The selective pressure of contraceptives

Interesting question, but the answer is simpler than you might think.

Antibiotics put selective pressure on bacteria. Bacteria resistant to that antibiotic evolve as only the resistant ones survive. But this is the key, there has to be at least some already resistant bacteria from which the new (resistant) population will emerge.

With contraception, this is not the case. There are no spermatozoids capable of penetrating condoms, for example, and you should also bear in mind that in most cases mild hormonal disbalance is enough to prevent conception. It's a very delicate process, and contraception is basically an overkill.

Even if some spermatozoids could penetrate condoms, that trait would have to be hereditary in order for evolution to occur.

If you'd want to prove that contraception constitutes selective pressure on humans you'd first have to prove that there are spermatozoids and egg cells that can beat contraception, and that it's hereditary.

Evolution doesn't work the way you think it does. If you kill a random person, even if you kill a million people, it's not necessarily selective pressure. There are rules to evolution, and one of them is that it has to be hereditary.

This is not.

It wouldn't even come close to being artificial selection, let alone natural selection.

Besides, there's 7.3 billion of us. More than ever. We can hardly say contraception is reducing the world's population.

You also fail to see one thing, that a person who uses contraception in teenage years still has kids as a young adult. Contraception just delays pregnancy until you're ready. In evolution, there's a concept of "surviving long enough to reproduce". You can both use contraception and be an organism with 10 kids - though not at the same time.


Relationship of bases in a gene to amino acids

Assuming that all 1200 bases in the gene code for mRNA, then 1200/3 = 400 is the correct calculation.

It's important to understand that a gene will only ever be transcribed from one strand of double-stranded DNA. Think about it mechanistically - first, DNA is transcribed to RNA by a polymerase that can only move in one direction. Second, the strand complementary to a gene's transcription start site is that sequence's complement and therefore not a start site itself. Hope that clears it up. :)


How would homologous recombination and mutations affect speciation?

Recombination occurs when homologous DNA sequences pair with each other and cross over, essentially swapping genetic material. Now, say that this crossover junction is in the middle of a gene, and we have some genetic differences in the top half and some in the bottom that distinguish the two alleles. If recombination occurs in the middle of the gene, then a new combination of alleles is created that didn't exist before. This new version of the chromosome can now be passed on as a single unit via sexual reproduction.

I left out a lot of details obviously, but this is the basic idea. The reason why recombination adds to genetic diversity and can lead to speciation is because it is essentially mixing and matching existing combinations to create new alleles.


Various adaptations help desert animals survive in dry and hot environments. These adaptations are not specific to Kangeroo rats in particular.

From Wikipedia :

  Metabolic water refers to water created inside a living organism through their metabolism, by oxidizing energy-containing substances in their food. Animal metabolism produces about 100 grams of water per 100 grams of fat, 42 grams of water per 100 g of protein and 60 grams of water per 100 g of carbohydrate.

  Some organisms, especially xerocoles, animals living in the desert, rely exclusively on metabolic water. Migratory birds must rely exclusively on metabolic water production while making non-stop flights. Humans, by contrast, obtain only about 8-10% of their water needs through metabolic water production.

  In mammals, the water produced from metabolism of protein roughly equals the amount needed to excrete the urea which is a byproduct of the metabolism of protein. Birds, however, excrete uric acid and can have a net gain of water from the metabolism of protein.

Also see Xerocoles - Water Conservation


The human has 46 double chromosomes or simple chromosomes?

Your first picture shows a chromosome that has been (1) condensed and (2) undergone DNA replication. During G1 interphase (normal cell activity; not dividing), your chromosomes actually do not look like either of the pictures. They look more like a mass of noodles (called chromatin; look at the image provided below); it is only during prophase (step 1 of mitosis, where the cell undergoes division) that the chromosomes condense into the form you have depicted in picture 1. Now, in G1 interphase, you only have single chromosomes. You have 46 of these, which can be grouped into 23 pairs—23 from your father, and 23 from your mother. Remember they aren’t condensed during this stage.

I have also included a diagram of the cell cycle:

In S interphase, DNA undergoes replication, and each of the 46 chromosomes create a double. This double sticks to the original chromosome at a point called the centromere. So long as the two “chromosomes” are conjoined at the centromere, the two “chromosomes” are considered as one chromosome, consisting of two sister chromatids (each like the “single chromosomes” you had previously). Again, in S interphase, chromosomes are not condensed, and look more like noodles than either one of your pictures.

During prophase, the chromosomes look like picture 1. Picture 2 depicts a sister chromatid during prophase (and metaphase), which is considered a chromosome after anaphase (when the two sister chromatids are separated from their centromere). Remember that when the chromatids are not conjoined at the centromere, they are considered each as their own chromosome.

Thus, the human body always has 46 chromosomes. They are “double chromosomes,” as you call them, during S phase of interphase to the beginning of anaphase of mitosis. They are “single chromosomes” from anaphase of mitosis to the beginning of S phase of interphase. As most cells spend the most time in G1 interphase (normal activity), you can say that most of the time their chromosomes exist as single chromosomes. Again, note that most of the time they don’t look like your pictures, except for the times that I mentioned above.

EDIT: To answer the question in your comment:

  If during interphase the DNA is not yet condensed and looks like a mass of noodles, then how can we know that there are 46 chromosomes (single ones in this case)?

During interphase, it is indeed difficult to tell how many chromosomes there are. It is only when they condense that they become visible to the eye and can be observed through a microscope. Chromatin, in its noncondensed form, is considered as euchromatin—that is, true (noodly) chromatin. When it is condensed, it can be referred to as heterochromatin. We can only count the number of chromosomes when they are in heterochromatin form; euchromatin is invisible to us. If we align all the chromosomes present, we will get something called a karyotype. Look below.

(You can see each chromosome in each of the 23 pairs are “double chromosomes.” These chromosomes were likely documented during prophase. Some karyotypes show "single chromosomes," most likely taken during anaphase or early telophase.)

In any case, double or single, we can observe that there are 46 chromosomes at all times. If we see "double chromosomes," we would find 46 chromosomes. If we see “single chromosomes,” we would still find 46 chromosomes. In both cases, we would find 46 centromeres, and ergo, 46 chromosomes.

References

Reece, Jane A., Lisa A. Urry, Michael L. Cain, Steven A. Wasserman, Peter V. Minorsky, and Robert B. Jackson. "The Cell Cycle." Campbell Biology. 10th ed. Glenview: Pearson, 2014. 232-50. Print.
https://micro.magnet.fsu.edu/cells/nucleus/images/chromatinstructurefigure1.jpg
http://www.everythingmaths.co.za/science/lifesciences/grade-10/03-cell-division/images/d62a6708a4a3942f21e003500ddf9664.png
https://study.com/cimages/multimages/16/karyotype_karyogram.png


Why does oxidative phosphorylation require complexes 2 and 3?

The numbering of the complexes in the respiratory chain is confusing, as it creates the impression that the chain is structured like

Complex I $\rightarrow$ Complex II $\rightarrow$ Complex III $\rightarrow$ Complex IV

... but this is wrong. There are in fact several ways of feeding electrons into the respiratory chain. They all begin with one enzyme E that oxidizes an electron carrier in the mitochondrial matrix, such as NADH, FADH2, or ETF (electron transfer flavoprotein) and transfers electrons to coenzyme Q, which is then processed by Complex III, after which electrons are handed on to Complex IV. Both complex III and IV pump protons. But there are several options for the first enzyme E:

Complex I (NADH dehydrogenase). This handles all electrons from NADH (from many sources in oxidative metabolism) and is typically the major source of electrons in the chain. It is the only enzyme E that also pumps protons itself.
Complex II (succinate dehydrogenase) accepts electrons from succinate (a step in the TCA cycle).
ETF dehydrogenase accepts electrons from reduced ETF, notably from fatty acid oxidation.
Glycerol-3-phosphate dehydrogenase accepts electrons from cytosolic NADH (from glycolysis) via the glycorol-3-phosphate shuttle.

There are more alternatives, but I think these are the most important ones. So you are absolutely correct that when NADH is the substrate, Complex II is not involved. There is in fact not one respiratory chain, but several possible chains with different starting points E,

E $\rightarrow$ Complex III $\rightarrow$ Complex IV

You might think of this as a "fan in" structure where the various enzymes E all converge on Complex III. (I don't have the energy to draw this :)

As for the proton pumping at Complex III, it is not the case that the H$^+$ pumped are exactly those derived from NADH --- the system is more complicated than that. The respiratory chain(s) convert chemical energy from the redox reactions into potential energy (a proton gradient), but most of the H$^+$ pumped are obtained from the mitochondrial matrix. The exact number of protons varies depending on the substrate: for example, the 2 electrons donated by NADH at Complex I is sufficient to pump up to 10 protons. Actually, the stoichiometry is not fully understood, and there isn't really an exact integer number of H+ pumped, because this pumping is an imperfect physical process --- there is leakage, protins slipping back into the matrix etc.


What is the transcriptome in layman's term?

There are three "omic" definitions that might help you.

The DNA is the long term storage of the information. You're probably familiar with this concept, and the study of this type of information is genomics.

One of the major functions of DNA is it's use as the blueprint for the production of proteins. Proteins carry out all sorts of structural and functional roles in the cell. Which proteins are present at a certain times and locations is known as the proteome. This is studied in proteomics.

Inbetween the DNA and the protein is an intermediate step. The DNA is transcribed to RNA, and then the RNA is translated to the protein. During the transcription of DNA to RNA, certain sequences of the DNA are not transcribed to RNA for a variety of reasons. The study of what exactly is transcribed at what time in which locations is transcriptomics.


What are the basic skills required to pursue future studies in theoretical ecology?

