term synaptosome to describe these fractionation-derived particles and shortly thereafter synaptic vesicles could be isolated from lysed synaptosomes


This stuff is so interesting! The instinctive behaviour is also known as a fixed action pattern or FAP which is a collection of well-defined motor patterns that are activated in response to a stimulus, i.e. a group more eleborate reflexes [2]. FAPs allow the brain to concentrate on other things as they don't need require time or energy to be thought about. The theory is they've been selected for because they decrease choice and decision time, which can be particularly important to survival.

There are some cool examples here (http://www.cerebromente.org.br/n09/fastfacts/comportold_i.htm).

the bird is continues to perform parental instinctive behaviour in the absence of a brood of chicks because the similar stimulus of hungry open-mouthed fish is present.

Another article draws comparisons between different animals as to how much of their behaviour is fixed/pre-determined [3]. There can be a correlation between the size of the cerebral cortex, used for thinking and problem solving, and the amount of innate behaviour (i.e. the bigger your cortex the less you need to rely on pre-determined behaviours in certain situations).

These patterns seem to be for the most part genetically determined, however some studies with song-birds in the 70's demonstrated that a learning aspect can modify the innate behviour. Birds which have been reared in an environemnt where they cannot hear other birds of the same species sing still sing their typical song, but when allowed to hear others sing the song becomes more complex.

Investigating the genetic basis behind innate behaviours involve searching for Quantitative Trait Loci (QTLs) or stretches of DNA that contain genes (complex traits require the concerted actions of multiple genes) or are linked to genes that are involved in determining a specifc trait (in this case a behaviour). Classically this involves crossing two animals that differ in the trait you're interested in and looking at the segregation patterns in the offspring to try and pinpoint the specifc region of DNA/collection of genes that control the trait. I think quite a lot of this has been done in insects and mice which have high breeding rates and can be studied easily in the lab.

...at this risk of making this answer ridiculously long I've just included a snippet from another website on behavioural genetics which details the OMIM and some of the traits you can search for[4]:

  Online Mendelian Inheritance in Man (OMIM) is a large, searchable, up-to-date database of human genes, genetic traits, and disorders. Each OMIM record contains bibliographic references and a summary of the scientific literature describing what is known about a particular gene, trait, or disorder. The following behavioral traits are included in OMIM. The six-digit number MIM number is used to uniquely identify each record.

Hand skill, relative (handedness): (139900)
Hand clasping pattern: (139800)
Arm folding preference: (107850)
Ears, ability to move: (129100)
Tongue curling, folding, or rolling: (189300)
Musical perfect pitch: (159300)

[2] http://books.google.co.uk/books?id=aQvGXLPjMPAC&pg=PA44&lpg=PA44&dq=fixed+action+patterns+difference+reflex&source=bl&ots=TxaSYeIpTs&sig=RfsmHLWVlNiF8B-dH928-F0I5M8&hl=en&sa=X&ei=Bs1WUZeCFYiZtAbZ_IHYBw&ved=0CDcQ6AEwAA#v=onepage&q=fixed%20action%20patterns%20difference%20reflex&f=false

[3] http://www.grandin.com/references/genetics.html

[4] http://www.ornl.gov/sci/techresources/Human_Genome/elsi/behavior.shtml


What are the lower and upper hearing limits of the human ear?

Short answer
Hearing threshold is 0 dB SPL at 1 kHz, and pain threshold is around 125 dB SPL at that frequency.

Background
Loudness thresholds depend on acoustic frequency (pitch), as depicted in the following figure:

Loudness contours in human. Source: Stanford Uni

When expressed in dB sound pressure level (dB SPL) the threshold of pain is approximately 125 dB SPL. The lower bound peaks at a hearing threshold of about -5 dB SPL at 4 kHz (maximum sensitivity). Outside that frequency, hearing sensitivity declines (and threshold hence increases).

Note that dB SPL references to a sound pressure of 20 µPa = 2 × 10−5 Pa. This sound pressure corresponds to the hearing threshold at 1 kHz and is hence defined as 0 dB SPL. (Stanford Uni).

Further reading
Why do humans hear better between 2kHz and 5 kHz


Why does throat 'burn' when you've got a common cold?

If you've been sneezing or coughing a lot it is probably micro abrasions in the throat. I don't recognize any other burning sensation.


How does sex differentiation work in Paracerceis sculpta, the sexually tetramorphic isopod?

Shuster, SM & C Sassaman (1997)
  Genetic interaction between male mating strategy and sex ratio in a marine isopod. Nature 388: 373-377

As described in this paper, the chromosomal system of sex determination in Paracerceis sculpta is ZW=females, ZZ=males. Genetic evidence indicates that the morph of a ZZ male is determined by a second locus, Ams (alternative mating strategy) which exists in three allelic forms whose dominance relationship is Amsβ > Amsγ > Amsα. So for example, to be an α type male, an individual must be ZZ Amsα / Amsα.

That's the end of the answer, what follows is supplementary information.

The paper also describes an additional layer of complexity in the sex-determining system of P. sculpta involving sex changes in both directions. This is explained by a model in terms of two other factors: an autosomal locus Tfr (transformer) and a cytoplasmic factor ECF (extra-chromosomal factor) which interact as shown in the Table below (taken from the paper). However, this doesn't really add anything to the Ams story as far as male morphs are concerned, except that some of them start as females.


What is the effect of temperature and carbon dioxide on the opening and closing of stomata?

I like the reference book Plant Physiological Ecology for stuff like this. I know one of the authors is Thijs Pons.

When temperatures become high, plants may close the stomata to conserve moisture. When the stomata are open, usually in daylight hours, the open stomata allow $CO_2$ to enter the leaf. This carbon is needed to form glucose and many other products a plant makes from photosynthesis. Most plants will not open the stomata in the absence of light.

(I use the above text as the reference. I can't give you pages right now, but I was reading this a couple of days ago.)


This may have to do with the fact that the cells require 'housekeeping genes', which are typically constitutive genes that are expressed in all cells of an organism under normal and patho-physiological conditions. Housekeeping and other essential genes are distributed uniformly across different chromosomes thereby making any chromosome indispensable.

