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Does making yogurt from non-pasteurized milk work against possible disease bacteria?
In the past, when there was no pasteurization, could making yogurt from milk lower the chance of getting infected by bovine tuberculosis (or other diseases from infected milk)?
For example, would yogurt cultures reduce the amount of "bad" bacteria or create a less hospitable environment for them?

In short, 'No.'
Yogurt, in and of itself, is the product of milk with specific strains of bacteria that are not particularly unique. Yogurt is just as hospitable to harmful bacteria as beneficial bacteria.
The two mechanisms which spring to my mind that would prevent infection by harmful bacteria in yogurt would be the following:
*The already dominant beneficial bacteria outcompete for the harmful bacteria, effectively limiting the capacity for harmful bacterial growth.
*The already present beneficial bacteria create extracellular products which damage harmful bacteria.
The second, if it happens at all, doesn't happen on a scale that I'm aware of. The first could happen, but I highly doubt it. It seems, to me, that it would be more likely to happen in cheese when most of the easy resources have been consumed, which in yogurt they haven't.
Yogurt, and all products stemming from milk, are inherently safer not because of any bacteria that take up residence, but because the mammary glands inside the animal producing the milk are effective filters for a variety of infections. Milk is a product that is constructed in the mammary glands, and the cells are selective about the output. Keep in mind, however, that it is by no means sterile. There are dozens of virii and diseases which can be imparted by breastmilk, and nursing women must adhere to guidelines concerning exposure to medications and diet. It's also possible for DDT and other compounds to become concentrated in breastmilk, resulting in harm to the child.
http://www.breastfeedingbasics.org/cgi-bin/deliver.cgi/content/Drugs/pre_pass.html
So, yes, while milk in and of itself is safer than other options, it is not risk free. A virus could easily infect the mammal or herd producing the milk for sale to humans, and only exhibit dangerous symptoms after the milk had been sold. This is why it's illegal to sell unpasteurized milk for human consumption in most U.S. states.

You should change that last paragraph from in most states to in most states in the US. Unpasteurized cheese and milk is legal and common in many countries in Europe for instance. I am so glad I live in a country where cheese from unpasteurized milk not only is legal, but it is considered (rightly) a delicacy. By the way, maybe I am misreading what you are writing, but pasteurized milk is NOT sterile either. If you need sterility you need to buy sterile milk, which is a different thing.

There have been studies regarding whether or not the bacterial load in yogurt (which would be the "Live and active cultures" part of yogurt - or the part where Jamie Lee Curtis talks about how you'll go back to pooping on schedule) helps protect the gut against the proliferation of certain pathogenic bacterias like C. difficile when we've otherwise wiped out the gut's natural flora - say with antibiotics.
So far, the results from that have been middling and inconclusive. And honestly, that's the best shot the cultures in yogurt have of showing a good effect.
In the scenario you ask about, you'd be trying to protect against diseases that haven't been handed a competitive advantage in the form of an obliterated gut flora, and have added in the risk of introducing pathogenic bacteria from the milk itself. A staggering proportion of milk-related food-born illness in the U.S. is due to unpasteurized milk. I'd say the chances of that being net-positive as slim, and more importantly I don't think you could slip that study past an IRB - at least in the U.S.
From Nico's question:
http://wwwnc.cdc.gov/eid/article/18/3/pdfs/11-1370.pdf Would be a decent place to start. Dairy is, admittedly, responsible for a small number of food born outbreaks overall - various fruits and vegetables, chicken and beef are still the top causes.
The issue is in how many outbreaks are caused by raw milk given how little of it is consumed in the U.S. The study I link above looks at known dairy outbreaks from 1993-2006. Of the 121 outbreaks, 60% of them were from unpasturized products, with a ~2 to 1 split between milk and cheese. All of them were caused by bacteria (addressing the idea that it might be a viral pathogen that wouldn't have been deactivated anyway).
The problem is though that many states prohibit the sale of raw milk products, and its relatively rare. If you weight the incidence of disease according to consumption patterns, one finds that the incidence per unit of dairy consumed is ~150x greater in non-pasturized products.
So while the overall numbers are not huge (though far from zero, and I've seen people consider lesser things public health emergencies), for such a rare product it's a big deal.
I've seen no suggestion that the patterns in Europe are different. For example (in Finnish) from this year: http://www.vsshp.fi/fi/7273/58327/ from this summer. But only the really massive outbreaks catch major media attention.

speaking of the proportion of food-born illness in the US due to unpaseurized milk, what makes you think it is the cause of that? Bad handling? Otherwise I cannot explain why the same is not true for the great part of Europe, where people eat Roquefort, Fontina, Gruyére, etc etc. Do you have any refs for that?

@nico Added information and some nuance to the answer. It's a "staggering proportion" given the volume of raw milk consumed in this country. I suspect the same is true for the great part of Europe - people eat food that will give them food-born illness all the time. Unless its a massive outbreak in a popular food item, you won't hear about it.

maybe there is some genetic part to it? Could it be that people, say, in France where it is extremely common to consume raw milk products are somehow "adapted" to them? On a side note, Slow Food even has a campaign in favour of raw milk

@nico I very much doubt there's a genetic component - the time scale we're talking about between the divergence from raw milk to widespread pasteurization is quite short. Odds are that people in France simply accept the risk, in the same way people in the U.S. accept the risk of say, medium/medium-rare hamburger.

@nico As to the Slow Food page, while I have some issues with it overall, whether or not raw milk is good 'on the whole' was not the question - the question was whether raw milk yogurt would represent a new positive prevention for disease bacteria. I'd argue that the weight of the evidence for that is still firmly "no".

that is my point. Say people in France "accept the risk" (and, in effect here people love their steak tartare with raw egg on top... :P) then there should be way more sick people when compared to the US.

@nico And you have not established that there are not. I pointed to a raw milk outbreak in Finland less than a month ago. There are others - your perception that they're aren't any doesn't necessarily mesh with reality. But foodborn outbreaks have to be very large to get much press, and raw milk products, even in Europe, aren't big enough to command that kind of attention. Also steak tartare has a very different pathogenic risk profile to hamburger meat ;)


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Do fake wasp nests actually fool wasps?
I have seen fake wasp nests sold as a deterrent against wasps and similar insects. Do they really work? Is there some scientific evidence for it?
A related link: http://www.scienceworld.ca/do-fake-wasp-nests-fool-wasps

I once heard someone who researches on wasps and he said that if you move the nest then the wasps get fooled and remain in the new location. I don't know about the fake wasp nests though.

Wasps are extremely territorial creatures. They also have great sight. Wasp colonies will send out foragers and scouts to look for uninhabited areas with food in which they can build a nest. Because wasps are so fiercely territorial, a scout wasp will generally stay away from an area with another colony already in it.
Because of this fact fake wasps nest works!!

Source: http://www.environmentalsociety.ca/main/wp-content/uploads/2011/05/Fact-Sheet-Wasps.pdf

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What is the difference between drought resistant non-succulent plants and plants that cannot be allowed to dry out?
What features make one plant able to withstand dry spells better than another with relatively similar structure? For instance, one of my Rudbeckias is wilting from drought at the moment, and an Oenothera next to it is not yet showing signs of dryness.
Or like jewelweed (Impatiens capensis), which wilts even while the soil is damp, in full sun, and ragweed (Ambrosia artemisiifolia), which will grow in very dry locations without being phased.
Is it caused by a faster transpiration rate in some plants than in others?

The difference may be related to how the plants fix carbon. While all plants convert CO₂ and H₂O to glucose and oxygen, there are at least three pathways that are used to do it. The C3 pathway is older and less efficient than the CAM and C4 pathways. Many drought tolerant plants use the CAM or C4 pathways because less water is needed. The C4 pathway is better than C3 in drier climates, hotter climates, and when CO₂ or nitrogen are limited. The hard part about this answer is that I'm not a botanist. Wikipedia lists some plants that use C4, CAM, and C3, but there is no comprehensive list, so I can't match up all the plants you mentioned in your question. In general, a higher percentage of monocots, especially grasses, use C4, but a wider diversity of dicots use C4. But you still can't draw conclusions about families of plants, because while corn and sorghum use C4, rice and barley use C3. Ragweed, a plant you say grows well in dry conditions, is a member of Asteraceae, which includes many plants that use C4. However, rudbeckias are also members of Asteraceae, but don't do as well in dry conditions. The C4 pathway has appeared and disappeared in several different plants, making any general claim hard to make. Here are some links that might help:

http://www.en.wikipedia.org/wiki/C4_carbon_fixation
http://www.en.wikipedia.org/wiki/C3_carbon_fixation
http://www.en.wikipedia.org/wiki/Crassulacean_acid_metabolism
http://www.brown.edu/Research/Edwards_Lab/reprints/sage_etal_2011jexb.pdf

If you know more about plants than me, that last link might be helpful, it's about the evolution of C4 pathway in plants and includes lists, but uses the formal species names I just don't recognize.

Plants in drier conditions usually have reduced surface area, thick waxy cuticle covering the epidermis, reduced number of stomata, and water storage tissues that presides in its roots and leaves.
This means that even if the plants are similar, one of them might express more of one of the features shown above.

But ragweed (one of my examples) has a large, thin leaf, barely any storage area, and no waxy cuticle, and withstands quite a bit of drought. Jewelweed, although it has a much reduced leaf area, and thick, watery stems, needs constant moisture.

i think this is a good answer inside, which is that there are lots of adaptations that cause drought tolerance.  i would avoid citing any particular adaptations as universal, though many are common.

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Why do some trees have a life span, while some don't?
I have heard that there is no limit on the growth of trees, but then why do some trees, such as boxelders and poplars, tend to live shorter than redwoods, for example? Some advertisements for improved lombardy poplars state that their trees have an extended life span, up to 75 years? The trees with shorter life spans seem to weaken at a certain age, and then contract diseases more easily.

do clones count as part of the lifespan? If so, many trees have an infinite lifespan. (I'm not hunting for technicalities, I'm just guessing that most trees die as a result of macroscopic effects like rotting out, infections, etc)

No. clones, once established and detached from the parent plants, become essentially new plants, and have a whole life ahead of them.