Theoretical ecology
From wikipedia

Theoretical ecology is the scientific discipline devoted to the study of ecological systems using theoretical methods such as simple conceptual models, mathematical models, computational simulations, and advanced data analysis. Effective models improve understanding of the natural world by revealing how the dynamics of species populations are often based on fundamental biological conditions and processes. Further, the field aims to unify a diverse range of empirical observations by assuming that common, mechanistic processes generate observable phenomena across species and ecological environments. Based on biologically realistic assumptions, theoretical ecologists are able to uncover novel, non-intuitive insights about natural processes. Theoretical results are often verified by empirical and observational studies, revealing the power of theoretical methods in both predicting and understanding the noisy, diverse biological world.
The field is broad and includes foundations in applied mathematics, computer science, biology, statistical physics, genetics, chemistry, evolution, and conservation biology. Theoretical ecology aims to explain a diverse range of phenomena in the life sciences, such as population growth and dynamics, fisheries, competition, evolutionary theory, epidemiology, animal behavior and group dynamics, food webs, ecosystems, spatial ecology, and the effects of climate change.
Theoretical ecology has further benefited from the advent of fast computing power, allowing the analysis and visualization of large-scale computational simulations of ecological phenomena. Importantly, these modern tools provide quantitative predictions about the effects of human induced environmental change on a diverse variety of ecological phenomena, such as: species invasions, climate change, the effect of fishing and hunting on food network stability, and the global carbon cycle.

Computational Biology
from wikipedia

Computational biology involves the development and application of data-analytical and theoretical methods, mathematical modeling and computational simulation techniques to the study of biological, behavioral, and social systems.1 The field is broadly defined and includes foundations in computer science, applied mathematics, animation, statistics, biochemistry, chemistry, biophysics, molecular biology, genetics, genomics, ecology, evolution, anatomy, neuroscience, and visualization.2
Computational biology is different from biological computation, which is a subfield of computer science and computer engineering using bioengineering and biology to build computers, but is similar to bioinformatics, which is an interdisciplinary science using computers to store and process biological data.

Field Ecology
Ecology can be studied empirically through data analysis, through lab experiments or through field observations and experimentations. Field ecology refers to this last point that is, it refers to empirical ecology in the field.
Conclusion
Potential Misunderstanding
In your post, you seem to suggest that field ecology is a subfield of theoretical ecology. It is not! Either you work as a theoretician or as an empiricist (and then eventually as a field ecologist). Of course many people do both theory and empiric work.
Note that whether you are theoretical or an empiricist working in ecology, you will need to have a good understanding of the theory behind the science of ecology.
Computational biology vs theoretical ecology
In opposition to empirical ecology and field ecology, computational biology and theoretical ecology do not have a hierarchical relationship. If you work in theoretical ecology you can make analytical modelling or numerical (computer) modelling. If you work in computational biology you could analyze data in genetics, you could model cell processes, you could simulate interacting populations in ecology and many other things.
What should you chose?
What skills do you need?

Do you like data analysis (statistics and R and python coding)? You will have to analyze your data whatever you chose!

Do you like numerical simulations (lots of coding, incl. languages like C++)? If no, then maybe avoid computational ecology!

Do you like analytical modelling (lots of math)? If no, then maybe avoid making analytical models in ecology!

Do you like messy, complicated, tiring field work? if not, then maybe avoid working as a field ecologist.

What would you imagine to work on?

What question would you like an answer to? Think about it and try to understand how you would address the question you are trying to answer.

My advice

Do not be afraid of any field, any technics, any programming language, etc... You are good enough and have enough time to learn what you do not know.

Do whatever you like most!


Modularity score comparison between different algorithms in network analysis

Since the goal of modularity estimation algorithms is to find the community structure that maximizes modularity, it is valid to compare different algorithms based on their modularity estimate. However, i) it is not the only consideration for choosing a community detection algorithm, and ii) the obtained modularity estimate will depend on the particular structure of each network, e.g. its number of nodes. For a principled comparison between several different algorithms, see Yang et al. (2016). Based on multiple criteria, they identify the multilevel (or Louvain) algorithm (Blondel et al. 2008) as the overall best choice.

References
- Yang, Zhao, René Algesheimer, and Claudio J. Tessone. “A Comparative Analysis of Community Detection Algorithms on Artificial Networks.” Scientific Reports 6, no. 1 (August 2016). https://doi.org/10.1038/srep30750.
- Blondel, Vincent D., Jean-Loup Guillaume, Renaud Lambiotte, and Etienne Lefebvre. “Fast Unfolding of Communities in Large Networks.” Journal of Statistical Mechanics: Theory and Experiment 2008, no. 10 (October 2008): P10008. https://doi.org/10.1088/1742-5468/2008/10/P10008.


What you describe is called a ring species. From wikipedia:

  In biology, a ring species is a connected series of neighbouring populations, each of which can interbreed with closely sited related populations, but for which there exist at least two "end" populations in the series, which are too distantly related to interbreed, though there is a potential gene flow between each "linked" population.1 Such non-breeding, though genetically connected, "end" populations may co-exist in the same region (sympatry) thus closing a "ring".

  Have this ever been observed?

While ring species is a classical theoretical concept, the cases of ring species is often open to some interpretation and limit case of what we want to call a ring species.

The question has been asked at Do ring species exist?, however the post is still left unanswered.

  And how would you classify C?

There is no obvious simple way to answer that question. The concept of ring species just shed light into the fact that the concept of species is an outdated concept and does not have a good formal definition. For much more discussion about the concept of species you should definitely have a look at the post How could humans have interbred with Neanderthals if we're a different species?.


Why does my room suddenly look 'reddish'? My eyes seem to adapt to color

Short answer
The phenomenon you describe can be explained by the negative afterimage effect, which indeed is elicited by adaptive processes in the retinae.

Background
In the retina there are three types of color photoreceptors, called cones. They are sensitive to red, green and blue, respectively. Colors are processed in the retina through a process explained by the Hering model. This model assumes that there are two sets of opponent colors, namely red - green and blue - yellow (Fig. 1).

This model assumes that in the red-green opponent channel the red cones inhibit the output of green cones and vice versa. In the blue-yellow channel the blue cones inhibit the green/red (= yellow) cone output and vice versa.

Now look at the visual illusion shown in Fig. 2. This illusion nicely illustrates the effect. After looking at the image for half a minute, your cones adapt to the color input. Particularly relevant to your question is that the green cones adapt to the green and become less responsive to green (this happens when you are in your "greenish blue shade acting as a sunlight blocker. This gives this entire place a greenish [blue] tint as shown. (Ref. 'area G')." Now this in turn lowers the green inhibition of the red-half of the red-green opponent channel. In turn, when you enter your "part of [the] house [with] a creamish tinge to it, [] 'area Y' []" the green channel will not inhibit the red-half and everything will have a reddish hue to it, akin to looking at the white half of the illusion after 30 seconds below.

Reference
- Sci Am, October 2013

Fig. 1. Hering model of color vision. Left panel: brightness coding. Right panel: opponent colors code for color, namely the red-green and blue-yellow channels. source: Bio.SE

Fig. 2. Visual afterimage illusion. Look at the fixation dot in the middle of the tripartite circle on the left for 30 seconds. Don't look away. Now look instantly to the white part on the right. If you don't see much, or only vaguely, try again. Blinking may help to shortly enhance the illusion. source: Sci Am


Will I hyperventilate if I breath twice as fast at an altitude with half as much oxygen as I am used to?

By definition, hyperventilation is a state of increased breathing where the exhaled $CO_2$ is greater than what is produced by the body.

Except in artificial condition or in disease process, breathing faster than the autonomously-dictated rate is going to cause hyperventilation. You have a fine-tuned control of respiration that will work out the correct breating rate for you.

Oxygen is actually irrelevant for this phenomenon, first because of the definition of hyperventilation, but also because oxygen is mostly transported through haemoglobin (98+%). This means there is a fixed quantity of oxygen that can be transported by unit volume of blood (and by breath, for a given cardiac output), and the maximum is already reached at normal breathing rate. Breathing faster does not allow for better oxygenation of the blood. (even at an higher altitude)

On the other hand, $CO_2$ is transported by the plasma, dissolved (7%), but also in the form of bicarbonate (93%) through the following equilibrium :

$$ H_2O + CO_2 \rightleftharpoons \underbrace{H_2CO_3}_\text{Carbonic acid}  \rightleftharpoons \underbrace{HCO_3^-}_\text{Bicarbonate} + H^+  $$

In the alveoli, a quantity of $CO_2$  will diffuse to the alveolar air, and be breathed out, the target being eliminating the quantity produced by the body. However, in opposition to oxygen transport, it is possible to overshoot by breathing faster, because removing $CO_2$ drives the equilibrium in direction of $H_2O + CO_2 \leftarrow  HCO_3^- + H^+ $ that is, eliminating additional $CO_2$ through the removal of bicarbonate from the blood.

This is hyperventilation, and leads to hypocapnia, causing that particular sensation of dizzyness. It is also leads to respiratory alkalosis, because, as seen in the reaction equation, this incurs the loss of protons ($H^+$).


The optimum pH for catalase can be found be a simple search. According to the Wikipedia entry for catalase it is approximately 7.

With the exception of extreme pHs, which can cause denaturation, the pH optimum of enzymes is often related to the ionization of the amino acid residues that participate in the reaction (and hence their pKa). Often what happens is that the reaction mechanism requires a residue to alternate between an ionized and non-ionized form, so that the optimum pH approximates to the pH of half-ionization. (This may not be the same as the pKa of the amino acid in solution, as the environment at the active site can alter this greatly.)

You need to understand ionization chemistry to appreciate this. If you do not, you could try this section from Berg et al. first. If you do, look at the mechanism of action of well-established enzymes like lysozyme and the serine proteases.

I cannot help you further with catalase. Apparently it is not well understood.


What Goes on in Photosystems at the Molecular/Atomic Level?

The energy transfer is achieved by a process called "resonance energy transfer". It needs the positioning of the donor and the acceptor in very close proximity to each other - the light harvesting complexes are optimized for this. This allows the collection of small amounts of light energy and still enables photosynthesis. The figure shows how this works schematically:

The figure is from this webpage, which gives a good introduction.


The localization of the protein kinase A (PKA) cannot be explicitly answered, since the localization depends on the activation state of the protein. Lets have a look at the protein itself first, as this is important for the activation.

PKA consists of four subunits, two catalytic subunits and two regulatory subunits. See the image from the Wikipedia article on PKA:

Each regulatory subunit R is binding two cyclic AMP (cAMP) molecules and dissociates then from the protein complex. This sets the catalytic subunits free, which can then transfer phosphate groups from ATP to serine or threonine residues of target proteins. Among the target proteins is also the Phosphodiesterase (PDE) which gets activated by phosphorylation from PKA. Activated PDE hydrolyzes cAMP into AMP which reduces the amount of free cAMP which is necessary for PKA activation. PKA is also inactivated by phosphorylation.