"Housekeeping genes are genes that are required for the maintenance of basal cellular functions that are essential for the existence of a cell, regardless of its specific role in the tissue or organism. Thus, they are expected to be expressed in all cells of an organism under normal conditions, irrespective of tissue type, developmental stage, cell cycle state, or external signal."
http://www.cell.com/trends/genetics/pdf/S0168-9525(13)00089-9.pdf

Intriguingly, chromosome X lacks housekeeping genes. A recent study suggested a possible explanation for this, as follows: "In the end, we have found the answer to be quite simple. Whereas most chromosomes operate in pairs, meaning there are two copies of each gene in every cell, in contrast, we only have one active copy of the X chromosome. This means it is not sustainable for highly active genes to be on the X chromosome. Housekeeping genes tend also to be highly active – they just couldn't survive on the X.”
http://www.bath.ac.uk/news/2016/01/12/x-chromosome/

Gene expression is regulated through transcriptional and translational regulation of genes to generate tissue-specific mRNA. Moreover, through alternative splicing a gene can code for multiple types of proteins. Alternative pre-mRNA splicing is widely used by (higher) eukaryotes to generate different protein isoforms in specific cell or tissue types. This means that the same gene can have different gene products in different cell types.

"Alternative splicing is a mechanism for generating a versatile repertoire of functionally different proteins within individual cells. The significance of alternative splicing is clearly evident in highly specialized cells such as neurons. For example, all of the main neurotransmitter receptors contain subunits that are alternatively spliced, which influences their localization, as well as their ligand-binding, signal-transducing and electro-physiological properties."
http://www.nature.com/nrn/journal/v2/n1/full/nrn0101_043a.html
http://nar.oxfordjournals.org/content/30/17/3754.short
http://genomebiology.biomedcentral.com/articles/10.1186/gb-2004-5-10-r74

Protein-coding sequences account for only a very small fraction of the genome (approximately 1.5%), and the rest is associated with non-coding RNA molecules, regulatory DNA sequences, LINEs, SINEs, introns, and sequences for which as yet no function has been determined. Furthermore, gene expression is controlled by regulatory elements that can be located far away along the same chromosome or in some cases even on other chromosomes. Genes and these regulatory elements physically associate with each other resulting in complex genome-wide networks of chromosomal interactions.
https://en.wikipedia.org/wiki/Human_genome
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2653627/

The genome is very intricate and consists of elements that interact with each other to regulate gene expression and to carry out various functions. Loss of any of these elements may affect other elements and disrupt cellular homoeostasis, resulting in cellular dysfunction, death or cancer.

I hope this somewhat answers your question.


Can DNA fingerprinting tell you if someone has been genetically engineered?

Could the technicians/scientists who perform the DNA fingerprinting procedure for the FBI be able to tell that this man is different from other humans?

If by different you mean genetically engineered, it depends on whether the loci tested have been engineered to such an extent that they are substantially different from other humans in order to arouse some kind of suspicion. There are other tests could be done that would show, at the least, that this individual's genome is abnormal.

Would it be possible for someone to be human and have a different number of chromosomes?

Yes, this is called aneuploidy and is the cause of many genetic disorders. Fingerprinting would not detect this.

Does all DNA fingerprinting appear as bar codes and mean nothing until compared to a sample?

DNA fingerprinting looks at sequence length polymorphisms and essentially tells you the length of certain regions of DNA in an individual. In fingerprinting, samples are compared to see whether DNA from two samples come from the same individual. A single sample obviously wouldn't work for this, but that doesn't mean it would tell you nothing.


How do I download entire human genome for local blast formatting and searching?

You can either download and concatenate the individual chromosomes from NCBI or make your life easier and download a single fasta file from Gencode (note that that's the primary assembly, if you want the one with haplotypes then it's here).

Having written all of that, the "human_genomic" files on the NCBI FTP server are the prebuilt blast databases for humans.


Repair of cloning vector nicks digested with antarctic phosphatase and ligated with T4 enzyme

The nicks are not repaired during preparation. Instead, the vector (which is circular, despite the nicks) is transformed into the host where it is repaired by endogenous mechanisms, likely through base excision.


It's a kind of loach. You have to include the location in your query.
i.e. a black khuli loach:

a weather loach:

http://badmanstropicalfish.com/profiles/profile103.html


Query regarding calculation of survival analysis

"0.003" is rounded up; the exact value is 1/380, which is 0.00263157894... (and some more decimal places).

If you calculate the table entries to a few more decimal places, you get 0.04873397172 (and so on), which rounds up to 0.049.


Well, the nucleus does not divide per se. Remember, the nuclear membrane dissolves during mitosis. It starts reforming after metaphase. Here is a review detailing the process and the mechanisms which are known. By extension, the Endoplasmic reticulum gets portioned as it is derived from the nuclear membrane.
Organelles also rely on the cytoskeleton and associated motor proteins for distribution between the daughters. A debated aspect in this regard is whether the organelles are distributed at random or is there an active process that ensures similar distribution between the daughters.
Finally, on to mitochondria. Till this point we have assumed symmetric cell division i.e. both daughters get almost equal amounts of maternal material. But in stem cell divisions, the non-stem daughter is smaller in size. Interestingly, this paper shows that the stem like daughter gets younger mitochondria (less damaged mitochondrial DNA).
As you can see, it is impossible to cover all the organelles in a single answer. And we are not even considering physiological differences between different cell types. Cheers!


From Wikipedia entry on thirst:

  In the mammalian brain, the posterior surface of the hypothalamus
  forms the front wall of the third ventricle (a cerebrospinal
  fluid-filled cavity) and clusters of cells (osmoreceptors) on this
  surface, notably in the organum vasculosum of the lamina terminalis
  (OVLT) and subfornical organ (SFO), signal this cellular dehydration
  to other parts of the brain, and thirst is experienced. Destruction of
  this part of the hypothalamus in humans and other animals results in
  partial or total loss of desire to drink even with extremely high salt
  concentration in the extracellular fluids.1

The entry on osmoreceptor says in part:

  When the osmotic pressure of blood changes (i.e. it is more or less
  dilute), water diffusion into and out of the osmoreceptor cells
  changes. That is, they expand when the blood plasma is more dilute and
  contract with higher concentration.

It also describes how the kidney measures chlorine anion flow through some nephrons, which triggers a cascade of messenger molecules resulting in increased blood levels of the hormone angiotensin, which also results in thirst messages originating in the hypothalamus.

1Derek A. Denton (8 June 2006). The primordial emotions: the dawning of consciousness. Oxford University Press. pp. 118–19. ISBN 978-0-19-920314-7.

2Walter F., PhD. Boron (2005). Medical Physiology: A Cellular And Molecular Approach. Elsevier/Saunders. ISBN 1-4160-2328-3. Page 872


Breeding laboratory mice with cancer; how does this work?

Cancer is a highly genetic disease, and much is known about how different genetic mutations contribute to the generation, growth, proliferation, metastasis, and control of tumors. Jackson Labs (commonly known as Jax in the research community) provides literally thousands of strains of mice, each bred/genetically engineered to have certain genotypes and/or phenotypes, a good proportion of which can be used for various purposes in cancer research.

