What creates the feeling of 'excess' blood pressure to an area of the body?

Arterial Baroreceptors felling the pressure.

Arterial blood pressure is normally regulated within a narrow range, with a mean arterial pressure typically ranging from 85 to 100 mmHg in adults. It is important to tightly control this pressure to ensure adequate blood flow to organs throughout the body. This is accomplished by negative feedback systems incorporating pressure sensors (i.e., baroreceptors) that sense the arterial pressure. The most important arterial baroreceptors are located in the carotid sinus (at the bifurcation of external and internal carotids) and in the aortic arch (Figure 1). These receptors respond to stretching of the arterial wall so that if arterial pressure suddenly rises, the walls of these vessels passively expand, which increases the firing frequency of receptor action potentials. If arterial blood pressure suddenly falls, decreased stretch of the arterial walls leads to a decrease in receptor firing.

The carotid sinus baroreceptors are innervated by the sinus nerve of Hering, which is a branch of the glossopharyngeal nerve (IX cranial nerve). The glossopharyngeal nerve synapses in the nucleus tractus solitarius (NTS) located in the medulla of the brainstem. The aortic arch baroreceptors are innervated by the aortic nerve, which then combines with the vagus nerve (X cranial nerve) traveling to the NTS. The NTS modulates the activity of sympathetic and parasympathetic (vagal) neurons in the medulla, which in turn regulate the autonomic control of the heart and blood vessels.

Of these two sites for arterial baroreceptors, the carotid sinus is quantitatively the most important for regulating arterial pressure. The carotid sinus receptors respond to pressures ranging from 60-180 mmHg (Figure 2). Receptors within the aortic arch have a higher threshold pressure and are less sensitive than the carotid sinus receptors. Maximal carotid sinus sensitivity occurs near the normal mean arterial pressure; therefore, very small changes in arterial pressure around this "set point" dramatically alters receptor firing so that autonomic control can be reset in such a way that the arterial pressure remains very near to the set point. This set point changes during exercise, hypertension, and heart failure. The changing set point (response curve shifts to right) explains how arterial pressure can remain elevated during chronic hypertension.

Baroreceptors are sensitive to the rate of pressure change as well as to the steady or mean pressure. Therefore, at a given mean arterial pressure, decreasing the pulse pressure (systolic minus diastolic pressure) decreases the baroreceptor firing rate. This is important during conditions such as hemorrhagic shock in which pulse pressure as well as mean pressure decreases. The combination of reduced mean pressure and reduced pulse pressure amplifies the baroreceptor response.

Although the baroreceptors can respond to either an increase or decrease in systemic arterial pressure, their most important role is responding to sudden reductions in arterial pressure (Figure 3). This can occur, for example, when a person suddenly stands up or following blood loss (hemorrhage). A decrease in arterial pressure (mean, pulse or both) results in decreased baroreceptor firing. Autonomic neurons within the medulla respond by increasing sympathetic outflow and decreasing parasympathetic (vagal) outflow. Under normal physiological conditions, baroreceptor firing exerts a tonic inhibitory influence on sympathetic outflow from the medulla. Therefore, acute hypotension results in a disinhibition of sympathetic activity within the medulla, so that sympathetic activity originating within the rostral ventrolateral medulla increases. These autonomic changes cause vasoconstriction (increased systemic vascular resistance, SVR), tachycardia and positive inotropy. The latter two changes increase cardiac output. Increases in cardiac output and SVR lead to a partial restoration of arterial pressure.

It is important to note that baroreceptors adapt to sustained changes in arterial pressure. For example, if arterial pressure suddenly falls when a person stands, the baroreceptor firing rate will decrease; however, after a period of time, the firing returns to near normal levels as the receptors adapt to the lower pressure. Therefore, the long-term regulation of arterial pressure requires activation of other mechanisms (primarily hormonal and renal) to maintain normal blood pressure.

This information from PhD Richard E. Klabunde lecture, that based on his book Cardiovascular Physiology Concepts (chapter 5, pages 93-123)


It is a common question

Statements of the kind "Evolution is impossible because of intermediate state" are common from religious extremists literature. There is therefore a lot of resource online that already debunk this type of statement but I guess, I'll just quickly write one more! Of course, I am not suggesting that you are taking an opinion-based position, you might well be genuily seeking for an understanding of the world.

Quickly speaking there are a series of concepts that are necessary to understand in order to answer this question.

Fitness landscape and fitness valley

The term "evolutionary midways" is not used in biology but one can rephrase it with the concept of fitness landscape and fitness valley.

Fitness landscape

The fitness landscape is the function that maps fitness (generally represented in y-axis) to phenotypic trait value (typically multi-dimensional but often represented on a single axis for simplicity). Fitness landscape may also refer to the mapping from genotype to fitness but we will not be concerned with that for this answer.

Fitness valley

A fitness valley refers to a region of low fitness on the fitness landscape. The movement from one locally high fitness state to another locally high fitness peak might well get through a region of low fitness. This is what you call fitness valley and on the fitness landscape and this is what you are interested in.

Is there always a fitness valley?

Let's first consider reasons for which a population might not experience such fitness valley

Logical Fallacy: Argument to ignorance

It is common for a layman to assume that intermediate states ought to be associated with low fitness. In reality the intermediate states might well be neutral or only slightly deleterious (and therefore be mainly affect by genetic drift) or might even be directly beneficial. It appears to be a mistake to assume such fitness valley are more common than they are in reality just because you fail to imagine how a trait may have evolved. In philosophy of logic, this is called an argument to ignorance. Of course, fitness valleys do exist. So, when they exist, do populations ever manage to get over them?

Assuming there is a fitness valley (for a given trait), can populations just "jump over it"?

Do populations need to get through an intermediate state?

Darwin framed his theory into the idea that evolution is a very gradual process. As we know today, this is far from being true. Evolution can actually occur through a big steps. There are single mutations that double the amount of genetic material, there are single mutations that completely affect the physiology or anatomy of an individual. There are cases of horizontal gene transfer (transfer of genetic material between species) as well that can cause sudden important change without having to get through intermediate stages. It is sometimes wrong to assume that there must be intermediate steps.

If there is a fitness valley and the population will not "jump over it"...

Let's assume a fitness valley (for a given trait, for a given population) and let's assume that the population will not "jump over it" thanks to a mutation of big effect.

Shifting Balance Theory

There are a number of different forces that affect evolutionary processes. Layman often think of natural selection as being the only force causing evolution but this is wrong. Genetic drift is another very important process that affect evolutionary process. Genetic drift refers to the random sampling of individual at one generation to build up the successive generation. The relative importance of drift to natural selection in driving evolution of a population depends on the effective population size. Have a look at Why is the strength of genetic drift inversely proportional to the population size?. Genetic drift can typically randomly yield a population toward a fitness valley, from which natural selection will yield the population to either come back or start climbing the opposite fitness peak. This concept is called shifting balance theory. There has been a lot of work on shifting balance theory suggesting that it well be much more common than previously thought.

Phenotypic flexibility

One may wrongly assumed that if a mutation occurs to make, say, a bone a big longer, then one organism would simultaneously need mutations that would make muscles, nerves and other tissues longer accordingly. In reality our developmental process is very flexible to an environmental change or to a mutational change. This flexibility is very much used in medicine and agriculture. If a bone gets a bit longer, muscle might just stretch a little more and end up developing in accordance to the new mutation. It would therefore be wrong to assume that because we are made of a complex interaction of traits, that a mutation cannot bring anything that would not be beneficial. If you are interested in the evolution of complex system you might want to have a look at the post How did the cardiovascular system evolve? for example.

Source of information

I would recommend that you have a look at a very short and introductory course to evolutionary biology such as Understanding Evolution by UC Berkeley for example and you will be able to understand much more about what evolution is and how it occurs.


"selective pressure" or "selection pressure"?

As far as online references are concerned, they should be equivalent (as "selective" becomes "making a selection"). The important difference in my understanding is that speaking in terms of biology, "selection" triggers associations with evolutionary terminology, whereas "selective" doesn't. Thus, as far as I am concerned, "selective pressure" could be referring to some machine that has a method of applying pressure to one thing but not another, whereas "selection pressure" immediately makes me think of factors benefitting the proliferation of one thing over another. Hence I would personally prefer "selection pressure".

Given the ambiguity, you probably won't be able to make all readers happy with either of the two. Thus, it might be best just to use a different phrasing as suggested e.g. by rg255 ("subject to selection").


What is the etymology of "moura" in Mourasuchus?

The original description of the species was given in 1964 by Llewellyn Ivor Price in:

  Price, L. I. (1964). "Sôbre o crânio de um grande crocodilídeo extinto do alto Rio Juruá, Estado do Acre". An. Acad. Brasileira Ciên. 36 (1): 59–66.

As such, it seems plausible that the name means 'crocodile of Moura', Moura referring to Rio do Moura, a river in the Brazilian state of Acre where the animal's fossils were discovered.


Pedigree Probability, Autosomal Recessive Trait

Here is my attempt!

Generation III

III3 is rR
II3 is rR and therefore III4 is rR with probability $\frac{1}{2}$ and RR with probability $\frac{1}{2}$.
Just like III4, III7 and III8 are rR with probability $\frac{1}{2}$.

Generation IV

Let's start with IV1.

IV1 is rR if ...

III3 transmits the r allele (probability $\frac{1}{2}$)
III4 is rR (probability $\frac{1}{2}$) and transmits the r allele (probability $\frac{1}{2}$). The total probability is $\frac{1}{4}$.

However, we have to remove the probability that both parent transmit the r allele as we know IV1 is not rr. This probability is $\frac{1}{2} \frac{1}{4} = \frac{1}{8}$. So, in total, the probability of IV1 to be rR is $\frac{1}{2} + \frac{1}{4} - \frac{1}{8} = \frac{5}{8}$.

Now, IV2

IV2 is rR if ...

III7 is rR (probability $\frac{1}{2}$) and transmits the r allele (probability $\frac{1}{2}$) or if III8 is rR (probability $\frac{1}{2}$) and transmits the r allele (probability $\frac{1}{2}$).