In the cell you will find PKA almost everywhere. The traditional belief is that the protein is activated in the cytosol and enters the nucleus where it phosphorylates targets like CREB which then subsequently binds the the CRE sequence in gene promoters and activates this genes. Reference 1 shows that PKA is also activated in the nucleus, meaning that also the inactive form is present there. Reference 2 gives a nice summary of the article.

The regulatory subunit of inactive form of PKA binds to a special class of proteins: The A-kinase anchor proteins (AKAP). These are membrane bound and allow the association of PKA to membranes, although the protein itself is not directly binding to the membrane. The AKAP family is rather big (at least 50 family members are known today), which probably allows the localization of PKA at different membranes. Have a look at references 3-5 for details on the localization and the anchoring.

References:

Regulation of nuclear PKA revealed by spatiotemporal manipulation of
cyclic AMP.
Protein kinase A activated in the nucleus as well as the cytoplasm
The where's and when's of kinase anchoring
Localization of A-kinase through anchoring proteins.
The biological functions of A-kinase anchor proteins


Signaling pathways with Receptor Tyrosine Kinase clarification

The active form of Ras should definitely be bound to GTP, to activate Raf. I don't see anything else wrong with the diagram. For reference, here is another useful diagram the pathway from Nature.


Even though you - or the problem did not clarify, I assume in my answer that you work with eukaryote system, even though the principle of the replication is the same.

dNTPs do have an OH group on their 3rd carbon atom (for eg. check this wiki-page for dCTP) so I don't think that's the issue here. My guess is that the first tube contains the radio labeled GTP and the second does not, so even the DNA is there, you cannot see it - even though the question specifically asked why DNA was not synthesized, my opinion is that it's a tricky question to confuse you.

For the second problem we need to dig into the replication process a little bit:

In the replication fork the two strands are synthesized differently. The so called leading strand is made continuously, without interruptions, however the other strand - the so called lagging strand is synthesized by ligating small fragments - aka Okazaki fragments. These small fragments require their own RNA primers that need to be removed after synthesis is done.
Now since the origin of replication is in the middle and replication can proceed both ways, on a linear fragment such as yours you can get two 2000bp fragment from the two leading strands. Would it be a circular DNA, then you could still get 4kbp fragments since the replication could go around the DNA circle.
The smaller 500bp fragments that are quite abundant in the tsr1 lane, are the fragments that cannot be ligated. That being said I must admit that 500bp Okazaki-fragments would by atypical for eukaryotes (usual is around 100-200bp). So the enzymes responsible for this could be:

DNA Ligase - the one responsible for ligating (joining ) the lagging strand's fragments.
Polymerase delta (Pol δ): That is responsible for lagging strand synthesis and primer removal - in this case the primer removal function might be defective, this causes that the primers stay on the DNA and complete synthesis and ligation cannot occur.
The last protein although it is not quite an enzyme is the DNA clamp complex (PCNA). This complex stabilizes the polymerase to DNA, but when reaching a previous fragment the polymerase should dissociate. But if the clamp is dysfunctional than the polymerase gets stuck on the end of the fragment thus no primer removal and ligation can occur.

If need more info read this wiki-page.


The answer to this is perhaps not as simple as you may think, in part because there are many different helicases in the human body. There is also some passive activity of a helicase that does not require ATP.

It is not clear exactly whether ATP is just involved in the translocation of the helicase or the actual unwinding.

For a RecQ helicase in E. coli, one study found that "The determined tight mechanochemical coupling of 1.1 ± 0.2 ATP consumed per nucleotide traveled indicates an inchworm-type mechanism." For more information see Sarlós et al. (2012).

Another study (Donmez and Patel, 2008) notes that "As compared with non-ring-shaped helicases such as PcrA (Dillingham et al, 2000) and UvrD (Tomko et al, 2007) that move on an average 1 nt for every ATP hydrolysed, the ring-shaped T7 helicase is three times more fuel efficient." This shows how there can be quite a bit of variation.

Bottom line - you can count on your fingers the number of nucleotides unwound by a helicase per ATP.


Current scientific theories for evolution of Cucurbita

You're right that modern species would have a hard time spreading group seeds, though you're not quite right about the reasons.  Cucurbita rinds are extremely bitter, so that modern mammals are reluctant to (or unable to) process the rinds to access the seeds.

According to a recent article (Gourds and squashes (Cucurbita spp.) adapted to megafaunal extinction and ecological anachronism through domestication), the explanation is that wild Cucurbita first co-evolved with North American megafauna, like mammoths and mastodons, who could tolerate the toxic/bitter rind. (The authors also suggest that megafauna also produced suitable habitats for their growth.)

Following the extinction of these megafauna, humans picked up the slack, with most wild Cucurbita going extinct and only domesticated versions remaining.

  Collectively, these results point to wild-type declines coinciding with widespread domestication. ...megafauna consumed Cucurbita fruits and dispersed their seeds; wild Cucurbita were likely left without mutualistic dispersal partners in the Holocene because they are unpalatable to smaller surviving mammals with more bitter taste receptor genes. ... Thus, anthropogenic landscapes provided favorable growth habitats and willing dispersal partners in the wake of ecological upheaval.


How precisely can we sense temperature differences?

Short answer
Temperature differences of 0.02 degrees Celcius can be distinguished, dependent on various factors including experimental conditions and bodily location.
Background
The ability to discriminate temperature differences depends on whether it is a cooling or heating pulse, the skin temperature, the duration of the temperature stimulus, age, bodily location among other factors. Unfortunately I cannot access the primary literature other than a few isolated smaller studies. However, Scholarpedia has a very nice entry and associated references, and I quote:

The thermal sensory system is extremely sensitive to very small changes in temperature and on the hairless skin at the base of the thumb, people can perceive a difference of 0.02-0.07 °C in the amplitudes of two cooling pulses or 0.03-0.09 °C of two warming pulses delivered to the hand. The threshold for detecting a change in skin temperature is larger than the threshold for discriminating between two cooling or warming pulses delivered to the skin. When the skin at the base of the thumb is at 33 °C, the threshold for detecting an increase in temperature is 0.20 °C and is 0.11 °C for detecting a decrease in temperature.
The rate that skin temperature changes influences how readily people can detect the change in temperature. If the temperature changes very slowly, for example at a rate of less than 0.5 °C per minute, then a person can be unaware of a 4-5 °C change in temperature, provided that the temperature of the skin remains within the neutral thermal region of 30-36 °C. If the temperature changes more rapidly, such as at 0.1 °C/s, then small decreases and increases in skin temperature are detected. [...]

You also were interested in the palmar skin: here average difference limens are 0.02 - 0.06 °C, dependent on the temperature step used. These values were obtained using cooling pulses. In other words, differences in two cooling pulses of 0.02 - 0.06 °C were discernible, with higher limens needed for higher pulses. Baseline temperatures (29 - 39 °C) had little effect (Darian-Smith et al., 1977).
Reference
Darian-Smith et al., J Invest Dermat 1977;69:146-53
Note
The Stevens, J. C., & Choo, K. K. (1998). Temperature sensitivity of the body surface over the life span. Somatosensory & motor research, 15(1), 13-28 article as commented on by Corvus is indeed a must-read, but my uni library does not have access to it unfortunately.


What makes tones sufficiently useful that it would lead to the evolution of tonal processing?

I think the whole issue is that you put all your focus into music. The ability to tell apart different tones hasn't evolved with the culture of music playing. It is much older.

Ability to distinguish different tones in non-human animals

Humans are of course not the only animals that are able to recognize tones. Mice for example can as well accurately tell the difference between two close tones (ref.).

Perceiving its environment

So why is the ability to tell different tones apart important. It is important because it allows one organism to better perceive the elements in its surrounding. For example, consider being in the savanna and you can't tell the difference between a lion roaring and a water fall. It seems to be a pretty important handicap.

Tones recognition in social contexts

A very large part of animal's communication is based on tons. Very primitive forms of language are mostly based on tones. Courtship display for example is often based on the tone of the other gender (the tone is correlated with the size of the organ producing the tone). A very large part of human's communication is based on tone as well. You might want to have a look at Albert Mehrabian.

If you have more questions about the importance of non-verbal communication you will need to ask your questions to psychologists (on CognitiveScience.SE) and not to biologists. Note btw, that the condition of being unable of recognizing different tones is called tone deafness.


According to this author (1) the human body emits radiation, mostly in the infared region. Human body temperature generally exceeds that of its surroundings and so there is a net flow of heat from the body into the environment, some due to convection and some due to thermal radiation.

This Czech paper suggests (2) human EM emission in a particular low-frequency band (0.5 - 30 Hz), but the writing is awkward and I do not think this is peer-reviewed.

A more comprehensive Russian paper (3) discusses, among other things, emission of photons (light!) from human skin. The energy of this light is not very high (1-3eV, which is 1-3 times $1.602~ \text{x}~ 10^{-19}$ Joules), but it's not nil.

This interesting topic has been studied extensively and this is a quick glance. Am adding the link furnished in a comment by OP above which does suggest that the body can emit energy via radioactive decay.

Also, this link (4) based on the paper by Toohey below discusses radioactive emission by humans in some detail, including radioactive decay of potassium-40. There is apparently a mechanism by which ambient gamma radiation can interact with atoms in cells (photoelectric effect) to produce x-rays, which are emitted from the body.

(1) Olivia Lee, Hong Kong Observatory, Sept. 2010

(2) Lipkove, Cechak, Human Electromagnetic Emission in the ELF Band,Measurement Science Rev. vol. 5 sec. 2, 2005

(3) Ignativ et al., Fields in the Electromagnetic Spectrum Emitted From the Human Body..., J. Health, Medicine and Nursing, vol. 7, 2014

(4) Toohey RE, Keane AT, Rundo J. Measurement techniques for radium and the actinides in man at the Center for Human Radiobiology. Health Phys. 44(1):323–341; 1983.


How to find out the when we had a common ancestor with a particular animal

TimeTree [http://www.timetree.org] is one site that allows you to look at times from divergence of various taxa. Their FAQ describes how they calculate the times by pointing to this paper: Tree of Life Reveals Clock-Like Speciation and Diversification, but in general they used standard molecular clock approaches. You ask about downloading their database: they say

  The TimeTree Database data is currently not available for download. Methods for making these data available in the future are currently under discussion.


