thermodynamics - How do warm-blooded animals keep their temperatures constant?

Since there seems to be several distinct sub-topics in your question, I will answer them one-by-one:

1). There are a variety of mechanisms that allow endothermic animals to maintain thermal homeostasis in a cold environment. The main ones are:

a). The shivering response: When the core body temperature of a endotherm drops below a critical value (36.8C in humans), it causes the posterior hypothalamus to stimulate certain skeletal muscle groups (especially around vital organs) to start to "shiver" rapidly, generating heat.

b). Compared to ectotherms, endotherms have more mitochondria per cell, thus allowing them to have a higher metabolism. Since metabolism always generates heat, an [general] increase in cellular metabolism will cause an increase in body heat.

c). Many endotherms have layers of insulating matter, such as fur, blubber, feathers…etc, allowing them to preserve body heat. In addition, endotherms can also route blood away from capillaries via vasoconstriction of arterioles, reducing the area in which heat can be lost.

d). As mentioned by Memming, brown adipose tissue also plays a role in temperature regulation. Thermoregulation-based metabolism in brown fat causes the P+ in the electron transport chain to go through thermogenin instead of ATP synthase. This process generates heat, but no ATP.

e). Some endotherms, such as penguins and arctic wolves have countercurrent exchange in their capillaries. This is when warm arterial blood "passes" some of its heat to cooler veinous blood. This feature allows some of the heat normally "wasted" into the air to be recycled back into the body.

Note: Though it is true that endotherms are able to keep their body temperature constant irrespective of their surroundings (ignoring extremes), they do this at a cost of requiring significant amounts sustenance. Most endotherms require much more sustenance than ectotherms.

2). Your second sub-question is very interesting. Though it is true that generating heat will require substantial amounts of carbohydrates/fats/...etc, it does not necessarily mean that the net consumption of sustenance in cold environments is greater than that in normal environments. In most cases, endotherms in cold environments will have exhibit significantly less activity than when in an optimal environment. The decrease in activity when in a cold environment will likely balance out the increase in thermo-regulation based metabolism. This likely explains why people tend to drink equal or slightly less amounts of water when in cold environments. One more thing: some reactions heat-generating reactions (like the alternate ETC pathway) do not require water. Glycolysis and Krebs actually generates water (not to say that there is a net gain in the body :))

3). In truth, nothing "prevents" ectotherms from generate heat. They simply do not have the cellular "machinery". Ectotherms metabolize in ways very similar to other organisms, using molecules like ATP, glucose, fat…etc. Unlike endotherms however, they spend very little of their energy on temperature regulation. As a consequence, their overall metabolic rates are dependent on the external temperature. The point is this: A substantial portion of endotherm sustenance is used to generate heat. Only a small (if any) portion of ectotherm sustenance is used to regulate heat. As a result, endotherms require much more nourishment than ectotherms.

4). I am not entirely certain what you mean by "evolutionary path", but I will just say this: In many ways, endotherms and ectotherms are organisms that have found different ways to the same problem; how to regulate body heat for maximal survival and reproduction. Basically,

ectotherm- more dependent on environmental temperature, requires less sustenance

endotherm- less dependent on environmental temperature, requires more sustenance

5). You are quite correct. The cellular and genetic components are very similar. Some morphological aspects seem to be shared as well.

Sources:

Cambell & Reece (2010) Biology (9th ed)

Swan, K. G.; R. E. Henshaw (March 1973), "Lumbar sympathectomy and
cold acclimatization by the arctic wolf", Analysis of Surgery 177 (3):
286–292,

Guyton & Hall (2006) Textbook of Medical Physiology. (11th ed)

Romanovsky AA. (2007). Thermoregulation: some concepts have changed.
Functional architecture of the thermoregulatory system. Am J Physiol
Regul Integr Comp Physiol. 292(1):R37-46.

chromosome - Coiling of chromatids during cell division

What is exactly coiling of chromosomes?
I just heard about the names i.e paranemic, plectonemic, orthostichious, anorthospiral.
I have ecaxtly no idea of what phenomenon is this.
Also what type of coiling occurs during meiosis and mytosis type of cell division.
Could it be explained in detail....?

cell biology - Experiments in vitro vs those with dead organisms and fixated tissue

Does the term in vitro necessarily imply that the organism/organs/cells of study are dead?

