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How does a tree trunk sprout and grow after being cut?
After I cut trees into logs and remove the branches in winter, they start growing. They sprout out and grow completely normal looking stems and leaves and maintain them all summer. The sprouts mostly appear around the cut branches.  Sometimes they last all winter and grow for another year. How does it find the energy and water necessary to maintain and grow these stems without ground connection and a water source?

I guess it is similar to what happens with onions, garlic, potatoes etc, that will sprout even outside of the ground.

Does this happen to other people? I've cut trees before, and never seen that happen... Exactly what trees are you talking about? From what part of the tree were cut the sprouting logs, top or bottom? Be more specific please!

From my experience this does NOT happen to people.

I encountered this in the context of a type of evergreen referred to in the vernacular as 'subabul'.

This is basically the same that happens after pruning and involves a basic hormonal regulation mechanism in the plants.
What happens is that the cut piece of the wood forms a new meristem which allows the growth of new organs. What’s important is that there is no other growth happening nearby, since that would hormonally inhibit any further growth. This is why such growths happen once you’ve cut the wood, not before (on the healthy stem). This inhibitory effect is known as apical dominance, which has now been disabled.
As to where the energy and water comes from, to some extent it is stored within the branches themselves. That’s why you need to dry them before being able to use them in a fire. However, this growth is pretty limited. Further water is probably collected by condensation of water vapour in the air.

Very interesting!

I would guess that the nutrients and water they need to survive are still in the logs.  This is Common with willow trees, and mulberry trees.  I’ve cut many of these species, and it always happens.  they are two very hardy trees.  Do you know what kind of tree you cut? It appears it is a willow.

Welcome to Biology.SE. While anecdotes are potentially interesting, speculation is not welcome on this site, particularly on subjects for which research is available — consequently your answer is much more likely to receive a favorable response if you [edit] it to include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion and thus is inappropriate for this site. ——— Please take the [tour] and then consult the [help] pages for additional advice on [Answer] effectively on this site and then edit your answer accordingly.

Also note that, it is generally best to avoid adding additional answers to questions unless you have something new and well-supported to add. As a new user you can find many unanswered questions, which I suggest could be a better use of your time.


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Do insects' muscles become stronger with exercise?
I am curious to know if insect muscles become stronger with exercise, because I have seen many insects get tired out, but I have never seen one get stronger. They always seem to become permanently weakened from excessive exercise. Do they get stronger like people do?

Would be interested to know how you might "see" one get stronger. As is the case with most wild animals, generally existing (scavenging, hunting, browsing, etc) requires exercise, and barring illness or old age, most animals are likely to be fit, but not fitter than necessary - building muscles becomes a waste of time after a certain point.

There are instances of insect muscle growth in response to increased use. The flight muscles of the tsetse fly (Glossina morsitans) have been observed to grow at a faster rate when subjected to enforced exercise (Anderson and Finlayson, 1976). Also larger mandibular adductor muscles (which power the feeding apparatus), and associated head capsule have been noted for caterpillars and grasshoppers feeding on particularly hard grasses (Bernays, 1986). However these examples occur immediately post-eclosion (i.e. after emergence as adults), and during immature stages respectively. Insect muscle typically grows during larval/nymphal (immature) stages, and often for a brief period at the start of adulthood - known as the teneral period. During immature stages, insects typically have a flexible membrane to allow for tissue growth and expansion, this can also be the case during the teneral period, before the inflexible exoskeleton has fully hardened. However at full maturity, insect growth is limited by the rigidity of their exoskeleton.
As far as excessive exercise is concerned, that some insects may be weakened permanently may be more to do with the fact that their life strategy is different to ours. Due to the vast number of offspring per adult, and subsequent low survival chance of any given individual, there could be an evolutionary advantage for individuals pushing themselves to possibly deadly extremes. This could lead to many deaths, whilst retaining a viable population and thus accelerate the emergence of a population of fitter individuals.
References

Anderson, M. & Finlayson, L.H., 1976. The effect of exercise on the growth of mitochondria and myofibrils in the flight muscles of the tsetse fly, Glossina morsitans. Journal of Morphology, 150(2), pp.321-326.
Bernays, E.A., 1986. Diet-Induced Head Allometry among Foliage-Chewing Insects and its Importance for Graminivores. Science, 231(4737), pp.495-497.

What about the butterfly ripping out from the chrysalis?

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If the xylem of a woody plant is composed of dead tissue, how does sapwood become heartwood?
If the xylem of a tree is composed entirely of dead tissue, then that means the sapwood is dead. If so, how does it transform into heartwood, and what starts the process?

I'm no expert, but I liked this question and did a quick literature search:
Xylem cells are certainly dead at maturity, and it is these cells that make up the majority of what we call wood. However, wood also contains other tissue types, some of which have live cells at maturity. From what I can glean here and here, it is ray parenchyma tissue that is responsible for many of the changes that take place during the transition from sapwood to heartwood. Ray parenchyma is formed at the vascular cambium, along with xylem, during stem secondary growth (wood formation). Ray parenchyma cells remain alive for years after the xylem cells in the sapwood die. Their functions are transporting nutrients radially in the stem, and storage of carbohydrates.
As the stem grows in diameter, there is a zone of transition from sapwood to heartwood where the ray parenchyma tissue begins to die. Before it dies, the cells undergo some metabolic changes and begin to synthesize secondary phenolic compounds (many different kinds) from stored starch or sugars. Then, as ray parenchyma cells die, they dump these phenolics into the surrounding xylem tissue, and the accumulation of these durable, decay-resistant compounds in the xylem leads to the formation of heartwood. In many hardwood trees this parenchyma death and phenolic accumulation is preceded by vessel-plugging, in which the ray parenchyma cells form balloon-like growths that block the flow of water through the xylem. So, once sapwood changes to heartwood there should be no living cells left, and the water transport capacity of its xylem is gone or greatly diminished.
There appears to be quite a bit of variability between species in when heartwood formation occurs and what triggers it. From what I could see in my brief literature search, it is all under fairly complex genetic and hormonal control that remains an area of active research. I would suggest (and speculate a bit) that the trigger has something to do with maintaining an optimum amount of sapwood as the tree grows in leaf area (which increases demand for water transport) and height (which increases demand for support, or stem diameter).

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Can a color-deficient person be made to visualize the missing colors?
Hope this is within the scope of this site.
Color-deficient persons lack the cells in their retina needed for differentiating some (or all) colors.
However, the part of the brain that actually processes images is not deficient.
Is it possible to somehow make a color-deficient person "see" the missing colors by directly activating that part of the brain responsible for processing colors?

@RoryM I would use "vision" instead of "sight" here? Do you agree?

@AlexanderGalkin Yes that would be more accurate.  As that tag also fits the other question I'll re-tag that too so that the tag persists after a month =)

It is a very interesting question and I did some efforts to investigate the literature on this topic, but yet I don't have a definitive answer for you. But let's start from the beginning.
First of all, the reason for color deficiency can be not only lack (rare) or impairment (more often) of certain types of color-perceiving cells (cones) in retina, but also brain injures: the central color blindness can develop after head trauma or as a result of some neurodegenerative deceases, like Parkinson's decease. In case of brain origin of the color blindness it is usually the complete color blindness (no color is percieved), whereas congenical primary color blindness (receptor-based) is usually just the unability to distinguish one or two colors, whereas the rest can be more or less separated.
I searched Pubmed for the literature on the topic and found a recent PNAS paper about the simulation of primary and secondary visual cortex on humans using intracranial electrodes. As they describe their results (bold font by me):

When percepts were elicited from late areas, subjects reported that
  they were simple shapes and colors....

But the paper investigated only healthy humans, no color impaired subjects were used for the tests, so cannot conclude from here whether we can elicit the perception of the color the person is incapable to see with the eyes using these stimulations.
I took this paper as the starting point and did some reference research, looking for the paper referenced there and for newer publications referencing this one: PNAS is one of the top journals in this area with very high impact factor and if there were a publication about brain stimulation and color blindness I would have definitely identified it.
During my investigations I came accross a series of interesting articles devoted to "cortical visual neuroprosthesis for the blind" (read this paper<1> from 2005 for review on this topic), but this is the treatment of conventional blindness, not the color blindness. There was no intersection in keywords or titles for color blindness and brain stimulation, both in the referenced articles and in the complete article database.
So, I would suggest that you address some talented experimentalist with your question and maybe one day, who knows, we will read your name under the Nature article dedicated to the novel way to cure color blindness.

<1> -- unfortunately not available publicly for free, I am sorry.

"no color is percieved" This is achromatopsia.

Yes!  And no.  But first, some background.
Your central nervous system has (or is believed to have, as do other primates) a number of different organizational structures.  Cells within a column (the cortex is composed of about 7 layers, and a column would be a vertical group of neurons from these layers) respond to stimuli with similar features.  There are also higher order structures of collections of columns, such as orientation pinwheels(1)
Note that in the above picture, color is used to indicate orientation and not what color the column responds to.  Color sensitivity itself is (as far as I'm up to date on things) simply known to occur in color opponency columns, see this paper by T'So(2) where for instance red and green color opponent columns would be found together more often than not.
The key point to take away from that is that your cortex has to develop these columns.  Without them you wouldn't have normal color vision, even if you circumvented the retina and LGN entirely.
That brings us to the "Yes!" part of my answer.  If you've got a person that lost their color vision late in life, they should have relatively developed color columns in their visual cortex and assuming that we could wire to those areas in a meaningful way, in sufficient resolution, and could manipulate their voltages in a directed manner (we can't) then they certainly should be able to see in color with direct cortical stimulation.
However if someone was born without color vision, I do not believe this would be possible.  Not without more work than simply sending a signal in, since there is strong evidence(3) that development of the columnar organization of V1 requires visual input during later stages of development.  I have read some cases where they took people with very simple retinal diseases (photoreceptor loss) and attempted to restore their vision.  There was an extremely strong positive correlation between how old the patient was when they lost vision and the degree to which any sight could be restored.
References:

 Ohki K, Chung S, Kara P, Hübener M, Bonhoeffer T, Reid RC. 2006. Highly ordered arrangement of single neurons in orientation pinwheels. Nature 442: 925–8.
 Ts’o DY, Gilbert CD. 1988. The organization of chromatic and spatial interactions in the primate striate cortex. The Journal of neuroscience : the official journal of the Society for Neuroscience 8: 1712–27. [pdf]
 Swindale NV. 1981. Absence of ocular dominance patches in dark-reared cats. Nature 290: 332–333.