Why does our voice change when we get affected by cold or cough?

The important point is that your voice is influenced by airflow, and your vocal cords. When we're sick, and it depends on what it is, a number of factors change the sound of your voice by influencing the two of these, either: By changing airflow due to respiratory tract swelling or fluid buildup, or by damage/swelling/alterations to the vocal cords. In a couple  of examples: A weak airflow might produce a higher pitch or weaker voice, or perhaps swollen vocal cords produce that hoarseness associated with decreased frequency of vibration.


There is only one segment between the thorax and the abdomen and the first segment of the abdomen is not elongated, which indicates this is a Formicinae.

Because the head width is similar to the thorax width from top view, this likely corresponds to a social parasite ant from the genus Lasius.

See ref below:

  Seifert, Bernhard. Die Ameisen Mittel-und Nordeuropas. Lutra Verlag-u.
  Vertriebsges., 2007.


How does paracetamol interfere with immune system?

First question: Yes. The immune system releases pyrogenic cytokines such as IL-1. Bacteria aren't typically used to 37C, they prefer working at under that temperature to function in the environment. Our body however can take a few degrees here or there however this severely compromises the bacterial enzyme activity. The same is true for other pathogen enzymes. The body also increases copper concentrations in the blood for similar reasons. Problem is of course if the body goes into overdrive and raises our temperature too much, this compromises our own ability to fight the infection so in that case antipyretics like paracetamol can reduce fever.

Second question. It isn't a side effect, however paracetamol works by blocking things like IL-1 that raise temperature. How IL-1 raises your temperature is quite interesting, it tells the hypothalamus (our thermostat) that it should be set higher. So we feel cold (so we try to keep ourselves warm) and the body thinks it's cold (so it increases the temperature by burning glucose mainly)


Code Golf!

This is my Python script, avoiding regex and not at all prettified.

def gettract(strand):
    #if strand is 1 then replace C with T and split on T
    #else replace A with G and split on G

    if strand==1:
        print 'top strand purine tracts:'
        aseq=seq.replace('C','T')
        tracts=aseq.split('T')
    elif strand==2:
        print 'top strand pyrimidine tracts:'
        aseq=seq.replace('A','G')
        tracts=aseq.split('G')
    sortedtracts=sorted(tracts,key=len,reverse=True)
    for i in range(5):
        print len(sortedtracts[i]), sortedtracts[i]

f=open('ec_dna.txt','r')
l=f.readlines()
print 'Sequence analysed is %s' % l[0][1:] #the header line
f.close()
seq=''.join([i.rstrip() for i in l[1:]])
print 'sequence length is %i' %len(seq)
print
gettract(1)
print
gettract(2)

And here is the output:

  Sequence analysed is E. coli K-12 MG1655 U00096.2 (1 to 4639675 = 4639675 bp)

  sequence length is 4639675

  top strand purine tracts:

  28 AGAGAGAAAAGAAGAAGAGAAAAGAAAA

  22 GGGGGAGAAAGGGGGGAAAAGG

  20 AAAGAGGAAAGGGGGGGGGG

  20 GAAGAGGAAAAGAAAGAAGG

  20 AAAAAAGAAGAGAAAAAAGA

  top strand pyrimidine tracts:

  29 TTTTTCTCTTTCCCTTTTCCCTTCCCTCT

  22 CCCTCCTCTTCTCTCCCTCCCC

  21 TTCTCCTCCTTCTCTTTTCTT

  21 TTTTTCTTCTCTCTTTTCCTC

  21 CTCCCCTTTTCCCTTTTCTCC

The longest purine tract is 29 bases long, and is on the bottom strand.

This script doesn't handle the problem that the E. coli genome is a circular molecule, so if the longest tract was split at the origin it would be missed - I leave that and obtaining the coordinates of the longest tract as an exercise.


Why is gene finding in Eukaryotes such a difficult task?

The main problem is that while most of the things you describe are necessary to have a protein coding gene (introns, the non-coding regions within a coding region, aren't actually per se, even though they're common), they are not sufficient. Additionally there are also genes for non-coding RNAs (including tRNA and rRNA), which obviously don't have a 'coding region' (and also usually no introns).

In order to classify something as a functional gene we usually require that is actually made into (at least) RNA, which requires regulatory sequences that lead to transcription of the gene, these are called promotors. In eukaryotes there are many different promotor sequences, so its very hard to predict them computationally, additionally there are evolutionary remnants in our genomes, which are called pseudo-genes, and while they still have the general structure of a gene, they are not actively used any more.


What determines the perceived pitch (frequency) of tinnitus?

Short answer
Perceived tinnitus pitch tends to resemble the frequency content of the loud sound that induced the tinnitus.

Background
Solid, laboratory-controlled studies to the perceived pitch of temporary, noise-induced tinnitus ("ringing in the ears") are ethically questionable, because researchers have to deliberately expose study subjects to potentially damaging loud sounds. Therefore, data on temporary noise-induced tinnitus are scarce and confined to a small handful of studies done in the 1960's (Henry & Meikle, 2000).

In one of these studies (Atherly et al., 1968) the authors exposed the study subjects to loud acoustic stimuli of various pure tones. The subjects reported to experience tinnitus pitched within a certain frequency band around the tonal stimuli received. The stimulus frequency and perceived pitch approached a 1:1 relationship, such that the tinnitus pitch was e.g. 4 kHz when the noise frequency was 4 kHz. Between-subject variability was, however, considerable. For example, at a stimulus of 6 kHz, the range of perceived pitch was 4-9 kHz.

The other study I found based on the review by Henry & Meikle (2000) showed that the perceived tinnitus pitch increased when the frequency of the loud tonal stimulus or frequency content of broadband noise increased (Loeb & Smith, 1967). Basically this confirms the data from Atherly et al. (1968). However, the perceived pitch did not coincide with the stimulus frequencies, and there was considerable variability between subjects. For example, some subjects reported multiple frequencies in their tinnitus, some reported a hissing tinnitus, while others did not develop any tinnitus at all (Loeb & Smith, 1967).

In all, your suggested perceived tinnitus pitch of 17 kHz is unexpected, given that noise-induced hearing loss (by loud music exposure etc.) typically results in a 4-kHz notch in the audiogram where hearing loss is greatest. Hence, tinnitus would be expected to occur around this frequency as well. But again, variability is very high and it may well be possible it is higher pitched in your case. Also note that 17 kHz is very high and near the upper audible frequency limit for humans (e.g., the sound an old CRT screen makes, i.e., hardly perceivable for many adults).

Most research on tinnitus has been done regarding patients with chronic tinnitus complaints that suffer from sensorineural hearing loss (i.e., damage to the hair cells in the cochlea). Typically, the perceived tinnitus pitch in this group is associated with their hearing loss. In other words, the pitch of the tinnitus generally matches a frequency range within the region of frequency loss (Eggermont & Roberts, 2004).

References
- Atherly et al., JASA 1968;44:1503-6
- Eggermont & Roberts, Trends Neurosci 2004;27:676-82
- Henry & Meikle, J Am Acad Audiol 2000;11:138-55
- Loeb & Smith, JASA 1967;42:453-5

Further reading
- What's the Frequency of the ringing in my ear?
- Can humans perceive sounds above 20 kHz?


What do we mean by MHC molecule diversity? Does each human have a variety of MHC molecule isoforms?

You're right that both polygeny and polymorphism contribute to the diversity of a given gene in the population correctly described what they mean individually.

However, you missed that the polygeny of MHC means that the human genome has 3 different loci/genes (called MHC-I A,B & C) in the haploid genome, meaning that any given human as actually 6 copies of the gene (i.e. 3 copies from each parent). All of these copies perform the same function of presenting peptides to CD8+ cells, but will have slightly different binding preferences for the peptides that they load. This is where the MHC diversity in a single human comes from.

Additionally each of the 3 MHC-I loci/isoforms is polymorphic, meaning that for each of them multiple alleles/variants exist in the human population. Since the number of these variants is pretty big (hundreds to thousands), most humans have different alleles on their paternal & maternal chromosomes and end up with 6 unique MHC-I genes.


What is the difference between "Bisphosphate" and "Diphosphate" in biochemistry?

[Source:Wikipedia]

As you can see in the above structure of ADP(Adenosine di-phosphate), the two phosphate groups in the compound are directly attached to one another. So it is named as di-phosphate. [Source] You can see this table for more examples.

[Source:Wikipedia]

In this structure of RuBP(Ribulose-1,5-bisphosphate), the two phosphate groups in the compound are not directly attached to one another, they are attached to first and fifth carbon, meaning they are attached to different atoms. Therefore, it is named as bis-phosphate. [Source](2nd comment)


How do PLINK files and HapMap Phased files differ?

According to http://pngu.mgh.harvard.edu/~purcell/plink/data.shtml#ped:

  The PED file is a white-space (space or tab) delimited file: the first six columns are mandatory:

 Family ID
 Individual ID
 Paternal ID
 Maternal ID
 Sex (1=male; 2=female; other=unknown)
 Phenotype

  [...]

  Genotypes (column 7 onwards) should also be white-space delimited; they can be any character (e.g. 1,2,3,4 or A,C,G,T or anything else) except 0 which is, by default, the missing genotype character. All markers should be biallelic. All SNPs (whether haploid or not) must have two alleles specified. Either Both alleles should be missing (i.e. 0) or neither. No header row should be given. For example, here are two individuals typed for 3 SNPs (one row = one person):

 FAM001  1  0 0  1  2  A A  G G  A C
 FAM001  2  0 0  1  2  A A  A G  0 0
 ...

And here is what I find in the begining of a HapMap .ped file I got a few years ago (hapmap3_r2_b36_fwd.YRI.qc.poly.ped):

 Y001    NA18488 0       0       2       -9      C C     T T     ...
 Y014    NA18519 0       0       1       -9      C C     T T     ...
 ...

So far, it seems to me than this is plain .ped format: the number of "header" columns is the same, and seems to conform to the specifications given in the above-mentioned web page.

Now let's have a look at the .map files.

  By default, each line of the MAP file describes a single marker and must contain exactly 4 columns:

 chromosome (1-22, X, Y or 0 if unplaced)
 rs# or snp identifier
 Genetic distance (morgans)
 Base-pair position (bp units)

  [...]