However, we have to remove the probability that IV2 is rr as we know this is not the case. The total probability is therefore $\frac{1}{4} \frac{1}{4} - \frac{1}{16} = \frac{7}{16}$.

Generation V

Finally, we get to your question

  [W]hat is the probability the offspring of IV1 x IV2 will show the recessive trait?

Both parents need to be rR which happen at probability $\frac{5}{8} \frac{7}{16} = \frac{35}{128}$ and both need to transmit the $r$ allele which happen with probability $\frac{1}{4}$. Hence the probability is $\frac{35}{512}$.


Is Parthenogenesis known as Sexual reproduction or Asexual reproduction?

Only a matter of definition

It is only a matter of definition. When it comes to sex, there is such a diversity of mating system that it is very hard to make a good definition that won't be challenged by limit cases.

Sexual reproduction can typically be defined based on the presence of meiosis (but again this will lead to limit-cases), on the need for two distinct parents + meiosis, or on the need for two distinct parents which have different gender (anisogamy) + meiosis.

Diversity of reproductive systems

At the end of the day, what one wish to call sexual reproduction does not matter too much as long as the definition is being made clear especially when dealing with potentially limit-cases.

If I remember correctly the intro book to evolutionary biolgy called Evolution by Futuyma makes a good overview of the diversity of reproductive system. Having a vague understanding of this diversity will help you undermine your hope of finding a clearly defined definition for sexual reproduction.

Applying the definition of wikipedia to parthenogenesis

Here is the definition from wikipedia

  Sexual reproduction is a form of reproduction where two morphologically distinct types of specialized reproductive cells called gametes fuse together, involving a female's large ovum (or egg) and a male's smaller sperm

Using this definition and applying it to the specific case of parthenogenesis, one would conclude that parthenogenesis is not a form of sexual reproduction (despite the presence of meiosis). Note by the way the even within the term parthenogenesis, there is quite a bit of diversity (see the wikipedia entry for parthenogenesis).

  what is the evolutionary explanation for this phenomenon(parthenogenesis)?

I will ignore this question because

A post should always be limited to a single question
This question is very broad
There is not a single answer to this question given the diversity of types of parthenogenesis.

For a start on the subject, you might want to have a look at Jaenike and Selander, 1979 for example.


Ok, Josh has PCD. That gives three possible genotypes for parents:- ( let the alleles be P and p)

1) Pp x Pp
2) Pp x pp
3) pp x pp

In (1), the probability for next child to be pp is 25% and to have the disease is 12.5%.

In (2) and (3), the probability of any parent to be pp is rare as the p allele is quite rare (discussions with swbarnes2 in comments). So the real probability will be only slightly higher than that of case 1 i.e. 12.5%


Is a set of chromosomes made up of many copies of DNA, or is one complete string of DNA broken up into one set of chromosomes?

A chromosome is one long molecule of double-stranded DNA.  As a diploid organism, you (almost certainly) have two copies of each autosomal chromosome; one from your father, one from your mother.  You (almost certainly) inherited one copy of the X chromosome from your mother, and you either have a second one from your father, or you inherited a smaller Y chromosome instead.


Transposition may occur at any given time in life, and in any cell. There are several cases known where transposition interests somatic cells (give a look here for reference). However, the frequency of transposition events is low, and the difference in amount of DNA between different cells in an individual is low. When you reason at the level of different individuals, however, the proportion of genome affected by transposable elements may be relatively high (give a look here for a reference)


why do overweight individuals sweat more than ordinary people?

Well there are some overall, simplified answers, but every individual is ..well.. individual.

First there is the ratio of volume to area. As interaction between two mediums normally is depended on their common/shared surface. If we state, that an overweight person A has more volume than a skinny person B of same height, A also has a larger surface as B, but not in the same scale the volume is increased.

The easiest way to describe is with spheres, let's assume bellies are kind of spherical ;-) . A sphere with diameter 2r=1d (hint: one dimension) has a surface of π4r²=πd² (hint: 2dimensions; 2nd power 2²=4; d²=(2r)²=4r²) and a volume of $$\pi\frac{4}{3}r^3=\pi\frac{8}{6}r^3=\pi\frac{1}{6}d^3$$ (hint: 3dimensions; 3rd power 2³=8).
So, if we manipulate r it's manipulated to the 2nd power for surface and to the 3rd power for volume.
So, if we double the radius, we have 4 times the surface, but 8 times the volume.

Humans are biochemical machines, we take an energyform we can exploit to fuel our processes keeping us alive. These processes also produce heat, which is kind of a nice sideeffect allowing us to operate in cold climate. But in hot climate we need to get rid of the heat.

As I stated before, interaction is surface based. Person A has a lot more heat producing volume than B, but the surface isn't that much bigger, so A's surface has a higher urgency to interact with the medium around than B's surface (so more sweat for example). Also more tissue produces more heat. But again disclaimer: different tissues have different activities.

Furthermore fatty tissue has an insulating effect, which reduce interaction even more. Other way round the heatloss of an overweight person isn't as dramatic as for a skinny person in sudden cold.

But these are simplified answers, there's much more to it. Like bloodpressure, thyroid, biological activity. Which can be influenced by so many more things.


Not well, they need  dextrose. Use YBT:

20 g Casein Peptone Tpe-M
10 g Yeast Extract
20 g Dextrose
17 g Agar

q.s. to 975 mls in di-water.

pH to 6.2 w 5M NaOH

q.s. to 1L with di-water.

Autoclave for 45 min at 121C

Aseptically dispense in Petri dishes.

Store at 4C for up to 12 weeks.

If you want to grow Co-culture do so in LB supplemented with 20g/L Dex.


How are the physiological properties of mitochondria measured?

A simple method would me to express a fluorescent protein in the cell that specifically localizes to mitochondria. mito-dsRed is a Red Fluorescent Protein which has that property; it can be expressed from a plasmid.

Using fluorescent microscopy and image analysis, you would be able to measure the geometric properties of the mitochondria. This can be done at a single cell level too (using confocal microscope) and non-destructively. Volume can be measured by what is known as Z-stacking— an automated technique by which the microscope takes several 2D snaps at different planes and stacks them to construct a 3D image.

You can implement this in live cells too; this method is called live cell imaging.


Average Nucleus size of human skeletal muscle cell

The average "length" for normal human myonuclei is 11.75 µm according to the abstract for:

Watkins, S. C., & Culien, M. J. (1988). A quantitative study of myonuclear and satellite cell nuclear size in Duchenne's muscular dystrophy, polymyositis and normal human skeletal muscle. The Anatomical Record, 222(1), 6-11.

If you can get access to this paper it should have more information for you.


What are the theoretical and actual (measured) minimum water potentials in plants?

Sodium Chloride (which I am here assuming to be the major salt in your solution) has a solubility of 6 Moles/L this corresponds to 12000 mOsmol, so the 2000 mOsmol you are measuring is not entirely implausible. However normally plant cells should have an osmolarity on the order of 300-400 mOsmol. In order to judge if your value was calculated correctly, it would be necessary for you to tell us exactly how you calculated and how you measured.
I am not aware of such literature but I am not a plant physiologist myself.


What does breathing through the mouth have to do with cracked lips?

You may notice waking up with chapped lips at times. It may be because of sleeping with your mouth open. So, of course you breathe through your mouth all night, leaving it exposed to continuous flow of your breath. Continuous airflow around the mouth region can cause chapped lips in many individuals.


(Reference request) Formal abstract theory of evolution?

Difficulties in your question

It is a little hard to know exactly what you're after because 1) the question is broad 2) some concepts you talk about are a bit unclear.

For example, by 'random change' I suppose you mean genetic drift but I am not sure. The term 'random mutation' is a little undefined (see this post). You list 'Random change, heritability, natural selection' as a list of assumptions (at least I think you mean those are assumptions) but those are typically not common assumptions of evolutionary models. Also, the list is not in any way intuitive, so it is unclear what you mean by it. The phrasing "selection criteria that are influenced by the mutations" is also very unclear. Of course, selection, by definition, is dependent upon the genetic variance.

From our discussion in the comments, I think you are attempting to group different fields under a single concept just because they have the same name. But it is not because they have the same name that they are governed by the same basic principles. For example, it is not because the concept of plasticity exists in both biology and physics that these concepts are in any way related and that there is a general theory of plasticity that encompass both fields.

Evolutionary genetics

That being said, you could gain from any good intro textbook to evolutionary genetics. I especially recommend Population genetics, a concise guide. You will find more such recommendation in the post Books on population or evolutionary genetics?.

Evolution of ideas, cultures, computer viruses, evolutionary algorithms

In your last question you mention 'evolution of ideas, cultures, computer viruses, evolutionary algorithms'. I think you are referring to these concepts so as to clarify that you are not so much interested in the biology of specific organisms but really into the process of evolution. I do not recommend starting reading about these concepts before having a background in evolutionary genetics. You might otherwise make the mistake to over stretch an analogy.

Note also that the field of memetics (evolution of ideas, cultures) is a young field in which very little empirical testing is possible. So, I don't think it is wise to start there if your goal is to increase your understanding of evolutionary biology.

In any case, I am not able to suggest a good book in any of these fields (Evolution of ideas, cultures, computer viruses, evolutionary algorithms).


The good news is: You don't need any agar in your plating media, since the bacteria grow on the surface anyway and the plate can take up some additional moisture from your plating media.

What I usually do is to dry the plates for a while (and also let them warm up, since they are stored in the fridge) with the plate upside down and opened a bit. Contamination is usually not a problem here.

Then I dilute the cells in an appropriate volume of media, then plate about 50 to 100µl on the agar and spread it with a Drygalski spatula. Put the plate in the incubator and everything is fine.


What is the effect of garlic on intestinal flora?

From studies,

  lactic acid bacteria were found to be more resistant to GP (garlic
  powder) compared to the clostridial members of the gut microbiota.
  While for most bacteria the antimicrobial effect was transient, the
  lactobacilli showed a degree of resistance to garlic, indicating that
  its consumption may favour the growth of these beneficial bacterial
  species in the gut. Once the strains of other bacteria (eg:
  Bacteroides ovatus, Bifidobacterium longum DSMZ 20090 and Clostridium
  nexile A2-232) became resistant, they retained their resistant
  phenotype upon sub-culturing. Garlic intake has the potential to
  temporarily modulate the gut microbiota (reference).