The answer to (this question) may be relevant to you. I didn't see your question until now, and it is very similar to a recent question I answered!

The answer that @Luke gave seems to apply very well to this question.

The answer to this could be that there are many factors contributing to the length of the life of tree species.
Climate: You can see that trees that have a reputation of becoming really old live in environments that have low moisture levels and much sunlight over the course of the year.
For example, you can see that the most long-lived trees in America are located in California, where the temperatures are relatively high, while moisture levels are low. If you have one without the other trees don't tend to live that long. Cold climates make growth
harder for each individual, yet hot and moist climates tend to help trees grow easier, but also die easier. Think of the amazon. It is one of the richest forests in the world, yet the growth of bacteria and high competition in the areas of the equator make life a lot harder for the longest living and slowest growing species.
As you can see, the vast majority of the longest-living trees are located in California, or other regions of the same latitude!
http://en.wikipedia.org/wiki/List_of_oldest_trees
Other species and the life around it/Its Ecosystem: Individual trees tend to be less likely to be destroyed by a fire, as they are less likely to catch fire. At some instances, forest trees or dried-out grass can catch fire and pass it on to other individuals.
Microbes and bugs found in some parts of the world are known to their abilities to destroy trees!
Current size of the tree: Larger trees are generally less likely to die of causes like drought or damage to their trunks, as they have greatly extensive nets of roots and thick trunks and thus are able to, even partly, recover these incidences.
If a rockfall for example causes damage to one side of the tree, some of the brunches will probably die, but the rest of them, that have their own network to the roots, will probably survive.
This means that luck is involved and if the tree is lucky enough to avoid dying for a certain amount of time, regular fluctuations in the environment do not kill it as they would kill a younger, less robust tree.
Biology of tree species: Debate is held as to whether tree cells have telomeres working the same way as they do in animals. Research published in 2001 suggests that telomeres don't work the same way, as plants developed without telomeres after six generations continue living and growing without problems. But even if they do use telomeres, they may use them in a different way. This is an area where research is still being conducted, though, and you may find controversies in the bibliography!
For example in the paper "Analysis of telomere length and telomerase activity in tree species of various life-spans, and with age in the bristlecone pine Pinus longaeva"
Barry E. Flanary & Gunther Kletetschka which can be found in the rep
http://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=2&ved=0CCgQFjAB&url=http%3A%2F%2Fwww.researchgate.net%2Fpublication%2F7709949_Analysis_of_telomere_length_and_telomerase_activity_in_tree_species_of_various_life-spans_and_with_age_in_the_bristlecone_pine_Pinus_longaeva%2Ffile%2F9c96052bcf0a51be49.pdf&ei=zzrCU9OcMIjV0QXmt4CwCQ&usg=AFQjCNH7853fvZ8yneznSfIQQPsxtIDQag&sig2=-PELK5RCQlAGTvQODoyZ2A&bvm=bv.70810081,d.d2k
we can see that sometimes, short lived trees have longer telomeres than long lived ones!
(Look in the second paragraph of the section "Results"). This means that actually, nobody really knows!! It may be the telomeres, it may be something else, it may be a combination of factors.
http://www.madsci.org/posts/archives/2002-04/1019349924.Bt.r.html
(notice that this post has links to pages that are no longer available).
Distillation and the most important point: The way that the tree is adapted to its environment determines its longevity in it. Planting an olive tree in the amazon is a great way of making sure it will not survive! Some trees are better at surviving in a certain climate (even if it is at your own garden) simply because they have evolved to live there.
That means that the trees probably don't have a defined lifetime in general, but the life expectancy is defined in each environment, depending on the circumstances!
This means that species we currently think of as short-lived can reach get really old:
http://www.ncbi.nlm.nih.gov/pubmed/11295506
What some companies may have done is   try to combine characteristics of individuals through selective breeding - and yes, it works for trees as well!- to match the climate and terrain characteristics found in the certain country or region! Or they may have selected for resistance against the most common pests in your area!
I hope I answered you question adequately!

Why do individual trees with no competition undergo a growth decline at a certain age, which lead to catching a disease, and the death of the tree? Some trees always do this. What is going on inside these trees?

Read the new section "Biology" in my answer!

Please change the !-. But looks pretty good.

Ya'll love explanation points!

Everything has a life span. When it comes to trees, there are significant variations between species (see here some examples).
Apart from the external factors, these variations seem to be related to telomeres length and telomerase activity [1]:

The results from this study support the hypothesis that both increased telomere length and telomerase activity may directly/indirectly contribute to the increased life-span and longevity evident in long-lived pine trees (2000-5000 year life-spans) compared to medium-lived (400-500 year life-span) and short-lived (100-200 year life-span) pine trees, as well as in P. longaeva with age.

Also, the lower metabolic rate of some trees increases life span [2]:

... the extremely high longevity of trees may be explained by the lower metabolism displayed by the stems. These results clearly reflect different energy allocation and energy expenditure rate strategies between leaves and stems, which may result in different senescence rates (and life spans) in these organs. They also suggest that, in contrast to animals, the ROL (rate of living ) theory of aging may apply to woody plants at the organ level, thereby opening a promising new line of research to guide future studies on plant senescence.

Leaf longevity is also correlated to shoot growth [3]:

These results suggest that leaf longevity is greater on shoots with low annual growth potential. Thus, a slow-growing tree at high elevation (low annual shoot growth potential) can have the same amount of foliage per shoot as a fast-growing tree at lower elevation.

References:

Flanary BE, Kletetschka G. Analysis of telomere length and telomerase activity in tree species of various life-spans, and with age in the bristlecone pine Pinus longaeva. Biogerontology. 2005;6(2):101-11. doi: 10.1007/s10522-005-3484-4. PubMed PMID: 16034678.
Issartel J, Coiffard C. Extreme longevity in trees: live slow, die old? Oecologia. 2011 Jan;165(1):1-5. doi: 10.1007/s00442-010-1807-x. PubMed PMID: 20963610.
Schoettle AW. The interaction between leaf longevity and shoot growth and foliar biomass per shoot in Pinus contorta at two elevations. Tree Physiol. 1990 Dec;7(1_2_3_4):209-214. PubMed PMID: 14972918.

On 'long-lived pine trees (2000-5000 year life-spans)', I haven't seen any evidence that there are trees older than about 4600 years old, but there are several trees of that age. I'm guessing there was an event at about that time that affected the trees. Those old specimens haven't been declining, so I think they might have a longer life span than people have thought. What are your thoughts on that?

Although most plants can potentially reproduce sexually, there are some plants that effectively always reproduce by shedding off branches which, when they fall in the right conditions, grow into new 'clones' of the same tree, which the exact genetic material. In these cases, it is advantageous for the tree to be able to survive as long as possible. Plants that reproduce sexually by the cross of two different individuals have a recombined genetic material in every generation, and the survival of that plant with that new genome is usually shorter.

why do you think that recombination of genetic material leads to shorter life span?

Because recombination is a mechanism to adapt to environmental changes. Then it is more important that nutrients, light and water are available for the "improved" next generation than for feeding yet unadapted elder individuals that might not survive long under new conditions.


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Why doesn't Fenoxaprop-P-ethyl damage cool season lawns?
For controlling bermudagrass, Cynodon dactylon, a serious perennial grassy lawn weed in my area, I use the herbicide Fenoxaprop-P-ethyl. It kills the bermudagrass rather well, without damaging the cool season lawn grass in the least.

I believe Fenoxaprop-P-ethyl acts by inhibiting the synthesis of fatty acids in the meristematic tissues of the weedy grasses (designed especially for bermudagrass).
How does this mode of action not affect the 'good' grasses (the fescues, bluegrasses, and ryegrasses popular in my area)?

Will get to this question hopefully before end of bounty :) interesting stuff!

A number of studies have been done that investigated resistance to Fenoxaprop-P-ethyl and related compounds. Most of these studies focused on resistance in crops (e.g., maize) or black grass. One of these studies (Kay et al., 1999) was particularly interesting as it focused on several possible mechanisms of herbicide resistance in Alopecurus myosuroides (Black-Grass). I quote from the abstract:

[...] Resistance at the whole-plant level correlated well with reduced acetyl Co-enzyme A carboxylase sensitivity (target site resistance) in two of the populations (one from the United Kingdom and one from Germany) but enhanced metabolism appeared to be the primary mechanism of resistance in the majority of the other populations. [...] We suggest that resistance in Lincs E1 may be explained by multiple resistance mechanisms—the expression of both insensitive acetyl Co-enzyme A carboxylase and an increased rate of detoxification. However, resistance in the population Clay from the United Kingdom could be explained neither by target site insensitivity nor by an enhanced rate of metabolism. These results provide conclusive evidence that a single resistance mechanism alone cannot explain insensitivity to fenoxaprop-P-ethyl in European resistant black-grass populations and that additional, as yet uncharacterized, mechanisms must also be present.

So based on these data, I think several mechanisms may play a role in the cool season lawn grass resistance (a species name may help to specify my, admittedly, broad answer).
Interestingly, Fenoxaprop-P-ethyl is an acetyl CoA carboxylase (ACC) inhibitor (Kay et al., 1999). Note that Haloxyfop (as mentioned in your question "How does Haloxyfop control young grassy weeds in fields of broadleaved crops?") is also an ACC inhibitor. From the answer on that question it appears that ACC inhibitors inhibit cell membrane formation and that monocots (grasses) are most susceptible and dicots less. Dicots are less sensitive because they have two ACC types at their disposal, one being insensitive to ACC inhibitors. Not surprisingly then, Bermuda grass, being a monocot is killed by this herbicide. Interestingly however, other monocots seem to survive, such as the cool-season lawns you mention.
I was not able to find conclusive evidence as to why some monocots survive ACC inhibitors. An educated guess is that resistance can be conferred by mutations in the ACC enzyme (Letouzé & Gasquez, 2001) that make the enzyme less sensitive to the herbicide. These mutations can be caused by repeated exposure to these herbicides, whereby strains become resistant to the material, much like the way in which (multi-) resistant bacterial strains emerge after repeated exposure to antibiotics.
References
Kay et al. Pesticide Biochem Physiol 1999; 65:169–80
Letouzé & Gasquez, Theoretical Applied Genetics 2001; 103:288-96


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How does Isoxaben kill newly germinating seeds, with almost no effects on established ones?
Isoxaben (N-[3-(1-ethyl-1-methylpropyl)-1,2-oxazol-5-yl]-2,6-dimethoxybenzamide) is a pre-emergent herbicide used in landscape beds before the application of mulch (my use for it, anyway). It kills the weeds as they germinate, while not harming most established plants.