  Note: Most analyses do not require a genetic map to be specified in any case; specifying a genetic (cM) map is most crucial for a set of analyses that look for shared segments between individuals. For basic association testing, the genetic distance column can be set at 0.

  [...]

  The autosomes should be coded 1 through 22. The following other codes can be used to specify other chromosome types:

 X    X chromosome                    -> 23
 Y    Y chromosome                    -> 24
 XY   Pseudo-autosomal region of X    -> 25
 MT   Mitochondrial                   -> 26

  The numbers on the right represent PLINK's internal numeric coding of these chromosomes: these will appear in all output rather than the original chromosome codes.

Here we have something that may be different.
The end of the .map file corresponding to the HapMap .ped file looks like this:

 26      rs28357376      0       15825
 26      rs2853510       0       15925
 26      rs2854125       0       16149

The HapMap .map file uses "plink's internal numeric coding" for the chromosome instead of the letter code (MT).

Otherwise, it looks a pretty standard .map file, with no genetic distance indicated.


This is one of the "chichen and the egg" quesitons about early origins of life. The answer is: we don't know. There is a RNA world hypothesis which suggests that RNAs were the primary versatile biomolecules before proteins. This idea stems from the fact that there are self-replicating RNAs and ribozymes (RNA-based enzymes). Also, the fact that the catalytic center  (peptidyl transferase) of the ribosome is RNA, is also used in support of the the RNA world. However, this is still an idea and we cannot conclusively say that an RNA-world existed.


Can Oxaloacetate cross the outer mitochondrial membrane?

In general the outer mitochondrial membrane is thought to be basically permeable (through porins) to small molecules such as OAA. As is typical in biology, the situation may actually be more complex -- see for example this paper. But I think the default assumption is that metabolites freely cross the mitochondrial outer membrane.

You might also ask whether either the mitochondrial MDH or the cytoplasmic MDH enzyme is likely to be found or be active inside the intermembrane space.


Such viruses have a natural host, which might get sick, but is usually not killed by the virus. From there, the virus can get zoonotic (jump over species barriers) and infect other animals when it comes to contact. For Rabies the reservoir hosts are different, for the US these are bats, skunks and racoons. For more details, have a look on this PDF.

Another example for this is the SARS virus (a corona virus) which most likely lives in bats naturally and has jumped from there onto birds and from there infected humans.


Lizards are sometimes called cold-blooded because they depend on their surrounding temperatures to keep them warm.

Just going to follow up on your thought here.

The fluidity of the cell membrane does vary with composition.  Off the top of my head there are four main components of the animal cell membrane:

1) proteins.  membrane proteins are responsible for the import and export of nutrients, waste, information etc from the cell, so lets assume that this needs to be fairly constant part of the composition while the seasons change.

2) cholesterol and similar compounds.  These are flat an inflexible compounds which will tend to lower the fluidity of the membrane.

3) unsaturated fatty acids and lipids.  These are long carbon chained compounds with some double bonds in them.  Because the double bonds cause the chains to be less mobile, but they don't pack well as they are not as flexible, so tend to make the membrane a bit more fluid.  Think about how butter (mostly saturated fats) is solid at room temperature while olive oil (monounsaturated oil) is liquid.

4) saturated fatty acids and lipids.  These are completely mobile carbon chains.  Without any double bonds, these tend to be the more flexible and can create a more tightly packed membrane, resulting in a stiffer membraine.

You can imagine for the cell to maintain the same flexibility at the lower winter temperatures (4) and (2) would tend to decrease and (3) might tend to decrease.

Does this make sense?


Why does strenous exercise cause vision of "lights"?

This is a common phenomena which most of us come across. Seeing flashes of light, stars and other shapes in the eyes occur when the body goes through stressful activities. For example while you are climbing the blood flow will be more to other prominent parts like hands and lower waist so brain and eyes will get less supply of blood as well as nutrients. Hence those flashes or stars are visible to us. This phenomena is called "Phosphene" and a phosphene is a phenomenon characterized by the experience of seeing light without light actually entering the eye.
Wikipedia/Phosphene gives an explanation for occurrence of Phosphenes:

Phosphene is "seeing stars", from a sneeze, laughter, a heavy and deep cough, blowing of the nose, a blow on the head or low blood pressure (such as on standing up too quickly or prior to fainting). It is possible these involve some mechanical stimulation of the retina, but they may also involve mechanical and metabolic (such as from low oxygenation or lack of glucose) stimulation of neurons of the visual cortex or of other parts of the visual system.

So seeing flashes of light can be due to:

Blood shifting.
Low blood sugar(causes weakness).
Head trauma.
Headache.

So to summarize this thing, we should have enough nutrients, water supply to the body whenever we come across stressful activities. Phosphenes are temporary stuff which do not harm eyes.


The wavelength of UV-C most effective at provoking mutagenesis in DNA is 260 nm, which has been shown to kill Cryptosporidium parvum at doses below 10 mJ/sq cm.

http://www.ncbi.nlm.nih.gov/pubmed/12834745

In units of lux, 10^5 lux of sunlight has been shown to kill 99.9% of Aeromonas salmonicida after two hours of exposure.

http://www.sciencedirect.com/science/article/pii/S0043135499001591


Do eye muscles relax when you close your eyes?

I would guess that the eye muscle relaxes when the eye is closed. After having the eyes closed, just in the moment after opening them, it seems that the focus is in the distance. It takes a fraction of a second before you can read some text on your computer screen for example . This focusing-duration seems to be shorter when looking into the distance after opening the eyes.

Another effect is when you look at an object in short range for quite a moment and then close your eyes. You can feel the relaxation.


Why don't we hear all the processes in our body and what prevents us from doing so?

The issue here is with the definition of the word "hear". We do hear most of this, that is our ears actually pick up and transmit this sound. But we don't hear it in the sense that our brain ignores it and filters it out of what we are aware of. Only a very small fraction of all the sensory data that comes into the brain ever gets processed. The brain does something called sensory modulation it filters through all the sensory data and decides what is worth paying attention too.

This happens at several levels, not surprising since we see these same levels of filtering in animals, as soon as you evolve sensory organs the ability to filter sensory information is an advantage. Some happens directly at the sensory organ, many have a threshold before a signal is sent. In the brain the reticular formation is responsible for much of it. But each sensory processing area also does some of its own filtering. Basically each portion of the brain contributes in some way. Attention and how it is controlled is greatly studied as it is central to how consciousness functions. A complete rundown of all sensory processing is tricky since some senses (like smell) skip some parts of the process, and there are so many ways it can be filtered. you can find a more detailed breakdown here.


Why pain caused by blunt objects vanish after some time and return at the event of touching?

BASIC REASON WHY THE PAIN DISAPPEARS FOR SOMETIME:

There are gating mechanisms involving pain both in the spinal cord and in the brain.

Although the pain gating pathways in the brain are multifold complex,the spinal pathway can be simplified.
The latter may be understood in a simplified manner in 2 ways:

When there is a nociceptive stimulus,the epicritic receptors are stimulated.Sensory fibres from them synapse with internuncial neurons which inturn transmits impulses via the ascending tract to the periaquiductal grey. This region is capable of inhibiting pain impulse transmission to the spinal cord or thalamus by modulating impulses via the descending tracts.
This type is called supraspinal control
Another spinal reflex-type gate control operates in which stimulus like rubbing over the pained area ,application of warmth or cold causes inhibition of pain.
This is due to the impulses by large type (myelinated)A-fibres which arises from the  rubbed areas synapse with the internuncial neurons which are already synapsed with the epicritic sensory neurons of the dorsal root.The ends of such type of fibres release neurotransmitters that inhibits transmission of pain impulses through the internuncial neurons .
This is termed as segmental suppression

WHY DOES THE PAIN RETURN AGAIN:

This is because the pain receptors are the slowest to adapt.It's exactly as you said because it keeps the body apprised of tissue damaging stimulus.
So when there is the return of the noxious stimulus we can understand the tremendous summation effect which takes precedence over the gate control.

This occurs by a greater output of neurotransmitters from the synapse of the pain sensory fibres which outdoes the inhibitory effect of the neurotransmitters favouring gate control of pain.


Catenation and decatenation by DNA Gyrase

Both DNA Catenation & Decatenation are crucial to the equal distribution of DNA to the daughter cells during the mitotic crossing over. While catenation plays structural role in chromosomal architecture , decatenation facilitates the separation of sister chromatids.


How is output of DNA assembler measured?

If you are interested on the topic of how to compare assemblers, have a look at assemblathon. That group has two papers and working on a third about comparing genome assembly algorithms.


Olympic's epidemiological impact on Zika?

Though I have not found direct access to a model (which is what I'm really looking for), I have found evidence of such modeling efforts.

The CDC apparently put out a risk-assessment report in mid July discussing the results of such epidemiological modeling (reported by FivethirtyEight, ABC and others).

The report (available here), suggests that the risk of accelerated zika spread due to the 2016 Olympics is low.

They cite two major reasons:

Low mosquito activity due to colder winter weather

and more importantly....

The number of increased visits to the Olympics will make up only a fraction of the number of people that travel to/from zika-affected countries on a regular basis.

  The estimated 350,000 to 500,000 international visitors and athletes
  from 207 countries who are expected to travel to Rio de Janeiro for
  the 2016 Olympic and Paralympic Games represent a tiny fraction --
  0.25 percent -- of total travel to and from Zika-affected countries,   according to the CDC report.

According to CDC director Tom Frieden:

  "Compared with all travel to Zika-endemic areas, the Olympics account
  for about one-tenth of 1 percent of travel from the U.S. and globally
  about one-quarter of 1 percent, so even if Olympics didn’t exist,
  99.75 percent would be the same risk."

I will contact the CDC directly and ask for additional information regarding the model they used for this report. I will update this answer with any additional information I can gather. However, I'm sure others are producing similar models using different criteria, so please feel free to add additional examples or provide direct links to any available models.


Why do doctors do chemo or transplantation for cancers that don't respond well to these treatments?

To long for a comment: Its more an ethical thing I would say.
I do research which is connected to melanoma - a cancer which is notoriously treatment resistant, once it started moving. Until very recently there was only one chemotherapeuticum which has pretty low (around 20%) response rates. It was usually tried anyway because its possible that the patients belong to this 20% which respond. If not, treatment was usually not prolonged.