Overall garlic can prove to be beneficial, because it seems to have more of an effect on detrimental bacteria like Helicobacter pylori (H. pylori), even when its strains were resistant to antibiotics. Overall garlic was found to be more detrimental to pathological bacteria when compared to normal gut flora (reference). Garlic’s diallyl disulfide has also been found to effectively cause cell death in Candida albicans which is a fungus in our gut which if not kept in check can cause health problems (reference).

Inulin and fructooligosaccharides present in garlic can also serve as nutrients for the probiotics colonizing your body (reference).


Expanding my comment into an answer as no one else has jumped in-

This fish closely resembles a sculpin of some kind. This is a very large and diverse family, but many of them share distinctive features. The quite wide head and horns that you describe and show are common in this family. Where I am from (Northwest USA), the Red Irish Lord / cabezon is a gamefish sculpin that can grow to be quite large, and closely resembles this picture of yours (a rather small specimen shown in Figure 1).

Figure 1.

Based on where you are in Vero Beach (Florida?), I have looked a little bit and there is a chance that it is a Gulf Toadfish (Figure 2) based on its appearance and where you caught it. Here is another fisherman's account (with pictures) of a similar fish.

Figure 2.

Hope that helps.


Linkage disequilibrium with multiple alleles and loci

LD describes the associations among alleles at different loci. For anything more than two bi-allelic loci, you need more than just one number to fully describe the associations. For instance, if we have three bi-allelic loci 1-3, we need the three pairwise LD coefficients, plus one extra three-way coefficient. In general, if we have $K$ loci, and the $k^\text{th}$ locus has $n_k$ alleles, there are $\prod_k n_k$ possible haplotypes, so to fully describe the state of the population we need $\prod_k n_k-1$ haplotype frequencies. If we instead want to use allele frequencies and associations, we'll therefore need $$\prod_k n_k-1-\sum_k(n_k-1)=\prod_k n_k-\sum_k n_k+k-1$$ LD coefficients. (Note that each locus is described by $n_k-1$ allele frequencies.) This means that things get complicated pretty quickly with many loci! If you want to dive into the details, check out Barton and Turelli (1991) and Kirkpatrick, Johnson, and Barton (2002).


Looking for university/graduate-level texts on RNA

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

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

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

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

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

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

This is another comprehensive review on ribozymes:

        Ribozyme Structures and Mechanisms

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


When does BLAST fail to align 2 DNA sequences?

BLAST works by finding a perfect match between sequences of a length equal to this "word length" and then enlarging it in a standard way -- yet there will be no alignment without this perfectly matched word.

So in your case, you must look for two 20bp sequences with no common 5bp sub-sequence; for instance:

AAAAAAAAAAAAAAAAAAAA

and

AAAACAAAACAAAACAAAAC


Why are lipid-soluble substances harder to excrete?

Short answer
If you understand why hydrophylic compounds can be excreted, than it's kind of straightforward why hydrophobic ones can't - because they are not hydrophylic.

Background
The kidneys, through the production and excretion of urine, are the major gateway of clearing the body from toxins. Some toxins absorbed in the gastrointestinal tract can be excreted by the liver through the gall system.

Urine is watery and kidney's excrete water through ion homeostasis. Hydrophobic compounds do not dissolve in water and hence cannot be excreted by the kidneys. The liver has an important role in making hydrophobic toxins water-soluble. Often hydrophilic groups are attached to it in the liver, making them hydrophilic. If that can be achieved, they can be excreted through the kidneys. Hydrophobic compounds that are resistant to chemical modification tend to accumulate in the body in fatty tissues like the nervous system, for example the notorious polychlorinated biphenyls (PCBs).

Reference
- Chen. Activation and Detoxification Enzymes: Functions and Implications, Springer Science+Business Media (2012)


Is there any possible way that hybrids can mate?

This is a hypothetical scenario which I think could be compared in parallel to hybrids like a mule (offspring of a male donkey and a female horse) or a hinny (offspring of a male horse and a female donkey) or zebroids (reference). In the case of the fertility of mules on wikipedia it is stated that

  A few female mules have produced offspring when mated with a purebred
  horse or donkey.

with examples being given as

  Since 1527 there have been more than 60 documented cases of foals born
  to female mules around the world. There are reports that a mule in
  China produced a foal in 1984. In Morocco, in early 2002, a mare mule
  produced a rare foal. In 2007 a mule named Kate gave birth to a mule
  son in Colorado. Blood and hair samples were tested verifying that the
  mother was a mule and the colt was indeed her offspring (reference).

In the case of a hinny fertility is much more rare but there is a documented case on Wikipedia

  In China in 1981, a hinny mare proved fertile with a donkey stallion.
  When the Chinese hinny was bred to a donkey jack, she produced "Dragon
  Foal," who resembled a donkey with mule-like features (reference).

The wikipedia page on hybrids will also be of interest in your research. In short, hybrids can procreate and give birth in rare cases. However, I wouldn't vouch on the survivability of the offsprings. Since your work is fictional, it is entirely left to your discretion on that topic. Btw, humazee or humzee makes a more intriguing name maybe. Good luck with the book.


I would like to start by suggesting you talk to whoever prescribed you the drug or your pharmacist. They should be most up to date with interactions and there are some interactions which may only affect you more seriously because of your medical history or current conditions.

Here are some sites that you can check drug interactions in order of popularity:

Medscape

Drugs.com

Healthline

WebMD

RxList


Does introgression require interspecific hybrids to be fertile? How is this possible?

Does this mean that the interspecific hybrid is fertile?

Yes

  But is it possible, that an interspecific hybrid is fertile?

Yes

You might be confused by the idea that by definition two individuals from different species should not be able to interbreed. If so, then you should have a look at How could humans have interbred with Neanderthals if we're a different species?.


Influence of temperature on transcription, protein binding and decay rates

This sounds straightforward when thinking about it but finding hard evidence is not really easy. As this is too long for a comment, I have to put it in as an answer. Just a few thoughts: All enzymatic reactions are of course temperature dependent and usually have a temperature optimum at the specific living temperatures. For yeast this is around 27°C, for thermophiles this is much higher. For transcription an number of other factors including accessibility of the chromatin and the availability of cofactors play an important role besides the higher activity of one enzyme. This paper might be interesting for you: "Direct measurement of transcription rates reveals multiple mechanisms for configuration of the Arabidopsis ambient temperature response".

DNA binding should be a statistical process between association and dissociation at a given binding site. At higher temperatures the turn-over at the binding site should be higher (because there is more energy available to promote dissociation). T

The thermodynamics of DNA structural motifs
Thermodynamics of specific and nonspecific DNA binding by two
DNA-binding domains conjugated to fluorescent probes.


This is a very ambitious project for a DIY-er. To explain why, I'm going to use the example of DNA polymerase I from E. coli.

DNA polymerase I is the most abundant DNA polymerase in the E. coli cell, but nevertheless is still only present at around 300 copies per cell

  Ishihama Y et al. (2008) Protein abundance profiling of the Escherichia coli cytosol. BMC Genomics. 9:102.

This was the first DNA polymerase that was ever purified, in the laboratory of Arthur Kornberg

  (Enzymatic Synthesis of Deoxyribonucleic Acid : I. PREPARATION OF SUBSTRATES AND PARTIAL PURIFICATION OF AN ENZYME FROM ESCHERICHIA COLI Lehman, MJ et al. (1958) J. Biol. Chem. 33:163-170.).

In this paper a method of purification is described that starts with 60 litres of culture. There is also this statement:

  "One kilo of E. coli yields less than 10 mg of the purified enzyme."

I'm guessing that you have no experience of protein purification, so I'll just tell you that this is very discouraging: these days, with overexpression, people expect to get mg quantities of their protein from just a few grams of bacterial cells.

This is a clear illustration of why it is pretty much unthinkable for you to set out to purify an enzyme like this using small-scale methods, and explains why techniques of overexpression and the use of affinity tags have revolutionised protein purification.

And it gets worse: even if you did manage to purify some DNA polymerase I from a bacterial source you would find that it is actually not very good at making DNA. This is because as well as extending primers in a 5'>3' direction, it is is very good at degrading DNA in the same direction. In other words as the enzyme moves along a template molecule, copying it, it will degrade any existing DNA that it meets "ahead" of its direction of travel. This is why the most commonly-used form of this enzyme in research is the "Klenow fragment", a fragment of the polymerase that lacks the 5'>3' exonuclease activity. This fragment was originally made by treating DNA polymerase I with the protease subtilisin, but it is now expressed from an engineered polA gene. Klenow fragment polymerase was used in the original PCR experiments (it had to be added afresh at every cycle).

I don't know how much money you have to spend on your projects, but in fact these enzymes can now be bought relatively cheaply.  I don't think that you can expect to make them for yourself, without this becoming the actual project.

Finally, if you can get hold of a strain of E. coli with an expression plasmid for Taq polymerase then you really could make your own very easily - I've done this myself (but I no longer have the strain) and the heat stability of the enzyme makes the purification trivial. It would be much easier to use your own Taq with a heated water bath than to try to make DNA polymerase I. But obviously it depends upon what you are trying to do: Taq polymerase may be unsuitable for other reasons.


Modeling yeast biochemical pathway using enzyme kinetics

You should take a look at SGD (the Saccharomyces Genome Database), and in particular YeastCyc. Some protein information pages at SGD give estimates of molecules per cell taken from this Nature paper.

Added later in response to some comments:

The question asks about levels of metabolites and of enzymes, not of transcripts. Microarray data can be, at best, only a guide to levels of proteins. Estimating the levels of metabolites from microarray data is a complete non-starter since there are entire layers of regulation that will be ignored. Just to give one example of a pitfall in this approach: you could have high levels of transcript from which you could you could infer high levels of enzyme, but that enzyme could be inactivated by a post-translational modification.