Here's the mode of action, as stated by Dow AgroSciences:

Isoxaben belongs to the Benzamide family of herbicides and inhibits cellulose biosynthesis in the cell walls of susceptible
  weeds (WSSA group 21). This means that cells cannot divide during the reproductive cycle; therefore, they cannot grow,
  causing death. While cell division does not occur, this mode of action should not be confused with mitotic inhibition that
  occurs with dinitroaniline herbicides.

How does this only affect germinating weeds, while not noticeably affecting weeds that have emerged from the soil (I have to hit those with another herbicide)?

As with your other question on mitotic inhibitors ("How does Trifluralin kill newly germinating seeds, with almost no effects on established ones?"), inhibiting cellulose synthesis will inhibit growth. Hence, an established plant will stand its ground, but newly germinating plants cannot grow without cellulose synthesis and hence will fail to germinate.


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What are the biological mechanisms behind the increase in cancer risk and alcohol consumption?
Alcohol consumption is known to be a risk factor for developing cancer. Compared to obvious causes like tobacco where one is exposed to known carcinogens, I don't see an obvious mechanism by which alcohol consumption would increase the risk of cancer.
Is there anything known about the mechanisms by which alchohol consumption affects cancer risk?

Am I missing something here or is it just for the rather obvious reason that alcohol is a strong cell toxin that, taken often, causes constant low-level inflammation and stress (and thus accumulating damage) in tissues?

Our pharmacology course taught alcohol essentially as "is an extremely unspecific molecule and doesn't really bind to anything, but we take it in doses high enough to drive random reactions everywhere" (its effects start at mM concentrations, 1000x higher than drugs tend to). It's tiny so I don't see a barrier preventing entry into the nucleus and randomly reacting with DNA.

Asian Glow is linked with cancer. Actually tackling alchol related cancer is a fairly hot topic these days.

There aren't many studies which associate between alcohol consumption and cancer to my knowledge. The association is more with metabolic diseases because the liver is affected.
Alcohol is oxidised to acetaldehyde by alcohol dehydrogenase. Acetaldehyde may also, in turn affect the cells by DNA damage if it is not metabolized quickly to acetyl-CoA (perhaps in a manner similar to formaldehyde or by formation of Schiff's base with nucleotides). The other way by which alcohol is metabolised is through cytochrome-p450 (CYP2E1) which produces ROS (Hydrogen Peroxide), that may lead to carcinogenesis.
You might want to check this review.

Welcome to the site. It would be great if you could provide citations for your statements if possible (e.g., low correlation between alcohol consumption and cancer).

@kmm.. corrected :)

I agree damaged is caused by acetaldehyde (also the cause of asian glow) but I believe that your selected enzyme is incorrect.

yeah.. i mixed it up slightly .. but cyt-p450 is also involved..


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How can I resuspend a cell pellet without harming the bacteria?
When using a preculture with Ampicillin in my protein expression, I have to get rid of the preculture medium to avoid carrying over too much beta-lactamases that will destroy the ampicillin in the main culture. To do this I pellet the cells and resuspend.
Which methods of resuspension are best suited if you need the bacteria alive afterwards? I'm not sure how much force I can apply without harming the bacteria, and resuspending very gently takes a very, very long time.
Which methods can be used to resuspend bacteria alive, and which ones are the fastest?

I wonder how many cells are even killed in a pellet?  It seems they always come back into log phase growth in a short time.

Assuming that you are talking about E. coli: As long as you are resuspending the cells in a suitable liquid, e.g. fresh medium or buffer, then from my experience you don't have much to worry about - the cells are very robust. I've found that different strains and growth conditions give pellets with very different qualities - some will resuspend quite well with vortexing. If the pellet seems clumpy then trituration is something that I always found to work - pipette up and down until the pellet breaks up.
If you were going to do some kind of physiological measurement with the resuspended cells then it might require some checking, but if you only intend to regrow and induce expression I would say that giving the cells some time to recover in the new medium (check that absorbance is increasing) before inducing expression should be enough.

Using a pipette is what I'm doing now, though I usually cut off the tip a bit to reduce the force when pipetting.

Pipetting up and down GENTLY, the slower you pipet and the thicker the tip the more gentle it is, or vortexing SLOWLY, high vortexing speeds result in shear stress on the wall, just like fast pipetting with small tips
Bacterias can take a lot, take more care with yeast and even more care with mammalian cells


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Which sequence characteristics influence the transcription efficiency of T7 polymerase?
The T7 polymerase doesn't transcribe all sequences equally well, the transciption efficiency can vary widely for different sequences. One well known requirement of the T7 polymerase is that the sequence should begin with 2-3 guanines for efficient transcription.
Is there any literature that quantified the effects of the sequence on the transcription efficiency? I'm mostly interested in the effect of the first few nucleotides, as changing other parts of the sequence is usually not possible.

Would be nice to know why some of my T7-promoter plasmids produce ~100 mg protein/L of culture and others maybe 2-3.

Well, the protein expression also depends on the strength of the ribosome binding site.

I'm doing in vitro transcriptions and I'm not translating the RNA anyway, so for me that part doesn't matter

This is not an answer, but a starting point. I found this article Bai L, Santangelo TJ, Wang MD. Single-molecule analysis of RNA polymerase transcription. Annu Rev Biophys Biomol Struct. 2006;35:343-60. that may contain the answer to your question. Lacking that, you may find good starting points in the references section.

By far the most important part is the very beginning of the transcript, especially the positions +1 and +2. The conservered consensus sequence in class III T7 promoters is GGGAGA, any changes in the first two nucleotides severely reduce the transcription efficiency. Changes at positions +3 to +6 have much smaller effects.
Additionally, changes that put many AU base pairs in that region (e.g. GGUUU) seem to affect the trancription efficiency negatively.
Other sequences that are problematic anywhere, not only in the beginning are long stretches of uridines or adenines. Sequences with eight or more uridines or adenines can cause the polymerase to slip, which results in transcripts with more uridines or adenines than in the template.
These characteristics are detailed in the paper from Milligan and Uhlenbeck from 1989.

Milligan, J. F. & Uhlenbeck, O. C. Synthesis of small RNAs using T7 RNA polymerase. Meth. Enzymol. 180, 51–62 (1989).


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Why is SOC medium recommended for transformations?
In pretty much every transformation protocol I've seen SOC medium is used to grow the bacteria for a short while after the tranformation and before plating.
I've usually substituted LB medium for this step for easy retransformations, but I gather that the SOC medium is supposed to make some difference in efficiency, or else the simpler LB medium would be recommended in the protocols.
Why is SOC medium used for transformations? What difference does substituting with LB medium cause for the transformation efficiency?

(Super Optimal broth with Catabolite Repression) SOC media contains glucose whereas Luria Broth (LB) doesn't. SOB also has a more delicate salt balance.
Naturally the glucose will help the cells recover and grow faster after the heat shock. Your transformation efficiency should improve since less cells will die.
On the other hand, the reason why SOC media isn't always used is because of the detrimental effects of having too much glucose. The glucose will be consumed in the Krebs cycle and produces a lot of acetate which can be pretty harsh on cells.

Do you have any literature source on that glucose helps the cells to recover?

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Are there issues with filling PCR tubes to capacity?
I'm planning to scale up a PCR reaction, and I'm wondering if filling the PCR tubes to the maximum volume of 200 ul would be a problem. It would mean a lot less pipetting as I would only need 1/4 of the tubes.
The typical protocols I've seen always use 50 ul for a PCR reaction, I'm wondering if there are any issues with larger volumes, e.g. differences in heat transfer, that could cause issues if I scale up the volume in one tube.
Is scaling up the volume problematic? Any specific aspects I should consider?

(Also too long for a comment.) This question reminded me about an anecdote told by Arthur Kornberg concerning the approach to scaling up that was adopted by Reiji Okazaki (discoverer of Okazaki fragments).
Here is a quotation taken from For the Love of Enzymes: The Odyssey of a Biochemist by Arthur Kornberg

Reiji’s research style is not readily gleaned from his publications,
  but it is vivid in my memory. One example I call the Okazaki maneuver. In purifying an enyme, he used a heating step: 10 milliliters of
  the enzyme solution was held in a test tube at 70°C for ﬁve minutes;
  then the coagulated impurities were removed by centrifugation.
  When he came to the point of scaling up the procedure to several
  liters, he simply repeated the original heating procedure several
  hundred times. I was embarrassed to have to report such an unsophisticated procedure in our publication. But then I realized that
  he was able to complete this step in a few hours and saw no point in
  wasting precious time and material in learning how to do the heating in a large beaker or flask. Later, when another of my students
  puriﬁed an enzyme with a heating step and had to scale up his
  procedure 2,000-fold from 3 milliliters to 6 liters, I advised the
  Okazaki maneuver: he added 3 milliliters to each of 200 test tubes to
  carry out the heating and centrifugation step, repeating the procedure nine times. Another student who tried heating a large volume
  of this enzyme in a single step lost it in a thick coagulum.