I think its something similiar here. The other problem for chemotherapy is that it is cytotoxic (until we got the small molecule inhibitors which are tested and used today) and the problem is to kill the cancer cells (all when possible) while you leave the rest of the body as unaffected as possible. To get this balance is hard (people tend to react differently to chemotherapy). The other problem is that cancers are not homogenous. So its possible that 99.9% of the cells present respond to chemotherapy and get killed, while a few acquired an additional mutation, which gives them an advantage. The conditions of chemotherapy are very selective.


Is diabetes mellitus a sex-linked disease?

Is either of them a sex linked disease? Can either one be inherited? My book says, "this disease is transmitted as a recessive genetic characteristic." What does this mean?

Neither are sex-linked. Type 1 can be directly inherited (in a non-Mendelian fashion), but Type 2 genetic factors mostly increase risks. "Recessive genetic traits" are traits that only express themselves when ONLY the recessive alleles are present in the organism (a dominant allele, if present, will 'overpower' recessive one).

Longer info:

Diabetes mellitus Type 1 (Juvenile Diabetes) is inherited, but it is autosomal with complex dominant/recessive rules:

  Type 1 diabetes is a polygenic disease, meaning many different genes contribute to its onset. Depending on locus or combination of loci, it can be dominant, recessive, or somewhere in between.

That results in some interesting, albeit complex, expressions:

  The risk of a child developing type 1 diabetes is about 10% if the father has it, about 10% if a sibling has it, about 4% if the mother has type 1 diabetes and was aged 25 or younger when the child was born, and about 1% if the mother was over 25 years old when the child was born.

Diabetes mellitus Type 2 does have genetic components, but the vast majority merely increase the risk of developing Type 2 Diabetes. Environmental factors play a large role in Type 2.

  Excess body fat is associated with 30% of cases in those of Chinese and Japanese descent, 60-80% of cases in those of European and African descent, and 100% of Pima Indians and Pacific Islanders.


Larger predators need a large range on which to find potential prey. An island might be bigger than the normal range of a predator, but too small to support a large enough breeding population (because of inbreeding, and because a brief lack of food, disease, or other insult could wipe out the entire population, rather than just a few individuals).


The tissue in the pharynx include:
Stratified squamous epithelium & mucus-producing glands.
However other cells that could be found would be other types of bacterial, is this what you're referencing?
Commonly scientists start with a gram stain to determine the classify the bacteria.
Gram+ bacteria have cell walls composed of thick layers of peptidoglycan. Gram+ cells stain purple when. Gram- bacteria have cell walls with a thin layer of peptidoglycan. Gram- bacteria stain pink.
The microbiome of a human consists of 100,000 billion bacteria. Therefore there are many types. E.g. Prevotella has been shown to be the most common type of bacteria in the human pharynx.
In a pharyngeal smear you would expect to find Stratified squamous epithelium, mucus-producing glands, bacteria and if a virus is present. Viral particles. This can be determined by RNA or DNA analysis.
E.g. COVID-19 is an RNA virus. If PCR analysis was completed on a sample obtained from a pharyngeal smear then we could confirm the presence of the aforementioned mammalian cells, bacteria and viral genetic material.


Why can cats interpret things on a monitor/tv, but dogs cannot?

Cats and dogs can both view tv screens & monitors ... though their viewing experience is a little different to ours thanks to differences in cone structure leaving them color blind and giving low acuity.

Both species have lower levels of color vision than humans. Cats see slightly more color (in the blue green and yellow end of the spectrum) than dogs do so they may get more of an immersive experience from watching TV.

Further, cats and dogs need a higher frame rate than humans to make it appear as a smooth film, a phenomenon known as flicker fusion, in humans we require 15-20 frames per second, dogs require 70fps and cats about 100. Before the frame rate of televisions increased in recent years it would appeared to them to be flashing images, similar to when you point a digital camera at a screen which may explain why the dog is not interested in the TV, it'd be like staring at a strobe for hours on end. Here is a paper which discusses flicker rates and color vision in dogs.

To summarize there are several factors which influence the "enjoyment" an animal can take from watching a TV - their response to TV imagery will depend on the frames per second, colors, contrast, clarity, movement, subject matter, and (perhaps most importantly in my opinion) the temperament of the animal, for all of which there are difference between the species.

From sciencenordic.com:

  "We humans need about 16 to 20 images a second to perceive what we see
  as continuous film, whereas dogs need about 70 images per second.

  So a few years ago, Fido was probably confounded by his master's
  behaviour of sitting for hours staring at a flashing succession of
  images. With modern resolution and quicker imaging, dogs have become
  potential television viewers.

  This has not gone unrecognised in the USA, for example, where hopeful
  TV producers have started special TV channels for dogs.

  If you have other pets, however, you need to think twice before
  placing them in front of the TV.

  Birds need at least 100 frames per second to see TV images as a moving
  picture. Having a bird in the same room as a TV with a lower frame
  rate than that will be very stressful for the creature."


I didn't believe this was a real thing, and I'm still very skeptical, but it is something that's claimed to happen!

  Their stems & leaves have a siliceous epidermis, so if rubbing b/n 2 horsetails occurs, a forest fire may be produced

--The Bottled Ocean of Biology, by Nisarg Desai, 2017

Why don't other plants show same thing? Another plant, bamboo, is supposed to do the same thing:

  How these fires originate is uncertain ... it has been suggested that a probable cause is the rubbing together of the silica-coated bamboo stems as they sway in the breeze.

--Burma, by R. Talbot Kelly (2004)

The same claim about bamboo is made in an Indian Government document on forest fire management.

What special thing about horsetail starts the fire? Apparently the claim is that it's the silica in the stems of the plant that is the important factor, and that horsetail and bamboo are both unusual in that regard. This does seem to be true:

  ... in general, ferns, gymnosperms and angiosperms accumulated less Si in their shoots than non-vascular plant species and horsetails.

--Phylogenetic Variation in the Silicon Composition of Plants

Bamboo isn't mentioned in that article, but the presence of silicon in bamboo is supported elsewhere:

  One of the advantages of bamboo over wood is that bamboo contains some silicon in both inner surface (pith-ring) and outer surface (rind) of the bamboo culm.

--Calcium phosphate formation induced on silica in bamboo

As I say I remain very skeptical. There's no evidence shown that this has actually happened. Is it telling that all these claims come from the same general region (India and Burma)? My guess is that this is an old wives' tale that's been written down and uncritically accepted, but if someone has actually seen this happen I'd be happy to be proven wrong, because the idea of plants sparking out flames in the wind is a pretty cool one.

Edit to add a link claiming that bamboo-on-bamboo generates sparks due to the silicates:

  The method consists of striking sparks out of  the culm of Schizostachyum bamboo with flint, broken pottery, china or even another piece of bamboo. The sparks that occur by striking the Schizostachyum bamboo are presumably generated by the high silica content in this genus of bamboo.

--Bamboo Strike-A-Light, by Tom Lourens, Ash Kivilaakso and Ed Read (My emphasis)

Edit to add that the overall concept of plants starting their own fires has been seriously looked at; the author is skeptical:

  Individual plant traits (such as leaf moisture content, retention of dead branches and foliage, oil rich foliage) are known to affect the flammability of plants but there is no evidence these characters evolved specifically to self-immolate, although some of these traits may have been secondarily modified to increase the propensity to burn. ... It is more parsimonious to conclude plants have evolved mechanisms to tolerate, but not promote, landscape fire.

--Have plants evolved to self-immolate?

Notably, in his list of factors potentially allowing self-immolation, he does not list silica, and horsetail isn't mentioned at all.


This is probably a large yellow underwing not finished pumping up its wings: https://en.wikipedia.org/wiki/Large_yellow_underwing


Your partly right both ways.  In a sense, the DNA clamp is a protein, in another sense, it's only part of a protein.  What it actually is is what we call a protein sub-unit, which is a protein, but which binds with other protein sub-units to form complex proteins.

In order to understand this, you have to remember what a protein is.  A protein is, in essence, a chain of amino acids.  Those can be short chains, long chains, medium chains: but they're all proteins.  Sometimes, a few short proteins (sub-units) will bind together to form one long protein (protein complex).  This is what happens in the case of a DNA clamp.

Basically, the DNA clamp is (an) independent protein unit(s) which has (have) the ability to encircle the DNA strand and travel along it.  They bind to the polymerase, which is why you don't see them on your diagram.  Their function is, very simply, to make it possible for the polymerase to stay closely attached to the DNA stand.

Sources:

DNA Repair (Amst). 2009 May 1; 8(5): 570–578


Identification of unknown bagworm (Singapore)

Is the plant Banana (looks similar)? If so, the bagworm (Psychidae) Kophene cuprea could be a possibility, since it is considered a pest on banana (Mosich & Larsen, 1978). The larval case is also supposed to be conical, but I cannot find an online picture for comparison.


If massive animals live longer, why do humans with gigantism die younger?

In short many things determine life expectancy and the interplay between different factors will determine an individuals life expectancy and a species' average life expectancy.
How life expectancy links to size:

Among mammals there is an inverse relation between heart rate and life expectancy (mammals tend to average 7.3+/15.6 x10^8 beats per lifetime which appears to be a symptom of the fact that heart rate is a marker of metabolic rate and so there is a fixed 'metabolic lifetime' for animals (source). This is somewhat substantiate by metabolism variants in C. elegans and the link between metabolism and free radicals and DNA damage (source).
Larger animals are thought to have a slower metabolic rate by weight (not overall) due to scaling laws (see Kleiber's law) and how surface area and volume relate and change temperature regulation metabollic requirements.

Other factors that change life expectancy:

In breeding: a reduction in genetic variation caused by inbreeding (e.g. many dog species though the extent to which they are inbred will depend on the species) can lead to lots of underlying health issues that may reduce the lifespan independent of metabolic rate
Stress: Higher stress will reduce life expectancy
Nutritional abundance: reducing caloric intake may reduce metabolic rate and extend lifespan, though starvation will decrease lifespan

Gigantism:

Whilst the life expectancy for a species may be higher in general people with gigantism may live shorter lives than possible because of non-metabolic related reasons. For example many forms of gigantism are linked to hormones which promote cell division and growth which are also linked to forms of cancer.


