microbiology - What does "cellular" mean in this context?

I came across a confusing word when I was reading a Scientific American story, “Controversial Spewed Iron Experiment Succeeds as Carbon Sink” (by David Biello). It goes like this:

“One key to the whole experiment’s success turns out to be the
specific diatoms involved, which use silicon to make their shells and
tend to form long strands of cellular slime after their demise that
falls quickly to the seafloor.”

I'm wondering what “cellular” means in this context. Does it mean “of (diatom) cells” or “porous”?

Could someone kindly enlighten me on this?

molecular biology - Do antibiotics attenuate immune response on subsequent exposure to same bacteria?

Edited for Clarity:

In order to invoke a memory response or create a memory response, there must be interaction with the Adaptive Immune System (usually CD40+ "Helper" T-Cells), and the interaction must come in the form of a protein since the MHC receptors only respond to proteins.

Antibiotics are usually smaller macromolecules that directly cause slower growth or kill the microbe. They will *not* create or illicit a memory response because they are not presented to the immune system to initiate the proper procedure, and may not be proteins and unable to be presented in the first place.

If you're asking about vaccines (which was my inference before the edit), then they stimulate what is basically the same memory creation mechanisms that normal infections do. Antibody counterparts recognized by B-Cells are paired with proteins from the disease you want to immunize against, called the Hapten and Carrier respectively. Then the protein is processed via the B-Cells, presented to T-Cells, and a memory response is made.

My apologies if the previous answer was more ambiguous.

evolution - Evolutionarily speaking, why do humans have 46 chromosomes

@nico is right. the number of chromosomes is the result of an evolutionary timeline, puncutated by sometimes spontaneous events which shape the DNA.

These events occur in the course of evolution:

1) Chromosomal rearrangements. Large sections of the genome can flip around or become integrated in other chromosomes. By homologous recombination, regions of the genome can clip themselves out or duplicate themselves as well. If you look at the alignment of human to say chimp, there are many segments that move relative to each other.

2) chromosomal breaking or combination. Two smaller chromosomes may combine to form a larger one, or a larger one may break into two smaller chromosomes. An example of this is human chromosome 2, which is found as two smaller chromosomes in the great apes (see figure in wikipedia). We infer that this is a combination event exclusive to humans by comparing the other apes on the evolutionary tree. Birds and reptiles tend to have lots of chromosomal breakage, even to the point where the number of microchromosomes (less than 20 million bases). Mammals tend to be more conservative and not allow viable chromosomal breaks - chickens have 78 chromosomes to our 23..

3) idiomatic chromosomal behavior. Sex determining chromosomes are examples of chromosomes where a pair becomes distinctly different in size and composition.
Another example is in trypanosome which has many tiny DNA segments which code for variant surface coat proteins.

4) @rwst points, what I clean forgot, that occasionally (like maybe just a few times) there have been whole genome duplications. This can be identified by chromosomal alignments within a single genome and has not happened very often since we became eukaryotic metazoans. Not sure how many times, but perhaps just once or twice in our lineage. If anyone knows about animals/humans that would be great. As you can see the link shows whole genome duplications in plants, which don't seem care how many chromosomes there are. Plants have polyploidy, you see, so such duplication events are much better tolerated. On the other hand plants can't play video games.

P. Dehal, J. L. Boore: Two rounds of whole genome duplication in the ancestral vertebrate. In: PLoS biology. 3, 10, Oct 2005, e314, doi:10.1371/journal.pbio.0030314. PMID 16128622. PMC 1197285.

You can see that these events happen at particular moments and help shape the species and the composition of the chromosomes. It is not a priori possible to predict the number or type of chromosomes just by looking at an animal, but only by looking at the related animals.

Fungi and Plants have even more variations in chromosomal composition than animals.

Is a minimum size/complexity necessary for an organism to exhibit territoriality?

With some bacteria (e.g.. Bacillus subtilis) when food gets scarce they will start trying to kill their neighbors. (See this arstechnica article) This appears to be a fight to the death between children and parents. That's a kind of territorial behavior, selectively applied only when there are not enough resources to go around. As there is no "recognition" of a specific territory being defended, just wherever the bacteria is currently, this might not meet a strict definition of territorial behavior. But the only thing simpler than bacteria are viruses.

Come to think of it, I bet there are viruses that, once they infect a host cell, will change the cell's membrane or metabolism in a way that reduces its chance of being infected again by a similar virus. Such 'behavior' could be compared to defending a breeding ground. Can't find any examples though.

nomenclature - What is the definition of "dry weight" and "dry cell weight"?

According to my Henderson's Dictionary of Biological Terms, dry weight is

The weight or mass of organic matter or soil after removal of water by heating to constant weight.

So yes, your definition is correct and it is also applicable to cells. The dry weight of cells is the weight left when their water content has been removed by heating.

genetics - What kind of event would cause the current Mitochondrial Eve to be replaced by a new one?

What would need to happen for a single woman's mitochondrial genome to be in all living humans ?

All other women would suddenly or gradually need to be eliminated from the gene pool. No other woman could enter the gene pool of this future humanity. So the most likely scenario is one where we would have to be reduced to a single woman at some point.

Genetic isolation was brought up, but the words 'all living humans' doesn't really say 'isolation'. In isolation, there are other people still carrying on somewhere else. Here we are talking about only isolation in the sense that the breeders are the only ones left to reproduce.