Classifying Polypeptides (and/or Proteins)

You can certainly refer to short peptides by their sequence. I don't know of any exact boundaries, but I've seen tripeptides referred to by either their three letter codes (Ala-Asp-Asn) or even the chemical name (alanylaspartylasparagine) although obviously that gets ridiculous pretty quickly.

  As the largest known protein, titin also has the longest IUPAC name of
  a protein. The full chemical name of the human canonical form of
  titin, which starts methionyl... and ends ...isoleucine, contains
  189,819 letters and is sometimes stated to be the longest word in the
  English language, or any language. However, lexicographers regard generic names of chemical compounds as verbal formulae rather than English words

For more than around 5 amino acids, just the sequence makes more sense. It would be interesting to analyse scientific paper abstracts to see how many have the sequence as the 'name', but anyway.

When we get to proteins, it would be unhelpful to refer to them by their sequence. They usually have names - enzymes are often named by what they act on (like 'alcohol') and how they act on them (like 'dehydrogenase'). In addition, there are structured names called E.C. numbers - sarcosine dehydrogenase is 1.5.8.2, for example.

As you point out, there are a very large number of sequences that do not correspond to proteins found in an organism. To name one of these is tricky, and if someone synthesises one then they would have to come up with some naming scheme to refer to it.


What kinds of cells does human saliva contain?

It contains white blood cells (leukocytes) and cells from the inner lining of the mouth (buccal epithelial cells). The DNA obtained from these cells is the basis of DNA profiling based on saliva samples.

Source: Salimetrics


New England Biolabs, which has an excellent reputation for well-tested, well-documented, and robust products, has a line of protein expression and purification products that I'd definitely take a look at. I've used the pMAL system for expression of fusion proteins in E. coli, and the PURExpress system looks just like what you're looking for. I have a personal (but not financial) connection with them, and I can vouch for their quality and technical support.

Pierce/Thermo is generally a good place to look when dealing with protein stuff. I've had good results with lots of their stuff, but I haven't done in vitro expression in ages, so I can't remember what I used. (BTW, I have no connection with them, I just tend to like their products.)

As Alan Boyd mentioned, lots of companies like Life Technologies, Promega, Qiagen, and Sigma have in vitro expression kits. Which one you pick will ultimately be influenced by what exactly you need your protein to do, the desired scale of expression, the type of tag(s) you want to put on it, what equipment and expertise you have in your lab, and how much time and money you want to invest.


Are there any non-mammalian species known that lactate?

Short answer
Technically, only mammals lactate. To lactate means to produce milk from the mammaries to feed a baby or young animal. Milk, in turn, is defined as the secretions from mammary glands. However, there are animals other than mammals that produce milk-like substances to feed their young.

Background
Both male and female pigeons (Columba livia) possess the ability to produce a nutrient substance, termed pigeon ‘milk’, to feed their young. A similar substance is produced by flamingos and male emperor penguins. The normal function of a crop is a food storage area located between the oesophagus and proventriculus where food is moistened before further break-down and digestion through the gastrointestinal tract (Fig. 1).

Fig. 1. Schematic of the location of the 'milk'-producing crop in a pigeon (left) and a pigeon feeding its chick from its crop (right). Sources: ZME Science and Bird Ecology Study Group

During the process of pigeon ‘lactation’, a curd-like substance is regurgitated from the crop to the chick. The dry-substance of pigeon ‘milk’ is 60% protein, 32-36% fat, 1-3% carbohydrate and some minerals, including calcium. It has been shown that pigeon ‘milk’ contains IgA antibodies, which provides evidence suggestive that it is more than a nutrients alone. The physiological mechanisms governing pigeon ‘milk’ production and delivery are unknown. It is well documented that the pigeon crop is responsive to the lactogenic hormone prolactin. However, the pigeon crop tissue during ‘lactation’ is structurally unrelated to the mammary glands in mammalians, because it is not glandular and secretory processes do not seem to be involved (Gillespie et al, 2011).

The similarity between this process and lactation in mammals is striking, but is a case of convergent evolution, where unrelated species independently evolve similar traits. 'Milk' production is also recorded in some fishes, where it is fed to their young in the form of a mucous secretion on the skin (Buckley, 2010). Certain amphibians shed skin cells that are fed to the young. But the 'milk' of pigeons and doves is thought to be the most highly specialized of any non-mammalian 'milk' (Australian Geographic, September 2011).

References
- Buckley et al., J Exp Biol; 213: 3787-95
- Gillespie et al., BMC Genomics (2011); 12: 452


How exactly does heterozygous sickle trait help patients survive malaria

Sickle cell anemia is characterized by the formation of sickle shaped red blood cells rather than the usual biconcave ones. For a double recessive homozygous genotypic person, i.e. an infected person, this causes severe lack of oxygen diffusion into the RBCs because of defective haemoglobin production.
In case of a carrier, he/she carries the gene for the defective version of haemoglobin but does not show the symptoms for the disease.

The malarial agent, Plasmodium uses haemoglobin, or more specifically haem as its main nutrient source The defective sickle haemoglobin induces the expression of heme oxygenase-1 (HO-1) enzyme in hematopoietic cells (those which produce erythrocytes, for example marrow of long bones). Carbon monoxide (CO), a byproduct of heme catabolism by HO-1, prevents further accumulation of circulating free heme after the infection by Plasmodium. This decreases the pathogenicity of the organism and prevents the disease from occuring.  Moreover, sickle haemoglobin inhibits activation and/or expansion of T lymphocytes (specifically CD8+T cells), which recognize the antigens expressed by Plasmodium and hence do not attack it. This is an immunoregulatory effect that does not involve the heme oxygenase enzyme.
This leads to the carrier person having innate resistance to malaria (or at least Experimental Cerebral Malaria )

And no, the RBC itself is not structurally different. Though there might be some
sickle shaped RBCs in the blood, their number is very less. The major difference comes from the haemoglobin in the red blood cell.

Here is the original paper which explains the phenomenon in detail.


Primer design and BLAST E value stringency

I never used BLAST for primer design, but often for finding out where a sequence came from.

From the FAQ of the NCBI:
http://www.ncbi.nlm.nih.gov/blast/Blast.cgi?CMD=Web&PAGE_TYPE=BlastDocs&DOC_TYPE=FAQ

"The lower the E-value, or the closer it is to zero, the more "significant" the match is. However, keep in mind that virtually identical short alignments have relatively high E values. This is because the calculation of the E value takes into account the length of the query sequence. These high E values make sense because shorter sequences have a higher probability of occurring in the database purely by chance. For more details please see the calculations in the BLAST Course.".

What they say in the papers is true, the size of your database matters in deciding how significant the match is. I can imagine that for primer design you want to be more careful with the E-values, as they often fall under: "because shorter sequences have a higher probability of occurring in the database purely by chance".

I hope this helps to make your decision for deciding your threshold, otherwise please give more information.


Why was not RNA completely replaced by DNA when the RNA world evolved into a DNA and protein world?

A related question is Why do some bad traits evolve, and good ones don't? Basically a strong selection pressure is necessary to filter out a trait.

Having said that, there is no strong argument in support of transcription being disadvantageous.

RNA has unique properties that makes it suitable for certain functions. RNA can adopt different secondary/tertiary structures that an equivalent ssDNA cannot. One of the reasons is that GU wobble pairs are stable in RNAs but not in DNA thereby allowing structural flexibility to the former. See https://chemistry.stackexchange.com/a/35224/5295

RNA also has a high turnover because of different RNAses. If there was DNA instead of RNA for carrying temporary messages and there were equivalent DNAses to increase the turnover of the "mDNAs", then the genomic DNA would also become susceptible to degradation by these DNAses, which would cause genomic instability. You can argue that protein synthesis could directly begin on DNA as a template instead of mRNA. I guess that it would crowd the DNA and clash with replication. Even transcription machinery clashes with the replication machinery; this is called Transcription Replication Conflict which leads to genomic instability. A hypothetical situation in which there are multiple ribosomes on a DNA, is likely to have higher chances of the conflicts with replication than transcription-replication conflicts, thereby causing higher degree of genomic instability. I am assuming so because a large number of ribosomes need to simultaneously be progressing through the gene in order to produce sufficient amount of corresponding protein (like in case of polysomes).

Another possibility is based on the RNA world hypothesis. If it is really true that RNA preceded DNA as a functional as well as a hereditary molecule then it is difficult to get rid of all RNAs that easily. Even if most of the functions of the archaic RNAs were taken over by DNA and proteins, they are still performing some vital functions. To replace RNA from these roles, an alternative should exist which performs much better than the RNAs.

These are just guesses. An absolute reason can not easily be attributed to many biological observations. This is because we do not know the actual evolutionary trajectory of how things happened. However, what is important to keep in mind is that evolution does to proceed towards some kind of global optimum. Evolution does not "aim" for perfection.


how to find full mitochondrial genome of plants in GenBank?

Is this one? http://www.ncbi.nlm.nih.gov/genome/38606?genome_assembly_id=233326

What I did was Google: "search mitochondria genome BLAST"

and clicked the first page for me "Organelle Genome Resources". I then selected

"Browse by Organism" on the lefthand side, which took me to a new page.

I then entered in the top left text box the phrase "Malvaceae" and up came a scroll down list from the text box of choices for the text field.

I chose the first "Malvaceae (taxid:3629)" and upon clicking that, 26 entries came up for organelles. Two of which were from Mitochondria under the "Type" column.

The other entry being: http://www.ncbi.nlm.nih.gov/genome/10704?genome_assembly_id=233221

Sorry if I  was totally off base, I am just a undergrad.


"Is it possible" has a carefully conditional "yes".  Do we have the expertise or technology to do it now? No.  One of the biggest difficulties is that nerve tissues (the connections between brain and rest of body) will take time to heal... time during which the brain cannot sufficiently give commands to the rest of the body to keep autonomic functions running.

Head transplants, however, have been "successfully" completed using monkeys.  The monkey lived for sometime after the transplant, but eventually died.  China has also been known to do a similar procedure with dogs.

Caution, this may be too explicit for some; I'm not sure ethics boards would allow it nowadays:
Monkey Head Transplant


How is it determined in a zygote state of foetus, that which side is mouth and which side is for anus?