Why is prothrombin time test not used for heparin

Thats because the mechanism of action is different between warfarin and heparin.
Warfarin inhibits the formation of prothrombin (also known as factor II) by inhibiting the metabolization of vitamin K (for extensive details have a look at the Wikipedia article about Warfarin).

Heparin inhibits the blood coagulation by binding to antithrombin III which functions as a inactivator of active clotting factors as factors V, IX, X, XI and XII. It also binds calcium which is important for the blood coagulation. For more details see the Wikipedia under Heparin.

Therefore Heparin interferes with the formation of Thrombin and the test does not work. A nice image of the coagulation cascade can be found here, which also shows the points where Heparin interferes. The test can be done with Batroxobin, see here.


What's the exact meaning of and how to derive the coefficient of the path from sire to offspring?

In The Method of Path Coefficients(Wright1934) Wright showed that the path linked two objects is the path linked their genetic constructions. Probabily "genetic construction" means sequences of loci rather than a locus. However, if we consider a genotype of a locus as a random varible, the total genetic construction of a germ cell will be a random vector. Hence something like correlation or covariance between genetic constructions of germ cells is usually in form of matrix or tensor rather than a real number $F$(which is Wright actually showed). Moreover, if germ cells are made of several chromosomes, the correlation between corresponded pairs of loci in two germ cells may be not equal to each other. (e.g. chromosomeI of $G_1$ and $G_2$ are from the same ancestor, but chromosomeII are not)

So I guess things were worked out in this way.

Suppose $G_1=(g_0,g_1,\dots,g_n)$,$G_2=(g'_0,g'_1,\dots,g'_n)$. If $g_i$ is mth chromosome's kth locus and original from an ancestor germ cell $G_A$. And let us only modify $G_A$'s mth chromosome's kth locus, then $g_i$ would get modified; $g'_i$ would also get modified if only $g'_i$ is also original from $G_A$; loci on $G_1$ or $G_2$ in other chromosomes or in mth chromosome but other loci would not get modified anyway.  Hence $\rho(g_i,g_j)=\rho(g_i,g'_j)$ for any $j \neq i$. Therefore $$cor(G_1,G_1)=cor(G_2,G_2)=\mathcal{I}\dots(1)$$ $$cor(G_1,G_2)=diag(\rho_{g_0,g'_0},\rho_{g_1,g'_1},\dots,\rho_{g_n,g'_n})\dots(2)$$

Since $1=\sum\limits_{i}{p^2_{G_1\cdot g_i}}+\sum\limits_{i\neq j}p_{G_1\cdot g_i}\rho_{g_i,g_j}p_{G_1\cdot g_j}$ and by $(1)$, $1=\sum\limits_{i}{p^2_{G_1\cdot g_i}}$. hence $p_{G_1\cdot g_i}=\frac{1}{\sqrt{n}}$ if we weighted every $g_i$ the same. And $p_{g_i\cdot G_1}=\rho_{g_i, G_1}=\rho_{G_1, g_i}=p_{G_1\cdot g_i}=\frac{1}{\sqrt{n}}$, Analogously to $G_2$.

Therefore $\rho_{G_2,G_1}=\sum\limits_{i,j}p_{g_i\cdot G_1}\rho_{g'_j, g_i}p_{G_2\cdot g'_j}=\sum\limits_{i}\frac{1}{n}\rho_{g'_i, g_i}=E(\rho_{g'_i, g_i})$. i.e. in this case the correlation between germ cells are just the mean of correlations between their corresponding loci.

So similarly the coefficient of the path from a sire to its offspring is also the coefficient of the path linked their genetic constructions. and in detail is from sire's  genetic construction to its components, then from components to offspring's construction's components, then to offspring's construction.

The derivation was given in the article. In fig6 the coefficient of the path from a sire to its offspring can be gotten from the product $p_{o \cdot G_s}p_{G_s \cdot s}$.

$p_{G_s \cdot s}=\sqrt{\frac{1+F_s}{2}}$; $p_{o \cdot G_s}=\sqrt{\frac{1}{2(1+F_o)}}$.
So $p_{o \cdot s}=\frac{1}{2}\frac{\sqrt{1+F_s}}{\sqrt{1+F_o}}$

If $F_s=F_d=F_o=r_{sd}=0$, then $d_{o \cdot s}=p^2_{o\cdot s}=d_{o\cdot d}=\frac{1}{4}$, $d_{o \cdot \bar{sd}}=0$ . Thus
$d_{o \cdot s}+d_{o \cdot d}+d_{o \cdot \bar{sd}}=\frac{1}{2}<1$. This result means  parents' genetic constructions are not sufficient to determine their offsprings'. But it is very normal the same parents have both sons and daughters. Which causes their difference in gender are random factors.


Are the brains of any herbivorous animals capable of utilising ketone bodies as an energy source?

My answer is limited to sheep.
Background
The metabolites referred to as ketone bodies (which I will refer to as ketones from now on) are acetoacetate and β-hydroxybutyrate. In humans these are produced in the liver when the amount of acetoacetyl CoA being produced exceeds the capacity of the TCA cycle. These acetyl groups are instead used to produce acetoacetate, and this can be reduced to β-hydroxybutyrate.
The production of significant amounts of ketones occurs during fasting (diabetic ketosis will not be considered here). Once glycogen has run out, the bodies requirement for glucose has to be met by gluconeogenesis (mainly in the liver) - glucose is synthesised from various carbon skeletons including glycerol and the products of amino acid catabolism (coming from muscle protein turnover). This means that in the liver the function of the TCA cycle shifts almost entirely to supplying oxaloacetate for gluconeogenesis, via the activity of phosphoenolpyruvate carboxykinase. Thus there is no oxaloacetate available for citrate synthase, so acetyl CoA cannot enter the TCA cycle. However, because fasting also results in fat mobilisation the level of acetyl CoA in liver cells goes up (acetyl CoA is the end product of fatty acid breakdown).
So what is going on here? During fasting the fuel economy of the body has to switch from being heavily glucose-based to one which uses carbon from fat and from protein. The ketones are the manifestation of this, and many tissues become heavy users of ketones during fasting as blood levels rise to 5 mM within a few days. This means that the glucose being produced by the liver can be directed towards tissues which are more dependent upon glucose. The classic example of such a tissue is the brain, but in humans even the brain begins to use ketones heavily during fasting.
In ruminants the situation is entirely different. Ruminants rely upon the bacteria in the rumen to metabolise carbohydrate in their diet and this results in large amounts of alimentary ketones entering the blood directly. For their glucose supply ruminants rely entirely upon gluconeogenesis, and the substrate for this is propionate, another end product of bacterial metabolism in the rumen: a lactating dairy cow will synthesise over 3 kg of glucose per day.
So, when I read this question my reaction was that the statement must be incorrect - surely it would make sense for sheep to use ketones in all tissues. However my intuition was wrong - according to

Pell JM.& Bergmane N(1983) Cerebral metabolism of amino acids and glucose in fed and fasted sheep. Am. J. Physiol. 244: E282-E289

cited in

Heitmann RN et al. (1987) Hepatic ketogenesis and peripheral ketone body utilization in the ruminant. J. Nutrition 117: 1174-1180
"Although there is some oxidation of ketone bodies by the brain tissues of humans and rats during prolonged fasting, Pell and Bergman ,using an elegant in vivo preparation, have shown no significant uptake or oxidation of ketone bodies by sheep brain."

I don't have access to the Pell & Bergmane paper so I cannot explain what they actually did. What is clear from the review by Heitmann et al. however is that fasting ruminants respond in the same way that we do, switching to hepatic ketogenesis, and presumably they also maintain gluconeogenesis, using not propionate, but amino acid carbon skeletons. The context of the statement quoted above suggests that even in the fasted state the sheep brain doesn't use ketones.


Sex biased gene expression in the X chromosome

You can answer this question for yourself using the modMine data warehouse for modENCODE datasets.  All you need is a list of female-specific genes (using your identifier of choice, although FlyBase FBGxxxxxxxx are the simplest). You can use their list tools to upload your own list of identifiers, and then there are a bunch of widgets that will tell you things like GO Term enrichment, PubMed references, and one is a histogram plot showing the chromosomal distribution of your genes, and a second histogram showing the "expected" distribution. Access to many modENCODE sites can be found at www.modencode.org

Okay, I went and did this myself.  modMine was quite slow, but fortunately the intermine server at FlyMine is working fine.  I downloaded Supplemental table 25 from Graveley et al., Nature, 2011 and cut and pasted all of the "Female Biased" IDs for those rows that had FlyBase Gene Identifiers.  This figure shows the chromosomal distribution of the 928 genes:

The Labels on the X-axis do not line up properly (for some reason), so here is a table with the Chromosome names and the counts:

Chrom     Actual    Expected

2L:     157      169

2R:     176      186

3L:     143      173

3R:     174      217

4:       0       10

X:     264      150


How can I extract ligand with neighboring protein atoms from PDB with complex?

