plant physiology - How does a tree trunk sprout and grow after being cut?

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.

structural biology - Which factors besides the thermodynamic stability are important for the hairpin in intrinsic transcription termination?

Intrinsic termination (rho-independent) relies on a stable hairpin with a subsequent uridine repeat. The common explanation on how these sequences cause the termination of the transcription are based on the thermodynamic stability of the sequence. The GC-rich stable hairpin together with the destabilizing U-repeat supposedly destabilize the binding of the polymerase enough to cause it to disassociate from the template.

What I'm looking for are specific requirements on the termination sequences that are not based on thermodynamics.

• Are there any specific requirements on the hairpin sequence beyond a certain thermodynamic stability.


• Are there any loop variants that are known to reduce the termination efficiency?


• Does the shape of the hairpin, e.g. any kinks or bulges in it, have an influence on termination efficiency?

The typical requirements I read are 5-14bp and GC-rich, and I'd like to know if there are any more specific requirements, especially ones related to the structure and not the stability of the hairpin.

human biology - Does consuming sodium benzoate (preservative E211) cause problems during pregnancy?

There is some evidence to support the idea that sodium benzoate may be detrimental to the development of the foetus:

TERATOGENIC EFFECTS: Classified POSSIBLE for human.

DEVELOPMENTAL TOXICITY: Classified Reproductive system/toxin/female, Reproductive system/ toxin/male [SUSPECTED].

^{MSDS for Sodium Benzoate}

This has been shown experimentally in rats by Minor & Becker in 1971. They introduced high doses of up to 1000 mgkg^-1 intraperitoneally and recorded reduction in foetal weight and "gross anomalies". Whilst I struggled to find a copy of their original paper, it is referenced in the Catalog of Teratogenic Agents¹ (Thomas H. Shepard).

There is some evidence to refute this, however. The Acceptable Daily Intake limits on sodium benzoate is a maximum of 5mgkg^-1, at this dose there is no noticeable effect of exposure. ^(2,3) The latter paper by EC food safety standards goes further:

There appear to be sufficient studies to conclude absence of teratogenic potential, with an overall NOAEL* for developmental toxicity of 500 mg/kg bw/day, based on effects on fetal weight.

*(No observed adverse effect level)

So the consensus from the food safety bodies suggests that E211 should not pose harm to an unborn child in the quantities allowed to be present as an additive.

---

1 Emire, Ronald J. "306: Benzoate, Sodium." Catalog of Teratogenic Agents. By Thomas H. Shepherd. JHU, 2004. 44-45. Google Books. Google. Web. 10 Feb. 2012.

2 Nair, B. "Final Report on the Safety Assessment of Benzyl Alcohol, Benzoic Acid, and Sodium Benzoate." International Journal of Toxicology 20.3 (2001). International Journal of Toxicology. Web. 10 Feb. 2012.

3 Scientific Committee on Food. Opinion of the Scientific Committee on Food on Benzoic acid and its salts. Rep. 24 Sept. 2002. EUROPEAN COMMISSION HEALTH & CONSUMER PROTECTION DIRECTORATE-GENERAL. 10 Feb. 2012

zoology - Why are (some) cats attracted by bleach?

I can't give a definite answer, and there's nothing in the literature about this specifically, but perhaps some relevant information and a suggested behavioural experiment will help.

Background
Firstly, I assume you are talking about sodium hypochlorite (which is usually what people mean by bleach)? If so, there are several compounds your cat could be reacting to. Chlorine is an obvious candidate, which is released as sodium hypochlorite decomposes in solution. Additionally, bleach can react with various organic materials to release a variety of volatile organic compounds (VOCs), which your cat might be able to smell. In addition to also releasing chlorine gas, the same suite of VOCs are released when the chlorine in chlorinated tap water reacts with organic contaminants (Odabasi, 2008). The VOCs include chloroform and carbon tetrachloride.

Next, cats are known to exhibit modified behaviour in response to a variety of compounds. Some are suspected pheromone components of cat urine, such as felinine (Hendriks et al, 1995) and its breakdown products, such as MMB (Miyazaki et. al, 2006).