I'll take a very basic example to walk you through the creation of a "cancer mouse." Say I've been doing research and have found through studying the DNA of many patients that the ABC123 gene seems to be associated with a certain type of cancer (skin, for example). I want to know more how ABC123 works, so one of the first things to do is to find out what (if anything) goes wrong when it isn't there - when it gets "knocked out." Using genetic engineering techniques, I create a sequence of DNA (called a vector) that matches the "wild-type" (WT) or normal mouse ABC123 gene sequence at the ends, but in the middle has a certain selection gene called Neo instead of the rest of the ABC123 sequence:

Neo makes cells that it is in resistant to a certain antibiotic called Neomycin or Geneticin, also called G418. I take my targeting vector and electroporate it into mouse embryonic stem cells (ESCs) that, if implanted into an appropriately-prepared female mouse, could develop into a normal mouse embryo. I then culture these ESCs in the presence of neomycin, which will kill any cells that haven't taken up and incorporated the vector into the genome.

Once I have some cells that I know have taken up the Neo part and are missing the targeted part of the gene (the exons marked 1, 2, and 3), I inject a few cells each into mouse blastocysts, where they divide and differentiate to form various parts of the new mouse.

This is a chimeric mouse, with different cells coming from different origins, either wild-type or ABC123-mutant. I try to generate a number of different chimeras to breed together in the hopes that at least some of my original injected mutant cells went on to form the gonads, and the mutant gene can be passed on to its offspring. I then breed the various chimeric mice to WT mates in hopes of producing heterozygous offspring, which have one copy of the WT-ABC123 gene (from one parent), and one copy of the mutant-ABC123 gene (from the other parent). These mice can then be bred together to produce homozygous "double-knockout" mice, which I can then use to study my gene's effects and its possible relation to skin cancer. This is the type of animal typically sold by Jax, although this depends very strongly on the gene being studied.

Now, there are many issues that can arise along the way, such as the mutation being embryonic-lethal, causing sterility, or other defects that don't allow you to produce true knockout mice. Much can still be learned, though, and scientists have gotten very inventive in producing functional animal models of previously-difficult mutations. For example, it is possible to engineer a strain that only becomes a knockout when you feed it a certain chemical in its water, or is only knocked out in certain cell types or tissues. Some gene functions are only apparent when two (or more!) genes are knocked out at the same time. Genetics is incredibly complex, but fascinating, and more and more complex tools are being developed all the time to assist scientists in their research and ultimately help people overcome illness and disease.


Can I breed the most productive hen by hatching eggs from the most productive ones?

In theory yes, so long as you maintain genetic variation within your flock of hens (e.g. by bringing in outsider males to prevent inherited diseases spreading), artificial selection will lead to a more productive flock.

However I don't think it would be predictable and not necessarily an improvement every generation, surely productivity would be influenced by lifespan? e.g. is it better to have a hen that lays 100 eggs/month for 24 months, or a hen that lays 120 eggs/month for 12 months? Not necessarily that important, but worth considering.

You would also want to keep more than one hen per generation, maybe 2 chick hens from each of the 3 most productive hens per generation, just in case you selected one that hadn't inherited the productivity traits.

I assume you've read about milk yields. And this looks like it covers the maths of heritability of egg production.


Why are bed bugs attracted to Carbon Dioxide?

It's nothing to do with what they breath, they're attracted to carbon dioxide because it's generally a good indication of the presence of a larger organism (such as a person) so they're simply following the "scent" (for want of a better euphemism) to their food (in this case you, or whoever happens to be in the bed), the traps in your links just take advantage of this to trap and kill them.


Help to identify this large, slow-growing mushroom?

This fungus is known as a puffball, although that is no longer a taxanomic order. Some of these fungi don't have small openings through which the spores disperse, but they burst open when the spores are ripe. This proces can be clearly seen in your last pictures. The brown stuff below the cracks are the spores. I think when you press it, the brown stuff will come out

Looking at the appearance, I think this is a Calvatia, but as I am unfamilair with the American fungi I can't name a species.


Egestion is the expulsion of undigested food which occurs typically via the anus. Although, interestingly or maybe just gross, flatworms must use their mouth has they have no anus. This is the non-metabolised material.

Excretion is the transfer of any metabolised material to the environment, including urine or carbon dioxide.


I would also go for d and g. All the others may vary. Strictly speaking, you may even have random, point mutations that have changed the genomic sequence between two given cells so even d and g might not be true in some cases.

I would also like to point out that recent evidence implies that differential expression of non coding, regulatory RNA molecules may play as, or even more, important a role as differential expression of proteins. See the ENCODE papers or here for a recent review.


Can I pellet DNA back from dissolved state?

No, you cannot pellet dissolved DNA with ultracentrifugation.

Yes, you can recover a pellet with additional treatments, similarly to how you got it in the first place; only instead of your input being homogenized cells, or tissue, or extract, or whatever you used to obtain your DNA, it would now just be your aqueous solution of DNA.

For instance, you may have performed a TRIzol extraction to separate your DNA into an aqueous phase, prior to spinning it through mini prep columns to elute your purified DNA in water. You could perform the procedure again and you'd have your pellet once more after the final alcohol (ethanol or isopropanol) precipitation step.

The key idea with pelleting DNA (or any nucleic acid) is to make it insoluble; this is achieved with by using alcohols and salts. If it is soluble, nucleic acids cannot 'come out of solution' to form a pellet.


Is there any kind of "unintended consequence" in evolutionary systems?

Preamble
Evolutionary systems do not have these exact terms as far as I'm aware (although I'm not a behavioral expert) This mainly is because generally speaking we must stop thinking about traits in terms of "advantageous" or "intentional consequences" when discussing evolution. However there are countless examples where a seemingly detrimental evolutionary trait flourishes, or when a seemingly beneficial trait can be exploited by other species. Here I point out two simple, well known examples that might be what you're looking for.
Physiological disease trait emerges
The most well known is sickle cell anemia (SCA); a disease that also reduces susceptibility to malaria. In areas of the world with high instances of malaria, there are also high instances of SCA (Piel et al 2010).
Behavioral altruistic trait exploited
For behavioral studies I think humans would be too vague... (okay, I know very little about sociology) But there is one story that springs to mind from another animal. Birds are ideal models for behavioral studies.
The cuckoo and warbler are an endless evolutionary arms race in terms of camouflage and behavior. The cuckoo parasitises the nest of the warbler with a single egg in a clutch of 3 or so warbler eggs. The warbler parents will watch the newly born cuckoo kick the other eggs out of the nest, and then continue to feed the cuckoo chick thinking it is their own. The reason is thought to be because the warblers respond to the feeding call of their chicks (altruistic, albeit from parent to chick), however the cuckoo chick can mimic this call much more intensely than an entire brood of warbler chicks (altruism is exploited)(Davies et al 1998). By the end, the tired parents are feeding a chick three times their size.


