Is the book "Bioinformatics for Geneticists" outdated?

I haven't read through all of it, but from the second edition, which I found available online here, it seems to me that it might be a good introduction, but (as expected from the publishing date) it is really missing out on all the next generation sequencing stuff. Which is important, not only because it is my favourite field.

I am not sure what you want to get from it? You say you have little genomics background, but then you got a book that expects you to know the genetics, but explains the bioinformatics.
There's a basic description of the background of sequencing at the NIH website, maybe that helps.


Independent contrasts with non-homologous traits

When you calculate the PICs of a trait, you are making a statement about how that trait evolved. The purpose of PICs is to account for phylogenetic non-independence. However, when you are comparing two analogous traits, those two traits are in fact phylogenetically independent of each other; they do not share a common origin. Thus, I think it would be an error to perform PICs on analogous traits because those traits do not share an evolutionary origin.

How to deal with this problem would depend on the specific question you are asking. One thing to do would be to perform PICs on each trait independently on just the portion of the tree that that trait occurs so you are not comparing analogous traits.

You've probably already read this, but I recommend that anyone who hasn't check out Felsenstein's 1985 paper describing the PIC method.


Is there a simple way to generate sets of sequences that re-capitulate the topology of pre-defined phylogenetic tree

Yes, what you are looking for seems to be an alignment simulator, which is quite commonly used in phylogenetics. Given a phylogenetic tree and a substitution model, you can use for instance INDELible or DAWG to simulate the extant sequences (N sequences at the tips). These programs can also simulate the indel process (gaps), which means your final sequences won't have, by default, the same length -- but you can change the settings to exclude insertions/deletions.

There is no absolute guarantee that the tree estimated from the simulated sequences will follow the "true" one (used to simulate the sequences), but they should be close enough if:

you don't simulate gaps
the branch lengths are not too short
the sequences are large enough


A mechanical vector just as biological vector transfers a parasite to its obligatory host but carrying it on the surface of its body while the host in phoresis is not necessarily carrying a phoront to an obligatory host (for parasitic interaction).

A parasite-mechanical vector relationship is possibly a kind of phoresis.


I would guess that the term "tissue patterning" could be an umbrella term for multiple different developmental processes. In precise (more modern) developmental terms it could be a old synonym or sub-type for "Regional differentiation"
https://en.wikipedia.org/wiki/Regional_differentiation
It also fits to the concept of X-inactivation in female mammals, but this phenomenon can not be observed by the bald eye.
https://en.wikipedia.org/wiki/X-inactivation
It is quite possible the term originated from pigmentation biology an early genetic discipline. The underlying mechanism are the Pibald mutations , which result in dysfunction in dorso-ventral melanoblast migration , a dominant mutation, that is a source of white spots and patches in many mammals.

These mutations are almost omnipresent in domesticated furry mammals (cows, dogs, cats rats,horses) as well as some wild species where it gives an evolutionary advantage.
You can also check out cat coat genetics its a lot of fun and relative easy classical genetics.
https://en.wikipedia.org/wiki/Cat_coat_genetics

Excurse biological definitions:
Many biological terms originated in the first years of biology as a science (<1820 ) when genetics, microbiology, evolution and developmental biology where not discovered as disciplines yet (Mendel, Pasteur, Darwin&Wallace where born later, Boviery, Speemann even later), so people (zoologists, botanists) just named the thing they observed, without knowing what the underlying mechanism was. So since they did not have the concept of mendelian inheritance, nor embryonic development, they just called it in layman's therms: "patterning".
Nowadays with the term "tissue patterning" is not totally clear anymore what an author means, if it has no proper context, in my opinion. We have clearer defined terms.


tissue-specific expression of homolog genes

The evolution of new genes is frequently associated with gene duplication. The paralogous genes are then free to evolve on their own into new functions over time. Sometimes (usually) the paralog will end up with a frame shift, or stop codon that inactivates it. But your question is lacking the element of time. At the instant of gene duplication, each copy is identical. However, one copy may lack the control elements (usually upstream), and not be transcribed. Or one copy may eventually evolve a new, tissue specific function. But whether the copy is inactivated, or evolves a new function, or remains active is not the same for every instance. It depends on how each copy changes under the influences of mutation and selection.


How long do your eyes need to adapt to darkness and reach full contrast?

Actually, the US Army and Air Force (and I assume the Navy) teach their life support troops about this (as well as the aviators), since so many missions are conducted at night.  It is actually some very interesting physiology involved in this.  This Army Instructional manual should be of help (PDF File).

  On an average it takes 30 to 45 minutes for your rods to be fully dark adapted to night vision.

It also covers things such as Mesopic vision and Scotopic vision, eye health, and how to actually dark adapt.  I suggest it as a good read.  It's less than 14 pages.


How do cellular conditions change the Gibbs free energy of a reaction?

To understand that, you must have a basic understanding of Gibbs-Helmholtz equation. it states-
$\Delta G'=\Delta G^{'o} +RT\,ln\,(Q) $
Here, $\Delta G'$ = biochemical free energy change & $\Delta G^{'o}$ = standard biochemical free energy change.
Suppose you have a reaction,
$x+FADH_2\rightleftharpoons xH_2+FAD $
So, $Q=\dfrac{[xH_2][FAD]}{[x][FADH_2]}$
Now let's assume that $\Delta G^{'o}>0$.
Hence the spontaneity of the aforesaid reaction (in forward direction) will be dependent on the $\Delta G^{'o}$, which is a function of reaction quotient (Q) as well as temperature (T).
Now, if the body is in lower energy state, i.e. fasting; $\dfrac{[FAD]}{[FADH_2]}$ ratio will be high. So, in order to make $\Delta G'<0$, the following condition must be satisfied $-$
$RT\,ln\,(Q)+\Delta G^{'o}<0$,
or, $RT\,ln\,(Q)< -\Delta G^{'o}$
or, $RT\,ln \dfrac{[xH_2][FAD]}{[x][FADH_2]}\,< -\Delta G^{'o}$
With this reasoning, be it any metabolic pathway; we can predict its spontaneity.


Why don't we have more cone cells (bigger fovea)?

We use central vision for a lot more things today than in the past. Peripheral vision is most important in navigation, so those who lose their central field retain the ability to navigate around objects. It is important that this is fast and sensitive in the dark as well as light. It isn't important for it to be in colour; this would mean it would be less sensitive in the dark and colour isn't important in navigation and also it would take longer. Navigation is of vital importance as it can be the difference between survival or death in the flight or fight response. Similarly it is important in the fight part, being able to see a foe.

Let's our foveas were bigger, well we would lose the above. What would we gain? The ability to see more at full resolution and colour. It's impossible for us to concentrate on more than we can see in our central field already. in fact we dart our gaze around to focus on many things because we can't focus on multiple things at once. By this I mean thinking about what we see not processing it. Of course we would also require a much larger brain to be able to process it all, processing the central field takes a lot of brain matter.

So in conclusion, it's not helpful.


I need help identifying a completely unknown plant for my biology class

I'm no expert on plants but it could be a kalanchoe. That's based mainly on the leaf characteristics and size.

There's some 120 or so species mainly originating from the old world. These are quite drought tolerant as yours seems to be. They are a common houseplant and there are ways to stimulate reflowering so that also makes it a good candidate.

Image source.


What in fast food fries have that regular fries don't?

I went through a longer winded explanation here:  https://biology.stackexchange.com/a/57877/19432.

In brief, food spoils if water is bio-available to micro-organisms.  In the case of a french fry from say, McDonalds. This fry has a very small volume to surface area ratio, and hence is able to dry out what little water is left after the frying process before micro-organisms can proliferate enough to visibly "spoil" the fry.

If, in your own kitchen, you were take a fresh potato, cut it into fries, and cook them in oil long enough to nearly dehydrate the fry, it would not spoil either in a dry environment.

Take either of those items that had been allowed to cool down and pick up micro-organisms (yeast and bacteria) from the air and place into a sealed ziplock bag with a little water and they would both spoil.

For your last question, in a dry environment, once something has become desiccated, decomposition stops and your fry would only decompose if the environment became more humid.  Think about naturally preserved mummies in an arid environment.

Edit: Light also can break bonds...and lend to further decomposition in the absence of micro-organisms. As can physical abrasion from wind, sand etc... So naturally mummified remains of great age would also have been protected from light and abrasion as well.


Can you use a cell in meiosis to create a karyotype?

Yes, you can, but it's way more difficult.

First of all, in order to see meiotic chromosomes, you need to colect young floral bud in the right stage of development (not too young, since you don't want microspore mother cell, and not too old, since you don't want polen), and that's not that easy.
Then, once you found the right stage and made a slide, you need good knowledge on all the phases of meiosis to understand what you are looking at. Bivalents and translocation rings can make it very difficult to really understand the chromosomes set you have in the cell, so you need a good sized sample and a lot of observation and analysis. If the species you are analyzing has small chromosomes, it's even more difficult to understand what you are looking at.


I accidentally wrote a lot!

I first discuss the term Darwinian evolution. I then describe the main evolutionary processes insisting on the two elements of interest in your question, that is mutations and natural selection. In the end, I directly address your two statements and bring a few more complications into the subjects.

Did you say Darwinian evolution?

Evolution is more than Darwinian evolution

The expression "Darwinian evolution" easily yield to misunderstandings. Darwin was probably the most important scientist and one of the first (if not the first) to develop the theory of evolution but evolutionary biology today is so much more than Darwin's theory of evolution.

Examples of very basic things Darwin did not know

We discovered the structure of DNA in the 1950s-1960s only with Miesher, Chargaff and most renowned Watson and Crick (history of the discovery). Darwin had no idea of the existence of DNA and had not even hypothesized about the existence of such a molecule (which came first by Erwin Schrödinger).
Darwin was not aware either that inheritance was through the transmission of "particles/atomic" and not through the inheritance of some kind of "fluid/continuum". In other words, Darwin did not know the Law of Segregation by Gregor Mendel (even if they lived in the same epoch).
Darwin had no idea about Evo-Devo, that is he had no idea about the similitudes in developmental processes among related (even distantly related) organisms.
Globally speaking, while Darwin managed to touch a little bit about many of the subjects of modern evolutionary biology (which is very impressive), he only manages to mention them and failed to provide any prediction. This is a large part because no one had no concept in genetics at that time.