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Why Does Salt Water Help Sore Throats?
I am having some trouble understanding how salt water, a simple solution, could so effectively remove the pains of a sore throat.
I do believe that the answer is closely related to hypo/hyper-tonic solutions, but why is this so, and how does this work?

Salt water may have anti-septic properties due to the effect it has on water potential.  Pure water has a water potential (Ψ) of zero.  A concentrated salt solution has a lower (more-negative) water potential.  The water potential of the salt solution is likely to be more negative than that of the pathogen's cytoplasm; the salt solution is therefore referred to as hypertonic.  Therefore water osmoses out of the cell (osmosis being the net movement of water from a higher water potential to a lower water potential across a semi-permeable membrane).  The loss of water from the pathogenic cells causes osmotic crenation - the cell becomes shrivelled and dies.
A hypotonic solution (for example cells placed into pure water) would cause the opposite effect - osmotic lysis.  This is the bursting of the cell due to the movement of water into the cell.  The bacterial cell wall would first have to be damaged (e.g. by penicillin).  This would not be the process by which a salt solution has effect, however.
The fact that the salt water is warm in order to improve solubility may also have the side-effect of causing vasodilation around the infection, increasing the rate at which white blood cells can arrive at the infection site.
It has been more difficult to find a theory as to why a salt solution would have analgesic properties, see the comments below & previous versions of this answer.

It is my understanding that a sore throat is sore because of inflammation. I had always thought that the analgesic effect of salt water was to reduce that inflammation by placing the inflamed tissue in a hypertonic solution. Do you have a reference that says that the salt water is actually killing the pathogenic cells or that this is the direct mechanism of action for why it "helps" the symptoms of sore throat?

It would be doubtful that any antiseptic effect as I described above would produce immediate "help" or pain relief. I agree that the solution would have anti-inflamtory effect, however as to the "sore throat being sore because of the inflammation" I must confess that I don't know.  If that is the case then of course that would be the direct mechanism that the op is looking for =)

Wouldn't it kill your own cells too and make the problem worse (at least temporarily?

Well it certainly wouldn't discriminate; I would propose that your own cells are less isolated, in that they will be near to a capillary with ready supply of water to replace any lost in the osmosis?

@Casebash It also helps to reduce inflammation by the same osmotic process - it draws the excess fluid around the cells thereby reducing the swelling. Reduced swelling would mean less irritation by the food/water entering the pharynx, as the contact surface is lessened.


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Is it the case that all changes in phenotype during life are not inheritable?
This came up in a talk with a friend. I wanted to clear this doubt. I've read about it before and did again after her remark (my thoughts didn't change: her concept is Lamarck's, not Darwin's), but wanted to clarify.
Regarding Evolution, nothing, absolutely nothing, that a person does to herself in life can be genetically inherited. It does not matter how much this person drinks, the changes they do to their body,  how dark their skin gets over life etc. Such changes can not be transmitted to their offspring in any way, correct?
*Summary:*Is the assertion "You can not change in life what will be genetically inherited in any possible way" true?

Yes, short of drinking mutagens every day to deliberately induce mutations

The assertion "You cannot change in life what will be genetically inherited in any possible way" is true, as you cannot (healthily) change the DNA in your germ cells.
However, the assertion "You cannot change in life what will be inherited in any possible way" is wrong, because of epigenetics. Parts of your DNA are marked (in different ways), and this can be inherited and have an effect. E.g. the only causal difference between these two mice is the diet of their mothers:

Image source and a further explanation: Nutrition and the epigenome.

–1, the paper didn’t actually provide evidence of epigenetic inheritance in any meaningful sense of the word, as is the more general conclusion: so far as we know, there is no single naturally occurring case of passing on of acquired traits. This isn’t unthinkable (see Prader-Willi syndrome), but remains yet to be demonstrated. I’ve written my take on the subject on Skeptics.SE: http://skeptics.stackexchange.com/a/7338/82

In general, Darwin's theory has been supported over and over again by experiments - our modern understanding of evolution is fundamentally what Darwin suggested. However, apart from appreciating many more details than Darwin ever could have, we also now know that Lamarck may not have been so crazy as he was later portrayed.
Inheritance in the Darwinian sense involves the digital information of DNA, i.e the sequence of bases. But we also know that DNA can be altered structurally - i.e. in the way it folds, or whether bases are methylated - and that these structural alterations can affect the expression of genes. In some cases, these epigenetic modifications can be trans-generational; they can be passed on to offspring.
Here are the mechanisms that I know of (perhaps others can expand on this):

X-chromosome inactivation (XCI): this is when one of two copies of the X-chromosome in females is completely inactivated by being packed into heterochromatin, preventing the DNA from being transcribed. Which chromosome (the maternal or paternal) is deactivated initially is random, but the decision can be inherited by all daughter cells. Skewed x-inactivation is when a cell very early in the cell line passes on its XCI decision, and can result in a particular phenotype being activated in a whole organ or tissue (such as patches in tortoiseshell cats). It has been shown that in mice and in humans, the somatic cells can sometimes have their XCI decision influenced by the mother, and that this can lead to early skewing of the XCI in the offspring, thereby passing on a decision about which alleles are present without affecting the DNA sequence.
Parental imprinting: in this case, individual alleles derived from one parent are preferentially activated or deactivated by methylation or histone modification. This change is passed on to the zygote, and alters expression in the offspring. Several human heritable diseases are associated with this kind of modification, such as Prader-Willi Syndrome.
Paramutation: first discovered in maize, this is when the presence of one allele in a genome can affect another allele in a heritable way. I.e. if allele A is present in the same genome as allele B for a single generation, allele A is permanently inactivated so that if you breed out allele B, allele A will not be active in the offspring.

Finally, there is also a phenomenon called structural inheritance, whereby a structural feature of an organism is inherited in a non-genetic way. There is less written about this, so the mechanism is not entirely clear as far as I know, but an example is that the 'handedness' of the spiral pattern on the shell of a protozoan Tetrahymena is inherited without any genetic change (Nelsen et al., 1989).
References:
Nelsen, E.M., Frankel, J. & Jenkins, L.M. (1989) Non-genic inheritance of cellular handedness. Development (Cambridge, England). 105 (3), 447–456.

Is the assertion "You can not change in life what will be genetically inherited in any possible way" true?
  No. Does not seems the case, as other people already replied.

Here, I just want to point to two recent research articles showing evidence against your assertion.
The first, published in Cell in 2010, is from Dr Oliver Rando, and suggests that you are what your father ate, too.

The second, published in Nature in 2011, is from Dr Anne Brunet, and argues that worms can inherit a 'memory of longevity' from long-lived parents.

That last paragraph is completely unnecessary. Anyone who knows what is going on would know this.

The purpose of peer review is not to detect fraud, so the peer review process did not fail 24 times for the same researcher. It's just that a researcher falsified his results. Unfortunately in science, as in all things, people can be deceiving. I don't think it's a reason to be any more skeptical about scientific papers than about anything else, and indeed scientific papers have other characteristics that make them, generally, the most reliable source of information we have.

Infections by a retro-virus (such as HIV) can, at least in principle, be inherited.
These viruses integrate their genome into the host's DNA, and these changes pass to next generations as the cells split. So if a germ cell is infected, all the cells in the child would be.
The question is whether there's a retro-virus that infects germ cells. I don't think HIV does (it can certainly pass from mother to child, but as a "normal" infection, not through the DNA).

There's a related review paper: "Beyond DNA: integrating inclusive inheritance into an extended theory of evolution" (PDF)

Very interesting, although this answer looks more like a comment to me.


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What conditions are necessary for HPL (human pancreatic lipase) to activate?
What conditions are necessary for human pancreatic lipase to activate? Is there an optimal temperature or pH? How quickly does it take effect?

Check this out: http://www.123helpme.com/view.asp?id=123079

There are several different lipases, you might want to specify which one you're interested in. It might help to add your motivation for asking this question, so that we might better understand what exactly you are looking for.

@Danielδ Oh my. That is almost exactly the experiment I did the other day, except I got no results. I'm wondering if my lipase was kind of smurfed.

@MadScientist I was using a 10% lipase solution; that was all the information about the kind of lipase that I was given.

Which lipase do you have in mind? From which organism(s)? There are over 90 lipase genes in the human genome.

Doesn't lingual lipase have an optimal pH  around 4 - 5? That's why it can still continue its catalytic activity even in the stomach...

I wasn't aware that most lipases needed any activation at all.  wikipedia says it is secreted from the pancreas in active form.  It might be pH dependent because its a digestive enzyme, but most lipases are....

If a lipase did not need activation, there is the risk that it would digest membrane constituents before compartmentalization and secretion. I'd expect most lipases to have a signal peptide, which needs to be cleaved prior to activation.

The protein referred to in the question is encoded by gene PNLIP, pancreatic lipase. From this annotation of the protein, I see that there is a signal peptide from amino acids 1 to 16. Thus, this signal peptide must be cleaved before the protein can be active in its digestion of emulsified triacylglyerides.
A paper describes the structural changes induced in human pancreatic lipase by lowering the pH. The secondary structure of the enzyme is stable within a pH range of 3.0 to 6.5. At this pH, a reversible opening of the lid controlling the access to the active site was observed. So, there is another aspect of activation - pH and the ability to open the enzyme lid so that the fat molecule enters the active site.