I reckon that picture as cauloma. Because it has a trichoms on epidermis. A_ corical parenchyma B_Phloem C_ xylem D_pitch. I hope it will help you.


Does a neuron ever generate an action potential without stimuli?

Neurones fire when they're sufficiently depolarised past their threshold. In the sensory system this is in response to an external stimuli which sets of a chain reaction. Then motor neurones may relay signals back and in this case the signal or initial depolarisation is occurring in the brain. However this is still caused by a stimuli even if indirectly. If we take an action it is generally because we thought which action we should take because of some sort of stimuli e.g. we are cold so we put a coat on.

But anything which depolarises neurones can set of an action potential. However there's always something which causes it to depolarise, perhaps a drug or a stimulus or another neurone. If any of these don't count as a stimuli depending on your definition, there's your answer.

Or perhaps if you consider cardiac muscle which can intrinsically depolarise. Not a neurone but there's an action potential. They just naturally depolarise over time and action potentials are set of regularly with no stimulus required.

As for learning, where the structure of neurones can change so they connect to new neurones or not to old neurones or vary in the strength of their connection.


There is a large variety of pupil shapes and ability to contract pupils in animals. The vast majority of animals can contract their pupils, including goats and mongooses. Prey animals tend to have horizontally slit pupil, like goats. Mongooses (carnivores) seem to be an exception in that respect. Here is a picture of a sheep's pupil fully dilated and fully contracted:

As you are particularly interested in mongooses, the paper "Characteristics of  the eye of the Indian mongoose (Herpestes auropunctatus)" reports the following concerning pupils dilation induced by topical application of pilocarpine: "The dilated pupil is approximately 3.80 mm in diameter and  slightly oval,  the long  axis  being  horizontal. [...] The constricted pupil is teardrop-shaped, with horizontal  and  vertical  dimensions of 2.5 and 1.1 mm, respectively,  the  narrow end of the  aperture being the nasal end." However that shape seems specific to Indian mongooses because if you search for images of mongooses you'll see that most of them have oblong pupils when contracted. But all of them seem to have almost circular pupils when dilated. Here you can compare the pupil of a mongoose during the day (strongly contracted) and at night (mostly dilated, the color comes from the night photograph):

Nellis, D. W., Sivak, J. G., McFarland, W. N., & Howland, H. C. (1989). Characteristics of the eye of the Indian mongoose (Herpestes auropunctatus). Canadian journal of zoology, 67(11), 2814-2820.


Is there a term for tool use in animals?

Having read this article on tool use in Chimpanzees in full, I am inclined to say that if such a term existed then either the article itself or the titles of any of the 30 articles referenced would have included it.

Searching a couple of online biological dictionaries and ethology sites hasn't yielded anything either, therefore until someone else points out that I'm missing the obvious I'd say you're free to coin the term yourself!


Is exon order always preserved in splicing?

After performing a quick literature search, I am, as with GWW, unable to provide any literature against this occurring, although this paper by Black (2005) states that exons in multi-exon pre-mRNAs are always maintained in order.

 Black DL. 2005. A simple answer for a splicing conundrum. Proceedings of the National Academy of Sciences of the United States of America 102: 4927–8..

Separate components of the spliceosome recognise sequences at the the start and end of each intron, along with a branch point adenine and some other conserved (highly in the case of yeast) regions upstream of the 3' end. The components seem to assemble in a particular order, which is 5' to 3' directional.

The general consensus seems to be that the spliceosome moves along the pre-mRNA from 5' to 3' removing the introns and splicing the exons together to form the mature transcript, ready for translation. The introns are subsequently degraded. In the case of eukaryotes some processing is required to transport the mRNA out of the nucleus to the ribosomes in the cytoplasm.

The mRNA would have a start codon near the 5' terminus and stop codon near the 3' end, at the boundaries of the CDS, and it isn't clear to me how this structure could be maintained if exon order didn't follow the 5' to 3' assemblage. I should imagine that the protein could be affected in much a similar way to exon skipping, possibly resulting in a truncated, inactive or ineffective protein. As protein folding is determined by the interactions between the amino acids, any change in exon order (secondary structure) is likely to result in a different tertiary structure.


How the vaccine based on "non replicating viral vector" is produced?

Complementing cell line (or complementary cell line) is a cell line which has been genetically modified to produce proteins necesary for non-replicating virus replication. It is designed to express exactly the genes which had been deleted from virus to render it non-replicating. The non-replicating viral vector can replicate only in complementing cell line and not in other cells.


Every atom produces a magnetic field, so the formally correct answer would be "yes" (assuming that viruses belong to the tree of life, which is disputed -- otherwise, one would not use the prefix 'bio').

However, biomagnetism as a science (and not pseudoscience) is concerned with more measurable effects. The biomagnetism of a virus will be negligible compared to all the surrounding cells, and hardly measurable.


Confusion about mitochondrial electron transport chain Complex I Wikipedia article title

I've changed the title of the article. The reason for the title was just poor writing (I agree that it seems to imply that the enzyme is ubiquinone) but also the fact that someone had previously tried to change the title to the accepted name tht @xusr has mentioned but they did so incorrectly.


Multistability in the lactose ultization network

The equation in the OP has been updated to $(y-a)^2(y-a\theta)$ which yields the correct expansion. Therefore, by equating the coefficients, we obtain
\begin{align}
\alpha &= (2+\theta)a\tag{1}\\
\rho/\beta^2 &= a^2(1+2\theta)\tag{2}\\
\alpha/\beta^2 &= a^3\theta\tag{3}
\end{align}
Using equations (1) to (3), we get the desired $\rho$ and $\alpha\beta$. Now the authors plotted $\frac{\alpha\beta}{\rho}$ and $\frac{1}{\rho}$.