Evolution is more than natural selection and mutations

Evolution is not only about natural selection. Even C. Darwin knew that evolution is way more than natural selection. It is for example very important to consider random events. One of them is mutation, another is genetic drift (I am not trying to list every process that influence evolution but only to give you a sense of why natural selection is different than evolution with a goal of explaining why a trait that is needed do not necessarily appear). Both mutations and genetic drift explain why a species will not necessarily be perfectly adapted to its environment. Evolutionary biology is a big field of knowledge and there is a lot to know about evolutionary processes.

Natural Selection and Mutations explained by the Lewontin Recipe

The Lewontin's recipe is a good way in order to understand what is natural selection and when it occurs. The Lewontin's recipe says that natural selection occurs whenever:

Individuals in a population vary in terms of a given trait
This trait has some (additive) heritability. Here is one of the several posts that explain the concept of heritability. It might be slightly a post that is a bit advanced for you though but shortly speaking it means that offspring are more similar to their parents more than they are to other non-kin individuals in the population.
The fitness varies (not necessarily linearly) as the trait varies.

Simple example:

In a population, there are blue pens and red pens
Reproduction is asexual and blue pens create other blue pens while red pens create other red pens.
blue pens make more offspring than red pens.

In such a situation, natural selection occurs yielding the frequency of the blue pens to increase in the population while the frequency of red pens will decrease.

Natural Selection

Natural Selection is the process by which variants of genes called alleles are selected and therefore increase in frequency. This selection result from a differential reproductive success.

Mutations

In the broad sense mutation is any change in the DNA sequence. Some changes are more likely to happen than other but in any case, the likeliness of these changes to happen is not dependent on the consequence they will have on the phenotype (shortly speaking, a phenotype is how an individual looks like) and on the reproductive success. So mutations occur randomly and the specific mutation that would be needed in the population may not occur. Therefore saying, if a trait is needed (in the sense of "if a trait would be beneficial"), then a mutation will occur to make this trait existing is wrong. Note that most mutations are deleterious (decrease the reproductive success) while few of them are beneficial (increase the reproductive success) and those that are beneficial are more likely to rise in frequency in the population.

Genetic drift

If the change in frequency of mutations would depend exclusively on natural selection, then I would not have said before that a beneficial mutation is more likely to raise in frequency but I would have said that a beneficial mutation will raise in frequency deterministically. An intuitive explanation of what is genetic drift can be found on this post. It will also allow you to understand why small population undergo a more random change in frequency of their genes than are big population.

Considering your opposing statements

Hopefully, the following is clear from the above discussion but I would like to directly address your statements.

  My friend said that Natural Selection is a mechanism inside the organism that mutates the DNA to make its offspring survive in an environment; that natural selection mutates the DNA beneficially and that random mutations are not useful (like blue eyes). But I disagree and think that it is closer to Lamarkian theory.

You are right that your friend is wrong!

It indeed sounds more or less Lamarkian. In any case, it is very wrong, as you said. Mutations are not caused deterministically under the pressure of natural selection to do specific things.

Are mutations completely random?

See Are mutations random?.

I do not want to go into too many complications. The sentence "mutations are random" is unclear. Does it mean that the mutation rate is random? Does it mean that the effect of a new mutation is random? And also the concept of randomness only make sense if we consider a set of a priori knowledge. So it is a little hard to fully answer this question and the easy, close-enough approximation for a starter in evolutionary biology is just to say that mutations are random (whatever that means). A slightly better approximation of reality is that mutation rate is an adaptive trait and can vary depending on the environment where the individual is found (adaptively or not). However, the effect of new mutations is really not deterministic.

The mutation rate varies with the type of sequence considered. For example, a microsatellite sequence is a sequence or repeated DNA. For example AATAATAATAATAATAATAAT etc.. (note that the genetic code is written with 4 letters, A, T, C and G). Such sequences are highly mutable. So a mutation is more likely to occur in this region than in the middle of a coding region. And it is more likely for a mutation occurring in a coding region to affect fitness than for a mutation occurring in a microsatellite (it is possible that a mutation occurring in a microsatellite will affect fitness).

Depending on the level of stress some organisms (plants mostly to my knowledge) can change their mutation rate. Consider for example an individual that is maladapted to its environment. If it mutates little, then the offspring will likely be as maladapted and in the long run, the lineage will disappear. If the individual is mutating a lot then, most offspring will have a very low fitness but eventually one will receive a beneficial mutation that will make it very strong and by itself, this offspring may save the lineage. This is what is called a bet-hedging strategy. The concept of bet-hedging can be summarized with the expression "Don't put all your eggs in the same basket".

You will note that the mutation rate is an evolving feature of an organism. This yield observation such as what is now called Drake's rule (original paper). Drake's rule indicates that the genome-wide mutation rate is always at the order of 1 (there is quite a bit of variation but it is a good approximation).

  I told him that DNA from male and female recombines and randomly mutates making a new "recipe" for the offspring (adding a new characteristic(s)). If the offspring is well suited for the environment, then it survives and passes on its characteristics to its offspring. If it does not have fitness for its environment, it dies. So, Natural Selection is were nature "selects" who survives and reproduces a lot.

Sounds quite right!

You pretty much nailed it. Mutation adds genetic variation and natural selection selects from the available genetic variation. Your wording is a little uncommon though :). For example, an individual, it is incorrect to say that an individual has fitness or not. Each individual has a fitness, that is some value that encompasses both its fertility and survival probability. In a simple model, fitness is simply the expected number of offspring.

Note also, that the majority of mutations that affect the fitness of the individuals are not so much dependent on the details of the environment. Many mutations are just bad wherever you are. Think about a mutation that would reduce the efficiency of energy production (ATP in mitochondria). Such a mutation will be deleterious regardless of whether the weather is hot or cold for example.

Introductory course to evolutionary biology

You probably want to have a look at an introductory course to evolutionary biology such as Understanding Evolution.


Why I have to pee more often in low temperature?

This phenomenon has been demonstrated in studies [1][2] which show a significant increase in urine output in the cold. The latter study shows the biggest increase is when a person is initially exposed to the cold rather than when they continue to be exposed or rewarmed up. In the study, the average urine out was 157 mL/hour when a person was initially exposed to the cold, 103 mL/hour when they were being maintained at that cold temperature and 70 mL/hour when they were being rewarmed.

The mechanism however is unclear. This study showed that the mean arterial pressure increases. It is well known that the cold causes our blood vessels to constrict (in order to keep the blood and therefore heat inside our core body). The thought was therefore that our kidneys try to lower our blood pressure by taking more fluid out and emptying it into the bladder. This is called cold-induced diuresis.

Other thoughts include that we lose the water we ingest by sweating (perspiring), pooping (defaecation) and peeing (micturition/urination). In the winter, we don't typically sweat as much, which ISN'T counterbalanced with a lower water intake, so we need to pee more.

Another possibility is that aquaporins (the pores that water comes out from our kidneys) are inhibited by the cold. This means more fluid would be filtered out. However there isn't really much research in this area that I am able to find.


Why is beta- D fructofuranose two different structures when in free form and as part of sucrose?

I'll try to explain this to you, but you should really look it up here: https://pubchem.ncbi.nlm.nih.gov/compound/beta-Levulose#section=3D-Conformer&fullscreen=true

This is the structure of beta-D-fructofuranose, as a 3D conformer. On paper, or as a 2D figure, we cannot visualize the -OH groups at positions 3 and 4.

They appear to be inside/outside the ring, but in reality, they're not really positioned that way. Both the -OH groups are oriented in an opposite manner, but in a plane perpendicular to that of the furan ring.

So when we flip it over to represent it in sucrose, the orientation of the -OH groups in the molecule flips too.

Think of it this way: if you have a piece of cardboard  (representing the ring) with a pin pierced into it (representing the -OH), and you flip the board over, the pointy side of the pin will face down too.

Moreover, if we represent it this way, the absolute configuration of the side chains at each of the carbons of fructose remain the same.
You could check that using their RS configurations.

For more on RS configurations, check out : https://chem.libretexts.org/Bookshelves/Organic_Chemistry/Supplemental_Modules_(Organic_Chemistry)/Chirality/Absolute_Configuration%2C_R-S_Sequence_Rules


What is it called when there is natural truncation selection?

Truncation selection

The term  truncation selection has been used a lot in theory papers because it is a simple model and because it is of interest to breeders. Truncation selection is most likely more common in a breeding setting than in nature and from wikipedia,  truncation selection is defined as specific to breeding

  In animal and plant breeding, truncation selection is a standard method in selective breeding in selecting animals to be bred for the next generation

However, as much as the definition fail to repeat animal or plant instead of just animal, IMO it fails to recognize that such notion could as well exist in nature. I would personally not be shock to read a paper talking about  truncation selection in wild populations.

Threshold model

If you really want to avoid talking about truncation selection, then you can eventually picture the phenotypic trait as a liability factor (as it is done in sex determination literature, see Perrin and Beukeboom's book) and selection acting as a threshold on this factor. Note that the concept of threshold and threshold model is very common and everyone will understand what you mean.


Why is there not an immune response to injected immunoglobulins?

If a head-to-head "match" between antibodies from two different people was to occur, a similar match would most likely have occurred already in the donor. People have the same tissues after all.
But in the donor; the B lymphocytes producing the antibodies had to go through the processes of "central tolerance" and "peripheral tolerance".
This would weed out the cells producing autoantibodies.
Theoretically, nasty autoantibodies in the recipient could react with innocent antibodies in the donor though.


How many primary oocytes in human female body at birth?

Short answer: The developmental process starts from oogonia as follows:

Oogonia(7million) in the foetus develops into primary oocyte(2million) in the foetus prior to gestation which again develops into primordial follicle(700,000-800,000)at birth.

From the second excerpt of your question I could understand that it said, "each ovary contains  approx. 400,000 follicles at birth." which is definitely correct if you consider that total number of follicles in both the ovaries would give 800,000.