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Are inflammation and anxiety connected?
I've been reading a curious paper about the use of cannabis, and one of the passages piqued my interest:

There’s also been a lot of work done on another constituent of
  marijuana, cannabinoid, which is not psychoactive by itself. A lot of
  research has shown that it’s a great anti-inflammatory, it’s a
  neuro-protectant, and it may be what gives medical marijuana patients
  relief from things like epilepsy and anxiety

Has there been any scientific evidence that links inflammation and anxiety?
Source:
Cannabis, Forgetting, and the
The Botany of Desire

See this paper on link between inflammation and anxiety.
Also, quoting one of the paragraphs of this paper

Clinical
  studies have shown increased serum inﬂammatory markers in patients with depression as well as a correlation
  between plasma cytokine levels and the severity of depression, and have described improvement in depression
  after anti-inﬂammatory treatment.

Even if you do a simple google search, you will get thousands of results on this.


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Which human body hormonal systems exhibit 24 hour diurnal cyclical activity?
I'm researching the possible connection between the dream content and the activity of various organ or hormonal systems within the human body. I'm looking for information on biological cycles within the human body that occur on a 24 hour cycle and may influence the sleep cycle, dream content or the overall state of awareness.
So far I was able to find:
Adrenaline, cortisol, testesterone - circadian endogenous cycle.
leptin, glucose, insuline  -  peak with awakening, decline with bedtime
What else within the human body is functioning on a predictable 24 hour cycle?
Thank you for any information!

Note that circadian cycle is not exactly 24 hours

Also, the fact that an hormone is produced in a circadian manner does not at all involve it in the sleep/wake cycle. I would be extremely careful in concluding anything about that.

Thank you for great info! There's anectodal evidence that eating before bed has an impact on the dream content. Would eating within 1 hour of bed trigger insulin/glucose elevation over the course of the entire night?

@leonardo: the situation is complex and not completely understood. Infradian and ultradian rhythms are modulated by circadian clock genes such as Clock, Bmal, Cry1/2 both in the suprachiasmatic nucleus and in the peripheral organs.

@leonardo: what I am saying is that just because an hormone is not secreted in a circadian manner it does not imply that its secretion cannot be controlled -or at least modulated- by circadian genes. A colleague of mine has recently published a review on the subject.

The real answer is probably more than you want, but its easy to do better than the list above.
I took a look through GEO for human circadian expression data and surprisingly I only found 2.
Looking at GSE2703 - the rhesus circadian expression experiment, they have shown 355 genes that are rhythmically expressed.  This is not a great experiment because they only looked over a single 24 hour period.  Its only the adrenal gland.  Nonetheless they found 355 genes which seemed to be circadian.  the table is supplemental data to the article,  listed below.
I see a fibroblast growth factor receptor, some hydrocarbon nuclear receptor components, sterol regulatory factors, bone morphogenic protein 2, glutamate receptor, thrombonspondin receptor, ryanodine receptor 3 (what is that?) , lysophosphatidic acid G-protein-coupled receptor 2, purinergic receptor P2Y, G-protein coupled.  You might find more if you know what you are looking for.
The other circadian study was on human muscle, which will no doubt give different answers.  I imagine circadian behavior is highly tissue dependent.
Reference: Lemos DR, Downs JL, Urbanski HF. Twenty-four-hour rhythmic gene expression in the rhesus macaque adrenal gland. Mol Endocrinol 2006 May;20(5):1164-76

Don't forget that many hormones and cytokines are translated in inactive forms (insulin is a great example) and are later cleaved to release an active peptide. Thus, mRNA production may be constant while active peptide levels may cycle.

Maybe there is only 2 in monkey, but the amount of data on mouse is huge.

355 genes is quite a lot to process at once. Thanks for the GEO Ascension viewer link, I'll investigate that!

nico is right - mouse and rat are going to be the strongest organisms to look at...


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What is the name of this tiny creature? It looks like a tiny piece of moving cotton?
By chance, I saw this tiny insect on my bag a few days ago in Sydney. Am I the first person who has pinpointed this animal?! If not can you please let me know its name?

From your image, it looks like it might be a woolly aphid. I just did a bit of cursory research, and it looks like they're often described as floating pieces of fluff, that seem to wander instead of directly heading somewhere. The fluff on their back is actually wax produced as a defense mechanism from predators and the like. I hope this is what you were looking for!

Welcome to Biology.SE! Nice first answer. Take the tour to earn your first badge and edit your answer with a link to the species description or a picture to get another one! Have a nice stay!

Though I agree this is some species of woolly aphid, you need to update your answer as suggested by LinuxBlanket. Please provide links/citations to support your answer. Species ID answers require you to show support since incorrect identification is so prevalent...Providing a picture is also always helpful for species ID answers. thanks.

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Why are riboswitches mostly present in bacteria and not in eukaryotes?
Riboswitches are a rather elegant way to regulate gene expression without any additional machinery. A small ligand binds to the mRNA and directly influences transcription or translation.
Most of the known riboswitches are found in bacteria, there are few examples of riboswitches in eukaryotes. There are no classical riboswitches in humans as far as I know (there is one example, but triggered by a protein and not a metabolite), it seems that more complex organisms tend to use other methods of gene regulation.
Are there any known reasons for this? What are the drawbacks of regulating gene expression with riboswitches compared to using regulatory proteins? Is there an explanation for the lack of riboswitches in more complex organisms?

You get higher accuracy and more timely control at a post translational level (think about the time it takes to affect a pathway with cofactor stimulation compared to gene expression stimulation). You also have more points of control throughout the pathway if you affect activity post translationally allowing for a more complex interaction between stimulating and repressing factors.

This may or may not be true. However it doesn't answer the question of "why bacteria and not eukaryotes?"


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Can you gain valid toxicological data about a detergent in cell cultures?
I just looked at a paper that in one assay tested a variety of chemicals and chemical mixtures against human cell cultures. They exposed HEK 293 cell cultures for 24 hours to the various chemicals.
One aspect I find dubious is that the chemical found to be the most toxic is a detergent. I only have negligible experience with cell culture experiments, but my assumption here would be that any kind of detergent would obviously disrupt the cell membrane and kill cells. And this kind of mechanism is not really transferable to actual humans, something that only disrupts cell membranes wouldn't be very effective against the entire organism.
How valid are toxicological experiments made in cell cultures with substances that are detergents or have similar effects? Does this make it impossible to draw any conclusions about toxicity as I suspect? Or can you still gain valid toxicological data about this kind of chemical from cell culture experiments?

I'm intentionally not linking to the specific paper as I want to focus on the general question, and I suspect this would side-track the discussion.


text:
Are red blood cells prokaryotic?
After searching "do antibiotics impact the immune system" I found out that antibiotics target prokaryotic cells. It all made a lot of sense thinking about all those yogurt recommendations you get after taking antibiotics: the collateral damage is on the prokaryotic cells that live with us, but are not "us" as such.
Except I remembered human red blood cells don't have nuclei, so where's my confusion?
(I'm only a biology enthusiast.)

Are red blood cells prokaryotic?

No!

There are many more differences between procaryotes and eukaryotes than just the presence of a nucleus. See DeNovo's answer for more information.
The terms procaryote vs eukaryote refer, not so much to the physiology of the cell but to a specific evolutionary lineage. Eukaryotes are individuals that belong to the monophyletic group of Eukaryota aka. Eukarya (see here for an intro to phylogeny). As such whether or not a eukaryotic loses its nucleus and start looking exactly like a E. coli won't change anything to the fact that this cell is still in the Eukaryota lineage.

When differences between prokaryotes and eukaryotes are taught in an introductory biology course, a generic prokaryotic cell and a generic eukaryotic cell are typically compared. Cells in a complex multicellular organism, like a human, are quite diverse. Human red blood cells are one example of a highly specialized cell with a mature form that is quite different from the typical eukaryotic cell. Keratinocytes in the epidermis are another example (see Ross Histology, Ch. 15). In both cases, these cells produce large amounts of a single protein, eventually, at their most mature stage, stopping protein synthesis, extruding their nuclei and most other organelles.
The absence of a nucleus or other organelles, however, does not necessarily make either of these cells more susceptible to antibacterial antibiotics. Antibiotics are targeted toward things that bacteria have (positive differences), rather than the absence of typical eukaryotic structures. Almost all antibacterial antibiotics have one of three targets (see Goodman and Gilman Chs. 48, 52-55):

The bacterial cell wall or membrane
protein synthetic machinery
specialized metabolites required by bacteria

There is (almost) no overlap between these structures in bacteria  and structures in any of the diverse array of human cells. The one partial exception is a similarity between the mitochondrial and bacterial ribosome, that may, for example, be responsible for some of the toxicity of chloramphenicol (G&G Ch. 55).

"antibacterial antibiotics" - never heard antibiotic qualified in this way. What's an example of an antibiotic whose intended target is a microorganism other than a bacteria?

@bishop antifungal and antiviral therapies both qualify as antibiotics. They have different targets, based on the properties of pathogenic viruses and fungi.

No.  Prokayotic cells are full organisms with their own DNA, red blood cells are not.

It's also hard to even call them living things, since they do not do most of what living organisms do. They are just half dead components with a single purpose: zombies so to speak.

Good answer. I expanded  a bit on the details.

@DanielGoldman thats not true. They consume organic matter, they reproduce, they have their own genetic instructions that produces proteins. What don't bacteria do that you would not consider them alive?

@JamieClinton he meant mature RBCs, which don't do what most living organisms do. They fulfill more than a single purpose, but otherwise, he's exactly correct. Once they reach maturity, they don't synthesize any more protein and can't reproduce.

Gotcha. Although I wouldn't call a cell in a multi-cellular being a 'living organism' regardless.

