CharonY

They cannot be translated, if that is what you mean. The lack the typical signal sequences of mRNA and presumably their tertiary structure will also inhibit translation. However, you could just look at the sequence and translate them using the genetic code, if you wanted to. I have no idea what information you would like to gain from that.

No, you have the same number of genes as you are ancestors. You will have different allele variants, though. The number of genetic loci is more or less fixed (not entirely true, but for this discussions close enough). You basically fill up the loci with the alleles (i.e. sequence variants at any given locus) from your parents.

I am not sure what you mean. Archaea are a completely different domain, distinct from bacteria. The evolutionary relationship is a bit tricky but it is a common misconception (presumably due to the name) that Archaea came before the bacteria. AFAIK the competing hypotheses are that archaea and bacteria share a common ancestor, another that archaea rose from bacteria. Bacteria have sex, but they do not use it for reproduction.

This is bound to be speculations and as such headed towards there.

I would need a bit more context to your question. Where examples given? The reason is that there are a lot of approaches (many now kind of obsolete), ranging from molecular biological techniques to crossing (or conjugation,in bacteria) and looking for phenotypes. The latter is hardly done anymore, though.

IIRC the claim that photosynthesis could be placed 3.5 billion years ago was only weakly supported and is rather disputed. See Rasmussen et al 2008 (Nature 455, 1101-1104 (23 October 2008), for example.

Regarding the OP: apparently the Virginia bill will be amended not to require the invasive transvaginal ultrasound (though ultrasound is still required). I was not aware that e.g. Idaho and Texas already had such bills My link. Technically the invasive option is not mandated per se, but since they are required to visualize the heartbeat, it is almost inevitable to do so during early stages of pregnancy. Also this makes me wish that it is all only a hoax: My link (the website with the full article appears to be down). At this point I would like to mandate some invasive for everyone before being to allowed to write and pass such laws.

I agree. Also I would have to wonder who would really count as a specialist in this field...

I assume you mean ferritin? What kind of column was used (not pertaining to the question really, but it is important to realize that you have a gazillion of column materials and running a column carries much less information than, e.g. saying one is running an SDS gel). That being said, depending on the preparation method albumin tends to multimerize. These tend to be very stable and are not easily resolved even in a denaturing gel. With better resolution you are likely to see also bands at e.g. 130 and around 190. Tip: use marker left and right of your samples to better assess smiling effects.

You can make a rough assessment based on the known sizes. pUC18 alone should yield a linear fragment. How big is the URA3 insert and if all the other sites in it, is it theoretically possible to yield the sizes you see? The accurate way is to get hold of the whole sequence and just check for restriction sites. But first make sure that the restriction actually worked.

Uncut plasmid DNA runs as supercoiled and will therefore run faster. You would have to linearize your plasmid first for correct size estimation. In most plasmid extractions you would include an RNAse step. But even without RNA rarely resolves as a clear band but rather than a smear towards the bottom. Plasmid DNA is usually seen in several conformations including open circle (single nick) as well as multimeric forms. Sometimes chromosomal DNA also gets co-purified.

You are still missing the point. A benefit is not a gracious gift by the employer. It is part of your compensation. Instead of paying you let's say 10-20k extra, he puts it into health insurance. So let us say you either get 40k cash or 30k plus benefits. Especially with large employers the total rate tend to be lower than individual insurance. It would be the equivalent of paying you the 40k and say that you are not allowed to use the 10k for certain things that I dislike.

Mutations are sudden in nature (either tthey are there or not). However, usually it is not very useful to look at at the rise of a single allele in a single individual. Instead you want to look at the frequencies in a given population. So basically how often does this mutation occur per generation and how it affects fitness. Also the population size is important. If the frequency of the mutation is low, it is only likely to persist if it carries a high increase of fitness (e.g. it is selected for) and vice versa.

Technically the whole gene pool is the result of mutations. Every single of our genes, regardless whether they lead to diseases or not.

I would counter that no a priori definition of life exists. All working definitions are based on descriptive parameters of things that we say are alive. Including borderline things like viruses and other mobile genetic elements. But as mentioned in basically all threads of this kind, biology is full of useful but not stringent distinctions that are not necessarily reflecting nature with absolute accuracy.

A limited form of transient multicellularity was most likely first developed in bacteria. An example of current bacteria is found in Myxococcus xanthus during fruiting body formation. It basically predates the formation of eukaryotes. Eukaryotes most likely arose from a fusion of an archaeon and a bacterium, so in a way they could be considered multicellular. However, individuality apparently got lost to a large extent so that one usually would refer to them as unicellular. Subsequently multicelluar eukaryotes developed (again most likely first with a transient, cooperative stage), still reproducing asexually. Sexual reproduction arose most likely later and is still a bit of a mystery. My favorite model assumes that the origins are found in mobile genetic elements (but that would take quite a bit to explain it in a clear way).