The gut tube is formed from endoderm that migrates through the primitive streak. Before this, however, the anterior-posterior axis of the embryo is defined by the formation of the streak at the beginning of gastrulation. In mice, which are phylotypic with humans at this stage, the streak forms posteriorly and then extends to the anterior. I'm not sure if you'll be able to find much research on humans, but mice and chicks are quite well studied. That said, I don't know the molecular and cellular mechanisms which define where the primitive streak forms. I don't even know if it is known. How much detail are you looking for? If I find the time, I can try and elaborate on this further. In the mean time, this review looks promising:

http://m.dev.biologists.org/content/136/5/701.long


This article by R. Aiden Martin doesn't have citations, but is a great read with a lot of detail on observations and mechanics of animals moving in water. If you trust the numbers the author gives, the top 10 marine mammals in terms of speed (in mph = 1.6 km/h) are:

  Dall's Porpoise (Phocaenoides dalli), leaping   34.5 mph

  Killer Whale (Orcinus orca)  34.5 mph

  Shortfin Pilot Whale (Globicephala macrorhynchus)   30.4 mph

  Blue Whale (Balaenopterus musculus) 29.76 mph

  Fin Whale (Balaenoptera physalus)   25.42 mph

  California Sea Lion (Zalophus californianus)    25 mph

  Pacific Spotted Dolphin (Stenella attenuata)    24.7 mph

  Common Dolphin (Delphinus delphis)  23.6 mph

  Bottlenose Dolphin (Tursiops truncatus) 17 mph

  Pacific Whitesided Dolphin (Lagenorhynchus obliquidens) 17 mph

As noted in the article, higher estimates of speed for, for instance, the common dolphin may be in fact records of them 'surfing' on the bow wave of boats (not propelling themselves through the water).


The diversity of fatty acids produced by an organism is limited by the diversity of enzymes which synthesize them. Unsaturated fatty acids contain carbon-carbon double bonds which do not isomerize. The capacity for humans to produce cis fatty acids is probably selected for because of their lower melting point which prevents arterial clogging. Cold blooded animals utilize cholesterol to increase membrane fluidity when their body temperature is low.


Are proteins a different shape in space?

Proteins are not made to be one way up or the other as they flow around and surround cells, so sea-level to space gravity gradient will not be the major cause of change to proteins at different altitudes.

Pressure is more of a factor on proteins, and it has been studies very much, both for protein shape and protein interaction with elements and other molecules.

http://www.annualreviews.org/doi/abs/10.1146/annurev.pc.44.100193.000513?journalCode=physchem

People have awesome health when they are born and raised at altitudes of 4000 meters, there are even people living at 4800 meters OK. the pressure gradient there is halfway in between sea level and space. 100m depth also stresses nitrogen toxicity and other severe effects more than proteins, but deep sea fish do have specially adapted proteins because depths at 10000 meters require different proteins than the surface.


What biological processes cause leaves to change colours in Autumn?

Here is a quite nice Chemistry of Autumn Leaf Color. And here is a less chemical, but more detailed explanation regarding the triggering of colour change, which is quite similar to the one from the University of Illinois that @Oreotrephes already gave.

As I understand it, during sunny days a lot of chlorophyll is broken down, but also built up. When after the summer the days get cold and dark, chlorophyll is built up slower (or not any more at some point) and you start to see the colour from the carotenoids and anthocyanins. A harsh change from sunny to cold and dark is supposedly bringing up the brightest colours. At some point, also the carotenoids break down and leaves get brown. The faster the change to cold and dark the larger is the frame between having all chlorophyll broken down and having the other colouring molecules broken down (-> bright colours).

But that's the amateurs explanation.


Do Osteichthyes fishes have any cartilage?

Yes, Osteichthyes do have cartilage. For example, Ancient origin of lubricated joints in bony vertebrates shows images of cartilaginous tissue in the joints of several bony fish.  More generally, cartilage is required for normal bone development, and Osteichthyes are no exception (e.g. Distinct patterns of notochord mineralization in zebrafish coincide with the localization of Osteocalcin isoform 1 during early vertebral centra formation).


What are parental antagonism & parental conflict?

You may inherit a gene, which is actually detrimental to your (most efficient) functioning and hence has a cost (eg. gene for being small when food is available from tall trees). On the other hand, you may inherit a gene which has a benefit for you (gene for being tall with food available from tall trees).

Sexual Antagonism:

  What’s good for the goose may not be good for the gander. Thistwist on
  an old proverb captures the notion of sexual antagonism.Traits that
  confer high fitness on geese (females) may confer lowfitness on
  ganders (males), and vice versa.

In sexually dimorphic species (like all common complex life), the evolution of males is usually decoupled from females. This is not as bad as it seems, as females and males may have different patterns of selection, different phenotypes of mutations all at the same time dodging pleiotropic effects. Hence mutations benefiting one sex will sometimes be deleterious to the other (i.e. their fitness effects are ‘sexually antagonistic’)

Sexual Conflict:

Males and females have divergent interests in reproduction that are rooted in anisogamy and lead to distinct roles, due to sexual antagonism. Sexual conflict occurs between the same or different genes,  when there are different optima for a trait expressed in both sexes (intralocus conflict) or when there is conflict over the outcome of a male–female interaction (interlocus conflict).

Intralocus sexual conflicts are potentially very common. Researchers have found a strong positive genetic correlation between male and female fitness at the larval stage in the fruit fly (when interests of the males and females are essentially the same -> survive and grow), but a strong negative genetic correlation between adult male and female reproductive success (when the sexes are expected to have different genetic interests). This is possibly due to sexual antagonism.

Interlocus conflicts occur when there is conflict over the outcome of male–female interactions, so that the optimal outcome is different for the two sexes,as occurs in yellow dung fly mating behaviour. In a rare instance, wikipedia does a good job of explaining the example:

  In the yellow dung fly Scathophaga stercoraria, females can be injured
  in the battles between males suitors. Males are selected to evolve
  traits for competitive ability that would increase their reproductive
  success, but females would evolve a set of antagonistic adaptations to
  reduce their chances of being injured in battles between the males.
  Therefore, there is an interlocus sexual conflict in males and females
  that could possibly lead to an "unresolvable evolutionary chase" when
  a novel trait in males increases their competitive ability while
  harming the females

[5,6]

.

Parental Antagonism:

An allele in a gene is said to be parentally antagonistic if it has an inclusive fitness benefit when derived from one parent (say the mother), but an fitness cost when derived from the other parent (in this case the father)

There are many different theories out there, but the gist of it is essentially some process creating an asymmetry between the genes that you inherit from your father and mother (patriGENIC and matriGENIC), that causes differential expression of alleles (silencing the other copy) [2]

Parental Conflict:

  When parent-offspring relations in sexually reproducing species are
  viewed from the standpoint of the offspring as well as the parent,
  conflict is seen to be an expected feature of such relations. In
  particular, parent and offspring are expected to disagree over how
  long the period of parental investment should last, over the amount of
  parental investment that should be given, and over the altruistic and
  egoistic tendencies of the offspring as these tendencies affect other
  relatives. In addition, under certain conditions parents and offspring
  are expected to disagree over the preferred sex of the potential
  offspring. In general, parent-offspring conflict is expected to
  increase during the period of parental care, and offspring are
  expected to employ psychological weapons in order to compete with
  their parents. [7]

Reading:

[1] Haig, David. "Parental antagonism, relatedness asymmetries, and genomic imprinting." Proceedings of the Royal Society of London. Series B: Biological Sciences 264.1388 (1997): 1657-1662.

[2] Patten, M. M., et al. "The evolution of genomic imprinting: theories, predictions and empirical tests." Heredity 113.2 (2014): 119-128.

[3] Patten, Manus M., and David Haig. "Maintenance or loss of genetic variation under sexual and parental antagonism at a sex‐linked locus." Evolution 63.11 (2009): 2888-2895.

[4] Normark, Benjamin B. "Perspective: maternal kin groups and the origins of asymmetric genetic systems—genomic imprinting, haplodiploidy, and parthenogenesis." Evolution 60.4 (2006): 631-642.

[5] Connallon, Tim, and Andrew G. Clark. "Evolutionary inevitability of sexual antagonism." Proceedings of the Royal Society of London B: Biological Sciences 281.1776 (2014): 20132123.

[6] Chapman, Tracey, et al. "Sexual conflict." Trends in Ecology & Evolution 18.1 (2003): 41-47.

[7] Trivers, Robert L. "Parent-offspring conflict." American zoologist 14.1 (1974): 249-264.


What is the connection between sleep requirement and age?

I believe the current theory is that it is related to cell loss in the intermediate nucleus of the human hypothalamus. They have shown sleep disruptions due to lesions of the hypothalamic ventrolateral preoptic nucleus in rodents, and found that the intermediate nucleus in humans is homologous and shows a reduction in size in older adults that is correlated with sleep disruptions. http://brain.oxfordjournals.org/content/137/10/2847


Is the sun's damage to skin sufficient to warrant protection anytime the average person goes outside or just for extended periods?

Because the website you link speaks of cancer, they probably go by the rule that a single exposure and even a single photon of UV may be sufficient to cause that one mutation in that one skin cell that will eventually lead to cancer.

In the end, they are right, because mutagens (UV, cigarettes, radiation) do not follow typical toxicological rules. There is no threshold dose of UV that does not cause cancer, as even a single short exposure may do the trick. Obviously, multiple exposures and longer exposures increase the chance. This, as opposed to toxic substances that generally feature a threshold dose. Below this threshold dose they are considered harmless.


Is it a valid generalization that kinases catalyse reactions involving energy transfer and utilization?

Your (original) description:

  a kinase helps chemically deliver or metabolize stored energy within a cell

sounds a little more like what many ATPases do: they are using the energy from ATP to do some energetically unfavorable work, such as moving molecules or ions against their concentration gradients. However, kinases have a broad range of different functions.

In some anabolic pathways, yes, kinases are helping to deliver stored energy in the form of phosphate groups onto 'building blocks' of other molecules, and this stored energy can be used for future reactions.