@DeNovo Even mature RBCs are living cells. They metabolize fuel and use the energy for repair and various other cellular reactions. They maintain their own membrane and ionic concentrations. They are no less of a living cell than the neurons in certain insects which lose their nuclei.

@forest I'm fully aware of the full range of erythrocyte behavior, which
is why i emphasized that they have more than one purpose. I was explaining Daniel Goldman's comment.

Not even an answer.

True; they do serve other purposes, but I don't think I would call [mature] RBCs alive. "Zombies" is still more appropriate.

@DanielGoldman how about a post menopausal female mammal?

@De Novo.  This is just what the world needs more of.  People openly saying that women who are not breeding are things. I wish I could delete my answer.  It disgusts me that it's being used to treat half the species like garbage.

@swbarnes2 That's not at all what I'm saying. Many attempts to define life start by considering reproduction. I was pointing out the problem with that, exactly because it is ridiculous and disgusting to consider an infertile individual to be a non living thing. I'm honestly shocked that someone would somehow interpret my comment as the converse (because these people are useless garbage, we can safely say that's a good way to classify cells). How would anyone think that?

@DeNovo: Although I'm just as surprised by swbarnes2's response as you are, I don't think your comment actually made that much sense even when taken as you meant it. Daniel Goldman didn't even bring up reproduction at all. I don't think it's controversial that some parts of the human body aren't alive (consider e.g. hair); someone can reasonably suggest that another part might be borderline without you needing to jump straight to a reductio ad absurdum counterargument.

@swbarnes2 As a species, we are able to reproduce. Individuals who cannot reproduce do not mean that they are not alive when, as a species, they are able to. Just think about a colonial organism such as ants. Their species can reproduce, letting them all be classified as life, even the drones.

To be clear, I never stated that a mature RBC was a zombie, simply because it cannot reproduce.

But they could have been said to be such before they threw out their kernels.

No, they are matured (broken) reticulocytes without the net structure and ribosomal DNA, which themselves are matured (broken) normoblasts that have lost their nucleus.
So basically they're the left over plasma membrane of a once-alive eukaryote cell, now filled with mostly hemoglobin, and little else.
(The above is not necessarily true for all animals, some have nuclei, but it's the case for mammals, and thus humans.)

Erythrocytes have very complex metabolism and maintain internal homeostasis. It's not fair to say that they are "once-alive, filled with hemoglobin and little else" considering they are still living cells.


text:
Why do hot water baths affect only males' fertility? Why not females'?
Here is the link where urologists are warning men not to take hot water baths.
Why does it affect only males' fertility? Why not females also?

@PeterMortensen By two tags, ignoring the question?

@PeterMortensen Posting xkcd links is fun but they should be actually relevant. A comic about memes popular in 2009 doesn't become relevant to a question about male fertility just because both involve pregnancy somehow.

For what it's worth, the article is making unsubstantiated scare claims that, as far as I know, have no basis in research. Temperature affects sperm production and viability but is not believed to have any adverse long-term effects on the body. There is (unfortunately limited in number of studies and sample size) research on contraceptive use, credited to Dr. Marthe Voegeli.

I dont know if baths last long enough to really reduce sperm count, but wearing synthetic underwear can elevate scrotum temperature enough to be used as a contraceptive. The effect is also reversible. Ahmed Shafik won the 2016 igNobel prize for reproduction for this research. Unfortunately, the study had a small sample size. Anyone care to reproduce (the study, not yourselves, obviously)?

@Ivana: Unless you like really, unpleasantly hot baths, I seriously doubt it's going to have any effect. It seems you need sustained temperatures above 37°C, which requires either really good insulation, ongoing heating or replacement of the water, or initial temperatures that would likely be scalding.

A mature human sperm has some mitochondria, a nucleus, an acrosome, and a flagellar apparatus. That's it. Because of the lack of other organelles in the sperm, they have to be kept in a kind of 'cold storage' so that they are viable for at least some time (usually a couple of days). The ideal temperature would be 1.8 °C to 2.5 °C below normal body temperature, i.e. 37.6 °C or 98 °F. If a man takes frequent hot water baths, his sperm count becomes low as the mature sperms get dessicated quickly.
The reason that women don't require this strict temperature regulation is that the mature ovum has the complete cellular machinery at its disposal- mitochondria, nucleus, golgi bodies, ER, the works. So it can remain viable for a much longer time (about seven days after ovulation) and has higher temperature tolerance than sperms.

can you add please some refferencis? Specially this "Because of the lack of other organelles in the sperm" made me quite suspicious.

@K Sai Harsha how do you know that this answer is scientifically correct let alone accept it?

I don't know about all other organelles but mature sperm certainly lack some of them, like endoplasmic reticulum. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2736672/ however it appears that has little do do with temprature sensativity, temprature appears ot be the regulator for sperm activity levels so they they can't remain dormant at highr tempratures. https://www.ncbi.nlm.nih.gov/pubmed/29963982

Well, the answer by @An J has already explained the prima facie of your question which is: sperms need lower temperature for development. But I will be explaining in my answer: Why do the sperms actually need a lower temperature for their development?
This is a debatable subject, but there have been several models or hypothesis about this. I found this literature on it, and it summarises the thing excellently. Hope it helps:

Throughout the Cenozoic, the fitness benefits of the scrotum in placental mammals presumably outweighed the fitness costs through damage, yet a definitive hypothesis for its evolution remains elusive. Here, I present an hypothesis (Endothermic Pulses Hypothesis) which argues that the evolution of the scrotum was driven by Cenozoic pulses in endothermy, that is, increases in normothermic body temperature...
The model argues that stabilizing selection maintained an optimum temperature for spermatogenesis and sperm storage throughout the Cenozoic at the lower plesiomorphic levels of body temperature that prevailed in ancestral mammals for at least 163 million years. Evolutionary stasis may have been driven by reduced rates of germ‐cell mutations at lower body temperatures...
The fitness advantages of an optimum temperature of spermatogenesis outweighed the potential costs of testes externalization and paved the way for the evolution of the scrotum. The scrotum evolved within several hundred thousand years of the K‐Pg extinction, probably associated initially with the evolution of cursoriality, and arguably facilitated mid‐ and late Cenozoic metabolic adaptations to factors such as climate, flight in bats and sociality in primates.

About the function of the scrotum from the article

The scrotum is a sac‐like thermoregulatory structure that houses the testes at a temperature lower than the core body temperature (Tb; Moore, 1926; Wislocki, 1933; Ruibal, 1957; Setchell, 1998). The cremasteric muscles in the scrotum contract and relax to draw the testes closer to or allow them to dangle further away from the body in order to maintain the testes at an ‘optimal’ temperature for spermatogenesis (sensu Moore, 1926; Tsperm) and sperm storage of 34–35 °C (Setchell, 1998; Gallup et al., 2009; Mawyer et al., 2012). In humans, the scrotal temperature is maintained about 2.7 °C lower than the Tb (Momen et al., 2010). Notwithstanding the relative fitness benefits of a cooled epididymis vs. the cooled testis, four nonmutually exclusive hypotheses currently dominate explanations for the evolution of the scrotum: the Cool Spermatogenesis Hypothesis (Moore, 1926), the Galloping Hypothesis (Frey, 1991), the Mutation Hypothesis (Short, 1997) and the Activation Hypothesis (Gallup et al., 2009).

Cool Spermatogenesis Hypothesis

...argued that Tsperm and the maintenance of sperm viability during storage in the epididymis is about 34–35 °C (Moore, 1926; Appell et al., 1977). Scrotal temperatures that approach those of the core Tbcompromise fertility (Moore, 1926; Bedford, 1978b, 2004; Setchell, 1998), particularly if evaporative cooling of the scrotum is impaired (Momen et al., 2010).

The Galloping Hypothesis

... (Frey, 1991)proposes a trade‐off between testes vulnerability (fitness cost) and the avoidance of strong intra‐abdominal pressure fluctuations during galloping which impair spermatogenesis in abdominal testes (fitness benefit).

The Mutation Hypothesis

... maintains that the testis is a ‘hot spot’ for germ‐cell mutations and that the lower temperatures of the scrotum reduce the rates of mutation on the Y chromosome through mutagenic metabolites (Short, 1997).

The Activation Hypothesis

... storage of sperm at a lowered temperature ensures that they undergo ‘thermal shock’ during ejaculation into the higher temperatures of the female, which increases their motility and hence the probability of a successful insemination (Gallup et al., 2009).

Finally somebody with refferences :D nice aswer :)

@user 33690 your answer lacks female's fertility

Hm, I thought that last hypothesis is closer to reality. That maybe after capacitation (which occurs in warmer environment) sperm have much shorter lifespan. Or that capacitation is limited in its time. So that it was lifespan-motility-scrotum tradeoff. But who knows.

@rus9384 yeah, I personally feel the same. But personal opinions are off topic in an answer so I considered adding all of them besides it's a hypothesis... nevertheless it's noteworthy that the male reproductive system has developed so much physiology to prevent early activation of the sperm, the last hypothesis is highly likely.

@KSaiHarsha I thought it was already there in An J's answer (& I have mentioned that)..what's the point in adding a second answer if I have to repeat the same content of the first answer

The thing is that activation is the case only for mammals (while birds do not have it). And scrotum as well. Also, wondering if difference between scrotum and body temperature is linked with sperm competition. This definitely would add points to the last hypothesis.

@KSaiHarsha Well... These four hypotheses are not applicable to women. Ova have quite a long lifespan; are not influenced much by the pressure; women do not have Y chromosome, so no mutations there; ova do not move really fast. I think this answer really explains the difference between male and female fertility under temperature influence.