Excerpts from the references that lead to the short answer above:

In the developing female fetus, oogonia become primary oocytes that begin the first division of meiosis. However, this division is not completed and the primary oocytes remain “frozen” in the prophase stage of the first meiotic division.
At birth, oogonia are no longer present. Each primary oocyte is surrounded by a single layer of squamous epithelial cells called follicular cells. The primary oocyte together with its follicular cells is called a primordial follicle. There are about two million primordial follicles with their primary oocytes in the ovaries at birth suspended in the first division of meiosis.
As the female grows, primary oocytes begin to die and disappear with their follicular cells. This process continues until puberty when there are only about 400,000 primordial follicles left in the ovaries. The primary oocytes continue the process of oogenesis after puberty begins.[Source]

The total number of primary oocytes at birth is estimated to vary from 700,000 to2 million. During childhood most oocytes become atretic; only approximately400,000 are present by the beginning of puberty, and fewer than 500 will be ovulated.[Source]

Primary oocytes reach their maximum development at ~20[6] weeks of gestational age, when approximately seven million primary oocytes have been created; however, at birth, this number has already been reduced to approximately 1-2 million.Recently, however, two publications have challenged the belief that a finite number of oocytes are set around the time of birth.[Source]

In the human embryo, the thousand or so oogonia divide rapidly from the second to the seventh month of gestation to form roughly 7 million germ cells.[Source]

REFERENCES:
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0008772


Is this a grackle with an unusually long decurved bill (Phoenix AZ, USA)

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

A crow with a deformed bill (reference)


It is not really making you vomit not directly, it is making you nauseous if you become too nauseous you vomit.(nausea has multiple triggers but for this I will stick to smell) Nausea exist to keep you from eating toxic food and to help you get rid of it if you do, the reflex is a balance between the biological cost of a meal(minimal) and the cost of being poisoned(extreme) so you can see why it might favor vomiting and losing a meal vs not vomiting and dying of poisoning than it would the two costs were not so drastically different.

Now your body can't really tell the difference between a smell coming from inside your mouth and one from outside, they both reach the nose by a roundabout course, and your mouth cannot smell. The closest your instincts can come is assuming a stronger scent is coming from the mouth since it is close and enclosed. That's why a stronger disgusting smell results in a stronger feeling of nausea. the stronger the smell the better the chance it is coming from inside your mouth.

Combine these two concepts and you can see how the stronger the smell and the more disgusting it is the more likely it is to make you nauseous it is the best protection our anatomy allows for. Now of course this is only the the current hypothesis, Nausea is not easy to study nor is it a in high demand for research.

Additional sources


Is one Short Tandem Repeat (STR) enough for a reliable identification?

One STR is certainly not enough for identification because the same STR could be shared by many individuals. Combinations of many STRs, however, would be sufficient for identification. The number needed would depend on how many variants of the STR exist in the population (or species, depending on what you are identifying), and what the mutation rate is (nuclear STRs mutate relatively rapidly compared to some other genetic markers, but they are still often used because they're cheap and easy to genotype).


Genetic variation in humans and model organisms (measured by SNPs)

SNP Density

Human = ~1.18 SNPs per kbases

  Based on CgsSNP, the average numbers of SNPs per 10 kb was 8.33, 8.44,
  and 8.09 in the human genome, in intergenic regions, and in genic
  regions, respectively.

Source: Investigating single nucleotide polymorphism (SNP) density in the human genome and its implications for molecular evolution. by Zhao Z, Fu YX, Hewett-Emmett D, Boerwinkle E.

Drosophila melanogaster = ~0.02 SNP per kbases

  FLYSNPdb provides high-resolution single nucleotide polymorphism (SNP)
  data of Drosophila melanogaster. The database currently contains 27
  367 polymorphisms, including >3700 indels (insertions/deletions),
  covering all major chromsomes. These SNPs are clustered into 2238
  markers, which are evenly distributed with an average density of one
  marker every 50.3 kb or 6.6 genes.

source: FLYSNPdb: a high-density SNP database of Drosophila melanogaster

Mouse(Mus musculus) = ~0.2 SNP per kbases

Source: Genome-wide single-nucleotide polymorphism
analysis defines haplotype patterns in mouse


Is there a name for this principle in biological contexts?

It may also be called as Idea of maximum parsimony. It is used in phylogenetics to construct phylogenetic trees which require the least number of evolutionary events.


What ecological niche do disk shaped fish exploit?

I believe what you're referring to are fish with the compressiform body shape (fish with a narrow flattened body). The advantage to this body shape is that it allows the fish to swim very quickly for short periods of time. This would, I assume, be an advantage both as predator and prey in that it can use a quick burst to escape from something else trying to eat it and also allow it to use a quick burst to catch food for itself.

--added--

I just re-read your question and caught the "ecological niche" part, which is different from evolutionary advantage. I'm not 100% sure regarding this (I'd say 80% sure though), but I don't think that an animal has to fill a specific ecological niche in order to survive - it just has to...survive. Surely animals that fill specific niches can gain an evolutionary advantage by filling a niche, but it is not (to my knowledge) a requirement.


What percentage of people today would likely be descendants a man born 4,000 years ago?

To what degree (if any) of accuracy could his descendants be traced?

I don't really understand this question. To what degree can we trace its descendants given we know what from this man? Do we have a blood sample?

  What percentage of the global population is likely a descendant of the man?

If $N_0$ was the population size 4,000 years ago and $N$ is the population today, then the expected number of descendent of any given person is simply $\frac{N}{N_0}$. However, there is a huge variance and this is where things get more complicated.

As coalescent processes are geometrically distributed (well approximated by an exponential distribution if we assume that the population is large; more info in this answer), then the variance in coalescent times is equal to the expected coalescent time.

The expected coalescent time in a diploid population of constant size $N$ is $2N$. Of course, the assumption of constant population size doesn't hold for humans due to the recent demographic explosion. When the population size is increasing the genealogy looks like a star as coalescent events are rarer and therefore, it is more likely for a given individual living in the past to live descendant today (Excoffier et al. 2009). However, I don't know how to calculate coalescent time in expanding populations.


What proportion of the people who lived 1000 years ago have genetic descendants alive today?

Expanding on @heracho's answer and Wikipedia, assume pi denotes the probability of having (exactly) i children, and that dm denotes the probability of extinction by the mth generation (note that this includes extinctions by all generations n with n < m). Then dm can be expressed as:

$\displaystyle d_m = p_0 + p_1 d_{m-1} + p_2 d_{m-1}^2 + p_3 d_{m-1}^3 + \dots = \sum_{i=0}^\infty p_i d_{m-1}^i$

with d0 = 0.

In other words, the probability of going extinct by the mth generation is equal to the probability of i children going extinct in m – 1 generations, summed over i. (The child lineages are assumed independent.) This recurrence relation allows you to calculate the extinction (and, by extension, survival) probability at any desired number of generations, if the values of pi are known. In simple cases it is also possible to work out the asymptotic value of dm by solving the fixed point equation dm = dm – 1 (see the Wikipedia page for an example).

In relation to your specific application, we can assume roughly 40 generations and use some empirical estimates of pi. The parity distribution of Denmark is given by Frejka (2008) as p0 = 0.127, p1 = 0.179, p2 = 0.443, p3 = 0.251 (where I simplify by assuming that people who have strictly more than 3 children actually have only 3 children). Plugging these parameters into the recurrence relation and iterating for 40 generations (see R code below), we get d40 = 0.17. Thus some 83% of the population can be assumed to have descendants in 1000 years.

I have taken Denmark as an example simply because it is the first country mentioned in Table 2 of Frejka (2008). However, to illustrate the dependence of the asymptotic value of dm on the parity parameters consider the case of Italy. From the same publication, we find p0 = 0.240, p1 = 0.235, p2 = 0.369, p3 = 0.156. With these values, we compute d40 = 0.41, obviously a very different situation.

I am not a mathematician, nor a biologist (nor a demographer), and the above logic obviously employs many ridiculous simplifications. It would be very interesting to know how all this pans out in a more realistic model.

Reference

Frejka, Tomas (2008) Parity distribution and completed family size in Europe: Incipient decline of the two-child family model? Demographic Research, 19(4): 47–72. https://www.demographic-research.org/volumes/vol19/4/19-4.pdf

R code

# get extinction probability (d) in generation m, given extinction
# probability in generation m-1, conditioned on probabilities
# of having 0, 1, 2, ... children (vector p)
extinctionprob <- function(d, p) {
  d <- d^(0:(length(p)-1))
  sum(d*p)
}

# iterate for 'ngen' generations
iterate <- function(ngen, p) {
  d <- 0
  for (i in 1:ngen) d <- extinctionprob(d, p)
  d
}

# usage example:
# iterate(ngen=40, p=c(0.240, 0.235, 0.369, 0.156))


What are the atmospheric requirements for large dinosaurs?

Oxygen levels have changed greatly throughout Earths's history starting with very little atmospheric oxygen and gradually increasing as photosynthetic activity appeared until all the oxygen sinks such as minerals had been filled, then taking off, reaching as high as 35% of the atmosphere during the carboniferous period 3. The reasons behind this sudden increase in O₂ has to do with the development of bark covered wooden plants, a feature made possible by the molecule lignin, which strengthens the trunks of trees and makes tall plants possible. However, lignin was hard for microbes to digest, and the dead trees built up, never returning their carbon to the atmosphere as CO₂. So the oxygen they had made while alive stayed in the air 4.

The plot shows the upper (red) and lower (green) estimates for O₂ concentration over time. The data for this plot was taken from a review of analysis of sulfur, carbon, iron, and manganese deposits 2. If you're interested in how isotopic analysis can give information about atmospheric oxygen, read that paper, it's detailed.

That spike in the plot is the carboniferous. This period in history is interesting because of the appearance of large invertebrates, such as 3 foot wide dragonflies and 6 foot long centipedes 5. Since these animals move oxygen through a series of tubes called trachea, where air just moves through by diffusion, it was speculated that the higher concentration of oxygen allowed this growth. Recent research indicates that insects can force air through their trachea, and that competition between predators and prey could have explained most of the size 6.