Too long for a comment: I would say it depends on the PCR. I have personally used maximum volumes of 50ul, if I needed to prepare higher volumes, I made one mix which subsequently got distributed to more tubes with 50ul max.
The problem with big volumes is to get a fast and homogeneous heating and cooling. If the outside of the tube is faster, the reaction there starts already while this may not be the case in the middle. This can lead to uneven denaturation and amplification of your template. The later is especially problematic when you amplify short sequences. There the amplification time might already be over and the PCR program is moving on before the template is finished, which will result in less of your full-length product and the enrichment of shorter versions.
There is another problem that might occur in big reactions: Due to gradients in reactivity because of temperature gradients I think it is possible that reagents (dNTPs, Mg-ions) can form gradients which further inhibit a good yield.
Finally I tested one thing on one of our PCR machines: The PCR tube is set into the heating/cooling block. It is not completely set into the block but stick out partly, so if you fill it up to maximum capacity, the upper 75-100ul (approximately) would be outside the heating block and we have a thermal problem. The reaction mix there would only heat up due convection.


text:
How do I read a sequence logo?
I'm looking at a paper that uses several sequence logos to illustrate the consensus sequence of certain sites.
Here is the most important of the sequence logos I'm interested in:

The explanations I found about the exact meaning of this visualization were rather abstract and mathematical. I understand that the height of the letter stack is indicating in some way how strongly conserved that position is, but I have some difficulty judging the absolute values.
When are the positions considered to be significantly conserved? The paper where this data is from mentions the positions 5 and 6 as characteristic for the consensus sequence, which is not really obvious to me from this graph.
How do I interpret the absolute value on the y-axis? What does it actually mean if position 16 has around 0.6 bits of information?
I'm not so much interested in an exact mathematical treatment, but a general guide on how to read these graphs and how to interpret them in practice.

For this kind of logo you compare a number of sequences. The height on the y-axis is indeed an indicator for the frequency of a certain base. The sequence logos I know use a height to 1 for  positions where only one base occurs and go lower for less conserved bases. I might have some papers about the generation of these logos in my database, I can look this up later today if you are interested.

Finally, Bioinformatics questions are coming in this site. Anyway, everything is in the main paper. I will be explaining in the answer soon!

DNA/RNA only has 4 nucleotides, and information content is often represented in log2 form. So a fully conserved site of, say, 10 sequences contains log(10/10/.25) = log(4) = 2 bits of information. The .25 is the probability of a given nucleotide, and the overall probability is represented by the height of the letter.

A very clear description is given in Wikipedia.
The starting point is an alignment for the region under investigation.
A. Basically, to get the height of the stack of letters for every position one has to calculate the degree of certainty about the residue (= degree of conservation) at this position in the sequences belonging to this class. I'll explain what it means:
The key parameter in this context is information. 1 bit of information can be understood as the amount "knowledge" you get when receiving an answer to one yes/no question.
Let's say we have equal proportions of all four bases at a certain position in a set of DNA sequences. To "guess" a base at this position in some sequence we have to ask two binary questions. For example: "is it Pyrimidine?" If 'yes' we'd ask "is it 'T'?" Otherwise: "is it G?". So, when the frequencies are equal we can get 2 bits of information from one observation of a base at this position in a sequence.
If the frequencies are distorted, we already have some ideas about the bases when coming to an individual observation. If we already know, say, that we have just G and A at this position with ratio of 1:1, we can just ask "is it G?", so we get clearly 1 bit. When the ratios are not even (or when the number of alternative states is not 2n), the analogy with the questions becomes much less clear and we have to resort to the very simple formula for Shannon entropy. Intuition and brief inspection of this formula would bring you the idea, that when the ratios of the residues are biased, we always have less information than for the case of equal frequencies (2 in the case of DNA).
Now to estimate the "the degree of certainty" we simply calculate the information based on the observed frequencies of different residues at this position and subtract it from the theoretical maximum (again: 2 in the case of DNA):
certainty = maximal information possible - actual information
This value defines the height of a stack of letters at each position.
The maximum value (2 bits) would be observed when we always have the same base, because "actual information" would be zero (there is no need to ask questions - we "know" the answer anycase). The minimum (0 bits) is when we have no idea about the base. One bit would be obtained if we had, say, just two equally frequent bases. And, for example, the value of 0.6 would be observed if you had, e.g. 68.5% of the time the same base A and in all other case C, G or T with equal frequencies of 10.5%.
B. As you probably already know: the proportions of all alternative bases are shown as relative heights of individual letters.


text:
Are human fetuses more likely to be male?
Question: From a physiological point of view, when sex is determined in a human fetus, is it equally likely to be male or female?
Studies in this area typically measure age at birth, where the data would have already been biased.  There's a slight imbalance in the human sex ratio, in that there's an overall tendency towards males.  However, this could be accounted for in numerous ways, such as abortion.
Fisher's principle suggests there would be an evolutionary tendency towards 50:50 chance.

@Dane Why are you marking the older question as a duplicate though?

@Dane Jan 23, 2012 vs Jan 11 2015?

Hi, as long as the newer question has an answer, it is accepted to close the older question. There are many such instances in meta.

http://meta.stackexchange.com/questions/147643/should-i-vote-to-close-a-duplicate-question-even-though-its-much-newer-and-ha

The Fisher's principle is not applicable to the fetuses because it has been formulated for parental expenditure and basically states that the ratio of male to female parents (implying that both parties have reached the age of fertility) will tend to 1:1.
There are several mechanisms that we can use and that are mentioned in the canonical paper by James (2007):

(a) there are equal numbers of X and Y chromosomes in mammalian sperms
  (b) X and Y stand equal chance of achieving conception
  (c)
  therefore equal number of male and female zygotes are formed, and that
  (d) therefore any variation of sex ratio at birth is due to sex
  selection between conception and birth.

James brings much evidence that none of these conventional beliefs is true. Rather, they are dependent upon many factors: exposure to stress during pregnancy, glucose level etc. He reports that there is an excess of males at birth in almost all human populations, and the natural sex ratio at birth is usually between 1.02 and 1.08. However, the ratio may deviate significantly from this range for natural reasons. (I really recommend reading the paper I linked, it is available for free).
Branum et al (2009) analyze birth statistics in the US taking into account many factors like ethnicity, gestational age and plurality and show that the ratio can increase even more with growing gestational age and has different values among different races.
So, taking everything together, I can say thay YES, the chances for human fetuses to be male are indeed higher.

Note there is a slightly higher mortality rate for males, which tends to bring the ratio towards 50:50 at reproduction age.

"the ratio of male to female parents (implying that both parties have reached the age of fertility) will tend to 1:1" Does this equal to that female parents and male parents would have equal mean amount of offsprings? But this is obvious claim!

The following paper(1) studies the trends in male to female ratios among newborns over the period 1950-1994 in 29 countries (20 major European countries, USA, Canada, Japan, and others). In all countries at any time point, the male to female ratio was always higher than one. In some countries (Mexico and a few northern eastern European countries) the male proportion has been decreasing over the 1950-1994 period, whereas in southern Europe and Australia it has been increasing. Overall, the ratio has remained constant.
The authors mention several factors that could contribute to the decrease of males. Among those factors are:

hormonally induced ovulation
maternal nutrition
environmental factors (like alcohol exposure of the fathers)

On another note, the increased male to female ratio in newborns could be explained with the size of the sex chromosomes. The X chromosome contains ~155 million base pairs, whereas the Y chromosome contains ~58 million base pairs. Thus, the X chromosome is heavier than the Y chromosome, and a sperm cell carrying the 22 autosomal chromosomes +Y chromosome will swim faster and have a slightly higher chance of fertilizing the egg. This explanation is purely my speculation.

Trends in male:female ratio among newborn infants in 29 countries from five continents

Could you provide some reference for the last paragraph, ie. that the ratio might be dependent on the weight of Y & X chromosomes?

@kate The last paragraph is my speculation. I can only support it my the reference I gave for the length of the sex chromosomes.

I see; thank you. It sounds really interesting, though.

@Gergana Vandova: then you should probably state it is just your guess in the answer. Right now it looks like a very (unsubstantiated) bold claim.

there is some evidence that the female reproductive system may also do some gender based selection and skew the chances of one or another outcome depending upon environment, if I recall the snake work correctly.
I found a recent (2002?) review:  West SA, Reece SE, Sheldon BC. 2002. Sex ratios. Heredity 88: 117–24.

Furthermore, in some of these cases individuals appear to show
  extremely precise control of their offspring sex ratio. For example:
  (a) in the Seychelles warbler (described above), females vary the sex
  ratio of their offspring from 90% female to 80% male depending upon
  environmental conditions.

It isn't so easily predictable what the outcome is for a given environmental set of conditions.  To me it is not surprising since sperm competition and selection in the oviducts is common to nearly all animals.


text:
How are arms different from legs?
How are arms and legs defined physiologically? For example, we say humans have two arms and two legs, while cats have four legs, and some monkeys (appear) to have four arms (although I guess they could be legs too). It's really unclear to me how we make these distinctions.
What is the physiological definition of both "arm" and "leg"? How are they different?

perhaps to do with whether or not they are walked on?

Why do they have to be defined physiologically? It is a matter of common everyday language, and human language is generally inconsistent and full of "because we've always called it this way" and "because they look similar" reasons. Do you have any example of any scientific research which divides appendages in "arms" and "legs" and proves results which are true for the one and not for the other? Maybe if you got to stuff which is about gripping, or bearing weight, but then you are back at the informal language level.

I don't think "arm" or "leg" is a matter of everyday language, and it just seems really silly that I don't know a) why my cat has four legs instead of two arms or b) how many legs/arms a monkey has.

I think that's more of a matter of linguistics rather than any scientific/physiological reason. For instance, in Portuguese, you wouldn't call legs to a cat or a dog's limbs. You would say they have 4 "patas" (roughly translated as "paws"). And calling them legs, in Portuguese at least, would be weird.
When veterinary doctors refer to animal limbs, they usually use anterior and posterior limbs. In fact, anatomically speaking, anterior limbs in cats and dogs (and probably in other animals too) have more in common with human arms (upper limbs) that with their own posterior limbs.