Some cats also react to externally-produced compounds with a particular response called the 'catnip response', which involves rubbing the face on the ground or other objects, shaking the head, rolling, etc. (Tucker & Tucker, 1988). Not all cats exhibit the response, around 50-50% do, and susceptibility is genetic and heritable. Some sources eliciting the catnip response include:

• nepetalactone released from catnip (Nepeta cataria)


• actinidine released from valerian (Valeriana officinalis)


• essential oil of Actinidia macrosperma (Zhao et al., 2006)


• the compounds epinepetalactone, dihydronepetalactone, isodihydronepetalactone, neonepetalactone, iridomyrmecin, boschnialactone, onikulactone, boschniakine, actinidiolide and dihydroactinidiolide (Tucker & Tucker, 1988)

In general all the catnip response elicitors share a two-ring structure, which is not to my knowledge shared by any of the volatiles given off by bleach.

A possible experiment
So, two obvious possibilities (regarding what type of behavioural response is being elicited) are that either:

1. your cat is interpreting the volatile as a pheremone and therefore as some sort of sexual or territorial signal, or


2. it is showing the catnip response

As a first experiment, you could check whether your cat (and any others you can get hold of - in an ethical way) respond to bleach and/or to catnip. If the cats do not exhibit the catnip response to catnip, they aren't exhibiting it in response to bleach, and thus some other explanation is more likely.

As a second experiment, you could make a detailed observation of the precise behaviour shown in response to bleach. Compare it to that exhibited when the cats encounter catnip (depending on the outcome of the first experiment) and when they are oestrous (if female) or encounter an oestrous female (if male). You could also compare to the response to the urine of other (male and female, familiar and unfamiliar) cats.

An experiment you shouldn't do
If you wanted to find out which chemical your cat is responding to, you could allow your cat to sniff pure chlorine which hasn't encountered organic contaminants, as well as chloroform, and carbon tetrachloride. However, all three of those compounds are extremely dangerous and could easily kill you or your cat, so please don't.

I general, I would caution against exposing your cat to bleach, because it can induce serious health effects depending on dose and mode of exposure, ranging from asthma to third-degree burns to carcinogenesis. If they are attracted to it, that is a good reason to keep it away from them to prevent them ingesting it, which is more harmful than inhaling the fumes.

I can't comment on whether the behaviour is acquired as result of domestication, but that too could be tested by comparing the reaction of a large sample of wild cats (!).

References

• Hendriks, Wouter H., Paul J. Moughan, Michael F. Tarttelin, and Anthony D. Woolhouse. “Felinine: a Urinary Amino Acid of Felidae.” Comparative Biochemistry and Physiology Part B: Biochemistry and Molecular Biology 112, no. 4 (December 1995): 581–588.


• Miyazaki, Masao, Tetsuro Yamashita, Yusuke Suzuki, Yoshihiro Saito, Satoshi Soeta, Hideharu Taira, and Akemi Suzuki. “A Major Urinary Protein of the Domestic Cat Regulates the Production of Felinine, a Putative Pheromone Precursor.” Chemistry & Biology 13, no. 10 (October 1, 2006): 1071–1079.


• Odabasi, Mustafa. “Halogenated Volatile Organic Compounds from the Use of Chlorine-Bleach-Containing Household Products.” Environ. Sci. Technol. 42, no. 5 (2008): 1445–1451.


• Tucker, Arthur, and Sharon Tucker. “Catnip and the Catnip Response.” Economic Botany 42, no. 2 (1988): 214–231.


• Zhao, Yun-peng, Xiao-yun Wang, Zhi-can Wang, Yin Lu, Cheng-xin Fu, and Shao-yuan Chen. “Essential Oil of Actinidia Macrosperma, a Catnip Response Kiwi Endemic to China.” Journal of Zhejiang University. Science. B 7, no. 9 (September 2006): 708–712.

Stabbing muscles when flexed and when relaxed

Well, if we look in very basic detail at how muscle contraction works within a myofibril of the sarcomere:

^{N.b. this isn't on a loop and only plays through seven times}

The red lines represent actin filaments whilst the blue lines represent myosin filaments. During muscle contraction the filaments move over each other:

As shown in the above diagrams the "more contracted" a muscle is then the smaller the size of the H zone (the area where there are just myosin filaments).

So if we consider a penetrating impact that went through a plethora of identically aligned sarcomeres (obviously this is not the case in nature) then we could presume that (et ceteris paribus) the object would not penetrate as deeply into a contracted muscle as it will hit more tissue on its route than in a relaxed muscle.

pathology - Is it harmful for someone to consume things full of bacteria if they don't get physically sick from the bacteria at all?

It really depends on what you consume, how much of it you consume, and the state of your immune system. Let me give you some examples. Yogourt is full of bacteria, and yet we can eat it without issue. The bacteria likely don't survive digestion, but if they do, they will quite happily live in our intestines contributing to the already existing population of good bacteria.