By plotting $\frac{\alpha\beta}{\rho}$ and $\frac{1}{\rho}$, we can re-create the plot in Mathematica with

ParametricPlot[{1/((1 + 2 x) (1 + 2/x)), (2 + x)^(3/2)/(
  Sqrt[x] (1 + 2 x) (1 + 2/x))}, {x, 0.01, 50 \[Pi]},
 PlotRange -> {{0, .15}, {0, 0.6}}, AspectRatio -> 3/4]

If you dont have Mathematica, here is some Python code that will plot it as well.

import numpy as np
import matplotlib.pyplot as plt

fig = plt.figure()
t = np.linspace(0.01, 25*np.pi, 5000)
x = 1/((1+2*t)*(1+2/t))
y = (2+t)**1.5/(np.sqrt(t)*(1+2*t)*(1+2/t))
plt.plot(x,y)

plt.show()

Here is the Python plot which has smoother lines compared to Mathematica's plot.


How is propagation of action potentials terminated once the "message" has been sent/received?

I'm not a Neurologist or Neuroscientist, so I can only share what I know about the subject!

TL:DR

Cease sensation
Neuronal recovery period prevents further signaling
Neurotransmitter inhibition prevents ligands from binding to receptors (usually Feedback mechanisms)
Neuronal hyperpolarization prevents signaling
Creation of signal (can be perceived as cessation of signal)

It's important to note, first and foremost, that a cessation of stimulation will result in a cessation of the propagation. This is one of the simplest ways that neurons can stop firing - you're no longer touching, tasting, hearing, seeing, smelling, or thinking of what you were previously.

Because of the way Neurons are constructed, and as far as I'm aware, signal propagation will persist as far down the line as possible. I don't believe there's a discrete point where an Axon will simply not send a signal once a dendrite on the same neuron has received the order.

What can happen is that a competing signal has exhausted the propagation potential for the next neuron in the chain (the neuron is still recovering), or a competing signal has released inhibitors that prevents the neurotransmitters from another Axon from affecting the target neuron. Competing signals is particularly common in the neurons of your eye, since the Amacrine cells fire depending on the competitive input of the Cones if I'm remembering everything correctly.

Then there are also substances like Benzodiazepines which block propagation by opening Cl- channels and hyperpolarizing a neuron's membrane, which prevents it from firing. Only a subset of GABA receptors have sites for benzodiazepines, but it's one more way that signals will cease.

Another way to cease a signal, or at least the perception of a signal, is to actually induce propagation. The Rods in your eyes only fire below a certain lumination threshold. What you perceive as light is them not firing, and darkness is what happens when Rods fire at full strength.

I'm not the last word on neurobiology, but I hope I've given you a good start!


What is the average speed of human sneeze?

Mainstream understanding is that a sneeze is 100 mph, or ~45 m/s. However, this isn't even close to being true..

A study in 2013 (see link below) was conducted where they investigated the airflow dynamics of sneezing and breathing, and discovered that the highest velocities of a sneeze are around 10 mph, or 4.5 m/s.

  ...the maximum sneeze velocity derived from these measured distances was 4.5 m/s.

So, about 1/10th the value of what most people believe.. just like the 10% use of our brain misconception, but reversed! (we use 100% of our brain.. not necessarily all at the same time, but we do utilize all parts of our brain)

Airflow Dynamics of Human Jets: Sneezing and Breathing - Potential Sources of Infectious Aerosols


Species don't live in isolation
As simple as the question seems, it actually contains some issue in the conceptualization of a species in isolation that affect or does not affect its environment.
Species do not exist in isolation from others. Many species have very important impact on their environment. These transformations would yield the environment to be unsuitable for the survival of the species over time if there were no other species to interact with. But by the existence of other species creating a cycle of, say oxygen for example, the transformation that the species is bringing to their environment is not seen as destroying the environment. In fact, if they were to disappear that could be an important problem. Let's go through examples
Example 1: Cyanobacteria and the Great Oxygenation Event
In the history of our planet, about 2.45 billions years ago, some species started to produce oxygen. Before that the oxygen level on earth was very low. We refer to this rise in oxygen as the Great Oxygenation Event. At the time, there was very few species that were performing respiration (breaking up oxygen and producing carbonic gas). Oxygen is a very reactive molecule and the rise in oxygen level was actually a MASSIVE environmental impact (arguably the most important life-induced environmental that had ever happen on Earth). It lead to an event of mass extinction.
The main contributors to this rise in oxygen were cyanobacteria. Cyanobacteria were most definitely destroying their environment. However, today, while modern cyanobaceteria are still producing loads of oxygen, we don't consider they are threatening the environment. In fact, they are fixing quite a bit of carbonic gas, which we rather tend to see as beneficial.
Example 2: Ants
I will not develop this example too much... Ants are greatly affecting forests of the world. Without ants, forests would be pretty different (see this non-peer reviewed source of information).
Ants are typically considered indicator of a "healthy" forest (see Segat et al. 2017; Lawes et al. 2017 and the book Gorb and Gorb 2003). Howe ver ants can also be invasive species that cause massive "destruction" on their habitat (Tsutsui and Suarez 2003; Lach 2003; Ness and Bronstein 2004).
"Destruction" is context specific
So, wether a species is "destroying" it's environment depends upon what other species are around. It also depends upon what you are aiming for (species diversity vs stable communities vs ...) but I won't go into these details.
Instead of asking

What species destroy their environment

it would not be 'more wrong' to ask

What species are present in ecosystem that are not adapted to their presence

or even (although that is a little of a stretch and some may argue on it)

What species have recently been introduced in a new ecosystem? / What species have recently changed their environmental impacts?

Always keep in mind, that no species can live sustainably on its own alone.
Do humans destroy their environment?
What do we mean when we say that humans destroy the environment, then? Human activities have changed drastically very recently. This is caused for two main reasons 1) our technology and, consequently our needs and therefore consumption have changed drastically ever since the industrial era. 2) we went through a demographic explosion.

So, yes we are pumping lots of carbon dioxide in the atmosphere. We get this carbon from forests we cut down, from large carbon reserves that have accumulated over millions of years (petrol, gas, peat and others). This change in our environmental impact is often seen (and for rather good reasons) as destructive.
Other modern species that destroy their own environment
Pretty much any invasive species would qualify as an example of a species that destroys its environment in a way that is not sustainable for itself over the long term. Among the invasive species that have important environmental impact that are seen as highly destructive, I can think of

Emerald ash borer (North America)
European starling (North America)
Feral hogs (North America)
Brown tree snake (North America)
grey squirrel (North America)
Zebra mussel (Europe and North America)
Japanese knotweed (Europe)
Cane toad (Australia and Latin Amercia)
Northern Pacific seastar (Australia)
Common wasp (Australia)
Rabbits (Australia and New Zealand)
Crown-of-thorns starfish (Indo-pacific and Australia)
Water hyacinth (global)
black wattle (global)
Argentine ant (global)

Many of these examples are from western countries because 1) that's what we tend to have most data on 2) because that's what I know having only lived in Europe, North America (and a little bit in Indonesia) 3) There are many examples from Australia and New Zealand because they are the world champions in invasive species and in bad policies concerning these invasive species!
Some readers will probably complain (and some with good reasons) about the species listed as what we mean by "destroy" is very subjective and my list is not intended to show the species that are considered "most destructive". Also, the locations of where these species are invasive might be inaccurate and I welcome anyone to edit them.
You can also consider any predator (incl. herbivores) and parasitic species that is leading it's prey / host to extinction such as

The experimental case with lizards in the carribean (Schoener et al. 2001)
The atlantic salmons leading shrimps to extinction (with the help of human activities) in the baltic sea
The red foxes affecting (with the help of human activities) hares population in Europe.