Also, as rg255 commented, maybe the reason behind the colloquial nomenclature is quite simple...
To (miss)quote Nancy Sinatra:

These "legs" are made for walking
And that's just what they'll do

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


text:
What cells don't have a primary cilium?
It is often stated that most cells in the human body have a primary cilium.
Which ones don't? For which cells is it unknown?

Thank you for the answer, @leonardo, but I was asking about unciliated cells in particular. I'll wait to see if anyone can provide a more authoritative answer saying there are none, or an example of cells with no cilia.


text:
Why can't plasma proteins migrate from capillaries?
Why can't plasma proteins shift from capillaries to connective tissue but WBCs can be very rich in connective tissue even though obviously the WBCs had to go through capillaries.  Another example: in alveolar sacs neutrophils are there in the lumen  despite the presence of epithelia of alveolar sacs,  and it can only reach there via capillaries. So, how can they get into lumen despite the epithelia lining? Histology textbooks say that no plasma proteins can enter or leave capillaries, but WBCs (which are much larger than proteins) can move to connective tissue via capillaries?

I believe the white blood cells that invade inflamed areas do so via the lymphatic part of the circulatory system.

WBCs typically invade inflamed tissue through post-capillary venules.

See Leukocyte extravasation.

Cells of the endothelium are joined by tight cell junctions which are impermeable or selectively permeable. Generally, proteins can only migrate through the endothelium via active transcytosis.
Leukocytes (specifically neutrophils, lymphocytes and monocytes) express various adhesion molecules and cytokine receptors which allow them to interact with endothelial cells and facilitate their movement (diapedesis) either between (paracellular) or through (transcellular) the cells. The process of leukocytes leaving the endothelial lumen is known as extravasation.

Carman CV. 2009. Mechanisms for transcellular diapedesis: probing and pathfinding by `invadosome-like protrusions'. J Cell Sci 122:3025-3035.
(C,D) The process of diapedesis, whether during intravasation or extravasation, can occur by two distinct pathways: paracellular or transcellular. (C) Paracellular diapedesis. Leukocytes and endothelial cells coordinately disassemble endothelial cell-cell junctions and open up a gap between two or more endothelial cells (Muller, 2003). (D) Transcellular diapedesis. Leukocytes migrate directly through individual endothelial cells via a transient transcellular pore that leaves endothelial cell-cell junctions intact. Note that the two individual endothelial cells in C and D are distinguished by different shades of pink.

Generally, for plasma proteins to enter the tissue space, they must be able to passively diffuse out of the vessel into the tissue. This requires sufficiently large gaps between the endothelial cells of the vessel wall (and if passing into the lumen, space between the epithelial cells forming the barrier of entry into the lumen.
However, under the proper circumstances, white blood cells can actively invade the tissue across the endothelial barrier, migrate through the tissue, and may even cross over into the tissue lumen. This is a active, highly coordinated process  allowing the white blood cell to bind the endothelium and push its way through a gap and allowing it to bind extracellular matrix proteins to migrate through the tissue to its destination.

Sounds very good, and plausible. There are answers opposed. Why don't you add some reference.

Let me add that during the process of inflammation (e.g., the skin has been infected), there will be foreign materials introduced into the body which are picked up by resident macrophages and dendritic cells, which are basically waiting for this stuff to happen. Once they engulf a foreign particle, they will become activated and start releasing inflammatory molecules which attract other white blood cells to come into the said interstitial tissue (you called it CT). They come in because the capillaries in those areas become permeable to the white blood cells due to WBC-endothelial cell interactions, like adhesins and also the capillary cells (endothelial cells) may separate slightly from each other, forming little gaps, that allow proteins, more fluids to come out with the WBCs. So that's why you get swelling if you injure yourself, like if you broke your bone.. or if you got a pimple and it filled with pus (that's all the WBCs and proteins and plasma coming out of the blood vessels into the interstitium).
The reason why we want WCBs to come out during these times is because they clean up debris (macrophages), kill bacteria (neutrophils, macrophages, T-cells, etc), and the proteins may come out like antibodies, anti-bacterial proteins like complement, etc.
tldr; WBCs extravasate through capillaries in certain situations where they are needed (i.e. inflammation). The process of leukocyte (WBC) extravasation has been described by the other answers so I won't go into detail about it.

welcome to Bio. Please add sources or references. Unreferenced answers don't allow users t background read on the topics discussed.

I'd be interested in reference on "the capillaries in those areas become permeable" which might be different from and opposed to "extravasation". Third, there seems to be uptake and release of protein - LDL, VLDL - via endothelial cells' receptors.  - Is there reference on local lymphocytes (Langerhans) already situated on lumen side, as "somebody's go to do the job" of signalling for permeability (in the first place)?


text:
Where are -HCl supplements absorbed in the human digestive system?
I see that quite a lot of drugs and dietary supplements sold in the USA have -HCl(hydrochloride) added to their name. For example pyridoxine hydrochloride for Vitamin B6.  I'm interested in knowing where in the digestive system -HCl compounds are absorbed? Is it in the stomach?
It would also help if I get a rough idea of how long it takes for -HCl supplements to be absorbed. Is it an hour or more?
Thank you for your input!


text:
Range of feasible coefficients in an unlimited growth model
If you are given an unlimited growth model in the form:
$\frac {dP(t)}{dt} = k P(t)$
Obviously the population growth would never be unlimited, but let's presume for the moment that we are introducing a species into an environment where there is the possibility for unlimited growth, at least on for a given time -- i.e. invasive species.
$k$ is some rate of growth of the population at time $t$, denoted by $P(t)$
What are some feasible values of $k$? In other words, if a number is way above or way below $k$, where would I know that the research I am reading is preposterously off-base?
I am sure it is different for different types of animals, including mammals, birds, bacteria, etc.

The feasible value for K depends on the growth rate and is variable. The good thing with using mathematical models is that you can provide a range of values for a parameter and observe the effect on the system.
You can get an idea of the feasible values based on literature evidence. You first decide what that invading species might be.

A solid limit: k must be greater than zero. Unless you're talking about some cannibalistic species or something that isn't suited to the model at all.
As long as the species is productive in the new environment: k is greater than 1. The population is probably growing or again you probably won't be using an exponential growth model.
As mentioned before you would need to know the species for more information. But if you look at generation times and litter sizes:

Some bacterial generation times (from here) range from 10 to
2000 minutes (33 hours). So that is $k=2$ per generation time. Per
day you're looking at a lower bound of 2 per day and an upper bound
of $k=2^{14}=10^{43}$ per day.
Mice are something like 12 week generation time and a litter of 10
giving something like $k=10^{10}$ per year.
Elephants are one young every 25 years. So $k=16$ per century or so.

Of course this is all based on gross assumptions. But you're looking for guidelines for a unrealistic model so hopefully they'll do.

Why k greater than 1?

If k is between 0 and 1, the population is dying out. Of course that is possible but the question seemed to be asking about growing populations, not dying populations.

"If k is between 0 and 1, the population is dying out." Certainly not, if k is between 0 and 1, the population grows exponentially. Likewise, k being negative does not mean cannibalism, only some death rate greater than the birth rate.

Hm. Yes you're right. I'll point out that this answer is 2 years old and I haven't thought about it since. I suggest you edit my answer or add your own as I've got it wrong.


text:
Energy use by muscles, actual work done by muscles and more
Lately, I've started exercising in the gym and outside. I've also started to look at the details of food I eat.
Food usually has a label saying the amount of energy is inside it. For example, some chocolate says it has 400 kilocalorie for 100 grams.
I have some questions about that:

Does the label say the amount of total chemical energy exists inside the food, which will be released if burned, or the energy available to the human body after digested, and because digesting requires energy, the food contains actually MORE energy then written?
When I'm riding on a static bike, it has a screen which counts the kcal I burn. It has a thing connected to my arm, measuring my heart beat. After about an hour of riding, it said I used about 700 kcal. Is it the amount of work I did, i.e if there was a battery connected to the bicycle, I'd generate 700 kcal of electricity, OR, the amount of energy my body LOST, because muscle efficiency is far from 100% (so, I lost 700 kcal, but generated only 150 kcal of electricity, for example)
When doing a physical activity, the heart beat and breathing rate increases. Lets say I'm riding a bicycle or running. Whats the ratio between energy consumed by the muscle to energy consumed by the lungs or heart?

Looking at the answers for question one it's hard to think of any other meaningful way to do it other than recording the energy released when burnt, any other measure would hardly be standardised between people.

I speak only for the U.S. regulations: the calorie labels on wrappers refer to the energy released when burned. Sometimes these are inaccurate. Many dieticians recommend calculating the calories based on weights of protein, carbohydrates and fats in the serving: 4 kcal in each gram of protein and carbohydrate and 9 kcal in each gram of fat in your food. Multiply carbs, proteins and fats by the appropriate value and add them up.
The reading on the bike does not take into account your pulse. Just the raw work done turning the pedals. Some very smart bikes do take pulse into account, but the often inaccurate heart monitors lead to inaccurate calculations of total energy.
The heart and diaphragm (muscle primarily responsible for breathing) do use more energy when exercising than when you are sitting still. But that increase is small relative to the increase in the primary muscle sets involved in the exercise. Your resting heart rate is probably around 70 bpm, your exercising heart rate is probably around 160-180 bpm. So it has increased its rate and energy consumption by about 3 times. Your skeletal muscles maintain a basal metabolic rate during inactivity (one purpose of this is your body needs the heat from slightly tensed muscles to thermoregulate itself) - but during exertion, their metabolic rate increases enormously. Exercise increases their energetic demands by whole orders of magnitude.