Streptococcus is a genus of bacteria that contains some species that live all over us. They are on our skin, in our upper respiratory tract and intestine. If the species, S. pneumoniae makes it into our lungs, this can cause a bacterial pneumonia. There are likely few bacteria making it into our lungs on a regular basis, and normally our immune system can fight this off without concern. If we some how become immune depressed or compromised (for a number of medical reasons) then that's when we become symptomatic and ill.

On a more extreme side, if we have a bacteremia it is called a bacteremia. There are benign cases of this every time your brush your teeth and bacteria are able to enter tiny cuts in your gums from the brushing action. A healthy person fights this off. If a bacteremia is left unchecked, because of a lack of immune response or trauma, this can develop into a sepetcemia, a toxic infection of the blood. This can be very life threatening and is quite serious.

In general, we always have bacteria all over our hands which we likely transmit to our food or otherwise ingest. This is normally not a problem, but there is an appreciable risk of getting some kinds of viral or bacterial infection (eg, strep throat or a cold). Washing with soap (and to a lesser degree, using hand sanitizers) minimizes this risk.

molecular biology - Why would we overexpress Sir2 by overexpressing its hypomorph (dSir2-EP2300) in C. elegans?

I have had a little time to look over this paper.

They do overexpress a native sir2 clone in high doses, called sir2.1 OE. Which seems to be native and also appears in high copy numbers. This strain was found in previous publication to have a high lifespan... that is old news.

This paper sees sir2.1 expression levels as an oversimplification of the causes of longevity. When they create crosses of the sir2.1 OE strain with wildtype, you can see the Outcross, which is verified to have a high level of sir2 expressed no longer has an extraordinary lifespan.

This can be seen in Figure 1. http://www.nature.com/nature/journal/v477/n7365/fig_tab/nature10296_F1.html

So this paper is now asking, if sir2 levels do not convey the information that creates an extended lifespan, then what does? It must be some modulation of some protein that sir2 affects. They implies that the actual cause of the lifespan increase may have been a mutation somewhere else in the organism.

"However, longevity was not suppressed by sir-2.1 RNA interference (RNAi) ... indicating causation by factors other than sir-2.1, either on mDp4 or elsewhere in the genome."

"This implies that lifespan extension is due to transgene-linked genetic effects other than the overexpression of dSir2."

In the second half of the paper (figure2) the investigators have moved on to drosophila work, where they look at how expressing constructs or inhibiting sir2 protein levels might affect lifespan. Although the dSir(EP2300) / + construct (drosophila sir2) with a wild type gene promoter did not live quite as long as dSir2(EP2300) with a fancy promoter (dSir2(EP2300) / tub-GAL4), the promoter construct (tub-GAL4/+) alone also had just as long a lifespan. How can this be? Not sure, but the expression of sir2 is clearly not the panacea we had hoped. Note however that the reduced power gene still gave the same boost to lifetime. This shows dramatically that sir2 activity alone does not drive the longer lifetime.

Lastly, deletion constructs (dSir4.5/1.7) , which should have lower than wild type protein levels for sir2 had completely normal lifetimes.

So the answer to your question; you need to test a hypothesis going in both directions - does increase of the protein really create a strong effect? Does decreasing it have a negative effect then? There are lots of other reasons to use knockouts and non functional genes in such an experiment, but those are the broad strokes.

cell culture - How long does antibiotic-dosed LB maintain good selection?

Various people in our lab will prepare a liter or so of LB, add kanamycin to 25-37 mg/L for selection, and store it at 4 °C for minipreps or other small cultures (where dosing straight LB with a 1000X stock is troublesome). Some think using it after more than a week is dubious, but we routinely use kan plates that are 1-2 months old with no ill effect.

How long can LB with antibiotic such as kanamycin, chloramphenicol, or ampicillin be stored at 4 °C and maintain selection?

botany - Do immature fruits perform photosynthesis?

Most immature fruits are green: peppers, pine cones, plums, lots of them. I want to know if the green is from chlorophyll in the cells. Do the fruit cells perform photosynthesis? When you cover a green stem or leaf, it will turn pale and stretch. That is because the stems have little need for chlorophyll in the dark, which is why they are pale. They stretch because the auxins in the stems are not destroyed by the photons, and the stems stretch out and topple over. If a green fruit is covered, will it turn pale and stretch like that?