You might find RCSB's Guide to Understanding PDB Data and the PDB file format documentation useful. I'll go over some of the information present in PDB files that seems relevant for you, using your example of 10GS.
Ligands are specified in the heterogen section:
HET    VWW  A 210      33
HET    MES  A 211      12
HET    VWW  B 210      33
HET    MES  B 211      12
HETNAM     VWW L-GAMMA-GLUTAMYL-S-BENZYL-N-[(S)-CARBOXY(PHENYL)
HETNAM   2 VWW  METHYL]-L-CYSTEINAMIDE
HETNAM     MES 2-(N-MORPHOLINO)-ETHANESULFONIC ACID
FORMUL   3  VWW    2(C23 H27 N3 O6 S)
FORMUL   4  MES    2(C6 H13 N O4 S)

These records tell you the identity of the ligands that are bound to the protein (VWW and MES), how many are bound (4 in total), the chemical name (in the HETNAM record) and chemical formula (FORMUL record). The HET record also gives the number of associated HETATM records (33 for VWW and 12 for MES). Here are the first five HETATM records for VWW of chain A:
HETATM 3265  N   VWW A 210      15.088  10.798  23.547  1.00 14.90           N
HETATM 3266  CA  VWW A 210      15.010   9.987  24.792  1.00 20.92           C
HETATM 3267  C   VWW A 210      16.115   8.924  24.830  1.00 21.55           C
HETATM 3268  O   VWW A 210      16.520   8.515  25.940  1.00 17.16           O
HETATM 3269  CB  VWW A 210      13.635   9.327  24.908  1.00 14.23           C

Each HETATM record corresponds to an atom in the ligand and gives the chemical coordinates for each on the X, Y and Z axes. For example, the first record specifies a nitrogen atom at coordinates (15.088, 10.798, 23.547).
The connectivity (ie covalent bonding) between atoms in a ligand is specified in CONECT records. Here are the first five from the PDB file:
CONECT 3265 3266
CONECT 3266 3265 3267 3269
CONECT 3267 3266 3268 3273
CONECT 3268 3267
CONECT 3269 3266 3270

This tells you that atom 3265 (the first nitrogen in the HETATM records above) is bonded to atom 3266 (a carbon). Atom 3266 is bonded to atoms 3265, 3267, 3269. Et cetera...
The atoms of the protein are specified in ATOM records. Like the HETATM record, these records give some identifying information (atom serial number and type, residue name and number, etc) as well as the coordinates in 3D space. For your purposes, it sounds like you can just loop through the atoms of the protein and find the ones which are within some threshold distance of an atom in a ligand (or the geometric centre of the ligand). However, this PDB file does already contain some information about the binding sites for these 4 ligands in the SITE records (here are the first four corresponding to site AC1):
SITE     1 AC1 15 TYR A   7  PHE A   8  ARG A  13  TRP A  38
SITE     2 AC1 15 LYS A  44  GLY A  50  GLN A  51  LEU A  52
SITE     3 AC1 15 PRO A  53  GLN A  64  SER A  65  TYR A 108
SITE     4 AC1 15 HOH A 229  HOH A 303  ASP B  98

The SITE records also have corresponding REMARK 800 records (which are given in the question). For example, site AC1 is described as BINDING SITE FOR RESIDUE VWW A 210 as identified by SOFTWARE. So in this case, these SITE records are a list of residues that make up the binding site of their respective ligands.
You may want to be somewhat wary of these SITE records because (1) as far as I know they are not mandatory records in a PDB file and therefore may not always exist, and (2) it is not entirely clear how they are generated. In this case they are software generated... but which software... or what algorithm? I have previously looked through the SITE record of a binding site in a protein I am very familiar with and noted some conspicuous absences from the list of residues, so take that for what it's worth.


Can allelopathy succesfully be used against algal blooms?

This has been tried and it sorta works.

Algae in general seems to be inhibited by rotting barley straw in the water.
There is also an observation (not universally accepted) that many plants in the water do not have as much algae.  This post is from April 2011, so it seems pretty current.


Antibodies stored in freezer instead of fridge

Most IgGs should be fine when stored in the freezer.

  Freezing at -20 or -80 in small aliquots is the optimal storage
  condition. Ali-quoting minimizes damage due to freezing and thawing,
  as well as contamination introduced by pipetting from a single vial
  multiple times. Aliquots are to be frozen and thawed once, with any
  remainder kept at 4 degrees C.

  Enzyme-conjugated antibodies, should not be frozen at all and should
  instead be kept at 4 degrees C. Freezing and thawing will reduce
  enzymatic activity in addition to affecting the antibody binding
  capacity.

  Antibodies of the IgG3 isotype are unique in their tendency to form
  aggregates upon thawing and should always be stored at 4 degrees C

Personally, I store antibodies I use at -20 (they are in PBS), and they work fine for the first freeze thaw cycle. I have never tried more than one freeze thaw, so cant comment on that.

http://www.abcam.com/ps/pdf/protocols/antibody_storage.pdf


What kind of microscope should be used to view biological structures (such as spores) roughly 5 µm in length?

I think you have a good question, but if you want to get a good understanding of the issues you raise with it, then you really ought to consider spending some time reading this optical microscope primer. In my opinion, you need not bother with taking an undergraduate course at a physical university. As an intro to biology (which is not really necessary if all you want to do is look at small things in a microscope and understand what you're seeing), you might want to consider enrolling in this free class, but if all you want to do is look at small things and have a basic understanding of what you're seeing, I think all you need to do is read the primer.

If it was me, I'd read at least some of the primer before investing the money in a microscope. Otherwise you're just taking a blind leap of faith from someone's (perhaps biased) suggestion.


Were dinosaurs 'hot-blooded' or 'cold-blooded'?

This is a question I have often heard and there is no one certain answer to it. There are several scientific hypothesis about the methabolism of dinosaurs, but none of them has been ever proved or completely disproved.

Arts of methabolism

First of all, the term "cold-blooded" and "hot-blooded" are not scientific. In biology the organisms are classified according to how constant their body temperature is:

homeothermic (from greek "hom(e)o" = equal, same) -- organisms, who manage to maintain constant body temperature.
poikilothermic (from greek "poikilos" = changing, changeable) - ogranisms, whose body temperature fluctuates over time. It is implied here, that  the body temperature follows the fluctuation of the environment temperature, even though this is strictly not correct (see below)

There is another orthogonal classification, which takes into account the metabolic properties of the organisms:

endothermic organisms actively produce heat in their bodies, whereas
exotermic organisms mostly rely upon external heat sources.

What do we know about dinosaurs' methabolism?

Unfortunately there is no one living dinosaur, so we can only reason about their methabolism basing upon the fossils (and possible DNA from moskitos trapped into ambers).

One of the most cited works here is the "Dinosaur Fossils Predict Body Temperatures" (link to the free full text), where the authors write:

  Perhaps the greatest mystery surrounding dinosaurs concerns whether
  they were endotherms, ectotherms, or some unique intermediate form.
  Here we present a model that yields estimates of dinosaur body
  temperature based on ontogenetic growth trajectories obtained from
  fossil bones. The model predicts that dinosaur body temperatures
  increased with body mass from approximately 25 °C at 12 kg to
  approximately 41 °C at 13,000 kg. The model also successfully predicts
  observed increases in body temperature with body mass for extant
  crocodiles. These results provide direct evidence that dinosaurs were
  reptiles that exhibited inertial homeothermy.

And exactly here we need the terminology I presented above to understand the findings:

Dinosarier were endothermic -- they were able to actively produce heat in their bodies.
The produced heat can only be taken away through their body surface. Due to the fact that the body surface increases quadratically (n2) with the size, whereas the weight grows cubically (n3), the bigger dinosaurs were the higher temperature their bodies reached. That could be one of the growth limiting factors and explains why especially big species preferred to live in water.
Even though the dinosaries were homeothermic, we don't know anything about their thermoregulation. Modern reptilia do not have the thermoregulation mechanisms that would keep the body temperature constant. Dinosariers, however, due to increased heat production might have less fluctuations in their body temperature, than smaller reptilia. This is termed as "inertial homeothermy" here.


Why do the hormones FSH and LH decrease when the follicle is maturing and does size of follicle change during menstruation phase

I find FSH and LH hormones do actually
  decrease during day 4-14. Is that because of increase of
  oestrogen？

You first need to note that during one ovarian cycle, multiple follicles are stimulated to grow at the same time by FSH. However, one follicle ends up being the dominant follicle, and it is the oocyte housed within this follicle that is released on day 14. The dominant follicle is the one whose cells express gonadotropin receptors the earliest and so have the greatest sensitivity to FSH. Its growth would outcompete the other developing follicles. During days 4–14, FSH begins to decline because the granulosa cells of the follicles secrete inhibin, which—just like in males—causes the release of FSH and LH from the pituitary to drop. Only the dominant follicle is capable of withstanding this FSH drop; the other developing follicles are thus eliminated.

  Also, another question is will follicle
  grow during menstruation, because on diagram,the size of follicle
  actually changes during Day 0-4, and FSH and LH hormones increases.

As user19099 explains, yes, follicles grow during menstruation. With the degeneration of the corpus luteum, the negative feedback effect of estrogen and progesterone (in combination) on the hypothalamus is relieved. Thus, GnRH levels increase, causing FSH and LH levels to increase (as reflected on the graph you included), and FSH will stimulate follicular development.

References

Marieb, Elaine Nicpon, and Katja Hoehn. Anatomy & Physiology. San Francisco, CA: Pearson/Benjamin Cummings, 2008. Print.


Why don't people seem to die from salmonella in bites?

Salmonella infect via the fecal-oral route. They have proteins on their surface that match our gut cell surfaces, allowing them to attach and invade the gut. Those cell markers aren't present when you are bitten. it's the same reason that plant virus dont make us sick.

https://www.ncbi.nlm.nih.gov/pubmed/17593246

this is a bit heavy if you dont usually read primary papers, but looking for "Salmonella route of infection" or similar will yield the same kind of information


PCR processes number of amplicons produced

This is a theoretical consideration, as PCR depends on a number of factors as optimal priming, salt concentration, enzyme activity, available dNTPs and so on. Ideally the number of DNA molecules is doubled with every cycle. So the general formula to calculate the number is:

$ n \times 2^{cycles} = $ number of DNA molecules at the end of the PCR

n is the number of molecules set into the reaction

So for our 600 DNA molecules with 25 cycles this would give:

$600 \times 2^{25} = 20.132.659.200$ or roughly 20.1 billion molecules of DNA.


Difference vector target and genomic target

Genomic DNA is a DNA that has whole set of genetic data of an organism. You usually extract it with a whole DNA extraction kit.

Vector DNA is a vector (usually a plasmid, it can also be artificial chromosome,...the type of vector depends on the species and strategy you are using) that has you desired string of DNA in it (for example a gene you want to insert in to a organism) and you are using it to get your recombinant DNA to the organism.

I hope it helps!


Can you help identify this tree from my garden?

It's a Juniper, genus Juniperus.

If will feel prickly, and if you run your hand along the branch from the out to the inside it will feel very prickly. If you run your hand in to out, it will be marginally less so, but still uncomfortable,

Crushing the leaves in your fingers will release a sharp, tangy, not unpleasant smell.

Juniper Juniperus communis is native to some parts of in England, Scotland and Wales, and north and west of Ireland, and in fact most of the temperate forest regions https://en.wikipedia.org/wiki/Juniperus_communis#/media/File:Juniperus_communis_range_map.png

The berries are used to flavour gin.

However there are many other species of Juniperus that are often planted as ornamental trees, so it could well be one of these. https://en.wikipedia.org/wiki/Juniper

Best way for a positive ID is take a small bit with you to a large garden centre, or arboretum, and head to the juniper section and compare the look, feel and smell of the specimens.