To keep sperm viable in natural body conditions, they are kept at a relative lower temperature than the body temperature, and this can achieved by the scrotum. As sperm is produced in testis, and testis are situated in the scrotum outside the main part of the body, a pouch like structure. This arrangement is going to help to achieve a slightly lower temperature relative to the body temperature. Definitely, frequent hot water bath will lower the sperm count by hampering spermatogenesis as it disturbs the normal physiological conditions inside the testis by increasing temperature.
Another side, in females, the body temperature is not going to affect the oogenesis (ovum formation process). Instead of that you will see an increase in basal body temperature (about 0.5 °C) during ovulation (release of ovum). That means a hot water bath isn't an issue for female fertility.

Hi, its good aswer, but can you add some refferences to your claims?


text:
Is it true that if a human lived long enough (up to 3-400 years), he/she would eventually develop cancer?
I have just studied DNA, but I am not so clear. So, I would like you to explain it more clearly.
This is what I think when a human grow older and older, his or her DNA repair mechanism would be weaker and weaker and eventually so weak that it couldn't repair the DNA damages and he or she would develop cancer sooner or later?
Is it true that if a human lived long enough (up to 3-400 years), he/she would eventually develop cancer?

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, questions should not be speculative — such questions lead to opinion based answers and are off-topic for this site. ——— We also encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). Thanks!

Every year we have a risk of cancer.  With enough rolls of the dice they will come up snake eyes.
That said, https://www.cancerresearchuk.org/health-professional/cancer-statistics/incidence/age#collapseZero highlights an interesting issue.  The incidence of cancer increases greatly from birth to seventies, then decreases.  If you are being optimistic enough to suppose a treatment could make you live for 400 years, I suppose you could assume your appearance and cancer risk would remain comparable to that of a teenager for hundreds of years as well.  If your cancer incidence is 0.2% per year (200 of 100,000 on the chart, 25-29 year olds) then your risk by the time 400 years have passed will be a little over 50%.


text:
How is heavy water detrimental to the human body?
Heavy water (D2O) is known to be lethal to humans and other life in large quantities. All I've been able to find on the toxicity is that it's similar to chemotherapy chemistry. I'd like to know precisely how having a single neutron in two atoms of an otherwise non-toxic molecule can cause the body to degrade. What's the root cause here?

Well, its vapors can give you super-speed.

The question is already answered by Armand. I am just going to elaborate on that by referencing the paper.

Different isotopes of chemical elements have slightly different chemical behaviors, but for most elements the differences are far too small to have a biological effect. In the case of hydrogen, differences in chemical properties among protium (light hydrogen), deuterium, and tritium occur, in part because chemical bond energy (the strength of a bond) changes  with changed mass of the nucleus–electron system. The isotope effects are especially relevant in biological systems because of the prevalence of hydrogen atoms in biological molecules (even deuterated water can have significant effects in the human body).
Note that enzymes have a finely-tuned network of hydrogen bonds, both in the active center with their substrates, and outside the active center, to stabilize their tertiary structures. In a deuterated environment, some hydrogen bonds will be replaced with deuterium bonds which have different strength (Ref. 3), so normal reactions in cells can be disrupted.
Studies and experiments* show that heavy water affects cell division(mitosis), cell membrane changes and cellular heat stability, possibly as a result of inhibition of chaperonin formation. Also noted among the presumably wide-ranging cellular effects was the display of an altered glucose metabolism under deuterated condition in cells. $D_2O$ is more toxic towards at least some malignant cells, but the difference in sensitivity vs. normal cells does not seem high enough for therapeutic use.
In ref. 2, you will find a paper which shows the biochemical and pharmacological effects of heavy water on humans. Basically, to study the effects of heavy water on the metabolism humans, $D_2O$ and deuterated drugs were used and various changes were noted. Have a look for more details.
References

Effect on biological systems (Wikipedia)
Kushner DJ, Baker A, Dunstall TG. Pharmacological uses and perspectives of heavy water and deuterated compounds. Can J Physiol Pharmacol. 1999 Feb;77(2):79-88. PMID: 10535697.
Steve Scheiner and Martin Čuma. Relative Stability of Hydrogen and Deuterium Bonds. J. Am. Chem. Soc. 1996 118, 6, 1511–1521 DOI: 10.1021/ja9530376

*Experiments with mice, rats, and dogs have shown that a degree of 25% deuteration causes (sometimes irreversible) sterility, because neither gametes nor zygotes can develop. Mammals (e.g. rats) were given heavy water to drink die after a week, at a time when their body water approaches about 50% deuteration. The mode of death appears to be the same as that in cytotoxic poisoning or in acute radiation syndrome , and is due to deuterium's action in generally inhibiting cell division.

Since "normal" water has around 156ppm of deuterium, and "D2O is more toxic towards malignant cells" does this imply a slightly beneficial effect of the normal deuterium found in water?

Great answer. It might make sense to add that the physiological effects are similar to those of chemotherapy (anti-cancer) drugs because chemo agents also disrupt cell division.

At 50% deuteration, half of the molecules would be $HOD$, a quarter $H_2O$, and only a quarter $D_2O$. At 25% deuteration, only $\frac1{16}$ of molecules would be $D_2O$.

@Acccumulation In the body, hydrogen atoms are constantly exchanging with or being incorporated into other molecules as well as water, so the calculation is not so simple. I'm not sure if the rat water deuteration reported above is a measured value or (as I suspect) a predicted or modeled value.

Substitution of deuterium atoms for normal hydrogen atoms changes structure and function at the atomic scale, disrupting normal biological processes. It causes changes in protein conformation and changes chemical reactions, as more and more $D$ replaces $H$, in water, substrates, macromolecules etc. "Stuff" doesn't work quite right and works less well the more the $D$. Remember, $D$ is roughly twice the mass of $H$, so it moves/diffuses very differently.
This QA at physlink.com reports:

The reason for these adverse effects is that replacing hydrogen with
its heavier isotope deuterium slows down the rate of any chemical
reaction in which the chemical bond to the hydrogen atom is broken.

(additional explanation at the link)
An actual scientific review, "Pharmacological uses and perspectives of heavy water and deuterated compounds" Kushner et al 1999  PMID: 10535697 seems to be pay-only access.


text:
What does the (-) in the molecule name mean?
I'm reading some text (purchase request) that has the following line in it.

(-)-Norepinephrine

What does the minus sign mean in front that is in parenthesis? Is this some kind of standard way of describing charge of the molecule or something? Or is this someone's way of representing something else? Or does this mean nothing?

The minus sign in parentheses here indicates the optical rotation, (+) means the molecule rotates linear polarized light clockwise, (-) means it rotates counterclockwise. Typically you would also write exactly which stereoisomer is meant (R or S), which is generally the more useful information.
The following are all valid names for the natural stereoisomer of norepinephrine:

D-norepinephrine
D-(-)-norepinephrine
(R)-norepinephrine
(R)-(-)-norepinephrine

I'd recommend that you take a look at the concept of Chirality if you're not already familiar with it.

And they have the article dextrorotation and levorotation as well.


text:
How can the Ames test detect a human carcinogen?
Using the Ames test, we add a mutagen to auxotrophic salmonella with mutations in the histidine pathway and rat liver extract to simulate metabolism.  How would we know if the carcinogen is a human carcinogen or not?
I'm guessing that if a mutagen showed no growth without the rat liver extract, but then growth with the rat liver extract this would mean that it is a human carcinogen. Is this true?

The Ames test aims to find out if a chemical (not yet known to be mutagen) is indeed a mutagen, either directly, or following treatment with liver enzymes (which may metabolise a chemical to mutagenic derivatives during "detoxification"). As you explain, the test involves looking for reversion of various histidine auxotrophic strains of Salmonella.
If the chemical is found to mutagenic in the Ames test then there is a good chance that it will be a carcinogen because of the link between mutagenesis and cancer. In practice further unrelated tests are needed to eliminate false positives.
In this review of the method

Mortelmans & Zeiger (2000) The Ames Salmonella/microsome mutagenicity assay. Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis. 455: 29-60

the authors state that:

...there is a high predictivity of a positive mutagenic response in the Ames test for rodent carcinogenicity...ranging from 90% to 77%...


text:
How can I normalize mRNA samples for sequencing?
Is there an easy, inexpensive, not too labor intensive way to normalise mRNA samples so that even though one loses information of gene expression levels, each of the transcripts in the transcriptome is equally represented in the sample for sequencing? This is to say, one has a uniform distribution of transcripts, so that the lowly-expressed transcripts still have a good chance of being sequenced.
I have seen a few papers mentioning protocols for mRNA normalization, but I can't tell if any of them are practical in real life wet lab situations.

I found the link to a commercial product by Evrogen here:
http://www.evrogen.com/technologies/normalization.shtml
They claim their method is compatible with nextgen sequencing platforms:

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

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


text:
What does 5' and 3' mean in DNA and RNA strands?
What are 5' and 3' in DNA and RNA strands? Please clarify with some images and please use simple English.

The 5' and 3' mean "five prime" and "three prime", which indicate the carbon numbers in the DNA's sugar backbone. The 5' carbon has a phosphate group attached to it and the 3' carbon a hydroxyl (-OH) group. This asymmetry gives a DNA strand a "direction". For example, DNA polymerase works in a 5' -> 3' direction, that is, it adds nucleotides to the 3' end of the molecule (the -OH group is not shown in diagram), thus advancing to that direction (downwards).

The five carbons in the ribose backbone are numbered starting from the O in clockwise direction* - therefore the carbon which has the base (A, T, C, G) attached is called 1'. The 2' carbon does nothing special, the 3' carbon has an OH group (downwards dash in the diagram), the 4' carbon connects the ribose ring to 1' via the O bond, and the 5' carbon is outside of the ring, attached to the 4' carbon on one side and phosphate on the other. PS: *) strictly, it's not after the ring direction but rather it comes from the linear configuration, i.e. when ribose is not in ring form.

@Armatus This comment is better than the answer.