So how does this affect dinosaurs? The carboniferous period was about 350-300 million years ago, which corresponds with the spike on the graph. Dinosaurs appeared in the Triassic, which was about 250-200 million years ago, but oxygen levels were at 16% of the atmosphere at the time 7 ( current O₂ levels are about 20% ) If we move into the Jurassic, about 200-150 million years ago, oxygen levels rise to about 26% 8. In the Cretaceous, about 150-65 million years ago, O₂ was at about 30% 9. The O₂ percentages are taken from the infoboxes on the right side of the wikipedia articles, which in turn take the number from a plot very similar to the plot I posted here, despite being in German 10.

I compiled lists of heaviest and lightest dinosaurs by going through the wikipedia article on dinosaur size 11 and going to the article on each dinosaur and checking if it was Triassic, Jurassic, or Cretaceous.
If we look at the heaviest dinosaurs, most of them appeared during the Cretaceous:

Heaviest Dinosaurs
Theropods                           Metric Tons     Period
Spinosaurus aegyptiacus             7-20.9          Cretaceous
Carcharodontosaurus saharicus       6.1-15.1        Cretaceous
Giganotosaurus carolinii            6.1-13.8        Cretaceous
Tyrannosaurus rex                   6-9.5           Cretaceous
Oxalaia quilombensis                5-7             Cretaceous
Acrocanthosaurus atokensis          5.6-6.2         Cretaceous
Tyrannotitan chubutensis            4.9-5.6         Cretaceous
Suchomimus tenerensis               2.7-5.2         Cretaceous
Therizinosaurus cheloniformis       5               Cretaceous
Tarbosaurus bataar                  4-5             Cretaceous

Sauropods                           Metric Tons     Period
Amphicoelias fragillimus            122.4           Jurassic
Argentinosaurus huinculensis        60-90           Cretaceous
Antarctosaurus giganteus            69-80           Cretaceous
Mamenchisaurus sinocanadorum        75              Jurassic
Sauroposeidon proteles              40-60           Cretaceous
Paralititan stromeri                59              Cretaceous
Brachiosaurus altithorax            28.7-56.3       Jurassic
Puertasaurus reuili                 50              Cretaceous
Ruyangosaurus giganteus             50              Cretaceous
Alamosaurus sanjuanensis            50-60           Cretaceous
Futalognkosaurus dukei              38.1-50+        Cretaceous
Turiasaurus riodevensis             40-50.9         Jurassic/Cretaceous
Camarasaurus supremus               47              Jurassic
Diplodocus hallorum                 30-42.5         Jurassic
Supersaurus vivianae                32-40.2         Jurassic
Elaltitan lilloi                    42.9            Cretaceous
Tehuelchesaurus benitezii           41.3            Jurassic
Apatosaurus louisae                 18-41.3         Jurassic

Ornithopods                         Metric Tons     Period
Shantungosaurus giganteus           9.9-22.5        Cretaceous
Iguanodon seeleyi                   15              Cretaceous
Saurolophus angustirostris          6.6-9           Cretaceous
Iguanodon bernissartensis           8.3-8.6         Cretaceous
Edmontosaurus annectens             3.2-7.6         Cretaceous
Brachylophosaurus canadensis        4.5-7           Cretaceous
Saurolophus osborni                 6.6             Cretaceous
Lanzhousaurus magnidens             6               Cretaceous
Parasaurolophus walkeri             3-5.1           Cretaceous
Charonosaurus  jiayinensis          5               Cretaceous
Barsboldia sicinskii                5               Cretaceous

Ceratopsians                        Metric Tons     Period
Triceratops horridus                5-14            Cretaceous
Triceratops prorsus                 6.5-11          Cretaceous
Titanoceratops ouranos              6.5-11          Cretaceous
Eotriceratops xerinsularis          10              Cretaceous
Pentaceratops sternbergii           3-4.8           Cretaceous
Pachyrhinosaurus canadensis         3-4.4           Cretaceous
Styracosaurus albertensis           4.2             Cretaceous
Agujaceratops mariscalensis         2.6             Cretaceous
Centrosaurus apertus                1.1-2.5         Cretaceous
Coronosaurus brinkmani              2               Cretaceous
Rubeosaurus ovatus                  2               Cretaceous
Achelousaurus horneri               2               Cretaceous
Pachyrhinosaurus lakustai           2               Cretaceous
Chasmosaurus belli                  2               Cretaceous

Thyreophorans                       Metric Tons     Period
Dacentrurus armatus                 5-7.4           Jurassic
Ankylosaurus magniventris           1.7-6           Cretaceous
Stegosaurus stenops                 2.6-5.3         Jurassic
Cedarpelta bilbeyhallorum           5               Cretaceous
Hesperosaurus mjosi                 3.5-5           Jurassic
Tuojiangosaurus multispinus         4.8             Jurassic
Wuerhosaurus homheni                4               Cretaceous
Niobrarasaurus coleii               4               Cretaceous
Stegosaurus ungulatus               3.5             Jurassic
Gobisaurus domoculus                3.5             Cretaceous
Nodosaurus textilis                 3.5             Cretaceous
Palaeoscincus costatus              3.5             Cretaceous
Sauropelta edwardsi                 3               Cretaceous
Edmontonia rugosidens               3               Cretaceous
Edmontonia schlessmani              3               Cretaceous
Edmontonia longiceps                2.3-3           Cretaceous
Tuojiangosaurus multispinus         2.8             Jurassic
Euoplocephalus tutus                2-2.7           Cretaceous
Jiangjunosaurus junggarensis        2.5             Jurassic

This isn't exactly a fair way to do it, but I didn't want to calculate average dinosaur mass over time. I know that some groups, such as the ceratopsians didn't appear until the late Jurassic, skewing the results, and I didn't make any attempt to differentiate between late or early periods. However I also noticed that many of the smallest dinosaurs appeared in the Cretaceous as well. Pay attention to the units, even the smallest sauropods are measured in metric tons.

Lightest Dinosaurs
Theropods                           kg              Period
Parvicursor remotus                 0.137           Cretaceous
Epidexipteryx hui                   .164-.391       Jurassic
Compsognathus longipes              0.26            Jurassic
Ceratonykus oculatus                0.3             Cretaceous
Juravenator starki                  0.34-0.41       Jurassic
Ligabueino andesi                   0.35            Cretaceous
Microraptor zhaoianus               0.4             Cretaceous
Sinosauropteryx prima               0.55-0.99       Cretaceous
Rahonavis ostromi                   0.58            Cretaceous
Mahakala omnogovae                  0.76-0.79       Cretaceous
Xiaotingia zhengi                   0.79            Jurassic
Mei long                            0.85            Cretaceous
Microraptor gui                     0.95-1.50       Cretaceous

Sauropods                           Metric Tons     Period
Pleurocoelus nanus                  0.5             Cretaceous
Magyarosaurus dacus                 0.75            Cretaceous
Europasaurus holgeri                0.8-1           Jurassic
Bonatitan reigi                     1               Cretaceous
Lapparentosaurus madagascariensis   1.4             Jurassic
Lessemsaurus sauropoides            1.8             Triassic
Lirainosaurus astibiae              1.8-4           Cretaceous
Shunosaurus lii                     2.2-6.7         Jurassic
Ampelosaurus atacis                 2.5             Cretaceous
Amargasaurus cazaui                 2.6-3.8         Cretaceous
Hypselosaurus priscus               2.7-8           Cretaceous
Euhelopus zdanskyi                  3.4             Cretaceous
Neuquensaurus australis             3.5-6.1         Cretaceous
Rinconsaurus caudamirus             4.1             Cretaceous
Atacamatitan chilensis              4.3             Cretaceous
Dicraeosaurus hansemanni            4.4-5           Jurassic

Ornithopods                         kg              Period
Gasparinisaura cincosaltensis       1-13            Cretaceous
Yueosaurus tiantaiensis             3.9             Cretaceous
Fulgurotherium australe             6               Cretaceous
Notohypsilophodon comodorensis      6               Jurassic
Yandusaurus hongheensis             6.6-7.5         Jurassic
Hypsilophodon foxii                 7-21            Cretaceous
Thescelosaurus sp.                  7.9-86          Cretaceous
Valdosaurus canaliculatus           10              Cretaceous
Haya griva                          11              Cretaceous
Agilisaurus louderbacki             12              Jurassic
Drinker nisti                       20              Jurassic
Changchunsaurus parvus              20              Cretaceous
Qantassaurus intrepidus             20              Cretaceous
Zephyrosaurus schaffi               20              Cretaceous
Oryctodromeus cubicularis           20              Cretaceous
Orodromeus makelai                  20              Cretaceous

Ceratopsians                              kg        Period
Liaoceratops yanzigouensis                2         Cretaceous
Yamaceratops dorngobiensis                2         Cretaceous
Psittacosaurus sinensis                   4.1       Cretaceous
Psittacosaurus lujiatunensis              5         Jurassic
Yinlong downsi                            5.5       Cretaceous
Micropachycephalosaurus hongtuyanensis    5.9       Jurassic
Chaoyangsaurus youngi                     6         Jurassic
Xuanhuaceratops niei                      6         Jurassic
Bagaceratops rozhdestvenskyi              7         Cretaceous
Psittacosaurus meileyingensis             8         Cretaceous
Psittacosaurus neimongoliensis            8-8.4     Cretaceous
Archaeoceratops oshimai                   10        Cretaceous
Psittacosaurus mongoliensis               12.1-20   Cretaceous
Psittacosaurus sibiricus                  15        Cretaceous

Thyreophorans                       kg              Period
Scutellosaurus lawleri              3               Jurassic
Emausaurus ernsti                   50              Jurassic
Scelidosaurus harrisonii            64.5-270        Jurassic
Animantarx ramaljonesi              300             Cretaceous
Struthiosaurus transylvanicus       300             Cretaceous
Struthiosaurus austriacus           300             Cretaceous
Gargoyleosaurus parkpinorum         300             Jurassic
Mymoorapelta maysi                  300             Jurassic
Minmi paravertebra                  300             Cretaceous

So what does this mean for the relationship between oxygen levels and dinosaur size? Higher oxygen levels in the Jurassic and Cretaceous probably allowed for larger animals to exist, however as time went on Dinosaurs became more diverse in general, including size. Many of them evolved to become smaller, despite being allowed to become larger by higher levels of oxygen. We should also note that even though oxygen levels were still lower than they were during the carboniferous, the animals were much larger, most likely due to their more efficient oxygen transport systems (lungs, 3(4?) chambered hearts, sealed circulatory systems, hemoglobin).