The actual value of the (energy used by heart) / (energy used by skeletal muscles during exercise) depends on what exercise you do and how efficiently you do it. The change in the ratio between inactivity and activity depends on how much muscle mass you have (more muscle uses more energy during inactivity) and how strenuously you exercise. But the point is that the increased energetic demands by skeletal muscles far outpace the 3x increase in energetic demands by the heart and diaphragm - so the latter accounts for pretty much all total energy consumption at even moderate activity levels.

to be clear one of the major sources of error in calories in food is fiber and other such material that will burn but not be digested. which is why many countries require carbs to show fiber content.

1) It depends on each country and your minister. In Finland, the thing is done so that it says the energy stored in food, which will be released if burned.
2) It is the energy pushed to the bike when the bike does not take into account your pulse. If the bike is smart one, it takes into account your pulse rate, then it tries to estimate the amount of energy released by your body. This is done differently among different manufacturers of those watches.
3) By the way heart is a bunch of muscles, a myogenic muscular organ! So consider instead heart and some part of lungs. Very broad problem otherwise.


text:
Why isn't the insertion of a single nucleotide destructive for DNA?
As far as I know proteins are built by sequentially reading triplets of nucleotides.
But if at a certain point a nucleotide is inserted in the sequence, the following sequence of triplets is completely different.
For example:

AATACGGTACCATTA ...

AAT ACG GTA CCA TTA ...

But inserting a nucleotide B at second place we get

ABA TAC GGT ACC ATT ...

Which is completely different.

However I know from theory that a single nucleotide insertion is not dangerous in most cases.
Could someone clarify my mind about this?

However I know from theory that a single nucleotide insertion is not dangerous in most cases. Do you have a citation for that?

@tel maybe I was remembering wrong.

A single substitution can often be silent, or at least not impact the structure and function of the resulting protein in a significant way. But what you describe is a frameshift, and that is one of the most destructive mutations. It will completely change the sequence of the protein after this mutation and disrupt the function of those parts of the protein.
Insertions or deletions that result in a frameshift are absolutely destructive mutations.


text:
Too few transcripts from transcriptome assembler Oases
I am trying to run Oases for transcriptome assembly. The result is far from expected, so I would like to ask whether I am running it in a right way? Thanks.
Here is my running command:
python scripts/oases_pipeline.py -m 25 -M 29 -o output -d " -strand_specific -shortPaired data/reads.fa" -p " -min_trans_lgth 100 -ins_length 300"

My library is strand-specific and pair-ended with length 67bp. The reads are shuffled as:
>0(left_mate_forwarded)
ACTC...
>1(right_mate_reverse_complemented)
TATA...

I got some transcripts, but are far from the transcripts annotated, also far from the result of Trinity. The longest contig from Oases is ~2500bp (vs. ~10000bp from cufflinks and ~6000bp from Trinity). The N50 value is also low. It only reports 20 contigs those cover full-length of some transcripts from Cufflinks (totally ~4000), while Trinity reports ~650.
The dataset I am using is a subset of S. pombe. Does it matter?
Could somebody help me point out whether something wrong here?

You mentioned that the result is far from expected--in what way? Is it just the number of transcripts, or the lengths of those transcripts?

Also, as stated in the FAQ: Questions on interdisciplinary subjects like bioinformatics are also welcome, as long as they focus on the biological part of the subject. I'm afraid if you can't highlight a significant biological component to you question, it's likely to be closed as off-topic.

Em, I tried to post to BioStar, but nobody answers me...

Here is the mailing list for Oases, http://listserver.ebi.ac.uk/mailman/listinfo/oases-users also there is a thread in SEQanswers http://seqanswers.com/forums/showthread.php?t=3877&highlight=oases some people also have problems to get Oases work.

Unfortunately, if nobody answered on Biostars, the chance of getting an answer here is very slim indeed …


text:
Why are sugars in whole fruits not digested the same way sugars in juice are?
In this paper of the WHO, it is claimed that we should limit our consumption of free sugars:

WHO recommends a reduced intake of free sugars throughout the
  lifecourse. [...]  Free sugars include monosaccharides and
  disaccharides added to foods and beverages by the manufacturer, cook
  or consumer, and sugars naturally present in honey, syrups, fruit
  juices and fruit juice concentrates.

At first, I was wondering if the sugars in a fruit can be different from sugars in a juice. According to the answer to my question here, the sugar molecules are exactly the same in both (in the case of a 100% pure juice).
So, why this recommendation? Why doesn't our body digest sugars from fresh fruit the same way as sugars from juice? To make it simple, my question only concerns 100% pure juice with no added sugars.
I tried to find an answer and, according to the answers of this question, because our body is slow to digest sugars from a fruit, it assimilates it better. Is it right? And, if it is the case, if we eat fiber and starch with our fruit juice, it should be the same as a fresh fruit, right?

Sugars in 100% natural fruit juices are chemically the same as in whole fruits. They mainly include glucose, fructose and sucrose:

Apple nutrition data (expand the carbohydrate section)
Apple juice nutrition data

Sugars in whole fruits are "incorporated" into the fruit, which means the digestive system first needs to physically decompose the fruit and then extract and absorb sugars, which takes some time. In fruit juices, sugars are "free," so they are absorbed quicker than from whole fruits, which results in higher blood glucose levels, which is a risk factor for diabetes type 2 (Defeatdiabetes, Diabetes.co.uk).
Also, fruit juices are liquid, so they pass through the stomach quicker than whole fruits, so they fill the stomach for a shorter time and may be therefore less satiating. This can make you drink more juice than you intended, which can result in unwanted weight gain.
If you eat foods high in fiber along with juice, the fiber will slow down the absorption of sugars from the juice (Nutrients). If you eat foods that contain mainly plain starch (white bread, cookies or rice, or potatoes) along with juice, the starch will be quickly digested and absorbed as glucose and will raise the blood glucose even quicker than the sugar from the juice.
The effect of nutrients from foods on blood glucose level after meals is expressed as glycemic index (GI): the higher the GI, the higher blood glucose (Harvard):

Glucose = 100
Cornflakes (mainly plain starch) = 81
Potato, boiled (mainly plain starch) = 78
White bread (mainly plain starch) = 75
White rice (mainly plain starch) = 73
Sucrose = 65
Honey = 61
Apple juice = 41
Apple: = 36
Kidney beans (high in fiber) = 24
Fructose = 15

In conclusion, natural sugars from whole fruits, fruit juices and artificially added sugars are all digested in the same way, but sugars from juices are absorbed quicker, which can result in higher blood glucose levels. Foods that contain mainly plain starch can raise the blood glucose levels much more than fruits and fruit juices.

It's interesting that Fructose has such a low GI... considering that honey is basically made of fructose (low GI) and glucose (high GI) it falls roughly in the middle of the two.  And for reference HFCS which is always mentioned as bad maxes out at 68 which is still lower than four of the foods on that list.

It's also interesting the apple juice is only about 10% higher than apple - probably not far off the difference between apples.

@ChrisH Yes, we've bred apples for a long time to make them the easily digestable sugars they are today (though evolution did it's fair bit even before us - fruits are carriages for seeds, "designed" as easy sugar) :) It's funny how thousands of years of breeding are now essentially being reversed, because we're no longer energy deficient by default. But there's still that one difference between juice and an apple - you usually eat one or two apples, but drinking a bottle of juice is something you easily do without even noticing (though I know people who eat apples the same way :D ).

Drinking the juice without the fruit can easily lead to over-consumption. It is after all harder to eat four apples than drinking 500ml apple juice.
As the liver breaks the fructose through lipogenesis it creates fat and can cause non-alcoholic fatty liver and obesity.
Since sugar (fructose/glucose/sucrose et al.) can be absorbed already through the mucus membrane, it also causes a rapid elevation in insulin levels leading to insulin-resistance. Insulin-resistance has an impact on depositing white adipose fat which in turn has several harmful effects on the hormone production of the body. Leptin resistance from insulin-resistance alone will cause you to be unable to regulate hunger properly, even further elevating excess fat storage in adipose fat.
You may notice you don't feel full when drinking sugars, but you do much more readily when eating them. WHO is recomending against all sugar beverages and juice is just as unhealthy as soda in this regard.

"You may notice you don't feel full when drinking sugars" I'd be quite interested in some numbers about this; I certainly do feel just as full when drinking sugars as when eating the corresponding amount of fruit (which is to say, "not much"). The main difference is that you're more likely to drink juice at the same time as eating your main meal, while you'd probably eat the apples as either a snack or a dessert after a meal. Insulin resistance is a real risk, but rather than sugar from apples and juice being different, I'd expect frequency has more blame - you can sip juice for hours.

@Luaan Liquids are readily absorbed by the body. "Sip" the same volume of carrots or similar fibers and you certainly will feel full. Sipping a liter of carrots will certainly not result in the same sensation as sipping a liter of juice.

Jan's answer is great, but I'm just going to quote the paper you reference:

The systematic review of the effect of intake of free sugars on body weight
  included 30 of the 7895 RCTs and 38 of the 9445 cohort studies initially identified
  as meeting the inclusion criteria. Meta-analysis of the five trials in adults with ad
  libitum diets (i.e. no strict control on food intake) found that reduced intake of free
  sugars was associated with a decrease in body weight (–0.80 kg; 95% confidence
  interval [CI]: –1.21, –0.39). Meta-analysis of the 10 trials that involved increasing
  sugars intake (mostly sugar-sweetened beverages) suggested a comparable weight
  increase (0.75 kg; 95% CI: 0.30, 1.19). Meta-analysis of the 11 trials that examined
  isoenergetic exchanges of free sugars with other carbohydrates showed no change
  in body weight (0.04 kg; 95% CI: –0.04, 0.13).

TL; DR:

If you keep the same energy intake, free sugars have no effect on body weight
If you eat without energy controls, reducing free sugar intake has a large effect on body weight

So in other words, it's not really that free sugars are easier to digest or anything; it's just that if your food has more free sugars, you're more likely to increase your overall energy consumption. This might have relation to feelings of satiation, blood sugar levels etc., but in the end, it's that simple - if you don't watch your energy intake, limiting free sugars in your diet will likely decrease your daily energy intake.