The no 5 and 3 are the carbon no of the carbon skeleton ring of deoxyribose  as similar as any other organic compound. In any nucleic  acid, RNA or DNA 3' refers to the  3rd carbon of sugar ribose or deoxyribose which is linked to OH group and 5' linked to a triple phosphate group. So these  5' and 3' group provide a directional polarity to the DNA or RNA molecule. Now a good question would be y 3' and 5' not 3 and 5. It is simply to differentiate sugar carbons from that of the bases which are also having a carbon skeleton and thus nos for their carbon


text:
What is the DNA/protein charge ratio?
To study DNA-protein interaction, I want to do a DNA retardation test by mixing the protein with DNA and afterwarts loading it on an agarose gel to see if the DNA migrates slower. I've found some articles where they do this and they state that they mix the DNA with protein in an 1:8 charge ratio, but I can't really figure out how to interpret this
Could anyone tell me how to calculate a DNA:protein charge ratio? If 1:8 is stated, how should I interpret this?

Could you please provide some more context, I'm having a hard time understanding what exactly you want to know.

I am guessing this refers to the isoelectric charge of protein molecules vs DNA molecules?

@Mad Scientist To study DNA-protein interaction, I want to do a DNA retardation test by mixing the protein with DNA and afterwarts loading it on an agarose gel to see if the DNA migrates slower. I've found some articles where they do this and they state that they mix the DNA with protein in an 1:8 charge ratio, but I can't really figure out how to interpret this

This is really sounds like a guideline, a starting place, not necessarily your best protocol.
In practice its hard to be more specific as MS says.  The pH of the buffer will affect the charge of the protein, and to a lesser extent the DNA.
Also the protein may have an ideal pH for binding which you could guess is in the range of 7.0-7.4, but might find that the strongest binding depends on unexpected pH and salt concentrations, or the addition of a small molecule.
The affinity of araC for instance is greatly increased by the presence of arabinose in sufficient concentration.
lac Repressor, in contrast releases itself from DNA in the presence of IPTG or  lactose.


text:
Why am I getting low transformation efficiency with DB3.1 E.coli cells?
I am making competent cells using DB3.1 E. coli cells. Even after following the exact protocol (Inoue method for ultracompetent cells) given in 'Sambrook and Russel', I am not getting transformation efficiency of more than 104. I am using a 5.1kb plasmid for checking transformation efficiency.
I will be thankful if any of you can share your experience in this experiment.

How are you storing the cells?  Competent cells can be very finicky.  In my lab, we usually flash-freeze them with ethanol/dry-ice and store at -81 degrees (long-term use) or we store them surrounded by ice at 4 degrees (short-term use).


text:
How to do western analysis to lung tissue?
I am working with lungs from mice, and I want to do a western blot analysis to my samples.
I am having trouble with this because my images turn out very "messy", with a high background.
Perhaps I should filter my samples following their homogenization?
Has anyone had this problem and knows how to avoid it?
What is the best method to homogenize the samples?

Doing westerns with primary tissue can be tough, especially because of the presence (sometimes at high levels) of extracellular matrix (ECM). This material can be quite resistant to homogenization and some lysis buffers. One method I have found to work is to snap-freeze the tissue in liquid nitrogen (not on dry ice or at -80°C) directly after removal from the animal, or after any sub-dissection you may wish to do. Then, when you are ready to prepare your sample, grind it thoroughly with a mortar and pestle in LN2, collect the dust and add a good lysis buffer like RIPA at 2-3X concentration, along with protease and phosphatase inhibitors, also at 2-3X. Then, instead of simply homogenizing, use a probe-tip sonicator (not a water bath one) and sonicate the lysate on ice with 8-10 pulses of perhaps 3-5 seconds each, ensuring that the lysate does not heat up too much, and making sure it does not froth up by getting the tip too close to the surface. Sonication sends very powerful shearing forces through liquid and is excellent at destroying membranes and breaking apart ECM. From here you can do your protein concentration assay (remember to use the same concentration of lysis buffer as your blank), aliquot the lysate and store at -80, or add SDS sample buffer and run your gel.
I routinely use sonication on all of my western samples, regardless of whether it's tissue or cell lines I'm dealing with, and I almost never get smeared lanes anymore. Sonication reduces the viscosity or "thickness" of the lysate, allowing you to pipette it much more easily and accurately. It is also useful when your sample "coagulates" after adding SDS sample buffer, and in this instance it doesn't matter if the sample gets hot, as you'll just be boiling it anyway.
I hope this helps, please let me know if you're still having problems. I used to do troubleshooting like this for a living :)


text:
Can animals use the nitrogen in chitin to build proteins?
Fungi and insects contain chitin, which is about 6% nitrogen.
Can an animal - like me - make use of this as a nitrogen source to build proteins?
Are there any animals that can do this?
Are there other uses an animal can put Nitrogen from this specific source to?

The first answer is that humans cannot.
Chitin is a major component of the exoskeleton of insects and other arthropods, the cell wall of fungi and bacteria, the perisarco of hydroids and is also present in the epidermal cuticle or other surface structures of many other invertebrates. After cellulose, chitin is the most abundant naturally occurring biopolymer.
Chitin is a polysaccharide consisting of multiple units of N-acetylglucosamine (N-acetyl-D-glucos-2-amine) linked together with a bond-type β-1, 4, of the same glucose units forming the cellulose. Therefore, the the chitin can be regarded as a cellulose in which the hydroxyl group on each monomer has been replaced a group of acetilammina.
Pepsin in the stomach cleaves peptide bonds that bind together the amino acids of proteins, thus forming small peptides and amino fragments.
From the organoleptic point of view, chitin is considered a fiber, like cellulose and chitosans, suggesting it is indigestible.
Some herbivores, such as goats and some ruminants can digest cellulose, breaking them down long chains of polysaccharides. Similarly, echinoderms can eat shellfish, sea urchins and mussels and digest chitin, breaking mechanically only ones with hard shells.

However, hydrogen bonds between adjacent polymer guarantee the substance a remarkable hardness. This feature, combined with its flexibility and the fact that it is degradable by endogenous enzymes, chitin is an excellent material for the production of wires for surgical sutures, bandages and also synthetic leather. Chitin also has the unusual property of accelerating the healing of wounds in humans, closely related to chitosan (a more water-soluble derivative of chitin) and to the immune system of plants and animals.
EDIT
Yes, @mart. Echinoderms use chitin for producing proteins, similar to how herbivores use plant cell walls, which consist mainly of polysaccharides (non-nitrogen compounds), to produce the proteins (nitrogen-containing compounds), that serve us also (since we are not able to digest the grass).

More sparing use of formatting might make your answer easier to read

Counted my bad English, I will very gratefull if you do it :)

Those animals that can digest chitin, do they use the contained N for protein building or other purposes?

This answer should not have been accepted in my opinion. It contains a ragbag of mainly irrelevant information and then it gets its key fact wrong. Humans have the potential to digest chitin as they have the genes for chitinase. The doubtful assertion that the the product of chitin digestion (Nacetyl glucosamine) is used for protein synthesis (i.e. converted to amino acids) rather than used for the synthesis of polysaccharides is not backed by any references or links so we cannot judge whether it is correct.

This article suggests a certain amount of chitin digestion is possible.
http://www.bio.unipd.it/agroecology/download/pdf/papers/2009/Chitin-Chitinases-Paoletti-From-Binomium-Chitnchitinase-Recent-Issues-Fp-Version.pdf
I can't quantitatively say how much of any of the myriad potential chitin sources (fungal, crustacean or other arthropods) would be digested within a 'normal' time frame in the human digestive system. That work should probably be undertaken, though.

You might summarize the key points of the article, including the fact that humans do have chitinase genes. I would cut your last line, which is a matter of opinion on research priorities. It's not the sort of work that I would fund.


text:
Are there any other animals that become attached to a non-living object?
Do any animals become psychologically attached to any non-living object that is not useful to the animal for any of its physical needs, like some children do to stuffed animals? Some children are so attached to their toys that they take them with them whenever possible, and are upset when the toy goes missing or is taken by another.

So, this is psychological attachment. From the question alone, I thought of physical attachment.
If you provide stuffed animals and human children, then I'd offer the television remote, a chair/sofa and the cellphone for human adults. In general, many adults are far too sedentary for their own health.
Some non-human primates have exhibited behavior similar to that which you describe with the stuffed animals-children example.
In terms of an inanimate object, you can add the Internet. Certain behaviors like over-indulgence in alcohol, sex, gambling, hand-washing, and the like, could, broadly speaking, fit within the question as posed.

Have you a reference for the statement about non-human primates?

This doesn't really answer the question, it gives more examples of human attachment and a vague reference to non-human primates. I think it would have been better as a comment.


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How can a plant resist glyphosate (Roundup) herbicide?
In my area, the most common weeds that strongly resists (N-(phosphonomethyl)glycine) (glyphosate) are the horseweed, or mare's tail, Conyza canadensis, and Canada thistle, Cirsium arvense There are several other weeds with similar resistance. I use the brand Roundup on jobs where a complete kill is necessary. However, I sometimes have to go through again, with glufosinate, to control these weeds. I'd prefer not to, as the glufosinate lingers much longer in the soil.

Glyphosate inhibits an enzyme used in the synthesis of the aromatic amino acids tryptophan, tyrosine,  and phenylalanine. It is taken in by the stomata in the leaves, and is moved throughout the plant to all the points of growth, acting fastest on those plants which are undergoing fastest growth.
I can't seem to find an article on how the weeds mentioned can tolerate this treatment. How do these weeds resist the glyphosate?

I found a paper investigating the mechanism of glyphosate resistance in Conyza canadensis. They used 31P NMR to investigate the fate of the glyphosate in vivo. What they found is that the resistant plants are able to transport glyphosate into the vacuole:

The following view of horseweed resistance to glyphosate emerges from
  the data presented herein. Glyphosate enters the cytoplasm of both R
  and S plant variants at the same rate. Within hours, however,
  glyphosate begins to occupy the vacuole in the R but not the S
  biotype. The identical pH values of R and S vacuoles speak against the
  possibility of a pH-driven process. This, coupled with the
  preferential movement of glyphosate from the cytosol to the vacuole in
  R tissue but not in S, suggests the presence of a transporter for
  glyphosate either specific to R or at a substantially greater
  concentration in R than in S tissue.