If we think about what could drive species to become larger, competition for food and protection from predators comes to mind. Sauropods that could reach the leaves in taller trees had distinct advantages over those who could not. Prey animals stood a better chance at fighting off predators if they were bigger. Likewise, predators could kill larger prey if they became larger too. Oxygen didn't drive them to become larger, it simply allowed them to.

To actually answer the question, could the modern atmosphere support animals as large as dinosaurs? It probably could. The heaviest living animal today is the blue whale, at an average mass of 110 metric tons, is heavier than all but 1 of the sauropods on the list I compiled. The heaviest land animal living today is the African Elephant, with average mass of 4.9 metric tons and as high as 10 metric tons, would be a respectable competitor with many of the dinosaur groups I listed 12.

Another interesting question is not how oxygen affected the size of organisms, but how it affects it their metabolism. Cold blooded animals don't need as much oxygen because they don't spend as much energy. Warm blooded animals must constantly expend energy to maintain body heat, and this requires greater consumption of oxygen. Obviously being large and warm blooded would force you to need even greater levels of oxygen than 1 or the other. It may be that the advantages of being warm blooded outweighed the advantages of large size, but I don't want to dig into that question right now.


Can trichoptera and lepidoptera be distinguished with the naked eye?

The etymology of the names will help you there: trichoptera means "hairy wings", whereas lepidoptera means "scaly wings".

If you can get a close shot (maybe with a powerful tele lens) of any possible trichoptera or lepidoptera, you can tell that it either has hairs or scales on its wings, without having to touch its wings.

Examples:

Note the hair visible above the wings. Taken from https://www.inaturalist.org/observations/18660283

Now, there are lepidoptera species that also seem to have hairy wings, such as the tussock moth:

Note the hair as well. However, the shape of the antennae would be a dead give-away: as far as I know, trichoptera shouldn't have feather-like antennae. Furthermore, the wings still have noticeable scales, besides the hair. Taken from https://www.inaturalist.org/observations/18652111

Other lepidoptera species may also seem to lack scales, such as the Syntomoides imaon:

Parts of the wings of the Syntomoides imaon are transparent. However, anywhere that has scales should exhibit some kind of iridescence. You can use your phone's flashlight and try to illuminate the insect from different angles, and you should notice some iridescence. Trichoptera wings, in contrast, should just reflect the light flatly, due to the lack of scales. Taken from https://www.inaturalist.org/observations/18652111

Also, (most) butterflies and moths have a proboscis (the "straw" that can coil up, used to suck nectar). That's usually easy to spot if you can look at the head from the side. Caddisflies don't have that. Instead, caddisflies have mandibles (used to chew through their pupal case as they emerge as adults).

I did mention using a tele lens at the beginning of this answer. Of course, that's not "naked eye" like you asked. The point is that you begin by using a tele lens. As you see more caddisflies vs moth/butterflies, you'll build up a sense of the cues to look at. And at some point you may be able to distinguish them with your naked eye (depending on how close you can get your face to the insect and how good your eyesight is).


Non-Salticidae with °oo° Eye Arrangements

It is pretty much unique to salticidae, although I did find some similar eye arrangements in sicariids and scytodids.

Salticidae:

Sicariidae:

Scytodidae:

Image source


Is the autonomic nervous system only activated by internal stimuli?

Short answer
External stimuli can drive autonomic responses.

Background
The autonomic nervous system is a visceral sensory and motor system. The viscera are the internal organs. Virtually all visceral reflexes are mediated by local circuits in the brain stem or spinal cord (Fig. 1). It is one of two major subdivisions of the nervous system; the other being the somatic (or voluntary) nervous system. The main distinction between the two is that the latter is involved in voluntary and conscious actions (e.g., movement, perception and cognition), while the autonomic nervous system is engaged in involuntary processes, such as regulating heart rate, breathing and bowel function (Fig. 1).

Fig. 1. Autonomic nervous system. Source: Austin Community College

Although by far most stimuli driving autonomous responses come from within (think muscle movements driving bowel movements, increased heart rates during physical exercise), outside stimuli do directly impinge on the autonomous system.

For example, the cilliary muscle in the iris is under the control of light coming into the retina. The pupillary light reflex test is based on this principle, and is routinely used to diagnose damage to the visual system. Also, production of saliva is controlled by external stimuli (smell and taste of food and see the striking example below from @anongoodnurse). And technically, the entire digestive tract can be considered to be outside the body, as it is continuous with the skin and lining of the mouth. Hence, the mechanical stimuli impinging on the intestines by a moving bolus of food that drives the waves of peristaltic movements can, arguably, be considered to be caused by external stimuli too. Lastly, the fight-flight-fright response involving the hypothalamic-pituitary-adrenal gland (HPA) axis is often initiated by external stimuli (loud sudden noises etc.).

The most important characteristic of the autonomic nervous system, as said, is that the autonomous responses are not voluntarily controlled. While you can decide to look or track a visual stimulus, you cannot decide to move the bolus of food back up to your stomach, or voluntarily constrict your pupil. The way the input is received may not be the best way to distinguish it from the voluntary nervous system.

Didactic answer
If you are left with questions, the first place to go to is your professor.

Reference
- Kandel et al. Principles of Neural Science 4th ed. (2000). Ch.49 The autonomic nervous system and hypothalamus. p.960-81


Viruses can infect any cell:

  a virus must have a host cell (bacteria, plant or animal) in which to live and make more viruses. Outside of a host cell, viruses cannot function.

Source

This includes the dendritic cells:

  Dendritic cells are antigen-presenting cells of the immune system. Their main function is to process antigen material and present it on the cell surface to the T cells of the immune system. They act as messengers. They don't actually release any antibodies.

Source

Quite simply, at the beginning of an infection, the viruses / bacteria will be destroyed by macrophages.

The dendritic cell will "pick up" some of the leftover pieces.

When it finds a T-Cell that has the same configuration, it orders lots of identical T-Cells to be made. These T cells have multiple jobs, one of which is activating the B cells. It is the B cells that release the antibodies.

So Ebola.

If the dendritic cells are "invaded", then the only line of defence is the macrophages. This is often not enough to stop an attack, and it multiplies out of control.

The reason the Dendritic cells can be invaded is because they are just as vulnerable as other cells. They haven't activated the T cells, and they haven't activated the B cells, so there is nothing protecting them.

Images Source (YouTube video)


What is the function of E-coli bacteria in our gut?

Nonpathogenic E.coli are a component of the gut microbiome of humans and many other organisms.

They are commensals, meaning that when they remain in the areas they have evolved to live in, and when they do not acquire virulence factors, they are benign. They live in our digestive tract and basically do nothing to harm us.

In fact, commensal microorganisms like E.coli can be considered part of the multicellular organisms innate immune system. They take up space on the exposed surfaces of internal organs such as the intestines and prevent the colonization of pathogenic strains of microorganisms.

Along with the endothelial cells and mucous, commensals form the barrier defenses that are the first line of protection against pathogenic organisms. Basically they are the good neighbors that don't cause problems and they don't leave space for bad neighbors to move in.

Problems can occur if they gain access to areas that are normally sterile. If the intestine is perforated and E.coli gain access to the thoracic cavity, they can become an opportunistic pathogen, as they will not be interacting with the host in a way that can control their proliferation. They can also come in contact with cells that are not expressing the necessary proteins to protect them from the E.coli.

You can also end up with the situation where a pathogenic bacteria or a bacteriophage carrying a virulence factor can transfer that virulence factor to the commensal E.Coli, turning them pathogenic.

But for the most part E.coli are there to take up space that could otherwise be colonized by harmful bacteria.


How copy number variation thresholds are defined in GISTIC

The best solution is to use only the broad alterations, using the file broad_values_by_arm.txt.

In particular, for each sample, the highest threshold is computed as the sum of the noise (low-level) threshold (e.g. 0.1) plus the maximum value of copy number variation for the sample over all the arms. Similarly, the lowest threshold is the minimum value for the sample over all the arms plus the negative noise (low-level) threshold (e.g. -0.1).


What are the internal surfaces of body cavities actually made of?

The peritoneum, the pleura, the pericardium, the tunica vaginalis testis and the tunica serosa uteri are made of mesothelium (simple squamous epithelium) [1].

The GI tube is made of a specialized tissue composed from four layers: mucosa, submucosa, muscularis externa and adventitia. The innermost layer (mucosa) has an epithelium that is stratified, squamous and non-keratinising, for protective purposes. The internal organs in the peritoneal cavity are covered with the visceral sheet of peritoneum which is the adventita layer [2].

Trachea is made of respiratory epithelium, which serves to moisten and protect the airways. It is lined with pseudostratified columnar epithelium with goblet cells that produce mucus [3].

Trachea, stomach and intestines are considered cavitary organs as opposed to parenchymatous organs (lung, kidney, liver).

References:

Wikipedia contributors, "Mesothelium," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Mesothelium&oldid=598055771 (accessed June 26, 2014).
Wikipedia contributors, "Gastrointestinal wall," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Gastrointestinal_wall&oldid=598338180 (accessed June 26, 2014).
Wikipedia contributors, "Trachea," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Trachea&oldid=613017631 (accessed June 26, 2014).


no none of the fungi in the nature is  autotrophic.
they are dependent mostly upon dead and decayed matter.
the reason that they are not autotrophic is that they lack any type of photopigment to carry out photosynthesis.
photopigments are necessary because the are the only components that can trap the solar energy and use it to extract the electrons from the inorganic source such as h2s or h2o by splitting them which are further used to prepare ATP and NADPHH+. these 2 are the assimilatory powers for the further dark reaction. so if these are not there then the processes of photosynthesis would not be there and therefore the organism will not be able to produce its own food in turn it would depend on other autotorphs for food (in case of fungi dead and decade matter).


What part of the brain controls depth perception?