I guess this is the link to the paper https://www.ncbi.nlm.nih.gov/pubmed/23321486 ; would you include it in your answer? There are several other systematic reviews that conclude pretty much the same: nutrients (sugars or other carbs, fats) are not fattening by themselves but only when they contribute to excessive calorie intake.

I'd challenge that "If you keep the same energy intake, free sugars have no effect on body weight". The liver has specific response to fructose through lipogenesis, so even if keeping the same energy intake, fructose has an impact on body weight. In fact, you have to have an energy depleted liver for fructose in isolation to have the same characteristics as other carbohydrates.

@PebermynteLars You can challenge that, but it's not my claim. I'm just quoting the WHO meta-analysis that the OP has a misunderstanding about.

@Luaan Have a read at the Harward Health letter quoted in my answer for an updated understanding of lipogenesis. The section "From fructose to fat" is quite clear on the mechanics. Not all sugars are equal.

@PebermynteLars I didn't claim all sugars are equal. The case the OP is asking about is about the same sugars, and regardless, my answer doesn't touch on that subject at all, because irrespective of the various mechanisms at play, the quoted meta-analysis found just one thing of statistical significance - free sugars make you more likely to increase your total energy intake. In the end, your answer says pretty much the same thing, just with an explanation of one of the mechanisms involved.


text:
Why do we not develop tolerance to endogenous factors?
In pharmacology, we studied the development of tolerance to the therapeutic effects of drugs. It is defined as the diminished response of the body to a drug as an adaptation to its continued presence.
However, the factors like enzymes and hormones (either autocrine, paracrine, or endocrine) are also continuously present throughout the body in a steady state concentration or fluctuating concentrations (depending on the function and homeostatic requirements). So why, and how, does the body not develop tolerance to its own enzymes and hormones?

I find your question unanswerable without your naming a specific example of a drug to which the body develops tolerance, and a specific example of  a (preferably similar) molecule (what you call a "factor") that you think should invoke a similar tolerance but does not, explaining why think it should. The key to this, in my opinion, is the molecular mechanism for this "tolerance". I suspect you and others may be approaching this from the wrong angle and the question to ask yourself is why should another compound have such a mechanism, not why it lacks this.

Tolerance is just a special case of homeostasis. There definitely is some level of "tolerance" to endogenous substances: down-regulation or desensitization of receptors that are over-activated, negative feedback loops, etc, are ubiquitous in biology.
The mechanisms that manifest as tolerance to exogenous substances are often part of endogenous homeostatic pathways.
Commenter bob1 mentions insulin resistance as a classic case of "endogenous tolerance", and it's quite an important one as it results in type 2 diabetes.
For another example, the most common excitatory neurotransmitter in the brain is glutamate; too much glutamate release or excitatory responses that are too strong result in seizures. There are several pathways that you could consider contributing to "glutamate tolerance", including particular glutamate receptors that downregulate other glutamate receptors: when neurons are exposed to a lot of glutamate at once, they reduce their responsiveness to glutamate in the near future. Failures in this regulatory/tolerance pathway are one cause of epilepsy.
A third generalized example is that of receptor-mediated endocytosis, which can serve to import specific things into the cell when they bind with a receptor, but is also important in regulating the overall strength of signaling pathways. Whether a ligand is exogenous or endogenous, when binding a receptor causes internalization of that receptor there is one fewer receptor available to bind additional ligand.

Bryan “…are often part of endogenous homeostatic pathways”. How many people will have a clue what this means? You work hard for this site. Give it a rest.

The classic example would be insulin resistance. This leads to hyperinsulinemia and can result in type 2 diabetes if the resistance gets too high.

+1. I think a pharmacology student should be able to understand your answer, however I doubt most lay persons will. Please forgive me for explaining it/dumbing it down.

@David "Endogenous" is in the question; "homeostatic/homeostasis" is linked in my answer and also in the OP - I think it's reasonable to expect someone to understand that word or read more until they do; "pathway" is, hopefully, a word that someone studying biology would encounter regularly.

This does not seem to provide a good reason to the actual question. Yes, the body regulates its internal functioning properly to achieve some usually near-optimal -- under the given circumstances -- dynamic balance. But why does it find a balance with endogenous substances, like endogenous opioids, which does not involve developing a tolerance, while a tolerance is developed for synthetic opioids? Saying "it's the usual mechanisms, nothing to see here" does not seem to cut the mustard. (Oh, I see you edited the answer in the meantime. It is a bit more specific now.)

@Peter-ReinstateMonica What makes you think there is not a balance found with synthetic opioids? It may not be the "desired" balance for someone seeking a euphoric drug experience or a physician using opioids for pain relief, of course. And, it may be desirable to have more tolerance than actually observed for some common side effects like constipation.

A balance, yes, but one that involves tolerance. As opposed to the balance found with endogenous opioids. (IIUC the endogenous ones are scrubbed quickly by receptors etc., which is why no tolerance develops. Such specific differences are causal.)

@Peter-ReinstateMonica Here's an example of a paper about tolerance to endogenous opioids: https://link.springer.com/article/10.1186/s40360-017-0193-y They claim evidence that tolerance of NSAID pain relief is mediated through reduced sensitivity to endogenous opioids. So, it isn't that tolerance can't or doesn't occur with response to the endogenous signals. Just that, when everything is "working properly", the body is somewhere near a homeostatic equilibrium. You need to perturb it or find a case of dysfunction to notice the regulation happening.

I suspect that the Emperor is naked. Bryan, just because the poster used an imprecise word, doesn't mean you should. I think this is an unclear question which according to SE policy should not be answered until the poster clarifies (as I comment to him). I respect your work on this site, but expected a hard molecular answer from you. And @fredsbend —  I don't think this is a technical question, but a naive question from a student who should be encouraged to do more preparation and give more precision to his thoughts.

@David I don't know, I think the question is a bit naïve to a biology professional, yes, but also insightful for a biology student given how these things are often taught in a biology/pharmacology classroom: it's likely that the concept of tolerance was introduced, and examples given, but the connection was not made between tolerance and regulation within biological systems more broadly. OP noticed that something didn't quite sit right, and asked a question about this conflict in their understanding.

I may be asking a naive question.  But I think the body has some ability to distinguish between foreign and self substances. It would probably perceive a foreign unusual drug as harmful and actually work towards building tolerance to it. A naturally found  substance in the body if useful will not stimulate body to build resistance Right? Otherwise people with allergies wouldn't have to suffer so much

Like the answer below says,  the body regulates endogenous factors so it is not noticed.  I think the body would create new receptors try to undo damage to the old ones and  more to reverse tolerance to something useful produced by the body. Otherwise hormone requirements and production should increase rather largely with age. Right? Insulin resistance is again a counter to what I said so IDK

Chemistry is chemistry. A given chemical is no different depending on how it's produced. Something exogenous might be different because it's in a different place or in a different concentration but otherwise there cannot be any difference in the effect of the same chemical. That doesn't mean that the response to any chemical is to respond less in the future - that's a response to "too much", wherever it's produced. Of course sometimes it's possible to get it "wrong" because our bodies are just chemistry, they don't have the ability to see the future.

Yes thats true. What i meant by foreign was something chemically similar or producing chemically simar effects as a substance produced by the body? Like body will probably promote tolerance, resistance to and removal of a drug but not whatever is it's analogue is in the human body.

@Aurelius Even endogenous neurotransmitters result in a regulatory response the same as tolerance, when they are present at a high concentration or for a long time. That's what I wrote in this answer. I'd suggest trying to grasp this concept rather than assuming it's not true. If you study biology you'll find these regulatory pathways absolutely everywhere. It's a basic defining principle of how biology works. See also the concept of "negative feedback loops".

@Brian Krause's answer is completely correct. I'm only going to simplify it.
Tolerance to drugs develops because the enzymatic pathways (which are already in existence in the body, i.e. "are... endogenous homeostatic pathways") responsible for its metabolism enabling its removal from the body are increased, either by increased rate of metabolism or increased production of the enzyme(s) responsible for the drug's metabolism, etc. One of the most widely known such enzymatic pathways is the Cytochrome P450 pathway. (These are not the only ways tolerance develop, just the easier ways to measure.)
Tolerance to drugs is more noticeable because most drugs are xenobiotic, i.e. substances foreign to the body (or "exogenous substances"), so we must ingest them to get the intended effect, and the effect is noticeable, so when tolerance starts to develop, the dosage must be changed. So it's easy to observe tolerance to drugs. However, substances produced by the body are regulated without our being aware of it, because we're not visibly or otherwise noticeably actively doing anything; our bodies are to constantly compensating for internal processes, e.g. regulating our blood pH, glucose levels, etc. In a healthy individual, this is normal homeostatis, e.g. through positive and negative feedback, up- or down-regulation of substances produces, etc.. You mentioned hormones; thyroxine is a good example. Thyroxine is needed by nearly every cell in the body. The pituitary gland monitors (and controls) blood levels of thyroxine through the production of thyroid stimulating hormone  (TSH) Low levels of thyroxine stimulate the  production of TSH, whereas high levels causes decreased TSH production. of We're just unaware of all the regulation our body does until it overwhelms our ability to maintain homeostasis and becomes a problem of some sort, e.g. hyper/hypothyroidism, T2D (type 2 diabetes.), etc.
Cytochrome P450 Structure, Function and Clinical Significance: A Review
Drug Metabolism
Physiology, Thyroid Stimulating Hormone

Thank you, this is a great companion answer. I think you stated the most important concept for OP to recognize when you write "the effect is noticeable, so when tolerance starts to develop, the dosage must be changed. So it's easy to observe tolerance to drugs". That seems to be the main difference with exogenous factors: they can be changed quickly and the effects observed. If you did the same with synthetic versions of endogenous factors you'd see the same behavior. The distinction is in the presentation of the factor rather than the response of the system.


text:
Why doesn't Clopyralid damage cool season lawn grasses?
I use Clopyralid (3,6-dichloro-2-pyridinecarboxilic acid) to kill broad leaved weeds in lawns. From my understanding, it works by mimicking an auxin which affects plant growth. Naturally this pulls the chemical to the growing points (stems, roots) of the plant and disrupts the growth, killing the plant.