Even so, any human woman will still be descended from MEve. That original Eve would still be the mitochondrial Eve, though the genomic record pointing to her would have disappeared.

A completely New Eve could happen if there were a woman unrelated to MEve were to come along, and her offspring were so much more successful than all other women that over time only this woman's daughters were chosen as mothers. She would be incredibly successful- like all her children were 6'6" and much smarter, attractive etc etc, then the rest of the gene pool could dwindle leaving only 'new Eve'. This could happen say if we got some Neanderthals going. They don't seem to be particularly likely to take over though.

This is similar to the scenario where one female lineage simply out-competes all other female lineages to assume the mantle of M-Eve. This seems less likely to me. This lineage would have to enjoy an advantage would have to out-weigh all over variants that exist at the time and would ever emerge over the following generations before our new M-Eve's final domination. Given the number of genes and possible variants, in the entire genome, that is statistically really improbable.

As far as a new Y Adam, this sort of thing nearly happened for men. Just to remind, the Y chromosome is transmitted exclusively from father to son, so a Y Adam would be the only ancestor of all men on the face of the planet.

A national geographic sponsored survey of genomes found that in central asia 8% of all men have the same Y chromosome. Over all humanity, 0.5% of all men have the same Y chromosome. The genetics point to the Mongol Warrior King, Genghis Khan whose campaigns across Asia to the doorstep of Europe included him bedding with one or more different women from the conquered peoples every night, one of whom is reputed to have killed him. Not incidentally killing many men too, eliminating much future competition for his progeny.

Still, all this is a mere fraction of the sort of effect you are talking about. 100% replacement by a single individuals descendants is hard to imagine in less than an extinction like scenario. Or a new race of superbeings coming from a single individual. Hard to imagine given the billions of people on the face of the planet now.

Its a little easier to imagine in the case of a new Adam only because a one man can have hundreds or even thousands of offspring in his lifetime. Even then, Male psychology seems to bring it up more than is rational. Its still extremely improbable (not going to happen).

Its also worth noting that few species have been able to come back from such a small gene pool and number...

Here's a tree of human Y chromosomes. You can see that fat grey blob which are descendants of GK.

human anatomy - Can any other animal choke on food?

The veterinarian in our group offers this: For humans, who choke much more frequently than other mammals, it is likely to be a cognitive problem. We talk and eat at the same time and so give ample opportunity to allow food passed the epiglottis and choking. Animals do choke - dogs can, cats can. Not all animals can vomit and this is particularly a problem for horses, whose stomachs will rupture instead of releasing contents through the mouth.

pharmacology - Does DHA increase the effects of clarithromycin?

I've read on this publication that every drug that induces CYP3A can reduce the effectiveness of clarithromycin. Clarithromycin inhibits CYP3A.

But it does not say anything about the opposite situation: does a low concentration of CYP3A increase the effect of clarithromycin?

This research shows how DHA can inhibit CYP3A.

Now the final question is: does a high concentration of DHA increase the effect of clarithromycin?

entomology - How many honeybees are there, and how has the number changed across time?

1 billion hives
(at 10,000-50,000 bees/hive this is 10-50 trillion bees)

Managed: 100 million hives

Based on country-level data from FAO, supplemented for a few countries with Apiservices, in 2011 there were about 80 million managed hives. Because FAO lacks any data for some countries, and other countries under-report (for instance US figures don't include hives kept for pollination service and hives kept by small-scale operators) a reasonable round estimate of managed hives in the world is 100 million. (This implies a 128% correction to the FAO numbers). (Aizen and Harder 2009 give context on FAO figures).

Wild/Feral: 900 million hives

Wild/feral hives of Apis mellifera are difficult to count via direct observation. Jaffe et al 2010 use a genetic sampling method, and also report a reasonably strong correlation between the total number of hives (managed and wild) per square kilometer and the mean annual temperature of the area.
I used the best fit line from their data to estimate the "hive-carrying-capacity" by country using (the admittedly very general) land area and mean annual temperature. Then I subtracted the number of managed hives from the carrying capacity to estimate wild hives.

Although this formula probably overestimates large, cold countries and underestimates Africa (the formula gives 211 million feral hives in Africa when literature suggests closer to 300 million), in general, it seems to give not unreasonable estimates in comparison to the literature. Globally, this formula gives an estimate of 984 million wild hives. Given that land area included desert and other unsuitable habitat, it seemed reasonable to round down, and I took 900 million as my estimate.

Historical Populations

1961-2011
FAO statistics date to 1961. I plotted their numbers, with the 128% correction for each year. I assumed that during this time the number of wild bees has remained virtually unchanged, at 900 million, because it was defined by mean temperature and land area, which have not changed.*

1650-1961
This period represents the globalization of Apis mellifera. Before 1600, there were no European honey bees beyond their native range (Western Eurasia and Africa). However, once established in new areas (the usually cited first beehive in the USA in 1622), Apis mellifera rapidly spread in both managed and feral populations, in North America (17th c), South America (18th c), Australia (19th c) and East Asia (20th c) (Crane 1999)
.

I used carrying capacity of native range countries (just about 35% of the carrying capacity of the globe, or 350 million hives) as a before-1650 estimate, and then assumed a geometric increase of about 2% per decade in available land area (ALA), as Apis mellifera bees and beekeeping made their way around the globe.