According to the article: Scientists uncover second depth-perception method in the brain:

  the neurons in the middle temporal area of the brain are combining visual information and physical movement to extract depth information

This Scientific American article states that there is a process involved:

  Visual-image processing from the eye to the brain happens in stages. Rudimentary features such as the orientation of edges, direction of motion, color, and so on are extracted early on in areas called V1 and V2 before reaching the next stages in the visual-processing hierarchy for a progressively more refined analysis. This stage-by-stage description is a caricature; many pathways go “back” from stage to stage—allowing the brain to play a kind of 20-questions game to arrive at a solution after successive iterations.

This process is discussed further in this article with what is known as the Laminart model.


You read right: it can only come from people already infected through:

sexual contact
contact with an infected person's body fluids (blood transfusions), although not all fluids carry HIV (saliva, tears)
from mother to child (pregnancy, breast feeding)

Having unprotected sex with multiple partners statistically increases the risk of stumbling upon someone infected.

A person carrying the HIV virus may not show symptoms of AIDS, because the HIV infection passes through a stage of clinical and symptomatic latency (the asymptomatic HIV or chronic HIV) which can last up 20 years (average of 8 years) when only uncommon symptoms like fever and weight loss show up.

Where it started? It is believed that HIV originated in non-human primates in West-central Africa and were transferred to humans in the early 20th century. The virus adapted and became strong, because the virus from primates is typically suppressed by the human immune system within weeks of infection.

HIV is a retrovirus that primarily infects components of the human immune system such as CD4+ T cells, macrophages and dendritic cells. It directly and indirectly destroys CD4+ T cells.

So it destroys the cells reponsible of its removal from the human body. Hard to believe that there are people whose immune can really destroy the virus. A virus lives inside the cell it parasite, so the immune cells must destroy one the other. Also the virus infects and kills them (the good ones). However, as MattDMo suggested an infected person may take antiretroviral drugs and the disease progression can be slowed down.

Source: Wikipedia - HIV, AIDS


After continuing to search I have located the name of this plant. It is Ipomoea alba or 'Tropical white morning glory'.
On locating the area of the Biome on a map where I had found it, I could conclude it grew in tropical and sub-tropical areas of South America and north of there. This narrowed down the search somewhat.
Thanks again to all involved for helping to identify!


denovo 2Gb whole genome sequencing on a small sequencer

Yet clearly the sequencers are never marketed like this and I'm
  struggling to understand why.

You don't see why two years of instrument reagent costs for a single project might be considered prohibitive?


Are probabilities of mutations symmetric?

The short answer is no, there is heterogeneity in the rate at which different nucleotides mutate into one another. This is generally a property of their differing chemistries (although I'm not an expert on this). Therefore, it doesn't really make sense to talk of alleles being $p$ or  $q$ like we do in most of population genetics, because the actual nucleotide (whether it's A, C, G or T does make a difference).
This is important in fields like phylogenetics, where people construct substitution matrices which describes the rate at which one base in a sequence changes to another nucleotide. Currently, it's possible to estimate the matrix parameters from empirically data relatively easily.
For example, in one of the earliest and most simple models, Kimura (1980) introduced a matrix which had two parameters - one for the mutation rate of transition substitutions (A/C -> G/T, more likely) and one for the rate of transversions (A/G -> T/C, less likely). Later methods got progressively more complex, which account for e.g. the different amino/keto properties of different nucleotides. Felsenstein's model (1981) accounted for the equilibrium frequency of the target nucleotide. These substitution values are also allowed to vary across time as well within a phylogenetic tree (e.g. Yang 1994).

References

Kimura, Motoo. "A simple method for estimating evolutionary rates of base substitutions through comparative studies of nucleotide sequences." Journal of molecular evolution 16.2 (1980): 111-120.
Felsenstein, Joseph. "Evolutionary trees from DNA sequences: a maximum likelihood approach." Journal of molecular evolution 17.6 (1981): 368-376.
APA
Yang, Ziheng. "Maximum likelihood phylogenetic estimation from DNA sequences with variable rates over sites: approximate methods." Journal of Molecular evolution 39.3 (1994): 306-314.


What's the correct name for the war of sexes in evolution?

Sexual Conflict is the word you are looking for!

Sexual Conflict occurs whenever the optimal mating strategy for the female and the male differ. For example, in Drosophila, it is beneficial for a male to mate as much as possible, while it is beneficial for a female to mate only a few times.


Why do flies leave dirty spots on shiny/glossy surfaces?

House flies (Musca domestica) prefer to rest on light colored surfaces, and what is lighter than windows, windowframes, glossy surfaces that reflect light, etc.? Where they rest (not eat) is where they defecate (or regurgitate), leaving marks politely called "fly specks".

  House flies also leave dark fecal and regurgitation spots on wall surfaces where they rest, and with a preference for resting on light colored surfaces, these spots can be quite noticeable when fly numbers are high.

If you ever visit an "open" barn, you'll notice the phenomenon is quite remarkable. If the number of flies is high, there will be specks everywhere, but the windows and other shiny surfaces will be more densely covered.


It is a bee in the genus Megachile, in the family Megachilidae, not Halictidae.

Megachile are leafcutter bees, and have scopal (pollen carrying) hairs on their bellies (ventral side of their abdomen).

Most bees in the family Halictidae have scopae for carrying pollen on their legs, though they may have hairy bellies with substantial pollen carrying capacity.


Do Yersinia genus spp have anything movement factors?

Yersinia enterocolitica does express flagella at a temperature around 25°C, but not at 37°C. Kapatral et al.
Besides that it can rely on peristaltic movement in the intestines.

Yersinia pestis is as far as I know nonmotile in the host, but motile if isolated Medical Microbiology.

As there are some other Yersinia species, including Y. pseudotuberculosis of course, I think you cannot totally generalize the answer for Yersinia spp., but searching for the Yersinia of interest with "flagella", "motility", "movement" or similar keywords on Pubmed might help.


What temperature should mammalian B-Cells be stored at outside of the incubator?

For the settling there's little you can do except agitation and using a taller thinner tube and larger suspending volume.

For the clumping however if the analysis permits it, adding serum to a [final] of 5% will help slow the clumping (in the short term). You can also filter out initial clumps by pushing the cells through a nylon mesh filter (they make these especially for flow-commonly used with fixed cells). I've analyzed cells on ice in dark probably as long as 6 hours after harvesting with little change in viability, however this is of course bad practice.


Definition of taxon (From ICZN glossary):

  A taxonomic unit, whether named or not: i.e. a population, or group of
  populations of organisms which are usually inferred to be
  phylogenetically related and which have characters in common which
  differentiate (q.v.) the unit (e.g. a geographic population, a genus,
  a family, an order) from other such units. A taxon encompasses all
  included taxa of lower rank (q.v.) and individual organisms. The Code
  fully regulates the names of taxa only between and including the ranks
  of superfamily and subspecies.

Birds are called Aves and that is a taxon. Cats come under Felidae. If you are asking - "Is a colloquial/vernacular name considered a taxon". Perhaps the group of organisms can be referred to by a colloquial name when they are not given any scientific name but in this case these taxa are well defined by a standard scientific name (according to the nomenclature codes such as ICBN, ICZN, etc).

So "cat" is not a taxon, but cats fall under the taxon called "Felidae".

In some cases certain groups are not even actual clades. A clade is a monophyletic group i.e. all its members have a common ancestor. The group — reptiles, is not a clade.


Selective breeding fluorescent sheep - possible?

Natural horizontal gene transfer in higher animals is possible, but still very rare.
If any transfer happens then it's usually from micro-organsims (viruses/bacteria) or parasites to the host animal (or the reverse). Transfer of genes from any other source to animals is almost unheard of, because the transfer needs to affect the germline (sperm / eggs) to last more than a single generation and anything that doesn't live inside an animal is unlikely to get there.

Therefore your example of getting GFP (or any other fluorescent gene) into a sheep is highly unlikely$^1$, even with a 1000 year timespan.
You'd need a virus or bacteria that has a fluorescent gene and naturally infects/lives in/on sheep. However, no natural bacteria or viruses have a fluorescent gene in the first place (they almost all come from corals or jellyfish). Another problem is that just having a fluorescent gene somewhere in the DNA, doesn't mean the any part of the organism is fluorescent; once its in the gene pool this should be achievable by breeding though.

You'd have to wait for HGT of a fluorescent gene from a source animal/life form to bacteria. (Time estimate is super hard, you can maybe house some of these jellyfish in a fish tank regularly sequence the bacteria that live with them to see if HGT happened.)
Then the genes needs to be transfered to a bacterial/virus strain native to sheep (This is relatively easy/fast, since bacteria are quite proficient at HGT between each other)
Lastly you need a 3rd round of HGT from the bacteria to the germline of the sheep. (Again this might take 'forever': most mammals don't like bacteria or viruses living in or near their reproductive organs. Also at least from this point on animal experiment laws will become a serious hurdle to your project).

1) This is a researchers highly unlikely: without trying this, its not correct to say impossible, but the chances are so low that for all practical purposes it might as well be impossible.


In your quotes, the terms spiking and firing are used as synonyms. Indeed, both terms refer to the same phenomenon of action potential generation and in this context there is no physiological functional difference between spiking and firing.

However, note that in some contexts there may be a difference, namely some authors distinguish between a neuron spiking and bursting; the former referring to a tonic firing mode, the latter to a bursting firing mode (e.g. Ramcharan et al. (2000)).

Reference
- Ramcharan et al., Vis Neurosci (2000); 17(1):55-62


Interestingly this effect seems to be true - there is one paper which claims that fasting for three days leads to the depletion of unused (and especially damaged) immune cells to save energy. When food is back at normal rates, the body starts to renew these cells which have been depleted before. This process also seems to enhance the self-renewal process of stem cells which start to replicate and further differentiate.

This works like in the figure below (from the paper below):

Although this renews a part of the immune cells, I wouldn't say that this improves the immune system. I think that here mostly naive cells (which haven't) come in contact with an antigen are shut off. If you deplete memory cells (which had this contact) this would be counterproductive, since these cells are important for a fast immune response.

Prolonged Fasting Reduces IGF-1/PKA to Promote
Hematopoietic-Stem-Cell-Based Regeneration and Reverse
Immunosuppression

There is as well an article in Science Daily, which summarizes the original paper. It can be found here.