My question is: Why doesn't this affect cool season lawn grasses (Winter rye, fescues, bluegrass)? It is also considered safe to use on some warm season grasses, but in my experience the results are not always good.

Auxins are a class of phytohormones involved in plant growth and behavior. Auxinic herbicides, such as clopyralid, induce an overinduction of the auxin response in susceptible plants (kelly & Riechers, 2007). From the Kelly & Riechers 2007 article I quote:

[Auxinic herbicides] cause various growth abnormalities in sensitive dicots, ranging from leaf epinasty and/or cupping and stem twisting, to thickening of stems and roots, and ultimately chlorosis and necrosis [...]. Lack of phytotoxicity in grasses has been attributed to several factors, including anatomical differences in vascular structure and differences in ability to metabolize the herbicide [...]

Hence, grasses seem to be protected due to anatomical and metabolic differences. Specifically, auxinic herbicides seem to kill dicots and spare monocots (Song, 2014). Song explains, and I quote:

However, the underlying molecular mechanism of how auxinic herbicides selectively kill dicots and spare monocots is not understood yet [...]. Early research has
  proposed that the selectivity of auxinic herbicide is because of either limited translocation or rapid degradation of exogenous auxin, altered vascular anatomy, or altered perception of auxin in monocots [...] The difference in vascular tissue structure between dicots and monocots may contribute to the selectivity of auxinic herbicides. In monocot stems, the vascular tissues (the phloem and xylem) are scattered in bundles, and lack a vascular cambium; in dicot stems, the vascular tissues are formed in rings and possess a cambium.

So in all, the exact mechanism of specificity between monocots and dicots is unclear, but may be related to structural and/or metabolical (pharmacokinetical) and/or different pharmacodynamical differences between monocots and dicots in general. Dicots are susceptible to auxin herbicides, while grasses, being monocots, are protected.
The complexity of the auxin hormonal system (Song, 2014) may explain why differences exist between grass species, but this is speculative.
References
Kelly & Riechers, Pesticide Biochem Physiol 2007;89:1–11
Song, J Integr Plant Biol 2014; 56:106–13


text:
How do some plants grow in salt water, while others die?
My question is basically out of curiosity and comes from observing how certain plants (such as mangroves or salt cedar) can grow in seawater. If this gives the plant an advantage, why haven't all plants that grow in coastal areas developed a salt tolerance? How can the plants keep from intaking salt, while absorbing other soluble nutrients through the roots?

It wouldn't be an advantage if there was no salt water near by.

A few things you have to realize when you ask 'why hasn't species x evolved trait y':

What is the cost of evolving this trait? If you gain one trait, you lose another (or others). Everything in evolution is a tradeoff: that's why you're not nine feet tall, you'd be able to beat up all your enemies great, but it would take so much food to sustain you, it wouldn't be worth it.
Not every trait can be easily evolved. When you're starting as a freshwater plant, there are many, many, many, many mutations that have to occur for you to become salt-tolerant. Every one of those mutations would have to give a fitness advantage to be positively selected. The chances of this happening are low, which means if it happens at all, it would take a long time.
Who knows, perhaps these plants are, slowly, becoming more and more salt-tolerant and you're seeing them at an intermediate point in their evolution. Everything is evolving all the time, if these plants were not in a salty environment until recently, mutation and selection haven't had time to work their magic.

Update from comment:

Can you flesh out a little on "How can the plants keep from intaking salt, while absorbing other soluble nutrients through the roots?"

Sure! I'll give you the simple answer first: there are different mechanisms for absorbing salt and for absorbing nutrients, so they can function largely independently.
Now the longer explanation: Salt and nutrients don't just diffuse (much) through cell walls, they have to be transported across by what are called transmembrane proteins. Think of the cell membrane (a layer inside the cell wall) as basically something like a layer of oil (it's called a lipid bilayer) -- you know oil and water don't mut, and for the different ions in salt (sodium ion and chloride), neither do oil and salt or oil and many nutrients so they get sort of escorted across that barrier by big proteins that form sort of a tunnel through it.
There's a different transport protein for different substances; the salt ones will only let salt through, and in fact there are different ones for letting salts in and letting salts out, and for the different ions (sodium and chloride) in salt.
Update from comment:

This makes me wonder how salt harms most plants, if it can't get in except by 'invitation'

Quite a bit of salt can diffuse in, the molecules are small enough (unlike most nutrients) to pass through the membrane via the channels that let water in. Every living creature has a quite sophisticated setup of "ion channels" to pump salt out. If suddenly its cells are in a very salty environment, these pumps can't keep up.
Update from comment:

So if salt can diffuse in, what do salt-tolerant plants have that other plants don't?

Mostly, if I recall correctly, three things: They will have enzymes that have evolved to work in higher salt concentrations, they will have cellular functions to "sequestrate" salt, i.e. store it in organelles called vacuoles instead of leaving it where it can harm other organelles, and of course they will expend more resources on ion pumps to get the salt concentration in the cell to an acceptable level.

Can you flesh out a little on "How can the plants keep from intaking salt, while absorbing other soluble nutrients through the roots?"

@proofreader Nice. Thanks for the info. This makes me wonder how salt harms most plants, if it can't get in except by 'invitation'.

@proofreader So if salt can diffuse in, what do salt-tolerant plants have that other plants don't?

@J.Musser Salt still enters the plant, they have the abilty to get rid of it. . and the term is Halophyte plants.

The white mangrove (Avicennia marina) does take up some salt but deals with this by excreting it from growing leaves and cramming it into older leaves that are about to drop.
Also, some fleshy maritime plants may exploit a high internal salt concentration as a way to hold on to extra water in dry periods.

Please add reputable sources to your claims so others can background read on your topic

Thanks for adding a source. Wikipedia is volatile, however, in the sense that its content can change quickly. In addition, it is notoriously badly referenced, and full of circular citations. Anyway, if you can back that second statement up too, that would be great; it isn't mentioned in the wikipedia entry.

PS, above answer didn't cite sources either, I know (I just dropped a banner), but criteria for posting were a lot looser back then


text:
Would a plant need light if the chemicals gained by photosynthesis were given through the roots or as a foliar spray?
If you took the chemicals a plant gains through photosynthesis and put it through the plants' roots or by injection, or used as a foliar application for intake through the stomata, would the plant need light? If not, how would it respond to the treatment?

Are you suggesting that someone would artificially supply a plant with sugar, proteins, lipids, etc. via the roots?  Isn't that sort of like putting a plant on a feeding tube?

Yes. Would it work?

This approach can be used to culture mycorrhizae http://www.jstor.org/stable/3760183

There are a couple autotrophic plants that parasitize other plants that kind of do this already. But you probably couldn't do it to any plant. But you could do it to some

Not exactly the same thing, but a species of algae has been genetically altered to allow it to  uptake glucose, bypassing the need for photosynthesis: http://www.unisci.com/stories/20012/0615013.htm

I doubt this would work for the vast majority of plants.  I think it would cause root rot as the microorganisms in the soil would out-compete the plant.  Also the transport systems of the plant might not be efficient in this direction.
I mean might there be a plant somewhere where this might work?  Sure.  Fungi that grow in the dark would be a lot like such plants, so its biologically possible.  There might be a primitive plant that doesn't need its chloroplast to be active to live.  I've never heard of one and wikipedia is not helping here...

http://en.wikipedia.org/wiki/Monotropa_uniflora


text:
Why do the sick and unhealthy trees leaf out first in spring?
It's spring. The time of year that trees start to leaf out. I have been watching them, and noticed an interesting pattern. The unhealthy trees of a species leafs out first. I've noticed this especially with the wild black cherries. The hollow and damaged trees and the ones in poor conditions leaf out a week ahead of the good ones. The last ones to leaf out are the strongest in the area. This is not just a casual observation, and I have kept careful track of it. What causes this?

-1 for use of the ambiguous (and unscientific) term "trashy trees"

The question is not clear. How a species of tree would be better than another? Why would a willow be worst than a oak or a black walnut? I think you're mixing two things: sick vs non-sick trees and trees of different species with different leafing times.

Be cautious about drawing conclusions from casual observation. There may be within-species variability in the timing of leaf-out. It is possible that trees that leaf out first are more likely to be infected (or to have been infected in previous years).

@nico No. My question is Why the softer and lower quality trees, especially of the same species, Leaf out before the healthier trees. I am not asking why they are different. I think many people will agree that an old oak tree is of higher quality than a willow scrub.

I clarified my question for you who didn't get the meaning the first time.

@jmusser: the market value of the wood of a tree has nothing to do with its leafing time. A 1 year old willow may be as good to its environment as a 300 years old oak tree: we may find it more valuable, but that is economy, not biology. I suspect that the pattern you are seeing there has to do with age rather than "wood quality".

How about the same species? Why do the unhealthy or rotted ones leaf out first?

Can you be more specific than "I have kept careful track of it"? Have you kept records? How do you quantify tree health? How many trees? Are they all approximately the same size? Do they grow in similar soil and light environments?

Trees that have been dormant over the winter exist on nutrients stored in their roots during fall. When a tree has been damaged or diseased, it may not have been able to store enough nutrients before winter, or may not have enough stored to heal the damage/disease. If the damaged/diseased tree has depleted its winter root stores, it must leaf out (earlier than others of its species) and resume photosynthesis in order to have enough energy to attempt healing itself.

This seems reasonable - do you have any references to support your answer?

Agree with @RoryM, it seems a reasonable theory, but I am not at all sure that this is true. It could be just as much about rising sap in the spring, carrying resources, reaching the terminal buds quicker, as there is less distance to travel, and so initiating bud burst earlier.  Also trees can't 'heal' themselves, as they grow they may occlude wounds and cavities, and compartmentalise decay to stop it spreading.