To estimate the number of managed bees during this period, I assumed a human:hive ratio of 35:1**, and modelled hives based on historical estimates of human population, multiplied by the ALA for the decade. The 1650 estimate was 5 million managed hives.

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*Although diseases, pests, and pesticides have been reported to affect feral populations, I didn't find any solid information on this. For instance, feral populations of Apis mellifera mellifera and A. m ligustica have been widely reported to be in decline in the USA, but at the same time, feral populations of Africanized honeybees (Apis mellifera hybrids) have been rapidly spreading. Even with 90% losses in the USA, Canada, Japan, and Europe (areas affected by varroa) my estimates would only be decreased about 10%. However, it's also possible that land-use change has greatly affected feral bee populations (Moritz et al 2007).

**This wasn't a totally wild guess. I first calculated the human:hive ratio for 1961-2011. This ratio was increasing - there were 71 people / hive in 2011, and 47 in 1961. Initially, I assumed the rate of change in the ratio to be constant, but this led to unrealistically large estimates for historically managed hives. However, the rate was clearly increasing (just, perhaps in a nonlinear way I didn't want to estimate), so I decided instead to compromise on a number less than 47 and greater than 4. I decided on 35, as it produced what seemed like a realistic estimate of 5 million hives in 1650, compared to around 20 million today for Eurasia and North Africa (excluding sub-saharan Africa where wild-harvest remains important and likely was even more so in the past).

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• Aizen MA, Harder LD. 2009. The Global Stock of Domesticated Honey Bees Is Growing Slower Than Agricultural Demand for Pollination. Current Biology 19: 4–4.




• Crane E. 1999. The World History of Beekeeping and Honey Hunting. Taylor & Francis. (Chapter 12).




• Jaffé RR, Dietemann VV, Allsopp MHM, Costa CC, Crewe RMR, Dall'olio RR, Rúa PPDL, El-Niweiri MAAM, Fries II, Kezic NN, et al.. 2010. Estimating the density of honeybee colonies across their natural range to fill the gap in pollinator decline censuses. Conservation Biology 24: 583–593.




• Moritz R, Kraus FB, Kryger P, Crewe RM. 2007. The size of wild honeybee populations (Apis mellifera) and its implications for the conservation of honeybees. Journal of Insect Conservation

virus - Changing the definition of life?

...many biologist/scientists say that viruses are not living because everything they do is just chemicals carrying out their predefined chemistry.

I don't think that's correct. Many definitions of life exclude viruses because they lack the apparatus to perform the life functions themselves, especially reproduction. They don't seem to qualify as parasites because, when they've infected a cell, they no longer occupy a bounding structure (other then the cell itself.)

When viruses are acting like a living thing, they look like misbehaving cell. Here's a similar puzzle; what organism is cancer? Viruses are basically rogue genes, just like cancer cells are basically rogue cells.

"Organisms carrying out their predefined chemistry," is basically saying that living systems are deterministic. The interesting question is, are very complex systems that emerge from stochastically-driven events themselves deterministic? Are organisms like a clockwork?

Probably you should check out Schrödinger's What is Life? to get started.

How is evolution possible in contemporary humans?

It is certainly not true that "all male humans have roughly 2.5 (or whatever the number) kids". First of all, male and female humans have exactly the same reproductive rate. For obvious reasons, every time a male has offspring, a female must have had also. Last I checked neither male nor female humans are capable of parthenogenesis (certain popular religious beliefs notwithstanding).

Second, let's assume that the 2.5 number is correct. That would be the average number of children per couple. That does not mean that all couples will have 2.5, or even that most couples will have 2.5. It just means that the average will be 2.5. If, for example you have one couple with 6 children, one with 2 and two with 1, the average will be (6+2+1+1)/(1+1+2)= 2.5.

On to the main point. What does selection mean? In its simplest form, that the individual most likely to survive (the famous "fittest") is also most likely to reproduce. This is a very simple concept, the longer you live the higher your chances of managing to have offspring. If you die two weeks after birth it is going to be hard to manage to reproduce yourself. This has not changed.

So, what does "fitness" mean? It can mean many things. If you are a warm blooded creature at the beginning of an ice age for example, it could mean being better at regulating your temperature than your peers. If you are a 21st century human, it could mean being funnier on twitter than your peers. The two are not fundamentally different. They can both be selected for or against. As long as one mate is chosen over another, selection is happening and the "fittest" (in each particular context) is most often selected.

Add in the process of culturally modified selection pressure, and it
seems to me that even an "unfit" male would end up having a couple of
offspring. The fittest male (or female) is no better off than his or
her contemporaries because of this "leveling" effect.

"Culturally modified selection pressure", as you call it, is still selection pressure. Cultural factors can change what it means to be "the fittest" but there is no objective gold standard of "fitness". While it may be true that in modern human society, different characteristics are selected for than was the case with early Homo sapiens, this does not mean that "evolution is not occurring". On the contrary, it is occurring but perhaps it is moving in a new direction. In fact, this is essentially a circular argument. By definition, "fittest" means most likely to survive and reproduce. It does not mean strongest or fastest or prettiest. It just means whoever is better at reproducing. If that happens to be those individuals who are best at square dancing, then it is they who are the fittest.