When you ligate two strands of DNA you build up a phosphodiester bond. To do so, you need energy, and this energy for the DNA ligase comes from the ATP (in bacteria this energy can also come from NAD+.
The enzyme metabolizes ATP to AMP + PPi and binds the AMP in its active center. Then the AMP is involved in the reaction itself and released afterwards. This page has a few illustrations on this process.
If you want to dive really deep into the topic, have a look at this review:

Eukaryotic DNA Ligases: Structural and Functional Insights


Will a Codon result in same amino acid across organisms

Although the answer to this question may be found in Mitochondrial Genetic code, because that answer is primarily about mitochondrial genetic codes, I shall give a more directed answer here.

Because the same genetic code that was elucidated in bacteria was found to apply to higher eukaryotes, it was initially assumed that the genetic code was universal, and was referred to as such. Subsequently it was discovered that mitochondria did not generally employ this ‘universal’ code, which is now usually referred to as the ‘standard’ code — indeed different mitochondrial codes were found in different organisms.

However the question seems to be more concerned with the genetic codes of  bacteria and the nuclear genetic codes of eukaryotes. Here also there are deviations from the standard genetic code, which can be found listed either on this Wikipedia page or at NCBI.

Below are some examples from the NCBI list (where references may be found) with the standard coding in parentheses:

 Mycoplasma
 UGA      Trp          (Ter)

 Ciliates, Dasycladacean and Hexamita
 UAA      Gln          (Ter)
 UAG      Gln          (Ter)

 Euplotidae
 UGA      Cys          (Ter)

 Candidate Division SR1, Gracilibacteria
 UGA      Gly          (Ter)

 Pachysolen tannophilus
 CUG      Ala          (Leu)

Finally, tRNAs for the ‘additional’ amino acids, selenocysteine and pyrrolysine recognize, respectively, the UGA and UAG stop codons in specific contexts.


What is difference between High quality and low quality proteins

"Low quality" vs. "high quality" protein does not refer to anything about the linkages between amino acids in proteins. Instead, these terms are used in a nutritional context to refer to whether an individual protein source is sufficient as a sole source of protein in someones' diet.

Essential amino acids are the amino acids that humans cannot synthesize; other amino acids can be synthesized from these, but they do not need to be part of the diet. Not all sources of protein have sufficient quantities of all of the essential amino acids. Low-quality protein sources are also referred to as "incomplete" and high-quality sources as "complete."

Meat products are typically "high quality" because they contain all of the essential amino acids together. Therefore, if you subsisted on various foods but only got your protein from one animal source, you would be okay.

Some plant products do not have all the essential amino acids in large concentrations. However, if you combine protein sources from different "low quality" plant sources that together cover these deficiencies, there is no disadvantage compared to a single "high quality" source.

In the digestive process, all you take out of the proteins you eat is the individual amino acids (generally): that means that only the amino acid composition matters, not the strength or quality of the bonds between amino acids. If someone tries to tell you otherwise, they are probably just trying to sell you something.

Here is a paper that talks about some of these issues, and addresses some of the myths about balancing proteins. The quick summary is that problems develop if you get your sole protein from a source that is low in a particular essential amino acids over a long time period, but there is no need to ensure every meal contain all the amino acids.

It is possible for people on unusual protein diets, either because they are avoiding animal products or using incomplete protein supplements, to develop a particular amino acid deficiency. Otherwise, as long as all amino acids are supplied, there is no difference on health or muscles to consuming "low quality" vs "high quality" proteins.

References:

Young, V. R., & Pellett, P. L. (1994). Plant proteins in relation to human protein and amino acid nutrition. The American journal of clinical nutrition, 59(5), 1203S-1212S.


How long human egg cell grow up until sperm fuse it?

Ovules are made while the female is still in the uterus of her mother. The ovules (in the form of ovarian follicles) are kept in the ovaries for a long time, and just a month before leaving the ovary (ovulation), the ovarian follicle (and the future ovule) gain in size. In other words, the ovules are slightly older than the age (counting from birth/labour) than the person carrying them. You'll find more information on wikipedia > ovule > ovule Development, oogenesis, and ovarian follicle.

Does it address your interest about alcohol consumption?

Now, I don't think this question/answer address your interest about alcohol consumption. Whether or not the ovule is create by a division that happen just a day before ovulation  or many years earlier doesn't change anything to the fact that this ovule has experienced alcohol consumption (either directly or in the lineage) before.

Where to ask the question that I suspect interest you the most

If you want to question the article you read about alcohol consumption, the best you could do is to go on Skeptics.SE, link the article, quote something from the article and ask "is it true?"


Molecular biology - fundamental questions

where does Protein come into play?

A Gene codes a protein.
DNA is transcibed into messenger RNA (mRNA). mRNA is translated into protein.

What do you call Genes that are spliced together to form something new?

Genes are not spliced together. One single gene can consist of introns (intervening sequences) and exons (expressed sequences). Transcribed introns in the RNA are spliced out and the exons glued together to form a functional mRNA.

What do you call a variable inside a Gene?

Genes are made up of DNA. DNA is made up of nucleotides.


Streptomycin or penicillin/streptomycin, and potentially amphotericin B. If you need a penicillin-free alternative, gentamycin is a good option.

I think streptomycin is a good candidate with a broad enough spectrum to target Gram positive, negative and yeasts. You can buy from Thermo Fisher a 1000X penicillin/streptomycin cocktail that you simply add at 1X to your medium, and the spectrum is broader. Due to penicillin allergy, you may need to find an alternative. Gibco markets gentamycin in 10mg/mL and 50mg/mL formats, but I think with gentamycin you definitely want to add amphotericin B. Use the same cocktail across all three types of control.

You can even go as far as to test your antibiotic cocktail in advance, in triplicate on your strains of interest, to ensure you have a valid positive control.

I find these compounds to be quite common and so there are other anti-fungals you could use, but I can't attest to their efficacy.


How important is dead wood to the ecology of a forest and how much dead wood should remain?

Dead wood is indeed very important to the food chain, and to the ecology and biodiversity of a forest. Lots of biota depend on the presence of dead wood; many species of insects and fungi only live on dead wood. See for example this study of fungi in Danish Beech forests.
The amount of dead wood present depends, apart from management, on the type of forest, the climate (and hence altitude!) and the age of the forest. This study provides a preliminary estimate of the amount of dead wood in British forests and might be very interesting to you. This study gives a review of dead wood in European (incl UK) Beech forest reserves.

I hope this will help you in the right direction. If you want any more information, please let us know. And preferably include some more information on the specific forest (type of trees, location) that you are interested in.

EDIT:
I recently stumbled across this project,
 that resulted in a systematic review of interventions that affected the occurrence of dead wood and saproxylic species in boreal and temperate forests.


In meiosis crossing over takes place which leads to variations
 in chromosomes while in mitosis no crossing over takes place


I almost got it right. The consensus as of 2018 appears to be that it's a Faustian pact between providing the CNS with our unique mental powers at the cost of poor damage repair. This is not an issue in the PNS where damaged neuron repair is, in the main, impressive.

Quote (1): Principles of Neural Science 5th Ed (2013) (Eric R Kandel et al)
“ ... the regenerative capacities in the peripheral nervous system are impressive.
In contrast, in the central nervous system regeneration after injury is poor.”
“Is it the ability of peripheral axons to regenerate that is unusual, or the inability of central axons to do so? It is in fact the latter.”
“Maintaining constancy in the face of small perturbations in connectivity may therefore have the unavoidable consequence of limiting the ability of central connections to regenerate in response to injury. In this view our limited regenerative capacity is the Faustian biological bargain we have made for the possession of many precisely wired circuits that underlie our superior intellectual powers.”

Quote (2): Transl Psychiatry (2017) 7, e1214; doi:10.1038/tp.2017.170 www.nature.com/tp
“Reticulon 4 receptor (RTN4R) [aka NgR and NgR1] plays an essential role in regulating axonal regeneration and plasticity in the central nervous system ...”

Quote (3): A.R. Walmsley, D. Bourikas And A.K. Mir, 15 - Myelin Neutralization For Spinal Cord Injury And Stroke, In CNS Regeneration (Second Edition 2008)
“ ... the environment of the CNS is highly inhibitory to axonal regeneration and plasticity. In recent years, great advances have been made in our understanding of the molecular components contributing to the inhibitory environment of the CNS. The majority of these have been identified as membrane proteins present in CNS myelin, such as myelin-associated glycoprotein, Nogo-A and oligodendrocyte-myelin glycoprotein, that inhibit neurite outgrowth by binding to the multimeric Nogo-66 receptor (NgR1) complex on the neuron ...”

Quote (4): https://en.wikipedia.org/wiki/Reticulon_4_receptor

Reticulon 4 receptor (RTN4R) also known as Nogo-66 Receptor (NgR) or Nogo receptor 1 is a protein which in humans is encoded by the RTN4R gene. This gene encodes the receptor for reticulon 4, oligodendrocyte myelin glycoprotein and myelin-associated glycoprotein. This receptor mediates axonal growth inhibition and may play a role in regulating axonal regeneration and plasticity in the adult central nervous system.


What is the difference between a DPY-10, DPY-11, and DPY-13?

Dpy is a class of genes. Usually they're written in lowercase when referring to a mutant allele. The name Dpy itself stands for dumpy and comes from the morphological change that occurs when one or more of the genes are mutated: the worms appear short and fat, or dumpy.

Another big class is Unc. Mutations in those genes cause uncoordinated movement.

For a description of the genes, see http://www.wormbase.org


What are the differences between a liposome and simple cell membrane

By looking on wikipedia I found:

About liposome

  A liposome is a spherical vesicle having at least one lipid bilayer. The liposome can be used as a vehicle for administration of nutrients and pharmaceutical drugs. Liposomes can be prepared by disrupting biological membranes (such as by sonication).

  Liposomes are most often composed of phospholipids, especially
  phosphatidylcholine, but may also include other lipids, such as egg
  phosphatidylethanolamine, so long as they are compatible with lipid
  bilayer structure. A liposome design may employ surface ligands for
  attaching to unhealthy tissue.