Coming back to the question

Is there any example of living beings destroying their environment?

Yes... other species than humans are "destroying" their environment. Estimating how much they are destroying their environment is really hard to both define and measure. Without a good working definition and without looking at actual data, I would personally be happy to consider humans as being the species that "destroys" the most today.


Why insects are so energy-efficient while flying?

Insect flight muscle is capable of achieving the highest metabolic rate of all animal tissues, and this tissue may be considered an exquisite example of biochemical adaptation.

Locusts, for example, may (almost instantaneously) increase their oxygen consumption up to 70-fold when starting to fly.  In humans, excercise can increase O2 consumption a maximum of 20-fold, and for birds in flight the figure is about 10-fold (Wegener, 1996; Sacktor, 1976).

As Wegener (1996) has put it (in his definitive paper):

  The aerobic scope (the ratio of maximal to basal rate of respiration) of insects is unrivalled in the animal kingdom

Flight is powered by ATP hydrolysis, and these impressive metabolic rates are achieved by very effective control of ATP hydrolysis and regeneration.

 Metabolism is aerobic, thus allowing for much more efficient ATP production from hexoses (as compared with, say, anaerobic metabolism).

 Flight muscle may account for up to 20% of body mass.

 In insects, haemoglobin and myoglobin are absent. Instead, gaseous O2 is transported to the tissues by a system of tubules and deposited so close to the site of consumption that (seemingly) it may reach mitochondria by diffusion.

Locusts fuel flight by burning sugars in the early stages, gradually changing to use lipids as fuel. (In bees, flight is totally fuelled by hexose consumption).

This is achieved by effective control of glycogen breakdown and glycolysis, by modifying the activity glycogen phosphorylase (glycogen breakdown) and phosphofructokinase (PFK), a key control enzyme of glycolysis.

There is an enormous literature on these topics, but suffice it to say, in the case of glycolysis, control is very efficiently achieved by allosteric regulation of PKF, where fructose 1,6-bisphosphate and fructose 2,6-bisphosphate play key roles (see Sacktor, 1976).

This allosteric control very effectively allows glycolysis to be (almost instantaneously) turned on and operate at a maximum value, and to be (almost instantaneously) turned off.

References

Wegener, G. (1996) Flying insects: model systems exercise physiology
Experientia May 15;52(5):404-12. (See here)

Sacktor B. (1976) Biochemical adaptations for flight in the insect.
Biochem Soc Symp. 1976;(41):111-31. (See here)


The main differences between RNA (ribonucleic acid) and DNA (deoxyribonucleic acid) is that DNA contains a hydrogen atom where RNA has a hyroxyl (-OH) group and RNA's uracil is substituted for DNA's thymine.  The below image shows several deoxyribose molecules bound together, and off to the side, a ribose molecule. It is the OH group on the bottom right of the ribose molecule that is exchanged for a hydrogen in deoxyribose.

The structures of RNA and DNA are almost identical, so there is no reason why you can't have double stranded RNA. Similarly DNA can be single stranded. In fact, for DNA replication and transcription, the DNA strands must be separated. dsRNA and ssDNA are most commonly found in viruses. Check out these lecture slides for more about them: http://www.columbia.edu/itc/hs/medical/pathophys/id/2009/viruses2Color.pdf


Does opponent process happen in the retina or in the brain?

Opponent process happens BOTH in the retina, and in the brain (Lateral Geniculate Nucleus).

Here is the excerpt from Vision Science: Photons to Phenomenology by Stephen E. Palmer:

In the brain (LGN):

  Physiological psychologist Russell De Valois (1965) and his colleagues (De Valois, Abramov, &
  Jacobs, 1966) measured responses in the LGN of macaque monkeys and
  discovered color-selective cells whose responses to wavelengths of
  light were incompatible with trichromatic theory but conformed roughly
  to the pattern predicted by Hering's opponent process theory. Some
  were excited by red light and inhibited by green (R+G- cells). Others responded in the opposite way,
  exciting to green and inhibiting to red (G+R- cells). In addition,
  they found cells that were excited by yellow and inhibited by blue
  (Y+B- cells) as well as ones showing the reverse pattern of responses
  (B+Y- cells). Together, these LGN cells can reasonably be interpreted
  as a neural implementation of Hering's opponent process theory.

In the retina:

  Further research has shown that these patterns of response are also
  present in the bipolar and ganglion cells of the retina. Output of R+G- opponent cells can be derived by combining excitatory
  input from the L cones and the inhibitory input from M cones,
  essentially computing the difference between the output of these two
  cone systems (L - M).


How compatible are mammalian digestive systems?

I think this would depend entirely on the diet of the host and donor mammal.

Assuming they are of similar size and diet, I don't see any reason why this wouldn't work. The gut tends to absorb more or less everything in the food.

If the diet of the two mammals differed significantly, I could see some problems with eating the correct foods. Herbivores with the significantly shorter carnivore gut would have trouble killing and eating things without carnivore teeth/claws/what have you, and the plants would not provide enough nutrition on their own. Rabbits, for instance, have a two-pass digestive system, so in order to use a rabbit gut the mammal would have to eat their own feces regularly. (Rabbits have digestive bacteria in their colon, but grass has to travel to the colon and then back 'upstream' to the absorptive part of the gut. So this is achieved by going around again.)


Confusion about the duration of different phases of the cell cycle such as G1, G2 & S

It depends on the conditions, cell type or state of the cell.

I don't think anyone here can do better justice to the question for a beginner than this web page.

To show you why your answer is not answerable, by way of example: some cells exit the cell cycle and enter a stage called G0. This can be a permanent state for some cells, or, for instance, others may return to the cycle if they receive (external) signals.