Take the example of a modern human with diabetes. Medicine allows diabetics to lead fully productive and largely normal lives. So, perhaps diabetes is no longer a selective criterion. This does not mean that the diabetic cannot be selected for or against based on their fitness on other scales.

Whatever the selective pressure, whatever it may be that defines a "good mate", if selection is present then so is evolution. The only way to remove a species from the process of selection would be to have all (or none) individuals of each and every generation reproducing at the same rate. This is clearly not the case with humans. Surely not everyone around you has, or will have, children? There you go, selection!

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UPDATE:

In answer to your comment, yes indeed, in order for a selective pressure to make itself felt and affect phenotype (at the species level), it needs to be constant across several generations. However, even the absence of selective pressure affects evolution. As others have mentioned below, active selection is not the only mechanism of evolution.

Your main question however seems to be the following: If modern society (medicine etc) allows individuals that would not survive in the wild to reproduce, how does that affect evolution? The main points in my answer, and all others here, are:

1. Even if we accept that modern humans have removed themselves from the purely "biological fitness"-based selection pressure (an assumption I am not at all sure is true), and assuming that this removal is constant enough over many generations (again unclear), even if all this is true, evolution is most certainly still occurring. It may even be faster since genotypes that would not survive in the wild persist in the gene pool, thereby increasing its diversity.




2. As you point out in your comment below, for such social pressure to make itself felt, it needs to be constant across many generations. We are probably not there yet.




3. Most importantly, as I said above, there is no such thing as an absolute biological fitness. When the ecosystem changes, so does the definition of fitness. Modern humanity's ecosystem, our habitat, is intimately connected with our culture and society. If an individual is better at reproducing in that context, then that individual is more fit.

Are human eyes equally sensitive to AC, and DC lamps?

Let's not confuse the type of power of a light emitting device with the type of light it produces.
_{This question is not about AC or DC current. It is about flicker frequency, light wavelength and their biological effects.}

Flicker frequency

The term "ache in the eye sockets" probably refers to asthenopia.

Human eye cannot detect flicker with a frequeny above 75 Hz. But many computer displays have a refresh rate of 60 Hz [1]. Out of focus and low refresh rate monitors are known to cause eye strain and asthenopia [2], favored by existing hypermetropia (and other vision issues).

Visual discomfort has been related to 1) the presence of flicker; the possibility to regulate, 2) brightness, 3) height; and 4) inclination of monitor. Asthenopia has resulted statistically correlated to the presence of flicker and to the impossibility of regulating height and inclination of monitor for both sexes. The possibility to regulate monitor brightness has not determined a reduction of visual discomfort either in men or in women [3].

Wavelength

Eye sensitivity is different (see spectral sensitivity):

"Cones SMJ2 E" by Vanessaezekowitz at en.wikipedia / Later version uploaded by BenRG. - Based on Dicklyon's PNG version, itself based on data from Stockman, MacLeod & Johnson (1993) Journal of the Optical Society of America A, 10, 2491-2521d http://psy.ucsd.edu/~dmacleod/publications/61StockmanMacLeodJohnson1993.pdf (log E human cone response, via http://www.cvrl.org/database/text/cones/smj2.htm)
Transferred from en.wikipedia to Commons by User:Richard001 using CommonsHelper.. Licensed under CC BY-SA 3.0 via Wikimedia Commons.

Light color and color contrast matter:

The study results showed that both visual acuity and the subjective visual fatigue were significantly affected by the color of light [4].

Images with excessive energy at medium spatial frequencies (Fernandez and Wilkins, 2008 Perception 37 1098-1113), or that have high color contrast and little or no luminance contrast (Wilkins et al, 2008 Perception 37 Supplement, 144-145) appear uncomfortable or aversive and can induce headaches in hypersensitive observers. Such stimuli are uncharacteristic of natural images [...] [5].

Blue light can also reduce melatonin levels and affect sleep and mood (the studies don't have a strong conclusion though):

Melatonin concentrations after exposure to the blue-light goggle experimental condition were significantly reduced compared to the dark control and to the computer monitor only conditions. Although not statistically significant, the mean melatonin concentration after exposure to the computer monitor only was reduced slightly relative to the dark control condition [6].

All light is not equal: blue wavelengths are the most potent portion of the visible electromagnetic spectrum for circadian regulation. [...] evening use of amber lenses to block blue light might affect sleep quality. Mood is also affected by light and sleep; [...] At the end of the study, the amber lens group experienced significant (p < .001) improvement in sleep quality relative to the control group and positive affect (p = .005). Mood also improved significantly relative to controls [7].

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References:

1. Wikipedia contributors, "Flicker fusion threshold," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Flicker_fusion_threshold&oldid=615159751 (accessed July 29, 2014).


2. Wikipedia contributors, "Asthenopia," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Asthenopia&oldid=617227613 (accessed July 29, 2014).


3. Rechichi C, Scullica L. [Asthenopia and monitor characteristics]. J Fr Ophtalmol. 1991;13(8-9):456-60. PubMed PMID: 2081858.


4. Lin CJ, Feng WY, Chao CJ, Tseng FY. Effects of VDT workstation lighting conditions on operator visual workload. Ind Health. 2008 Apr;46(2):105-11. PubMed PMID: 18413962.