However, when a kinase phosphorylates another molecule (often a protein) to regulate its function, I wouldn't really say that it is delivering energy, just that there is some energy cost to doing the business of flipping cellular light switches, and ATP is readily available as a source to do that. One big advantage of using kinases in these sorts of reactions is that, because a fairly large energy input is required, such reactions don't occur easily by mistake or just due to thermal energy.


How can I preserve hair or saliva for future genome sequencing?

Full genome sequencing is only one of many experimental approaches. It's important in the field of genomics and useful in transcriptomics and proteomics.

It's best to extract DNA as soon as the sample has been removed from the living organism since all kinds of physiological processes start breaking down DNA in dead tissue. Kitchen refrigerators are not ideal for storing extracted DNA because they operate at about four degrees celsius. In the lab, minus eighty degree freezers are used. The lower the temperature, the better. Minus eighty degrees, however, is good enough.

Contamination is a big problem, so the more technical repeats you run, and the more biological repeats you have, the better your chances of getting reliable results. Biological repeats refer to, for example, taking three strands of your hair for analysis, while technical repeats refer to, for example, carrying out three PCR experiments on material from the same strand of hair. Once you've used tissue to extract DNA you don't keep remaining tissue because it gets contaminated during experimental preparation. That is why you may want to have biological repeats. It's also important to take precaution when removing the sample from the organism. This means wearing latex gloves and even using dilute ethanol to sterilize the sample before placing it in a sterile container. The problem is that ethanol can interfere with DNA extraction and be a contaminant itself. Balancing contamination prevention with quality results is important in the lab.

There are additional biological information such as DNA methylation events that occur intermittently on a genome and are inheritable. This information cannot be predicted from the sequence composition of your genome, but there are experiments meant for elucidating methylation patterns that can be carried out using uncontaminated biological samples (such as hair and saliva) stored in eppendorf tubes at minus eighty degrees celsius.


What is the cause of the packaging capacity limit of recombinant adeno-associated viral (AAV) vectors?

It's not the size that counts, it's how you pack it (sorry couldn't help myself).

Wild-type bidensoviruses do a lot of interesting things to pack genome like splitting its genome into two virions(1), inverted terminal repeats (ITRs) that form panhandles that can stack instead of hairpins (2), and overlapping positive and negative ssDNA strand ends (2 and 3) that clip closely together.  So on the whole, I don't know that it's a fair comparison.

Also remember that you can go too small with AAV genome size, not just too large (if you go too small you will even get 2 genomes per virion).

If you want to orderly pack ssDNA (or DNA in general), you have to use some nucleoproteins to help.  Free ssDNA has the added problem of being unstable.  Going back to basic biology, you can think of nucleosomes allowing the packing of eukaryotic DNA at a much higher density than would otherwise be energetically favorable.

Viruses use a wide variety of methods to pack genetic material, one of which is through binding directly with the capsid as with AAVs.  One should remember that the capsid proteins also are tasked with entry into the cell, trafficking, and entry into the nucleus.  All while protecting and packaging the genetic payload.

AAVs, being small (wt is ~4.7kb w/7 proteins), only have the capsid proteins VP1-3 to work with.  The ITRs are known to be the cis active sequences of the genome (4, 5), and these ITRs form normal hairpins.

A portion of the AAV ITR binds (hooks onto) an interior facing portion of the VP3 gene (6, 7).  But the virus has to push in this ssDNA, and it uses the Rep proteins to do it (8).  The Rep proteins (Rep52 and Rep78 specifically), are larger than the capsid proteins, and bind the ITRs at multiple sites.

While the exact insertion pore hasn't been identified at the structural level, the way I like to picture it is a series of hairpins have to bind on spokes of the Rep proteins to be pushed into the virion, where in turn the hairpins have to hook onto the inside of the capsid.  If you put too much ssDNA between your ITRs, then you lose the ability to be passed along (or bind) to both proteins in packaging.  You start to lose the tight packing onto VP3 found in wt virus, and instead get more sporadic VP3 binding (every 3rd as opposed to every other).

It would be incredibly hard to just "increase" the size of the capsid without messing up the assembly and the other functions of the capsid.  The VPs only oligomerize in the cytoplasm (9) suggesting that host proteins are required for proper assembly.  I think the process of successfully increasing the optimal genome size would be quite a task and achievement if done.  One would likely have to optimize additional ITRs, the internal binding bind sites on VP3, and the structure of Rep52 before such a thing would be possible.  Alternatively bringing in a novel or chimeric packing mechanism, but again this would be exceedingly difficult (probably prize worthy).


All animals develop in this way, whether they are oviparous (developing in an egg) or viviparous (developing inside their mother, or live-birth).

From Wild Birds Unlimited:

  All mammals have navels or belly buttons where the umbilical cord distributes nutrients between a mother and her fetus. After birth, the umbilical cord is cut and a scar develops on the abdomen where the hole closes.

  Of course avians or birds hatch from eggs which are virtually self-contained life-support systems that only require warmth and oxygen to develop properly. Instead of an umbilical cord scar, birds have yolk sac scars at hatching. This is where the chick embryo is attached to the yolk sac. But don’t look for any bird belly button rings. The scars usually heal and become virtually invisible.

As for their umbilical cord, it looks like it falls off when the chick hatches if it is not fully absorbed along with the yolk sac, along with everything else contained in the egg (although there is not a lot of material left within the egg by the time the chick is ready to hatch).

  Inside a bird's egg there is a tiny cord that connects the developing embryo to the yolk sac. When the egg cracks open, the hatchling does in fact have a miniscule residual scar where the cord was.


DNA extraction from plants and algae don't use phenol. Why?

CTAB is for removing polyphenols and polysaccharides which are found in plant tissues. Animal cells/bacteria don't have these. You can do an additional phenol-chloroform extraction if you want.

See this protocol by Monsanto.

  Weigh out 6g of processed tissue into a 50ml conical tube appropriate for centrifugation. Note: For unprocessed tissue, weighing
  m ay occur prior to processing as long as entire processed sample is
  transferred to the conical tube.
  For each 6g sample add 25ml of a solution consisting of 24.25ml, pre-warmed (55°C) CTAB extraction buffer, 0.5ml 2-mercaptoethanol
  (2-ME), and 0.25 ml of 10mg/ml proteinase K for a final concentration
  of 2% (2-ME) and 100µg/ml (proteinase K).
  Incubate the tube for 60 minutes at 55°C. Cool the tube briefly on bench (10 minutes)
  Add 20ml of phenol:chloroform:isoamyl alcohol (PCI, 25:24:1).  Cap the tube and mix vigorously by vortex or inversion.
  Centrifuge for 10 minutes at 13,000×g and 20-25°C to separate the aqueous and organic phases. Transfer the upper aqueous phase to a
  clean 50ml conical tube.
  Repeat extraction two times for a total of three extractions (steps 4-5).
  Transfer upper aqueous phase to a new tube and add approximately 2/3 volume of -20°C isopropanol and gently invert the tube several
  times to mix.
  To precipitate the DNA place the tubes at -20°C for at least 30 minutes and up to three days.
  To pellet the DNA centrifuge the tubes at approximately 13,000×g for 20 minutes at 4°C.
  Redissolve the pellet in 4 ml of TE pH 8.0. Transfer to a 13ml Sarstedt tube and add approximately 40µl of 10mg/ml RNase, then
  incubate at 37°C for 30 minutes.
  To extract the DNA add 4ml of chloroform:isoamyl alcohol (CIA, 24:1).  Centrifuge for 10 minutes at approximately 13,000×g at room
  temperature.  Transfer the upper aqueous phase to a clean Sarstedt
  tube.
  Repeat step 11 then add half volume of 7.5M ammonium acetate, gently mix by inversion/pipette and add 2 volumes of 100% ethanol. Mix
  by inversion/pipette and place at -20°C for 30 minutes to overnight.
  Centrifuge at 13,000×g for 20 minutes at 4°C to pellet the DNA.


Proteome patterns between treated and control cells

If I understand you did a treatment to some cells and compared them with non-treated ones. Instead of running the four experiments at the same time, you did one treated and one untreated at a time. Then you did proteomics for each sample. Is the treatment the same in all four experiments?

Edit after the further comments of the OP: So, since the four treated samples are the same and the four untreated also (same conditions except from the treatment and the treatment is the same), then the way to go is as what your collaborator did.

Identification and quantification of the detected proteins is one thing and every sample of the four are replicates. Comparison between the two conditions is another thing.
The software he uses for ID can combine the same samples and already perform the statistical analysis, so the list you have now has higher credibility in terms of the proteins it includes and their levels for your cells when they are treated or not.

Using only one of your replicates, although it might give you different number of detected proteins or different amounts of each, has lower credibility, because it's only one sample out of four. In plain words, the presence or absence or the amount of a protein might be an artifact or insignificant.

What has to be clear is that the comparison between treated and untreated conditions is done after you have received the statistically correct list of detected proteins.

Thus, and in accordance to what I had said before the edit, if you take the list for each treated sample and compare them with any of the lists of the untreated ones, it will lead to conclusions that won't be as statistically significant as when you combine all treated together and all untreated together (as your colleague did). In plain words, your conclusions will have a higher chance to be wrong.

Every statistical analysis you do yourself for each sample should eventually lead to a similar consensus as your colleague got using the statistical analysis of his software.

As a sidenote, considering how many types of proteins are in a cell, now that you have a quite short list might not be a bad thing at all and you can proceed by:

Concluding that the treatment had minor effect in the proteins that you expected it would affect (if they are not present in your lists as significant different)
Trying to understand, identify and hypothesize on the role of the proteins that made it in your comparison threshold, as they have a much higher probability of being indeed different between the two conditions.

Splitting the samples in your analysis might have a point if the conditions of the experiment were not exactly the same or the treatment level is different etc. In that case you could split the samples accordingly, but that would definitely reduce your certainty level for your conclusions.


What biological systems are affected by Vitamin B6 (or B vitamins in general)?

The main effect, of vitamin B6, is neurological, becouse  moderate variations in the intracellular concentration of pyridoxal 5'-phosphate (PLP), the biologically active form of vitamin B6, can have pronounced modulatory effects on steroid-induced gene expression. So you cannot get the effect of stress hormones.