Here is a very loose approximation, circles are to scale with respect to cycle time. Notice, for instance, the human circle is for an immortalized cell line under laboratory conditions, rather than for cells in your body. A neuron (brain) or an enterocyte (gut) have vastly different cell cycle states, so it's impossible to give you a single straight answer without misleading you totally.

Bonus food for thought: notice that the fraction of time cells spend on G1, S, G2 and mitosis is also different between different cell types.

Bonus food for thought #2: In fruit fly embryos (pictured bottom right in the above picture), you have an extreme example of unconventional (non-textbook) cycling. Rather than synthesizing new cytoplasmic materials, the size of the developing embryo is constant except for the replication of the genetic material. This happens in the growing larva for ~10 cell divisions, in thousands of cells. One of these cycles takes about 8 minutes to complete fully. That's an impressive time to copy a genome; most* bacteria can't do it this quickly!

(*any that I am aware of)


Why do restriction enzymes tend to have an even number of bases in their recognition site?


Is it possible to lose synapses over time?

Regarding your question about losing synapses; yes, synapses are regularly lost in a process called Synaptic Pruning. From the Wikipedia article:

  A decrease in synapses is seen after adolescence reflecting synaptic pruning, and approximately 50% of neurons during development do not survive until adulthood. Pruning is influenced by environmental factors and is widely thought to represent learning.

Synaptic pruning is most significant during development due to "excessive" Neurogenesis that creates a large number of neurons, many of which will later be pruned. It's not excessive in a bad way, it's simply the case that more neurons are generated than necessary and thus pruning is needed to keep the connections efficient. There's no "measure twice, cut once", instead pruning is used to refine connections.

Synaptic Pruning really doesn't have anything to do with forgetting; Forgetting is natural and simply happens because connections (via Recall/Rehersal) are not made strongly enough to fully encode memories into Long Term Memory.

Note that Synaptic Pruning is not the cause for Alzheimer's or other age related degenerative disorders. From Wikipedia again:

  Synaptic pruning is classified separately from the regressive events seen during older ages. While developmental pruning is experience dependent, the deteriorating connections that are synonymous with old age are not. The stereotyped pruning can be related to the chiseling and molding of stone into a statue. Once the statue is complete, the weather will begin to erode the statue and this represents the experience independent deletion of connections.

Synaptic Pruning is a normal process of development and occurs in all individuals. Alzheimer's is a very visible disorder due to media focus, but not part of normal developmental/aging effects.

Instead I suggest you read more specifically about Alzheimer's disease, there's quite a bit of information on it.


What is (roughly) the net charge of the DNA in an average human cell?

That reasoning seems to work for Harvard's bionumbers database. They use a charge of -2 per base pair, and then estimate the linear charge density as 2e / 0.34 nm, where 0.34 nm is the length of a base pair. There are approximately 3.08 billion base pairs in the human genome, so you could run the same calculation: $2e \cdot 3.08 \cdot 10^9 = 9.86 \cdot 10^{-10} C$.


What is the use of an antibody that is non-neutralizing?

The term "neutralizing" depends on context. In virology, it generally (not always) means it prevents the virus from binding to its receptor(s) and getting its genetic material inside the now-infected cell. Other antibodies can bind other epitopes besides the sites of binding between capsid and receptor (or enveloping membrane and receptor), yet still contribute to the immune response. Such antibodies are often opsonizing. Still more antibodies are just ineffective, a byproduct of the antibody maturation process.


How to determine which is the nucleotide sequence of a gene?

You run a blast of your sequence. Then explore the results and you'll see somewhere that says "strand"  and is indication whether is plus/minus.

https://blast.ncbi.nlm.nih.gov/Blast.cgi

Also blast has a graphical interface in which you'll clearly see the matching and non-matching bases. Therefore it should help you to identify the differences between the 2 sequences.


NCBI EUtils. Get Homolog infromation using Gene ID

From Entrez Programming Utilities Help [Internet]:

  Input: Any Entrez text query (&term); Entrez database (&db);
  &usehistory=y; Existing web environment (&WebEnv) from a prior
  E-utility call

To avoid the error messages, web1, and key1 can be used as terms (these are usually being used to associate with other searches), however this returns no data, probably because the ID you supplied was simply "9", and it remains unclear exactly what you're searching for in the context of other queries.

For example:

esearch.fcgi?db=<database>&term=<query>&usehistory=y

# esearch produces WebEnv value ($web1) and QueryKey value ($key1)

esummary.fcgi?db=<database>&query_key=$key1&WebEnv=$web1

So whilst view-source:eutils.ncbi.nlm.nih.gov/entrez/eutils/efetch.fcgi?db=homologene&geneid=9&WebEnv=web1&query_key=key1 is a valid query, it's not pointing to anything.


Does transplanted heart have full sympaticus without medication?

The parasympathetic supply to the heart is by nerves and that is truncated during surgery as pointed out.

The sympathetic supply to the heart is by two means:

Through sympathetic nerves from the sympathetic trunk
From the adrenal medulla which secretes both adrenaline and nor-adrenaline directly into the blood stream

The heart contains the beta receptors for the sympathetic system, especially the ventricles and nodes (SA) and conducting fibers. These receptors respond to the presence of adrenaline and nor-adrenaline in blood. Thus the sympathetic response is preserved while the parasympathetic responce is lost.

There is a minimal level of nor-epinephrine in blood at all times which thus influences the heart.

Receptors in Heart:

The heart contains adrenergic (sympathetic) and cholinergic (Parasympathetic) receptors. When the heart is transplanted, the donor heart also contains the same receptors. The only thing missing are the nerves.

The sympathetic system does not suffer as much as the parasympathetic system, because of the adrenal medulla which secretes the nor-epinephrine (same as nor-adrenaline) into the blood, which upon reaching the heart can stimulate the beta receptors on the heart.

There is no organ which releases acetyl-choline into blood, (fortunately, as such a release would be disastrous leading to shock and rigor, possibly death). So the parasympathetic receptors in the heart do not receive any stimuli.

Edit 1:
In response to your edit, yes there are polymorphisms in all receptors. But the structure of adrenaline and nor-adrenaline are pretty much constant. This means that the donor heart will be at a similar level of sympaticus as it was in the donor when (s)he was alive. Although this will not be the same as the recipients pre-surgery sympaticus state of the now removed heart.


Open databases for copy number variations similar to TCGA

The ICGC has CNV data for many different cancer types. It has many both restricted and open data sets. The DCC releases page will let you hunt through them - those that are public are easily downloaded. They also have matched expression, SNV, DNA methylation, and structural mutation data for many samples.


The urogenital system as a cohesive functional unit probably evolved very early in vertebrate history. Hagfishes and lampreys have separate systems for reproduction and excretion. More derived groups of fishes use kidney tubules and ducts for sperm delivery outside the body (Helfman et al. 2009).