5. Juricevic I, Land L, Wilkins A, Webster MA. Visual discomfort and natural image statistics. Perception. 2010;39(7):884-99. PubMed PMID: 20842966.


6. Figueiro MG, Wood B, Plitnick B, Rea MS. The impact of light from computer monitors on melatonin levels in college students. Neuro Endocrinol. Lett. 2011;32(2):158-63. PubMed PMID: 21552190.


7. Burkhart K, Phelps JR. Amber lenses to block blue light and improve sleep: a randomized trial. Chronobiol. Int. 2009 Dec;26(8):1602-12. doi: 10.3109/07420520903523719. PubMed PMID: 20030543.

dna - How is instinctual information encoded?

Web spinning in spiders is a complex behavior and probably involves a number of different factors, genetic and environmental. Genetically there are surely many different genomic regions underlying the development and expression of the behavior.

Is the algorithm for web spinning directly encoded in the DNA? Not directly. There is not a single region of contiguous DNA sequence that codes for all the steps involved in building a web. Instead, there is a sequential and parallel developmental process beginning at fertilization (earlier if you include parental epigenetic modifications) - encoded and regulated by the genome and its products - that, without too many errors, generates a viable and fertile web-spinning organism. But the DNA sequence involved in that algorithm is spread all over the genome and includes coding genes, non-coding (ncRNA) genes, and regulatory regions. And the genome alone will not carry out an effective algorithm without proper environmental inputs like nutrition and parental provisions.

The act of constructing a web, when and where, and the design of the web is likely carried out via brain architecture and neuronal patterning, but of course these structures are built based on the DNA-based, developmental algorithm. In that sense, there are many nested levels of algorithms.

One of the best models used for studying behavioral genetics is the fruit fly Drosophila. Many different behaviors have been studied at the genetic and molecular level in Drosophila including courtship, foraging, sleeping, and memory-related tasks. A popular science book on behavioral genetics worth checking out is Time, Love, and Memory by Jonathan Weiner. It details the work of Seymour Benzer and provides a lot of background and easily understood explanations of how genes and their products can work together to exhibit complex phenotypes like sleeping patterns. It includes a detailed (though not up-to-date) description of circadian gene circuitry and how it develops.

At the moment, the best that I can think of for an algorithm directly encoded for by DNA is the sequential activation of HOX genes for animal body plans. But even in this case DNA code does not progress through correct development without other factors.

dna - Why can't we observe haplotypes directly?

The difficulty of reading haplotypes 'directly' lies in the difficulty of reading any long sequence of DNA, and this is for technical reasons.

Short DNA fragments are sequenced using a variety of methods. Gel electrophoresis can pull these fragments apart by length, but all the fragments have to be relatively close in size to get the accuracy needed to tell fragments that differ by one base pair apart. It's easy to separate a 16-bp segment from a 17bp segment easily, but it's much harder with a 516bp segment and a 517bp segment. Modern sequencing can sequence reads up to about 5kbp in length at a time. The 'reads' are then reassembled.

There are next-generation methods(pyrosequencing, etc) that can read a long dna molecule one base at a time, but for practical reasons sequencing an entire chromosome this way is cost and time prohibitive. As a result, there are always going to be fragments that you need to reassemble computationally, no matter how the sequencing is done.

human biology - How do omega-3 fatty acids reduce cholesterol at the molecular level?

I found this research paper (pdf) by D. Roger Illingworth, William S. Harris, and William E. Connor (Journal of the American Heart Association, 1984) that offers some help. Its abstract says:

Diets rich in omega-3 fatty acids derived from fish oils lower the plasma concentrations
of low density lipoproteins (LDL) and very low density lipoproteins in humans. The present study was designed to examine the mechanism(s) by which diets enriched in omega-3 fatty acids reduce plasma LDL cholesterol levels in normal subjects.

In the Dicussion part, you will find your answer:

Reductions in the plasma concentrations of LDL in human subjects consuming diets rich in long-chain omega-3 fatty acids from fish oils or omega-6 fatty acids from vegetable oils may be due to a reduction in LDL synthesis, an increased fractional rate of catabolism of LDL, or a combination of both... The present study indicates that the hypocholesterolemic effects of long-chain omega-3 fatty acids present in fish oils results from a reduction in the rate of LDL apoprotein B synthesis and that such oils do not stimulate the fractional rate of catabolism of LDL. These observations imply that the incorporation of omega-3 fatty acids into cellular or lipoprotein lipids does not enhance the rate of receptor-mediated catabolism of LDL as has been observed with omega-6 fatty acids in vitro.

I could not find a paper on its exact mechanism, so I'd rather say that the process is still not clear. Yet, as the paper suggests, the main effects of omega-3 fatty acids are reducing LDL synthesis and/or increasing fractional rate of catabolism (FRC) of LDL.

A similar article can be found here:

Omega-3 fatty acids have been shown to lower triglycerides, which are a type of fat in the bloodstream. Experts aren't sure of the exact mechanism. Omega-3 fatty acids may also slow down the growth of plaques in the arteries and reduce inflammation throughout the body.

A number of studies going back years have shown the benefits of fatty fish. In an important review of studies, researchers found that getting daily omega-3 fatty acids from fish oil could lower triglyceride levels by 25%-30%. The results were published in The American Journal of Clinical Nutrition in 1997.