About cell membrane

  The cell membrane (also known as the plasma membrane or cytoplasmic
  membrane) is a biological membrane that separates the interior of all
  cells from the outside environment.The cell membrane is selectively
  permeable to ions and organic molecules and controls the movement of
  substances in and out of cells. The basic function of the cell
  membrane is to protect the cell from its surroundings.

  It consists of the lipid bilayer with embedded proteins. Cell
  membranes are involved in a variety of cellular processes such as cell
  adhesion, ion conductivity and cell signalling and serve as the
  attachment surface for several extracellular structures, including the
  cell wall, glycocalyx, and intracellular cytoskeleton. Cell membranes
  can be artificially reassembled.

So the major difference seems to be the presence of "embedded proteins" inside the cell membrane.


Looks to be either a chestnut-tailed starling (AKA grey-headed myna, Sturnia malabarica) or a Malabar starling (Sturnia blythii) in the Sturnidae (or starling) family.

S. blythii was previously considered a subspecies of S. malabarica.

 S. malabarica, Source: universebirds.com

 S. blythii on the left and S.malabarica on the right.

Description: Adults are approximately 20 cm long. They have grey heads/neck, blackish remiges, and reddish-brown (i.e., "rufous") belly and undertail. Their beaks are yellow with pale bluish bases.

The poor coloration in your photo seems to show the base of the beak being a paler grey color (vs. the yellow of the rest). I'm going to guess that this was really at least slightly bluish in hue and the color did not show up in your low-quality photo.

Range: As you can see in the map below, they are present throughout most of India:

 Source: Natural Earth and Myself

According to here, S. blythii is more constrained to just southwest India.

You can see videos of specimens here.

Further References:

Fina a list of most (all?) species of birds in India on Wikipedia.
Here is a good site with hundreds of photos of Indian bird species.


Can a strand not be synthesised in 5' -> 3' direction?

It sounds like your guess was right and the exception is the lagging strand. The statement is phrased poorly, but it seems like they were going for the lagging strand. Either they meant for you to think that
-the lagging strand is growing 3' to 5'
or, more likely,
-the polymerase is only synthesizing on one (leading) strand at a time
While technically the book was correct, it was a trick question and phrased unfairly.
You are completely right that DNA is synthesized from 5' to 3'. I don't know of any exceptions to this, but hesitate to say anything overly definitive because there are so many rare exceptions in science. I can say with some confidence that DNA polymerase cannot ever synthesize in the 3' -> 5' direction. If you haven't already, I highly recommend checking out the Khan Academy article, Molecular mechanism of DNA replication! Nature Education also has a pretty good article on the topic, Major Molecular Events of DNA Replication.


The manufacturers of each component should have information available on their website regarding storage temperatures, along with recommended protocols on how much of each component to add to the PCR reaction. I would not try to reuse the polymerase, as depending on the kind you buy it may be a complex of proteins, and it may not be functional after purification. However, you're welcome to experiment all you want, it's your stuff!


What's a mouth ulcer/canker sore "made of", and why do they develop?

The redden area around the grayish-white indentation of the canker sore isn't filled with anything. This circular area is simply inflamed. The grayish-white area in the center is not filled with puss or anything else as well. This is an area of dead cells but underneath this layer of dead cells the tissue red [1],[2],[3].

Canker sores, Aphthous stomatitis, is an ulcer. An ulcer is a break in the membrane. That is, you have an open sore in your mouth. As with any open wound, pain and discomfort will occur but the mouth is how we consume our food. Since we intake our daily bread in this manner, what we consume can cause the pain to increase; for instance,

acidic foods
spicy foods
abrasive foods

The cause of canker sores is not entirely known, but according to the Mayo clinic [2], possible triggers are

A minor injury to your mouth from dental work, overzealous brushing, sports mishaps or an accidental cheek bite
Toothpastes and mouth rinses containing sodium lauryl sulfate
Food sensitivities, particularly to chocolate, coffee, strawberries, eggs, nuts, cheese, and spicy or acidic foods
A diet lacking in vitamin B-12, zinc, folate (folic acid) or iron
An allergic response to certain bacteria in your mouth
Helicobacter pylori, the same bacteria that cause peptic ulcers
Hormonal shifts during menstruation
Emotional stress

Canker sores may also be caused by the following diseases as well [2]

Celiac disease, a serious intestinal disorder caused by a sensitivity to gluten, a protein found in most grains
Inflammatory bowel diseases, such as Crohn's disease and ulcerative colitis
Behcet's disease, a rare disorder that causes inflammation throughout the body, including the mouth
A faulty immune system that attacks healthy cells in your mouth instead of pathogens, such as viruses and bacteria
HIV/AIDS, which suppresses the immune system


Basic reasons as to why cats shed fur can be found in this link and this link.
An elaborate understanding of shedding in animals including cats can be obtained from this link. Hope that helps.


What is the relationship between protein-protein interaction networks and metabolic networks?

In short, proteins in Protein-protein interaction networks perform a function by directly interacting with one another.  They may for instance bind to one another forming permanent or momentary complexes (e.g. insulin binding to insulin receptor or the pieces of F0-F1 ATPase combining), or they may chemically modify one another (e.g. protein kinases adding a phosphate to the residue of another protein).

Proteins in a Metabolic network might never be in physical contact one another. They effect one another by producing chemical compounds which are utilized by other enzymes, forming a network of chemical transformations.

Of course an enzyme in a metabolic network might also have its activity modulated through interacting with other proteins in a protein-protein network.  The two terms are of course not mutually exclusive, but describe different sorts of relationships between proteins.


You want to isolate the cfDNA, and leave anything else in the plasma out of your analysis — essentially, the lysis step is part of the purification.
(See here)
(I'll elaborate with edits shortly)
Edit:
Actually, it looks like lysis is not a good idea in cfDNA isolation — lysing cells in your sample will result in contamination by genomic DNA, as discussed here. It would be better to stabilize/fix cells to prevent them from lysing, to avoid this risk.
In other words, your initial instincts were correct!


This is mostly a guess and loose suggestion, since the picture is not very clear (would need to see the larvae in more detail). However, Bagworm moths (Psychidae), Case moths (Coleophoridae) and Caddisfly larvae (Trichoptera, almost exclusively aquatic) all build similar cases. They construct their cases out if silk and often include debris, pebbles and other materials. I wouldn't be surprised if the larvae in your picture belongs to one of the first two taxa. Bagworm moths and Caddisflies generally include lots of external materials in their larval cases, which could point to Case moths for your specimen (which seems to have a weaker case mostly made of silk).

Here are two pictures of first a UK Case moth larvae (Coleophora deauratella) followed by a Bagworm moth (Dahlica triquetrella), just as comparisons. If you do google image searches of "group name + larvae" you will see many examples of what they can look like.

And just as a cool example - the larvae often use random material lying around to build their cases, which can give the following result, if caddisfly larvae are bred in a tank containing pieces if gold and pearls. For further information see this link.


Are cells really the basic unit of all life?

According to Gerry Joyce: "Life is a self-sustained chemical system capable of undergoing Darwinian evolution."

From a meta-analysis of 123 definitions of life: "Life is metabolizing material informational system with ability of self-reproduction with changes (evolution), which requires energy and suitable environment."

According to Alexander Oparin: “Any system capable of replication and mutation is alive”.

At hand are some key elements in order to match these criteria. Maintaining a Darwinian cycle requires replication, mutation, and selection. Thus, we can break down the above into 5 criteria (personal communication with Gerry Joyce).

Life stores information
Life reproduces its information
Life alters that information
Life does something with that information (uses energy)
Life does all of this in a self-sustained manner

I would point out that the above criteria is quite different from what is currently on wikipedia described by metabolism and homeostasis. There are certainly additional criteria that certainly raise the threshold for what may be considered life. The common discussion revolves around viruses which do many of these things but not in a self-sustained way.

The question at hand then asks if cells are the minimum unit of life? What makes a cell a cell is that there is compartmentalization. The underlying reason behind this compartment is due to the necessity of tying the phenotype to the genotype. Paraphrasing using our definition of life, it links the information with the function that the information carries out. In the modern biological scheme, it keeps the proteins (phenotype) with the DNA (genotype).

The necessity of compartmentalization is negated when the phenotype is already linked with the genotype. The most frequent example is RNA where the material that carries the information is also the material that carries out its function. It tend, is reasonable to hypothesize that life can be made entirely with RNA without the need for compartmentalization (although compartmentalization certainly helps see Paegal and Joyce and Chen and Szostak).

Recent experiments by Gerry Joyce and others have been able to satisfy several of the requirements of life. The have self-replicating RNAs, that store information, that reproduce their information, that introduce alterations to their information, and do it in a self-sustained manner. What Gerry and his colleagues agree on is that their current self-replication Ribozyme system doesn't do anything particularly novel. However, by introducing a larger variety of functional elements to their ribozymes perhaps they will.


Comparison of humans and other primates in milk production amount

The comparison to non-human primates and the behavioral question kind of threw me, but I think this is an X-Y problem. If you're asking:

  Are humans capable of producing more milk than they need to feed their own offspring

The answer is yes

There is some data I don't think we'd be able to get anymore, but in Chapter 5 of Nutrition During Lactation, they break it down.

  Several studies indicate that potential milk production in humans is considerably higher than the average intake by single infants. Kaucher and colleagues (1945) measured maximum milk output with intrusive and tedious mechanical methods to extract all the mother's milk and reported that production averaged almost 1,200 g/day at 6 to 10 days post partum. This level is much higher than the 500 to 700 g/day consumed by breastfed infants at the same age (Casey et al., 1986; Saint et al., 1984).

Kaucher's methods may not have been particularly good, because others showed limits more than twice that

  Women who express surplus milk for a milk bank have been shown to produce as much as 3,000 g/day (Macy et al., 1930).

As my wife and many lactating mothers who use a breast pump will be able to confirm, this isn't a relic of the 30s and 40s. If you keep pumping, you keep getting milk.

  In two separate studies, milk production increased by 15 to 40% when a breast pump was used to remove additional milk after feedings (Dewey and Lönnerdal, 1986; Neville and Oliva-Rasbach, 1987).


There is a yearly contest on cell tracking organized by the IEEE International Symposium on Biomedical Imaging, and the associated data sets are freely available.

See for example: http://www.celltrackingchallenge.net/