If not, is there an alternative latin term to refer to studies of dead biological matter ? (e.g. in Connectomics where the tissue is biologically dead, and has been fixated and sectioned with a microtome)

genetics - Non-monotonic knock-out effects in prokaryotes

Typically, when performing gene-knockout, the experimenters select one gene to remove/replace-with-junk and then see if the prokaryote can still undergo fission. If it continues to reproduce then the gene is labeled as non-essential; if the organism cannot reproduce then the gene is labeled as essential; and some-times (if the organism can reproduce but only for a certain number of generations) the gene is labeled as quasi-essential.

Typically, if gene X is essential, and you knock-out both gene X and some other gene Y then the organism still dies; this is an example of monotonic behavior. However, this doesn't always have to be the case, it could be that gene X is essential only in the presence of gene Y (for instance if the two proteins produced are in a delicate feedback loop). Is there examples when knocking out gene X makes the organism nonviable, but knocking out gene X and Y maintains viability? In the most extreme case, is there an example where both gene X and Y are essential, but if both are knocked-out then the organism is still viable? I am primarily interested in simple prokaryotes (an answer for Mycoplasma genitalium or Escherichia coli would be best) but more complicated organisms are preferred over no answer.

bioinformatics - Expanding the SETI initiative to seek intelligent data within DNA sequences?

Let's extend your idea a bit... Ok, there are conserved sequences that we may not know what their function is. Let's assume that they are indeed not functional and are some kind of message left by an ancient form of intelligence.

How would you go about detecting that? It is already given that they are highly non-random, but this is not surprising and many "non-message" sequences have this property. Also consider that these sequences are quite short, meaning that they will have low information content. This means that if you check enough conversion codes and use imagination, you would probably be able to find several "messages" which are "hidden" there (e.g. "bible codes" etc). In other words, as I am a scientist that deals with probability and pattern recognition frequently, you will have a very hard time trying to convince me that you found a real hidden message... Formally, you don't have a satisfying background model.

The main difference from SETI is that there they know that their background is essentially random noise, so it is much easier to detect "intelligent" messages.

microbiology - How do I measure bacterial growth in agar dishes (either by cell mass or by cell count)?

The most simple way is seeding the plates with a suspension of bacteria ensuring that you spread the solution properly. Then you can count the number of colonies, wich would be equal to the number of single cells.

If you want to mesure the growth speed, usually it's simpler to just measure the diameter of the colonies, always ensuring you inoculate the plates with the same amount of inoculum.

Lastly, it's even easier to estimate the growth if your culture is un liquid media and you measure the optic density with an spectophotometer.

genetics - How many nucleotide pairs code one gene?

You seem to have some confusion, so let's clear things up.

A gene is a stretch of DNA (or RNA) that codes for a polypeptide (protein), that is a series of aminoacids bound together.
Each gene consists of nucleotides bound together, which are interpreted by the cellular machinery in groups of three, called triplets.
DNA is first transcribed into messenger RNA (mRNA), which is then translated into proteins.
Each triplet codes for one aminoacid not one gene! In fact genes are not "coded" by anything, they are the code!

Now, what I just wrote is extremely simplified, there are other important details that I omitted, but hopefully it cleared your doubt.

To give you some further detail: not every single nucleotide in a gene will code for an aminoacid. There are regulatory elements such as the promoter of the gene, which allows the enzymes that transcribe the DNA to attach to the gene (essentialy it says: "hey, start transcription right here!"). Similarly, enhancers and silencers can tune up or down transcription of the gene.

In eukaryotes there are big stretches of DNA called introns that are not coding for anything but have big importance for regulating transcription. In fact a single mRNA can be used to code more than one protein, using a process called alternative splicing.

There are also regions of DNA that code for RNA sequences not translated into proteins at all, but which have all sorts of regulatory functions in the cell.