The vertebrate nephron may be homologous to the invertebrate nephridia (Ruppert 1994). The genetics underlying the development of vertebrate female reproductive organs shows many homologies with invertebrate reproductive organs (Kobayashi and Behringer 2003)

I would hypothesize that the both the reproductive and extrectory systems of vertebrates show corresponding homologies to invertebrate organ systems (at least genetic and developmental homologies) but evolution of the urogenital organ system did not evolve until the early vertebrates.

Literature Cited

Helfman, G.S. et al. 2009. The Diversity of Fishes. Biology, Evolution and Ecology. Wiley-Blackwell, Oxford, UK.

Kobayashi, A. ad R.R. Behringer. 2003. Developmental genetics of the female reproductive tract in mammals. Nature Reviews Genetics 4: 969-980.

Ruppert, E.E. 1994. Evolutionary origin of the vertebrate nephron. American Zoologist 34: 542-553.


Why are some housekeeping genes considered better?

Yes, it does matter. Gene expression varies a lot thoughout tissues and living conditions, so you need to test a variety of genes and choose the ones with the smallest variation in the expression between sample and control.

If you don't find any, you have to test other genes for this purpose. This is important, as this can severly affect the outcome of your experiment, since you normalize to the housekeeping genes. If these are not constant, it will cause problems. Have a look into the references, this helped me a lot.

References:

Accurate normalization of real-time quantitative RT-PCR data by
geometric averaging of multiple internal control genes.
The normalization of gene expression data in melanoma: investigating
the use of glyceraldehyde 3-phosphate dehydrogenase and 18S
ribosomal RNA as internal reference genes for quantitative real-time
PCR.
Normalization of qRT-PCR data: the necessity of adopting a
systematic, experimental conditions-specific, validation of
references.


Should I design a primer to detect virus based on NCBI genebank?

Any other database better than NCBI ?

A lot of people overlook some sub-databases inside NCBI and search the main nucleotide database only.

If You never tried it, you can blast the HIV sequence which You have found, against other databases. On the ncbi blast webpage, just choose the options other than nucleotide collection (nr/nt). I tend to find new sequences in Expressed sequence tags (EST), Genomic survey sequences (GSS) or Whole genome shotgun contigs (WGS). Some of these databases cover unfinished sequencing project and should be a source of new data.

(I am a plant person, not virus person, so maybe you will find out, that different databases are worth searching for you. Or you will find it a waste of time.)

BTW, now some time had passed since your question. How did you solve Your HIV sequence problem ?


As far as online dictionaries (Medical Dictionary, Merriam-Webster) and a popular-scientific site on hormones (Your Hormones) go, LH and ICSH are the same. ICSH mainly pops up in the older literature; e.g., Lostron & Johnson (1966) and Louvet et al. (1975). My understanding is that LH is currently the more accepted term for the hormone.

I get the impression that historically, LH has been used in relation to female reproduction and ICSH to the male reproductive systems. In males, LH stimulates Leydig cells in the testes to produce testosterone. In females it stimulates the ovarian follicles to produce oestradiol, and it induces ovulation.

References
- Lostron & Johnson, Endocrinology (1966); 79: 991
- Louvet et al. Endocrinology (1975); 96(5): 1179-86


What could account for an apparent loss of mass at death?

Snopes.com gives a discussion of possible issues with the original experiment.  Evaporation or bowel or body movements for instance.  I think the biggest complaint about the experiment is that it has not been reproducible and that the original experiment was flawed.  MacDougall only took six measurements and he threw two of them out in his original work.  The Wikipedia link you give cites a paper where sheep were found to gain weight at least for a time after death.  Dogs are found to have no weight change.

MacDougall and his contemporaries were inclined to interpret their results such that animals simply do not have souls, or have different sorts of souls.  But if you look at an average of all experiments cited, it could also be said that the average weight loss up on death averages to zero.  3/4 of an ounce of a human being (or a sheep) over the course of something like a death is not an easy measurement.  You can't give them a drink of water, you worry that they are breathing too much and losing water.  Its not an easy experiment, at least for human beings where you can't control the circumstances of death so well.

In any case this really needs to be measured better.  In 90 years it doesn't seem that there's been a real rush to do it.

I just stumbled across this blog post that talks about an effort to measure a change in blood flow to the brain when in intense mental activity popularized in the late 19th century.  The investigator Mosso claimed he measured a difference, but the result is disputed today.  It could not have been more than a few grams. In any case a description of how difficult this measurement can be.


What is this plant in the Butler, Pennsylvania area?

That looks like a bit like a Smilax to me, possibly Smilax herbacea.

Make sure you have a positive ID on any wild plant before you eat it, but if this is Smilax it looks like you don't have to worry about it being poisonous: from Flora of North America entry on the genus Smilax:

  Smilax has numerous uses. Sarsaparilla, a beverage and medicinal used
  against rheumatism, is obtained from the rhizomes of various species... All species of Smilax are excellent wildlife food and are also browsed, or the rhizomes dug
  and eaten, by domestic stock.

For you, or for other Pennsylvania people, note that the Pennsylvania Flora Project of the  Morris Aboretum is a great resource. You can download species lists by county, and just that and some google image searches can often substitute for a field-guide of your county.

If you want to identify plants the hard way, and are willing to deal with special botanical vocabulary, the Flora of North America that I linked to above is the definitive resource.


Is the affinity of an enzyme or transporter for its substrate or solute influenced by the amino acids at the binding site?

In a reaction which follows a saturation kinetics, KM is basically the concentration of substrate/ligand at which the rate of the reaction is half of the maximum rate (or the binding sites are half saturated).

The biophysical meaning of KM would depend on the underlying model. For example, in the equilibrium approximation of Michaelis-Menten model, KM is same as dissociation constant (of enzyme and substrate). In the Briggs-Haldane model (quasi steady state approximation), it is slightly complex: KM = (kr + kcat)/kf.

Overall, the thumb rule is that lower the KM faster will the reaction saturate.

  Is affinity always a function of the protein structure of enzyme? If
  someone study same enzyme in two different species and observe that
  the enzyme has different affinities in two species, then does it
  indicate that there might by slight difference in key amino-acid
  component at the binding sites of the enzyme between these two
  species?

Almost every property of the protein (not just affinity towards a ligand) is because of its chemical composition and structure. Although they are directly involved in binding, the amino acids at binding site are not the sole contributors to the affinity. The other amino acids that are critical for the overall structure of the protein are also important in preserving the function.