Also neurological damage has been reported on doses from excess of 500 mg/d. Check this papers http://www.ncbi.nlm.nih.gov/pubmed/2661220 and http://www.fasebj.org/content/8/3/343.short


Why is there no way to remove an immune response?

It is an interesting question. The reason for why new immune responses can be launched but the memory of old ones are not deleted is based on the concept of irreversibility of certain chemical reactions.

Launching an immune response involves clonal expansion of cells expressing the epitope sensors such as the immunoglobins and T-cell receptors, accompanied by maturation of these receptors. Some of the reactions involved in this process are irreversible, which include VDJ recombinations, class switching and affinity maturation.

In an overall sense, immune response is analogous to natural selection- in the presence of the antigen the best binders are selected and expanded. Now to make a species extinct you would have to find each individual and kill it. Or you may have to develop a technology that will identify and kill a certain species in an automated manner. This is difficult to implement; how to engineer a mechanism that will precisely seek and destroy all the epitope sensors for a particular antigen. In contrast selection happens spontaneously because it does not proceed with a reason. It just selects the best from available stock.


How well is gene A annotated? Do you have the gene A sequence (after post-transcriptional modifications)? If you do, you can order it from a company like DNA2.0 and they will synthesize it for you for like $0.35/base. Then you can transform the cells with this plasmid and do a knockout of gene B by inserting some sequence at the ~200bases overlap.

Also, I guess you can transform the immediate transcript (without modifications). It will also be modified once it is in the cell. But it will be longer and more expensive to synthesize, but there are a few methods you can use to do that.

Let me know if this idea appeals to you. I can give you more info if you are interested.


what is the difference between osciloscope and electrocardiograph?

I would say that electrocardiograph is a specific case of oscilloscope. The main difference, perhaps is that "oscilloscope" is a device for visualization on a display ("scope" from greek "look out"), whereas "electrocardiograph" is primarily used to record ("-graph" from greek "to write").

Oscilloscope is design to visualize an electrical signal, that changes in time (generally speaking). Nature of that signal is not important, it can be radio signal, electrical signal from some device (Arduino), or sensor (thermometer). You can detect earthquakes if you have particular sensor for vibration.

It is just that these devices should output signals of particular frequency, usually general laboratory oscilloscopes are designed to work with signals up to few MHz. If you attach sensor that "feels" muscle contraction, you will have a tool for electromyography.

Electrocardiograph, by definition, is a device that visualizes electrical signals acquired via electrocardiography. It is just that usually when people and doctors perform electrocardiography, they use specialized devices, not general-purpose oscilloscope. For example, cardiac signals are usually well below 0.5-1KHz, you can save a lot of money and complexity by not having to worry about higher frequencies in your device.


Downloading specific yeast genes in an automated manner?

These sequences do not have any standard i.d. The information in Saccharomyces Genome Database is also obsolete (2005) and does not have these identifiers.

These sequences can be found here (in the same site).

Each species has a short name:

ORGANISM        Short Name
S.cerevesiae    Scer
S. bayanus      Sbay
S. paradoxus    Spar
A. gossypii     Agos

.... and so on.

First letter of genus name in uppercase + first 3 letters of species name in lowercase.

The fasta file (for all ORFs) is:
 www.broadinstitute.org/regev/orthogroups/nt/<Shortname>.fasta

From there you can use grep to retrieve the sequence.

So, if you have saved shortnames and gene names two separate files you can do something like this:

for shortname in `cat shortname.txt`; do wget -O tmp.fa "http://www.broadinstitute.org/regev/orthogroups/nt/"$shortname.fasta; grep -A 1 -f ids.txt tmp.fa >> $shortname"_Select.fa"; done


How did the first sexual animal come to exist?

This is a very broad field, with many complementing, overlapping, and contrasting theories. I suggest that you read this part of the Wikipedia article on this topic:

http://en.wikipedia.org/wiki/Evolution_of_sexual_reproduction#Origin_of_sexual_reproduction

Here is what I got from the Wikipedia article (this is just one hypothesis, read the article for all the others):

There are many advantages to sexual reproduction, two main ones are greater genetic variation and recombinational DNA repair (occurs during meiosis).

There are certain species that can reproduce both sexually and asexually. They choose to reproduce sexually during times when the environment is uncertain (changing). This provides evidence that greater variation is one reason for sexual reproduction.

Asexual organisms only have one copy of each gene, therefore if this copy is mutated in a bad way, they are out of luck. Organisms that sexually reproduce have two copies of each gene, when one goes bad, they can use the other copy to repair the original copy, during meiosis.

As you may know, stress has many harmful effects, one being that it leads to DNA damage. There are certain species of bacteria who, in response to stress, uptake/integrate nearby bacteria cell's DNA into their own. They can then use this new copy to repair their own copy in case they experience DNA damage.

This "trait" of up taking/integrating other's DNA may have been evolutionary selected for (because these organisms repaired their DNA, they survived and passed on their genes), therefore eventually leading to organisms that sexually reproduce.


Can anyone (urgently) tell me if this is a bed bug

This is not a bedbug. This is a hemipteran called a leaf-footed bug in the Coreidae family. (Note: bedbugs are also in the order Hemiptera, but in a different family).
Species similar to yours found in Poland include Coreus marginatus (or "dock bug"), which [according to Wikipedia], is found throughout Europe.

 Adult male and nymph shown from dorsal and ventral views. Source: Wikipedia
C. marginatus is typically 13-15 mm long (which matches your updated length) and has a widened abdomen as does your specimen. Additionally, the antenna of C. marginatus is typically red-orange with black ends (as is also seen in your specimen). A more complete description from Wikipedia:

The head, pronotum and abdomen of an adult dock bug are speckled reddish brown. The antennae are composed of four segments, red-orange in colour except for the final fourth segment which is black. Between the antennae are two small projections, known as antenniferous tubercles, which can be used to distinguish this species from other superficially similar species.[6] The pronotum has angular upward facing projections and the scutellum is clearly visible. The rounded edge of the abdomen has lighter coloured markings. Adults are between 13 and 15 mm long and males are typically smaller than females but have longer antennae.

See here for an additional picture showing a specimen with less prominent abdominal markings as in your specimen.
C. marginitus tends to be found in thick vegetation, so unless you've bee around hedgerows, wasteland, or other densely-vegetated areas, it's possible you have some other closely related species.
I haven't been able to find a better matching specimen, though it seems likely I have only gotten you to the right family without being certain of the genus or species. I'll update if I can find more info...
Notes:

Your specimen does not appear to be another common hemipteran found in Poland:  Leptoglossus occidentalis, which is native to the western United States but has invaded Poland for over 10 years [Surce: Lis et al. (2008)1]

You can find a guide to this family of insects (with pictures) for the neotropics (not immediately useful to you, but a good resource) by Fernandes et al. (2015)2

 1 Lis, J.A., Lis, B. and Gubernator, J., 2008. Will the invasive western conifer seed bug Leptoglossus occidentalis Heidemann (Hemiptera: Heteroptera: Coreidae) seize all of Europe?. Zootaxa, 1740(1), pp.66-68.
2. Fernandes J.A.M., Mitchell P.L., Livermore L., Nikunlassi M. (2015) Leaf-Footed Bugs (Coreidae). In: Panizzi A., Grazia J. (eds) True Bugs (Heteroptera) of the Neotropics. Entomology in Focus, vol 2. Springer, Dordrecht


Why add hydrogens in molecular dynamics simulations?

The RCSB Protein Data Bank (PDB) presently has 137,917 structures deposited in it, of which less than 10% have been solved by nuclear magnetic resonance (NMR). Most techniques in structural biology simply cannot resolve the positions of hydrogens in macromolecular structures; only NMR and neutron diffraction provide the positions of hydrogens "by default." Therefore, all-atom molecular dynamics force fields, the most notable of which are the OPLS, CHARMM, and AMBER series, require that the positions of hydrogens be deduced from the starting macromolecular structures and geometric criteria and patterns, that hydrogen bonds are known to generally follow, if the starting structure doesn't have hydrogens. "Generally" is an important word to point out here, as there often is no unique, unambiguous way to place the hydrogens in a structure. This is especially true of histidine, where the local environment of residues and/or cofactors may perturb its pKa in often unexpected ways. Simulating histidine in the wrong protonation state, when that histidine is an active site and crucial to the mechanism and process under study, may lead to spurious, misleading, and/or potentially nonsensical results. Hydrogens are required for a faithful, (relatively) realistic description of macromolecular structure, simply because they are always present in macromolecules and are crucial for macromolecular structure and functioning - recall that hydrogen bonds stabilize the secondary structure of proteins, the DNA double helix, etc., moreover, they often mediate intermacromolecular recognition and function. Thus, an explicit representation of hydrogens is required. The so-called coarse grained force fields, the most popular of which I believe are the various versions of MARTINI, group hydrogens along with heavier atoms to achieve an increase in the simulation time step and to reduce the number of particles in the system, but these force fields are a very poor choice when modeling specific recognition and interactions.

The ambiguities of protonation are not a matter of opinion, I'm afraid. One can go through all the structures in the PDB, only to find that the majority of  them have no hydrogens at all. One can explore the link to the PDB I've provided; one will find that out of the 131,917 structures in the PDB, 123,461 have been resolved by X-ray crystallography, of which only 10,749 have a resolution below 1.5 Å. To resolve hydrogens, a resolution below 1 Å is required. Indeed, high resolution crystal structures, NMR structures, and neutron diffraction structures (only 60 in the entire PDB!) are less than 20% of the entire structural archive. Techniques like electron microscopy have resolutions between 4 and 10 Å; in such cases, people are unsure about the positions of the heavy atoms; they don't even dare think about the hydrogens. So, it's not just the titratable groups that are problematic, in most structures one can't see ANY hydrogens. Of course, for backbones and alanine side chains, one probably has a pretty good guess where the hydrogens are, given the positions of the heavy atoms. But to answer the question - in MD, most often one needs to add hydrogens everywhere, not just in the titratable groups, because the starting PDB structure doesn't have any hydrogens. In fact, often times structures from the PDB have missing heavy backbone or side chain atoms, because those couldn't be resolved; sometimes termini are missing, sometimes large stretches of protein; these often need to be modeled-in.