Another paper titled "Two non-target mechanisms are involved in glyphosate-resistant horseweed (Conyza canadensis L. Cronq.) biotypes" found a different mechanism for glyphosate resistance in addition to the sequestration into the vacuole.

Glyphosate was metabolized faster in the R (C004) biotype than in the
  S biotype. The herbicide disappeared completely from the R (C004)
  biotype by conversion into glyoxylate, sarcosine and
  aminomethylphosphonic acid within 96 HAT.

The resistant plants seem to be able to metabolize glyphosate more effectively.
It is of course not guarenteed that these are the only mechanisms for glyphosate resistance, there are likely more variations.

authors: Деррик Морган


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How does MSMA kill crabgrass with only minimal damage to lawn grasses?
I use MSMA (Monosodium methyl arsenate) to kill crabgrass in lawns. I am not certain of the mode of action.

How does this chemical work? How does it target the annual grassy weeds, without damaging the lawns much?

Please consider this a sort of comment — I tried looking up for articles related to MSMA mode of action but almost all the articles are about its toxicity in mammals.
By what I understand, trivalent arsenates act as phosphate analogs and therefore interfere in phosphorylation reactions including DNA synthesis [Ref].
The weed is affected perhaps because of its relatively higher growth rate. Also the already established lawn grasses would have good population size to regrow out of the damage.


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What is the number of cells in a line of a fingerprint?
I have been reading a little about the size of cells and was curious as to how small they really were.
I have noticed that on my finger, the outlines of the fingerprint are made up of thin lines. In fact, some of them are so thin that I have difficulty imagining anything thinner I can make out with the naked eye.
I have read that the naked eye has a resolution of 0.1 millimeters = 100 micrometers, whereas eukaryotic cells range in diameter of 10 - 100 micrometers.
Putting this information together, would it be reasonable to conclude that the lines on my fingers have a width ranging from 1 - 10 skin cells? Is there any satisfactory method to verify this without fancy equipment? Is it even true?
P.S.
Are there also more scientific names for these "finger lines" so that I can look it up somewhere? Googling "finger lines" brings up a lot of stuff about palm reading.

Are you just asking how large is a typical cell?

I think the scientific term is friction ridges

@Kevin More or less. But it doesn't have to be as large as "a tpyical cell". I am looking for something encountered in everyday life that I can use as a ballpark to compare with other things. I have heard stuff about how "so and so" many cells could fit in the tip of a needle, but it seems silly to think that way because a metal needle doesn't have any cells.

@math4tots I agree that the needle isn't a great size reference because the size of the tip isn't an "everyday life" kind of thing. However, I don't see why something has to be made up of cells to act as a reference for judging the size of cells. http://scaleofuniverse.com/ might be interesting to you for relating magnitudes of scale. Make sure to catch the human blood cells (~10 micrometers) between the micrometer and millimeter markers.

I am not sure that this can be accurately estimated because the outer layer of skin is ill-defined in terms of cells and cell boundaries. The outer layer or epidermis is composed of dead cells and dead cell parts that is tough and interconnected by design. Individual cells are not readily discernible.


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What is the origin of "melting" in molecular genetics?
I'm reading some papers about prokaryotic transcription mechanisms, and I've come across a term I haven't heard before: DNA melting or promoter melting. After reading a bit, it's pretty clear that they're referring to the separation of DNA from the double stranded form to single strands.
Maybe it's just because chemistry isn't my thing, but when I think of melting I think of a solid gaining enough energy to become a liquid. How did the term melting come to apply to DNA in this way? Does the term melting have a more general definition in terms of thermal chemistry?

What if you just consider melting where the intermolecular forces (here, base pairing) give way?

Nick T But intermolecular forces "giving way" is not melting. Melting (in physics) refers to the phase change undergone by a substance from solid to liquid.

From a statistical thermodynamics standpoint, DNA denaturation and renaturation is certainly a phase transition. The question is going from which phase to which? I would argue that the description of a rigid polymer going to a freed fluid polymer sounds like a solid to liquid transition to me.

The melting temperature (Tm) of a double stranded DNA tract is defined as the temperature at which 50% of the DNA molecules are dissociated into single strands (and 50% form duplexes). Sure, it has a different meaning than in physics... but it is a really common term in molecular biology and I doubt people will stop to use it anytime soon!
There is a vast amount of literature about the calculation of Tm, which is very important also for practical applications, such as designing PCR primers. This page has some explanations and references about the maths behind it.
I am not sure when the term first appeared, but it has clearly be used since the dawn of molecular biology.
DNA denaturation/renaturation dynamics were first studied in the '60s.
See for instance:
STRAND SEPARATION AND SPECIFIC RECOMBINATION IN DEOXYRIBONUCLEIC ACIDS: BIOLOGICAL STUDIES - J. Marmur and D. Lane - PNAS, 1960
Although Marmur and Lane do not talk about melting temperature, we can find the term already two years later in this 1962 paper:
Effect of Concentration on the Formation of Molecular Hybrids from T4 DNA - Andrzej W. Kozinski and Michael Beer - Biophys J., 1962
Evidently the term was already common there, as they don't care to define it (it's even in the abstract).
Who first used it? I'm not sure, if anyone knows feel free to add a comment or edit the answer.

Don't get me wrong. I'm not critical of the terminology, nor do I think it's inconsistent. I'm simply interested in the origins of the terminology, and whether it's at all related to other uses of the term, such as in thermodynamics.

The original researchers working on DNA knew nothing about its structure, but I assume they noticed when you got it above a certain temperature it got much runnier, and named the process accordingly?


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Is there a tool to find the action of an enzyme in a metabolic pathway?
Is there any tool to search the biochemical action of a particular enzyme in a metabolic pathway of an organism? In other words, how can I find if enzyme "E"  is involved in the metabolic pathway for organism "X".

I think the KEGG pathway database may be of some use to you.
Link is here: http://www.genome.jp/kegg/pathway.html
This a database of manually drawn pathway maps, I have used the site myself and it is very useful in determining if your enzyme is in a pathway and where it lies in it. This is assuming though, your enzyme is in the database and has been mapped.


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What is a pA(2) value?
I saw this article http://www.ncbi.nlm.nih.gov/pubmed/16710314 and it mentioned pA(2) values and I had no idea what they were. What are they? What do they mean?
If possible it'd be just dandy if you could cite some journal articles/books/other reliable sources for me to dig up.

I don't know enough about this to write a good answer, but you can find an explanation here. A p(A2) value describes the affinity of an antagonist for its receptor.

Below are responses generated using the isolated guinea-pig ileum preparation to determine a pA2 value for a sample of the cholinergic antagonist homatropine.
Responses are expressed in millimetres +/- SDM (n =4). Plot the data and then determine by Schild analysis the pA2 value and Schild slope. What conclusions can you draw; does the experiment/data fulfil the criteria for a valid Schild analysis?
Acetylcholine      ACH Alone    ACH +Homotropine       ACH +Homotropine   ACH +Homotrop
Concentration                     3x10^-9 M              1x10^8M            3x10^-8M
[Molar]
3 x 10^-9            3+/-1
6 x 10^-9            8+/-3            Not Response
3 x 10^-8            28+/-6             10+/-4             No response
6 x 10^-8            38+/-8             21+/-9           5+/-2                                                    No response
3 x 10^-7            55+/-5             43+/-7                27+/-9             10+/-4
6 x 10^-7            56+/-5             52+/-3              38+/-7             20+/-7
3 x 10^-6              -                55+/-4              53+/-6             43+/-6
6 x 10^-6              -                   -                56+/-2             54+/-5

This is a well-written answer; however, it does not answer the question being asked. If you could state what exactly it is as opposed to how it behaves when tested on a guinea pig that would be helpful. Also, it is advisable that you put in references. Aside from this, you did well for a first answer and I welcome you to Biology S.E.! If you have additional questions, please visit The Help Center.


text:
Why Is Most Life Symmetrical Externally But Not Internally?
Mammals, reptiles, arachnids, insects, etc are all as far as I am aware symmetrical in appearance.
Take a human for instance, make a line from the top of our head right down the middle. However, internally it is not the same. Our organs excluding the kidneys, lungs, reproductive organs, etc are not symmetrically placed in our body.

Why do we not have an even number of each organ so it can be placed symmetrically?
If we have a single organ why is it not placed in the middle like the brain or bladder is for instance?
Is there some evolutionary advantage that led to this setup?

I am not sure I completely agree with your conclusion that we are not symmetrical internally.  There are exceptions but I would say we are more symmetrical than not.

@DQdlM, yes, there are exceptions to organ symmetry. However, externally there are no exceptions to symmetry. Why are not all organs symmetrically placed? That is what I am trying to understand. Why full symmetry is not internal as well?

The question of why there are no major exceptions to external symmetry is subtly but interesting different from why are we not symmetrical internally.  I am interested to see the answers you get.

Flounder fish aren't the most symmetrical guys. Just thought I should point out that external symmetry is not essential. http://www.google.co.uk/imgres?imgurl=http://www.dnr.state.md.us/fisheries/juvindex/flounder.jpg&imgrefurl=http://www.dnr.state.md.us/fisheries/news/story.asp?story_id%3D130&h=480&w=640&sz=28&tbnid=_PWh1T3gGBB50M:&tbnh=92&tbnw=122&zoom=1&usg=__lSMRjlJzASOX2hcwsLpOoXtKSjY=&docid=Qy-9gfEvf_FxcM&sa=X&ei=ReScUcOdJYmp0AXwuoGwAQ&ved=0CD8Q9QEwAg&dur=1064

This question was first asked by Sir Isaac Newton: "Can it be by accident that all birds beasts & men have their right side & left side alike shaped (except in their bowells) & just two eyes & no more on either side the face & just two ears on either side the head & a nose with two holes & no more between the eyes & one mouth under the nose & either two fore leggs or two wings or two arms on the sholders & two leggs on the hipps one on either side & no more?"