BUT, I would also like to point out that the question itself "omega-3 fatty acids found in fish are a good way to prevent/reduce cholesterol problems" seems to be a matter of debate because of articles like this:

New data presented this week provide clues as to why eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)--both components of omega-3 fatty acids--have differential effects on LDL cholesterol.

Presenting the results of the laboratory study here at the National Lipid Association (NLA) 2011 Scientific Sessions, senior investigator Dr Preston Mason (Brigham and Women's Hospital, Boston, MA) said that EPA is an inhibitor of lipid oxidation at normal and elevated cholesterol levels in the presence and absence of DHA, while DHA seems to have no real effect on lipid peroxidation. This trial was one of a number of studies that attempted to address the clinical question as to why LDL-cholesterol levels increase in patients treated with the triglyceride-lowering omega-3 fatty acids. In his trial, Mason et al compared the effects of EPA and DHA--alone or in combination with statins--on lipid peroxidation in polyunsaturated fatty-acid– and cholesterol-enriched vesicles.

evolution - Would ovoviparous to viviparous mutation have been gradual? How would that work?

I happen to have seen a talk by an anthropologist who was working on this (i can't reference them here i'm sorry to say - forgotten her name). I can only give an example from their work...

If you look at old world and new world primates, there is a large difference between the gestation time. If you look at the table in the link, lemurs have half the gestation time that humans and gorillas have.

What I can recall is that the lemurs placenta lacks many of the structures that primates have (see section 5). The lemur placenta is supposed to be primitive and a lot more like an egg sac which was internalized as opposed to a more articulated womb that primates have. So her thesis was that eggs would start out being internalized and subsisting only on their own internal structures, still isolated from the mother, then later placental structures would come about that nourish the fetus and enable it to enjoy longer gestation and better development pre-partum.

The stage I'm describing is only the divergence between primitive wombs and 'more advanced' wombs in the sense that they were capable of supporting the fetus for 9 months rather than just 4. That development happened over about 30 million years. The divergence of mammals is thought to have happened about 270 million years ago.

So the rough answer would be hundreds of millions of years for the whole shebang, but internalized eggs and live birth would be a relatively smaller amount of time.

microbiology - Which strains of C. diphteria are causing Diphteria toxin?

Real simple: Beta! Often called "phage beta" b-prophage is a more modern way to write it. I knew that one off the top of my head, but I like to refer the general public interested in bacteriology to Tadar's online text.

It's nicely done, and I wish that it had been around when I was studying bacteriology.

Specific to your question:

Hence, Corynebacterium diphtheriae can only produce the toxin
responsible for the disease if it carries a temperate virus called
phage beta. Only lysogenized streptococci produce the erythrogenic
toxin (pyrogenic exotoxin) which causes the skin rash of scarlet
fever; and some botulinum toxins are synthesized only by lysogenized
strains of C. botulinum.

hematology - Why does blood come from mouth when people are shot in the chest area?

Substances such as blood trigger the Cough reflex, so if for any reason blood accumulates in the airways, it will be ejected this way.

If you have a look at chest anatomy, you can see how this could be caused (look at Trachea down to the lungs, aorta and the carotid arteries above the heart). A shot through the chest can peforate many large blood vessels, along with the airways, and cause leakage inside.

I would consider it quite hard to hit the aiways like that though, the bullet would have to enter the chest quite near the centre as the cough reflex is not triggered by substances in the lung itself, only in the airways. There may be other ways of blood getting into the airways, but I would assume that a scene with a shot near the breast and then blood coughing would be unrealistic.

Image source: Micheau, A (2010) ANATOMY OF THE MEDIASTINUM: ILLUSTRATIONS AND CROSS-SECTIONS. From: http://www.imaios.com/en/e-Anatomy/Thorax-Abdomen-Pelvis/Mediastinum-Illustrations

human biology - How reversible is decerebrate posturing caused by brain stem damage?

This is a follow-up question to How likely would Abraham Lincoln be to survive his wounds today?

You don't have to see a CT scan or autopsy to know if the brainstem is
injured (directly or indirectly), if it doesn't work right.

The description of the first doc at the scene mentioned that Lincoln
was not breathing, and one pupil was dilated (the latter a clear and
unequivocal sign of dysfunction of the third cranial nerve or the
upper brainstem, from where it comes). Unfortunately, the second doc
described the enlarged pupil being the right one (it's extremely
unlikely to have been one and then the other - one of the doc's was
probably mistaken as to the side).

By 3 hours after injury, both pupils were fixed and dilated, and
Lincoln showed extensor (decerebrate) posturing - again, all signs of
profound brainstem dysfunction (but not yet brain death, though pretty
close to it).