Auxotrophic complementation test with yeast

If the yeast strain A is auxotrophic for AA 1 and the yeast strain B is auxotrophic for AA 2, neither would be able to grow in minimal medium by itself. But combined they complement the lack of AA1 in strain A by strain B and vice versa. That is metabolic complementation.


What's it called when a male seahorse gets "inseminated"?

Short answer
I think that "egg deposition" by means of the female "ovipositor" seems the most commonly used terminology.

Background
A cursory Google search yielded quite a few alternatives, ordered here from the most fancy to the least:

...that are deposited directly into the brood pouch ... (Look et al., 2007)
...transferring their eggs directly into the male brood pouch... (Masonjones & Lewis, 1997)
...the female injects her eggs into the male’s pouch using her penis-like ovipositor
...once all the eggs are inserted

References
- Look et al., J Exp Biol (2007); 210: 432-7
- Masonjones & Lewis, Copeia 1996; (3): 634-40


How long does it take for DNA to degrade

Degradation of DNA is gradual, but continuous, even in the freezer. However, they can sequence DNA from ancient animals in permafrost, or Neanderthal teeth. Fresh is always best, but there is no reason not to try PCR on your samples.


The processes that occur at the ER membrane in eukaryotic cells take place directly at the bacterial plasma membrane. Phospholipids are synthesised and inserted at the plasma membrane, and there is a protein translocation apparatus for translocation of proteins into the periplasmic space and insertion of transmembrane proteins into the plasma membrane.


Are there any bacteria that can receive ultrasound signals?

I'm going to post a quick answer here, really a thought piece.

Usually to detect a sound wave you need a sounding board about the wavelength of the sound.

Bacteria are on the order of a few microns in length.

Ultrasound frequencies range from 2 to 200 MHz (and up I assume).

To have a wavelength on the order of 3 microns, a 100 MHz wave would be needed.

So only on the very high end of the range.  If bacteria make sound though, they probably are on this frequency range.

I wonder if this has been looked at?  Not sure it has.  While in biology you never say never - if a bacterium really needs to pick up a wave it might have a clever adaptation to do so, but in the 100MHz + frequency range seems more likely.


In the linked paper, the authors discuss this as sex-based gene expression that evolved by sex-specific selection. The expression is not limited to one sex (which are sex-limited genes). Sex-biased genes are expressed by both sexes, but differently between sexes.


Why we shiver/tremble/shake while performing some work which requires high accuracy?

If you thread needles often - like a dozen times a day for many days - you will eventually be steady as a rock, because practice improves the process (you will also unconsciously maneuver to steady both hands.) It's not inevitable that all people have involuntary muscle movements with very fine motor skills; it's a matter of ability/practice for most.

The steadying of larger muscle groups like the upper arms - especially against gravity - is less controllable (e.g. threading a needle with arms fully extended), but not even closely outside the realm of possibility. Think of what great athletes, dancers, craftsmen are able to do that is "impossible" for mere mortals.


Advantages of bisexual reproduction over asexual one toward species promotion?

Those are very good questions. Unfortunately answers are not easy and ask for writing a lot! But maybe someone else will give it a try and make it better than I can. Note that the evolution of recombination and of sexual reproduction are not quite the same thing. Also, evolution of sexual reproduction is not the same than evolution from various reproductive system. Finally there are also questions concerning the evolution of sexual determination system. You might have more chance to get useful answers  by splitting up your question and to ask for evolution between different reproductive system. Hermaphroditism vs Bisexual reproduction. Asexual vs sexual. And finally on another post you may add the "conservation" part of your question.

What do you mean "animals that have two or more sexes"? Do you mean hermaphrodites?

You may have a look to other posts on this sites that discuss the question. I don't think there is one post yet that really goes in depth though.

I think that would be great if someone could post an easy-to-read source of information on the subject. Here is one but it is in french only. This presentation by Sally Otto will probably interests you.

Some hints in very short: One issue with hermaphroditism is selfing and its associated concept inbreeding depression. For conservation purposes, note that if one beneficial mutation occurs (at any locus) before another beneficial mutation had time to reach fixation, then  the frequency of one of the two beneficial mutations will necessarily goes to zero. You may be interested in the two-fold cost of sex. Müller's ratchet is also a concept you may want to learn about. There are several very interesting quantitative models on the subject and it is still an ongoing debate. You may be interested in the work of S. Otto and B.& D. Charlesworth. You may be interested in E. Charnov's book although it is a bit old now.


When the neuron reaches threshold, this is the trigger that leads to sodium channels opening and this creates a positive feedback process causing the neuron to become less negative and more positive, triggering more sodium channels to open until it is inevitable an action potential will be reached. During an action potential, the neuron cell becomes more positive compared to the outside for a very short period(ie, 1 millisecond or less).

Yes, depolarisation does mean the inside becomes less negative in this context.
You would expect the inside of the neuron to be at +55mV (or perhaps more) during an action potential, as the depolarisation of the neuron grows closer to reaching the sodium equilibrium potential which is estimated to be around +58mV. However, during the phase leading up to an action potential, potassium channels also remain open. The diffusion of potassium ions can lead to the cell becoming more negative. In other words, it limits the voltage of an action potential to around +33mV instead of +55mV.

Sources:

(1)https://www.khanacademy.org/science/biology/human-biology/neuron-nervous-system/a/depolarization-hyperpolarization-and-action-potentials

(2)https://opentextbc.ca/anatomyandphysiology/chapter/12-4-the-action-potential/


Why is compensatory negative supercoiling generated in a positively supercoiling ccDNA?

For a piece of topologically constrained DNA, Lk is constant. Since Lk = Wr + Tw, if you increase Wr in one area, it can be compensated by decreased Wr or Tw in an adjacent area. You may ask why the unwinding is concentrated in the adjacent region and not spread throughout. This is explained in the paper you link to:

  Although any superhelical strain generated by DnaA-mediated wrapping would be expected to spread throughout the topological domain that contains the origin, it may preferentially affect the nearby DUE, which is unstable and prone to spontaneous unwinding.

The DNA unwinding element (DUE) is unstable because it is AT rich:

  …the opening of individual AT/TA base pairs in the three DUEs investigated differs from that of GC/CG base pairs in at least two respects. First, the opening of AT/TA base pairs is significantly more favorable, kinetically and energetically, than that of GC/CG base pairs. Second, the opening of AT/TA base pairs is affected by long range effects of the DNA base sequences, whereas the opening of GC/CG is insensitive to the base sequence beyond that of nearest neighbors. The first difference confirms the earlier proposal that the high content of AT and TA base pairs is necessary to lower the stability and enhance the dynamics of the three DUE sites. The second difference suggests that the sequences of these AT and TA base pairs have been selected by evolution as a means to modulate the energetic stability of the three DUE sites according to their location and function in the origin of DNA replication.


I found out that this is on of the most common specious from this family in whole Euroupe called Bombylius major. From wikipedia article (same with picture):

The adult is 14 to 18 millimetres (0.55 to 0.71 in) in length, squat and very hairy, with a wingspan of around 24 mm (0.94 in). It has dark patches on the anterior half of the wings and long hairy legs that dangle while in flight. The very long proboscis is used to feed on the nectar of many species of flower, especially primroses. While its wings continue to beat its front legs grip the flower and its long rigid beak is inserted to collect the nectar.[2] Despite its fearsome appearance, the beak is quite harmless.[2]
Bearing a mimetic resemblance to bees their body is stout and furry, with the top of the thorax being black and shiny and the pile either brown, yellow, or white. They have long spindly legs as well as a long rigid proboscis found in the front of the head. Their boldly patterned wings have a distinct dividing border through the horizontal middle between the dark and clear portions. Their antennae are typically very short and pointed. In the field they will be seen hovering and darting above bare ground or flowers, in an up-and-down movement, accompanied by a high-pitched buzz.


How many allele for one gene are found inside our cell?

In short. Yes.

Each diploid cell has 23 pairs of chromosomes (22 of which autosomal)

In relation to the genotype part of the question. The "Tt" refers to each allele on the chromosome and wether it is dominant or recessive. Take for instance, hair colour. On one chromosome, there would be an allele from one parent and on the other an allele from the other parent. This is why two letters are needed, to show the allele given by each parent.

You can think of dominant and recessive in terms of how powerful the copy of the gene(allele) is. An allele that is able to overpower and mask traits is called dominant, one that is not strong and cannot mask traits is called recessive. This is why you need two recessive alleles for recessive disorders, otherwise the dominant allele would cover it up.

As this is a homework question I have tried to explain this in simple terms which you should understand. Hope this helps.


What's the point of glycolysis in fermentation?

Remember that glycolysis yields 2 NADH as well as 2 net ATP. This NADH can be used to a terminal electron acceptor to produce an end product with a net gain of ATP. End-products of fermentation can include lactate, acetate, butyrate, propionate and ethanol, all of which generate different amounts of additional ATP.

The exact pathways involved vary according to the organism, but anywhere between 1 (or even 0.5) and 4 additional ATPs can be generated, even without the involvement of oxygen. In the case of aerobic respiration of course, the NADH feeds into the electron transport chain and yields ATP.

EDIT: It's perhaps worth noting that the 2 ATP is gained. See @SatwikPasani's answer for the math.


Why doesn't life produce diamond, graphene, nanotubes, etc? Could it?

Biology does not have too many uses for super hard but brittle materials like a diamond. The hardest biological materials are also very tough as well since they need to form complex shapes for maximum utility. Limpet teeth are the hardest biological material known but are also incredibly strong, stronger than steel, not super brittle like diamond1.

As for graphene, the big problem there is reactivity; graphene is a great substance except it is pure carbon and has a huge surface area. If you put it in a solution full of carbon reactive chemicals, it starts doing weird things, and it has particularly weird interactions with cell membranes. Structurally, it is far more trouble than it is worth in something made of cells2.

You also have to remember that, in evolution, it is generally about "good enough", not perfection. Making a pure carbon structure would be an incredibly costly process in a biological (and thus aqueous) environment.

References:

Extreme strength observed in limpet teeth
Exploring the Interface of Graphene and Biology