It is worth noting most animals ARE symmetrical internally, One which are not tend to be highly derived and very different from their ancestral body plan, animals like tetrapods or mollusks

First, I think it worthwhile considering 'Why would internal symmetry be beneficial?' Developmental simplicity jumps to mind immediately. You can also consider relationship to external organs; the stomach and esophagus are lined up with the mouth which is symmetrical about the sagittal plane. Or maybe even balance; the lungs are large organs and if put to one side would likely cause locomotive issues. (Perhaps this is even an interesting topic for another question.)
That said, I feel, at it's core the evolutionary advantage which led to the lack of ubiquitous internal symmetry is space. Simply put, there is only so much room inside an organism and every little counts. Thus, if there isn't a need for a particular organ to be mirrored about a plane then there is a benefit in putting elsewhere: utilization of space.
I think a fantastic example of this is the human digestive tract. The key factor in the shape of the intestines is utilization of space, which directly affects the point at which is connects to the stomach, itself contributing to the asymmetrical shape of the stomach. One could envision other configurations, sure, and nature has. However, this configuration works quite well and the extraordinary use of limited space seems to outweigh all benefits of symmetry.
To directly respond to your questions above:

Question: Why do we not have an even number of each organ so it can be placed symmetrically?
Response: Each organ addresses (or addressed) a need of the organism. Addressing that need with multiple organs working in concert has benefits and consequences, as does addressing the need with a single organ alone. These benefits and consequences are balanced throughout the evolution of an organism.
Question: If we have a single organ why is it not placed in the middle like the brain or bladder is for instance?
Response: I feel space. Again, there are benefits to symmetry but there are many other factors at play. Some of which, it seems, are more important than symmetry at times.
Question: Is there some evolutionary advantage that led to this setup?
Response: I hope this has been addressed - I don't claim to have 'answered' anything, this is a question for discussion.

Other fuel for discussion:
In thinking through this question I found myself able to rationalize why internal symmetry isn't necessary. However, I'd be interested in seeing opinions on why, then, external symmetry is so prevalent.

External Bilateral symmetry permits streamlining, favors the formation of a central nerve center, contributes to cephalization, and promotes actively moving organisms.

@Mew: Why and how?

So our body is a iPhone 7plus

This works just as well on external symmetry, locomotion is a lot easier if you are symmetrical.  you will not most asymmetrical animals are asymmetric in something not involved in locomotion.

Building on the answer given by Sean Connolly above, it would be very easy to imagine evolutionary scenarios where organs are more likely to develop asymmetrically than symmetrically.
For instance, imagine an organism that has a simple digestive system that consists only of a single undifferentiated intestine that runs directly from mouth to anus in a straight line, as in primitive annelids. Let's say that there is also only one enzyme present to break down the food particles, and that this is present throughout the intestine.
Now, perhaps for space issues, or for reasons that are entirely unrelated to internal organs, the intestine itself becomes asymmetrical. This could be because a longer intestine is needed to dissolve and take up more of the food, but the organism cannot become longer (for instance, it might live in dead coral reefs, and the size of the hollows cannot be controlled by the organism itself, so there is an external limitation to how long the organism can become). One way to solve this would be to fold the intestine, which can make it asymmetrical.
Now, because food particles that enter the mouth are exposed to the single enzyme throughout the intestine, the gut fluid will be less and less nutritious the farther posterior it gets along the gut. Possibly, more anterior parts of the intestine will become specialized in breaking down and absorbing more frequent kinds of food, while more posterior parts will become specialized in less common foodstuffs. This could lead to differentiation of secretory organs along the intestine, and if this is already bent because of external selection pressures, it is not impossible that a given secretory organ will develop asymmetrically simply because the intestine at the point where the enzymes secreted by this organ are to be used is not near the mid-line of the body.
For instance, if we needed to absorb substance X from our food, but substance X only became abundant in the gut fluid at a distance from the mouth that corresponds to a place when our intestine is located on the left side of the body, it is not unreasonable that development of this excretory organ would develop on the left side of the body. This could then be self-reinforcing, as a more ready access to substance X may mean that this substance becomes more important for us, and the secretory organ may become larger and more dominant, and eventually we have a large organ that exists only on the left side of the body, without ever having existed in a symmetrical form.
This is, of course, pure speculation, and I know of no example of this, but it is one that is not at odds with evolution in general, and could certainly be plausible. The same could occur if differentiation of enzyme secretion organs occur in a symmetrical gut, which later becomes asymmetrical and the whole secretory organ becomes displaced to one side. Retaining a symmetrical pair of secretory organs on each side of the body, but having the enzymes work on food only asymmetrically would imply that one of the secretory organs had a very long duct and the other had a very short one. It is reasonable to assume that over evolutionary time, the one with the long duct would become less important and may disappear.
A similar reasoning could be applied to the blood circulation system and any organs relevant to that.

There are many examples of external asymmetry throughout the animal kingdom. Many decapods, for instance, have asymmetrical claws that are used for different purposes (feeding in lobsters, for instance). Several genera of bird lice (e.g. Struthiolipeurus, Bizarrifrons) have asymmetrical heads, which probably have something to do with how they attach to their hosts' feathers. I believe that many groups of sessile invertebrates have anal openings displaced to one side, but that may be caused by internal asymmetry or because it is less efficient to have our anus situated so that feces is filtered into your mouth again.

Thanks for the response. It was very difficult choosing who to accept, so opted to just choose the highest voted one. If I could choose multiple answer I  would have chosen yours as well. I did upvote!

You change one thing and you have to change everything else to compensate.
Lets look at what organs are not symmetric in tetrapods, the heart and the digestive system, everything else is symmetric. Note these are symmetric in more basal vertebrates like fish.
the heart starts symmetrical in vertebrates but that changes when animals evolve independent circulatory systems, that is flow of blood to the lungs that is separated from the flow to the body, allowing for differential blood pressure. that evolved by having one side of the heart supply the lungs and the other supply the body, since they have vastly different blood pressures it would make sense the sides of the heart creating that blood pressure would also be different. this change in shape forces some asymmetry on the lungs that have to share space with the heart.

The digestive system is even easier, again it starts as a straight tube, but two major changes occur. first a longer digestive track allows you to extract more nutrients, and making a human (or nearly any animal) long enough to hold a straight digestive track of the same length would be incredibly wasteful. For scale the human digestive tract is about 10 meters long.
The other change is the development of the stomach (which not all vertebrates have). having a portion of the digestive system dedicated to storage and soaking is useful by allowing animals to eat larger quantities when situations allow without having to hurry it through the digestive system and lose most of the benefits. And again the only good way to enlarge a section of a straight tube without elongating the body is to have it turn and be offset, this forces many other organs out of place (liver and spleen) which attach along the digestive tract's length. Note in many fish this is all still symmetrical, but this changes when they evolve away from a tall thin cross section into a more rounded cross section which is favored in shallow water and eventually life on land. Once that happens you can't simply stack everything up along the mid-line without wasting a lot of space.

you can see how changes to the digestive track might evolve in many different lineages that change the shape of the body like crabs or molluscs. which are the other groups with asymmetric internal organs. Note these other two groups are often externally asymmetric as well. Snails in particular because they changed a  long straight shell into a compact coiled shell, which forces asymmetry on many systems.

I would like to add an answer here to explain how the internal asymmetry of animal organs might be consistent with their external symmetry.
Here's my argument:
1) In the case of vertebrates the important internal organs are protected by the animal's skeleton.
2) The internal organs are soft matter and so their physics is very different from how they would behave if they were nearly rigid bodies.
3) Internal asymmetry isn't a big issue because the mass distribution is approximately symmetrical in a bilateral sense.
To make this concrete I mean:
a) If you should try slicing a vertebrate down the middle you will notice that the left and right sides of a vertebrate have approximately the same weight
b) The left and right sides of the vertebrate's head have approximately the same weight...etc.

Imagine that the intestine is a long, symmetric, flexible tube, about 20 feet long.  Now imagine what the tube would look like if it were packed into a 5-gallon bucket.  It would be literally, mathematically, impossible to pack it in symmetrically.  In physics we call that "spontaneously broken symmetry".  It would take a lot of genetic instruction to pack a long intestine into a small volume even approximately symmetrically.  Of course this doesn't explain all the asymmetry you're wondering about, but does explain some of it.


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Is there a scientific proof that smoking spoils face skin?
I saw that cigarettes-smokers (more than 3 cigarettes per day) often have the skin of the face which is a little bit spoiled.
Is there any scientific proof that cigarette smoke (or the nicotine inside it) is a damaging fator for face skin?
Or it is just due to the skin-smoke interaction casued by the smoke that the person breaths out from the mouth?

This page is pretty complete with examples and references.
In summary a lot of the evidence is empirical - you look at smokers and the quality of their skin and compare to non-smokers and the differences are statistically significant and reproducible.  It seems as if this is old work, dating from the 1970s.
So in many cases these are only observed correlations.  But they are pretty strongly agreed upon by medical people.  Given the fact that we still don't know exactly what causes cancer, I think this is not an unusual level of explanation for medical conditions.
As you can see some theories would include direct effects of the smoke and some indirect effects.

It is not certain exactly how smoking causes early ageing of the facial skin. Theories include:

Heat from the cigarette directly burning the skin
Changes in the elastic fibres of the skin
Narrowing of blood vessels (vasoconstriction), which reduces blood supply to the skin and can cause changes in skin elastic fibres and
  loss of collagen
Reducing Vitamin A levels and moisture of the skin