Now, what is decerebrate posturing? See http://en.wikipedia.org/wiki/Abnormal_posturing#Decerebrate

Decerebrate posturing is also called decerebrate response, decerebrate
rigidity, or extensor posturing. It describes the involuntary
extension of the upper extremities in response to external stimuli. In
decerebrate posturing, the head is arched back, the arms are extended
by the sides, and the legs are extended.[6] A hallmark of decerebrate
posturing is extended elbows.[12] The arms and legs are extended and
rotated internally.[13] The patient is rigid, with the teeth
clenched.[13] The signs can be on just one or the other side of the
body or on both sides, and it may be just in the arms and may be
intermittent.[13]

A person displaying decerebrate posturing in
response to pain gets a score of two in the motor section of the
Glasgow Coma Scale (for adults) and the Pediatric Glasgow Coma Scale
(for infants). Decerebrate posturing indicates brain stem damage,
specifically damage below the level of the red nucleus (e.g.
mid-collicular lesion). It is exhibited by people with lesions or
compression in the midbrain and lesions in the cerebellum

ecology - Statement about Tropical Rainforests

There are many websites which describe this phenomenon. They all seem to confirm the basic premise of the question: in tropical rain forests most of the minerals are held in the biomass and rapid decomposition contributes to the recycling of these nutrients for new growth. One example is here.

Tropical rainforests are noted for the rapid nutrient cycling that occurs on the ground.  In the tropics, leaves fall and decompose rapidly.  The roots of the trees are on the surface of the soil, and form a thick mat which absorbs the nutrients before they reach the soil (or before the rain can carry them away).  The presence of roots on the surface is a common phenomenon in all mature forests; trees that come along later in succession win out in competition for nutrients by placing their roots over top of the competitors, and this pattern is seen in the temperate rainforest as well.  What does not occur in the temperate rainforest, however, is a rapid cycling of nutrients.  Because of the cold conditions and the acidity released by decomposing coniferous needles on the forest floor, decomposition is much slower.  More of the nutrients are found in the soil here than would be the case in a tropical forest, although like the tropical forest most of the nutrients are held in the plants and animals themselves.

I looked for actual evidence of these differences in rates of decomposition and I found this:

Salinas, N. et al. (2011) The sensitivity of tropical leaf litter decomposition to temperature: results from a large-scale leaf translocation experiment along an elevation gradient in Peruvian forests. New Phytologist 189: 967-977

These authors reported a comparison of rates of decomposition at various elevations in Peruvian forest. The parameter k is the decay rate of dry mass, year^-1. The following data are taken from Table 3.

site          elevation (m)   mean k (yr-1; 15 species)
Tambopata     210             1.753
Tono          1000            1.424
San Pedro     1500            0.968
Trocha Union  2720            0.546
Wayquecha     3025            0.424

and this:

Jacob, M. et al. (2010) Leaf litter decomposition in temperate deciduous forest stands with a decreasing fraction of beech (Fagus sylvatica) Oecologia 164:1083–1094

These authors studied leaf decomposition in a deciduous forest in Germany, with emphasis on the effect of proportion of beech trees upon overall rates of decomposition. Using data from Table 1 and Figure 2 (values converted from mg^-1 g^-1 day^-1 to yr^-1)

% beech yr-1
  96    0.2555
  67    0.657
  21    1.022

My Conclusion

Rates of decomposition can be much higher in tropical rainforest (k=1.753 yr^-1 for the Tambopata site in Peru, k=0.256 yr^-1 for a beech-rich forest in Germany). However, at higher elevations tropical rain forests are characterised by much lower rates of decomposition (Wayquecha k=0.424 yr^-1), comparable to those in deciduous forests.

These are all measurements of loss of dry mass from leaf litter. This will be dominated by loss of carbon, and I would expect that minerals will leach from the decaying litter more rapidly than these values. Nevertheless it seems plausible that relative rates of mineral recycling will reflect these k values.

chromosome - Is it more likely that the very first living organisms had a linear genome?

I would say this is a question that might not be resolved yet.

Going back to the earliest days of DNA - a billion years ago - its hard to imagine circular DNA being the first sort to show up. Its speculated that in the transition from RNA world to DNA world, early on each gene had a separate piece of nucleic acid coding for it which would not have been circular. It's been proposed for example that RNA viruses might have been a next step to cellular life. Although I can see an old electron microscopy reference, not it does not seem as if any RNA viruses with circular RNA have ever been found. How the first DNA chromosomes came about and what they looked like seems unclear to me.

In any case, though not typical, its not unusual to find linear chromosomes in prokaryotes. I could not find reference to archaea with linear chromosomes, but in prokaryotes, the link above points to the observation that even close relatives can have linear or circular chromosomes.

A remarkable property of the 8.2-Mb chromosome of S. erythraea was that, contrary to the expectations and the earlier data (Reeves et al., 1998), it proved to be circular. The chromosomes of its close relatives, Streptomyces coelicolor and Streptomyces avermitilis, are both linear, as is the chromosome of Rhodococcus sp. strain RHA1. These chromosomes are the largest in actinobacteria (8.7, 9.0 and 7.8 Mb respectively) and comprise some of longest DNA molecules in the prokaryotic world. In contrast, the shorter chromosomes of other actinobacteria are all circular.

It seems that linear vs circular genomes are a 'lifestyle' choice or connected to selection critera we don't understand yet:

Hence, it was tempting to speculate that the linearity of streptomycetal chromosomes was somehow linked to and perhaps beneficial for the maintenance of these extremely long DNA molecules, even though it resulted in the instability of their termini. This idea has been contradicted by the discovery of equally long but circular chromosomes in the acidobacterium Solibacter usitatus (9.97 Mb), δ-proteobacterium Myxococcus xanthus (9.1 Mb), cyanobacterium Trichodesmium erythraeum (7.8 Mb), and, now, in the actinobacterium S. erythraea.

