Genetic effects on personality - Biology

The problem you are looking for is called the "Nature vs nurture" debate. Lots of scientists have written lots of books and papers and done lots of studies on the subject. As you can see, the title of the debate already includes the two main concerning factors: nature (genes) and nurture (environment).

These of course each include a variety of ways in which they influence personality. Genes provide the biological basis for your personality, they determine how everything in your body works¹. At the same time, these genes build a system that has a life of its own - your brain.

It consists of neurons, and nobody knows how personalitites comes about from them exactly but somehow they do. Neurons reshape all the time in ways that no other cells do. The connections between them, synapses, are formed, destroyed, reinforced or weakened all the time - in response to things that take effect on them, for example the things that you see and hear, smell, taste and feel. A very interesting subject in this field is the study of neuronal networks, giving some insight into how memory and learning may work.

But while this may seem like external factors must then be more important for personality, it depends on the setup provided by your genes how your neurons respond to certain influences - what concentrations of neurotransmitters they produce and secrete etc.

As you can see, the only thing that is really safe to say is that it is not "either or", both definitely play a role.

¹But even the biological development of the body has non-genetic influences - at the moment I can think of epigenetic inheritance though this seems to be disputed (see comments). Apart from that as far as I know there are uterine influences on embryonic development. And then there are the more or less obvious external influences such as cutting things off before they develop.

human biology - Why do people have darker skin in sunnier climates?

One of the important pigments that the earlier answer hinted at is melanin. Melanin is a brown pigment with photoprotectant properties.

As you correctly identified in your question, exposure to EM radiation (particularly UV and shorter λ waves) is damaging (indirectly) to DNA, which can cause mutations and therefore possibly cancer. Melanin production is one of the defence mechanisms the body has evolved to deal with this threat.

When DNA is damaged by the UV-B radiation, melanogenesis (the increased production of melanin pigment) is induced.⁽¹⁾ Therefore, people often exposed to more UVB (i.e. in sunnier climates) are likely to have more melanin in their skin, which makes it appear darker in colour. It is likely to be the increased incidence of melanin proteins in your skin which leads to the formation of a tan.

Melanin and its derivatives work as photo-protectors (protecting the body from the damaging effects of ultra-violet exposure) by absorbing UV-B photons and converting them into much less damaging infra-red wavelengths (heat energy). It does this extremely rapidly by internal conversion and extremely efficiently - efficiency in excess of 99.9% has been reported.

As the melanin removes the danger posed by the UV within a few femtoseconds (x10^-15 s), the more melanin that is present in skin tissues (and consequently the darker the skin), the lesser the chance of the UV damaging molecules in the skin so the lesser the risk of developing skin cancer.

mrna - Has anybody used Evrogen's DSN-normalization protocol for cDNA normalization?

I found the link to a commercial product by Evrogen to normalise cDNA samples for gene discovery projects here:
http://www.evrogen.com/technologies/normalization.shtml

The most up-to-date reference seems to be this Curr Protoc Mol Biol. paper by Bogdanova et al.:
http://www.ncbi.nlm.nih.gov/pubmed/20373503

They claim their method is compatible with nextgen sequencing platforms:

cDNA normalization using duplex-specific nuclease (DSN) is a highly
efficient approach that can be applied for normalization of
full-length-enriched cDNA (Zhulidov et al., 2004; Zhulidov et al.,
2005). The resulting cDNA contains equalized abundance of different
transcripts and can be used for construction of cDNA libraries and for
direct sequencing, including high-throughput sequencing on the next
generation sequencing platforms (Roche/454, ABI/SOLiD or
Illumina/Solexa).

Has anybody successfully used it for next-gen gene discovery projects?

cell biology - How are chromatids correctly segregated during mitosis?

It's a spatial constraint. As the DNA is replicated, the two resulting chromatids are kept stuck together by cohesin proteins. The DNA sequence that corresponds to the centromere then coalesces the kinetochore. It seems that the DNA-protein interactions at the centromeres creates a particular structure along the chromosome. Since the two chromatids have their kinetochores pointing in opposite directions, when a spindle microtubule attaches to the kinetochore, it is nearly impossible for another microtubule from the same spindle to attach to the opposing kinetochore.

zoology - Is there a term for tool use in animals?

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

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

statistics - What is the base cancer rate for an arbitrary carcinogen?

To answer this question in its entirety we have to split it into two questions:

What are the underlying mechanisms of carcinogenity?

One of the main mechanism behind carcinogenity is the mutagenity of the cancerogens, i.e. the ability to cause mutations, that are abberations of the cell DNA leading to uncontrolled proliferation. This classical paper investigates the relation between cancerogenity and mutagenity.

One should mention here that there are many types of mutations possible, mutations are not equally dangerous for cells and some mutations can be successfully repaired using the intact strain.

Therefore the following parameters of the source substances need to be measured to estimate the cancerogenity:

1. Substance concentrations or absolute amounts (both being indirect measures of their chemical activities, the lower concentration is needed for causing cancer the higher is the chemical activity and vise versa).


2. Substance radioactivity (for the mutagenesis due to radiation).

How can we measure the carcinogenity of different substances?

The most general approach here is to introduce certain amount of cancerogen into the animal body or to the cultured cell and to see the effect. The effect is calculated as the percentage of cells that undergo the transformation from normal into cancer cells. Two metrics are available here:

DT = Tumorigenic Dose (the amount of substance causing certain
percentage of cancer in treated animals, all treated animals are taken
for 100%)
CT = Tumorigenic Concentration (same, but adjusted for
concentration and used in cell cultures).

(They are written CT and DT because in science people tend to used Latin abbreviations where the adjective actually follows the noune).

The common metrics are DT5/CT5 (5% cells/animals get cancer) and DT50/CT50 (50% of the animals). Those are similar to other common metrics, the most common is LC50/LD50 -- lethal dose for 50% of the animals/cells.

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Unfortunately I couldn't not find any pre-compiled list with most known cancerogens and their TD/TC values. These seem to be interesting primarily for scientists. But going back to your question: you are absolutely right: some cancerogens are much more potent in causing cancer than the others!

physiology - What are the effects of caffeine on the mammalian circulatory system?

I can't speak to the causes of hypotension, but you are indeed correct, caffeine is a stimulant. As a stimulant, there is a well documented acute period of hypertension that lasts for up to 4 hours. Interestingly, there is no causal link established between caffiene consumption and chronic hypertension leading to cardiovascular disease (see here and here).

Having said that, caffeine is also a diuretic, which could cause someone who is already fairly dehydrated to exacerbate that state. It's possible to faint from a result of severe dehydration but I think it would have to be pretty severe.

It's possible someone is prone to fainting for non-medical, purely physiological reasons, such as standing for long periods, standing up too quickly, hypoglycemia, or some other predisposition.

evolution - How did viruses come to be?

I found a book chapter for you here

Quick summary:
3 hypotheses to Origin of viruses

1. From pre-cellular world (virus first hypothesis)


2. From reductive evolution of parasites (reduction hypothesis)


3. From fragments of cellular genetic material (escape hypothesis)

Drawbacks:

1. virus require cells (to infect) so how can they come first


2. virus do not look like known reduced parasites from Bacteria/Eukarya/Archaea


3. unlikely that genetic fragments form complex viral structures for viral function

Because of these drawbacks, the problem of virus origin was for a
long time considered untractable and not worth serious consideration

The rest of the chapter looks more in-depth into the 3 hypotheses