(2) is also not guaranteed, especially if you are an experimental scientist, as that depends on whether you get funding. (3) I agree. (4) depends, in reality it tends to translate in working 60+ hours a week, so in reality you have less average flexibility (in a 40h work week you would have 20 hours more to do other things). (5) I am not sure what it means and you can have (6) in many jobs, especially with a big ego.

You think so? Then you haven't seen this:

This is an unanswerable question. Even with selective pressure you would have no predictive knowledge how things are going to evolve, especially considering the stochasticity of the mechanisms involved. But they are led off by a major misunderstanding (or simply lack of knowledge) of what mechanisms pertain to changes in a given gene pool. Really, read up on Hardy-Weinberg equilibrium (even on Wiki). This is essentially the baseline (or null, if you want).

The first part does not make sense. And again, selective pressure are not the only elements that can eliminate alleles. Stochastic events are biologically relevant, especially in small populations as well as non-random mating. Also certain alleles may by themselves reduce fitness of their carriers without an external selective pressure. Also, technically all alleles can survive some time unless they are lethal, result in sterility etc.. Selective sweeps are not absolute.

A very stable environment still could have selective pressures. Plus stochastic events and sexual selection among others still shape evolution. Again Hardy-Weinberg would be the situation where the gene pool would remain constant.

Just a few things. For starters, AEI is a conservative think tank, so it is clearly partisan. Just for reference, the publication they referred to is this one My link (which is not peer reviewed). Now, there are several issue with this. First, the correction for accidents is not trivial. For one, healthcare also affects survival rate of those incidents. Ignoring that the authors used regression analyses to estimate life expectancy instead of removing deaths and re-calculate the life expectancy. Thus the numbers are at best suspect. Note that estimations of life expectancies are a tricky business at best. Regarding infant mortality, there has been much talk about that, too. However, a number of the studies actually have taken the different ways to count infant deaths into account. But let us look at the life expectancy at age 65 instead. This will remove many of these factors (as accident levels are highest at young age, and obviously infant mortality does not factor in anymore). Looking at OECD from 2007 (I have not found a newer data set that includes the US My link) data the US has a life expectancy of 20.3 years for females, which is better than UK (20.1) but worse than e.g. Germany (20.7), Canada (21.4), Australia (21.6) or Japan (23.6). For males USA ties with UK and Germany (17.4) but is lower than Canada (18.2), Australia (18.5) or Japan (18.6). According to some reports the US is falling further behind since 2007, but since I was not able to find the source quickly I have omitted those. Note that at that age people become eligible for medicare. Nonetheless it is clear that despite much higher costs the outcome in the US is not proportionately better than the other systems. Also note that several studies have shown that the health outcome is much more income-dependent than in other countries (for obvious reasons). I also have a comment regarding the survival rate of cancer. In the US certain screens including mammography as well as PSA test (screen for prostate cancer) are fairly common and occur more often. However, one should note that not all positive detections (which would go into the statistics) result in adverse health effects. In the case of prostate cancer it has been estimated that more men die with prostate cancer than from it. Now this could be seen either way. Early detection in the US helps in intervention and thus increase survival rate. The other is that for the comparative purpose a lot of people are added that have a positive cancer detection, but are finally not at risk from dying from it. There are studies that these early screens do not, in fact, save lives (which would support the latter hypothesis), but there is still some controversy going on and I do not think that a consensus has been reached yet. See e.g. Schröder FH, Hugosson J, Roobol MJ, et al. Prostate-cancer mortality at 11 years of follow-up. N Engl J Med 2012;366:981-90 Schröder FH, Hugosson J, Roobol MJ, et al. Screening and prostate-cancer mortality in a randomized European study. N Engl J Med 2009;360:1320-8 Andriole GL, Crawford ED, Grubb RL III, et al. Prostate cancer screening in the randomized Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial: mortality results after 13 years of follow-up. J Natl Cancer Inst 2012;104:1-8. Andriole GL, Crawford ED, Grubb RL III, et al. Mortality results from a randomized prostate-cancer screening trial. N Engl J Med 2009;360:1310-9.

Homeopathic porn. You know, diluted pornographic images. Like this one: · BTW, downvoting posts that one does not understand is generally not a nice thing to do.

As mentioned in the article, race is a delimited based on perception and a limited number of traits. As mentioned already (and also in the linked article) it is not valid as a genetic concept. To be precise, if we used the whole genome, we would not be able to draw meaningful boundaries.

Well, having a high immune response is generally not a very good thing. While it may reduce the incident of smaller infections resulting in full blown diseases, a stronger infection can result in a very strong inflammatory response or trigger autoimmune responses. You can think of it as delaying a cold in exchange for something really nasty.