I really doubt the instability of the chromosomal terminii is a real consideration - there must be genes that help maintain those, just as there are in eukaryotes. S coelicolor is a soil bacterium that is so common most people can find it in the dirt right outside their door - its not hard to live with a linear chromosome as a bacterium.

Were any brain fusion experiments ever conducted?

The odds of that are really very slim. "Growing brains" in vitro is rather difficult, and it appears that no one has created the brain of a real organism, but they have created "brains" from cultured dissociated neurons.

Fusing brains is complicated by the fact that you need to make the appropriate synaptic connections between neurons, and what exactly are the appropriate connections is still being worked out. As a side note, this is one of the goals of the BRAIN Initiative.

The closest I believe people have come to anything approaching fusion are brain transplants in non-human animals. This might be the closest thing to an in vivo fusion, especially if it is only a partial brain transplant. This is discussed a bit here.

genetics - When can a virus modify DNA in every cell of a living organism?

The answer depends on two factors:

• The type of vector (virus) you are using


• How well your vector can be integrated.

The bottom-line is that there is no guarantee the vector will work even if you start from the embyro.

As far as I know, the problem of using vectors in general is that the vector you are using might not be integrated into the genome of the host. (Not necessarily get into the DNA, but just keep replicating during each S phase.) Therefore doing it earlier gives you a better chance to actually get them in the organism.

For example, there is a linear vector used in C. elegans that was injected into the oocyte even before fertilization. The cell later treats the vectors as broken DNAs and linages them so they could be pull to one side of the cell during mitosis. However, the huge chunk of vector DNA is mosaic. (i.e. only some of the cells in that worm have the vectors.) Other vectors like engineered HIV have better chance to integrate themselves.

dna - What happens when cells in your body run out of telomeres?

During mitosis the genetic material in the cell is replicated to produce a copy of the genome for each resulting daughter cell. Due to the nature of the process, the ends of the chromosomes are not completely replicated, resulting in a slightly shorter copy of each chromosome after each round of replication.

Telomeres are extensions to the end of chromosomes that prevent damage or loss of genetic information during cell division. Telomeres are not replaced (in 'normal'/somatic cells), which gives rise to a replicative lifespan; the number of times a cell can divide before permenantly leaving the cell cycle (known as cellular senescence).

• This is generally viewed as an anti-cancer mechanism to protect against errors creeping in to the genome through many cell divisions. In order to become cancerous, a cell must first overcome its replicative lifespan [ref.]. This is achieved by activating the (normally inactive) telomerase enzyme that extends the telomeres - embryonic stem cells are one of the few cell types that normally express this enzyme, so they have unlimited replicative potential - a very important trait for stem cells.




• So a rapidly proliferating cell would indeed 'use up' it's telomeres before a different cell type. The cell would then either enter a state of senscence (permenant cell-cycle arrest), or apoptose. There are a lot of factors governing which outcome is realized, but the senscent cell population increases with age, and is proposed to contribute to many aging phenotypes (there is a recent fascinating study published in Nature where the authors remove all the senscent cells from aging mice, and the mice actually get healthier! Can't wait for studies that relate to human aging and senescent cell clearance (ref.)).

I have elaborated on the function of telomeres in the context of organismal aging in my answer to this question.

zoology - What was the reason for some plant and animals to become giant in course of evolution?

Thanks for asking an interesting question which made me think.

The short answer is that something evolves if there is an advantage to the genes involved, and, by 'advantage' I mean it produces more copies of the genes in the next generation so more individuals with that characteristic will be present in the population.

As to what particular advantage increased body mass had to any particular species that would depend on the particular species and its environment at the time. There is almost certainly not a 'one-fits-all' answer.

Most very big land mammals are herbivores and there is an advantage in having a large digestive tract when you eat a lot of plant material with a fairly low nutrient level. However, when there are also predators around, getting big and slow might be more of a disadvantage than staying small and fast. With evolution there is often a balance of competing forces which are traded of against one another.

Where large mammals have become isolated on islands with no predators, such as a species of now-extinct elephant on the Flores Island, they tend to become smaller so this suggests avoiding predators by simply being too big for them to kill might be an important factor.

And of course with many species we have the effect of sex-selection. If females select for the biggest males, there will be a selection pressure towards greater size.

With plants it could be something else entirely. Trees, for example, have long trunks basically for one of two reasons.

Firstly to put their leaves and seeds out of the reach of herbivores, so we have a kind of arms race like that between giraffes and acacia trees in Africa.

Secondly, when they grow in close clumps like woods and forests, there will be competition for sunlight and soil resources like water. A species which can reach higher and put it's leaves above those of it's neighbours will win the competition and there will also then be pressure on it's neighbours to evolve longer trunks. Long trunks mean that water must be pumped a long way to the leaves so the tree with the longest trunks will also need bigger root systems. Again a trade off between making a long trunk and dominating the water supply underground.

Many trees are also believed to have formed symbiotic associations with fungi in their root systems which help them take in the nutrients and water required to 'service' a long trunk and high-up leaf crown so they may be the only types of plants capable of doing this anyway.

One thing you might like to think about is why some whales are very big and some are relatively small (dolphins, porpoises, killer whales). What is the difference in their life-style, food, habitat, and so on, which could drive these evolutionary differences.