CharonY

What, precisely, do you think neurotransmitter are, and what is their role?

The reason why AP travel in a specific direction is due to the kinetics of the involved ion channels. Once they they have activated, they do not react for a given time (refractory period). This prevents the AP running into the opposite direction. However, if you stimulate the middle of the axon, for example, the channels in both directions can be opened. Hence, from the depolarized area the AP can move into both directions. Neurotransmitter are only relevant to eventually create AP in the postsynaptic cell.

Algae in this context is usually used as a catch-all phrase which includes cyanobacteria.

Actually, part-time work for kids between 14-16 is not that unusual and is imo a rather good idea to give them a first taste of real life, provided the workload does not impact on their time to get education.

I agree, the language was a bit inaccurate in that sentence.

Profitability (or lack thereof) is still one of the biggest issues. The yield per dollar is still too low and quite some funding has been pulled out of that area because of this (and other issues).

I assume you mean lac promoter (the whole operon is not needed and lacI is often provided by the host strain)? IPTG induces the lac operator, acting as a lactose-analog (essentially by binding to the lac repressor). The induction with IPTG is dependent on the host strain. The trick here is the use of the T7 promoter. In order to express the gene insert under control of the T7 promoter, the viral T7 RNA polymerase has to be present. This is done by having a host strain carrying it. If the T7 RNA polymerase is under control of a lac promoter, but is repressed by LacI, IPTG would induce T7 polymerase expression, which in turns results in expression of the insert in the plasmid. Thus, the control of induction is not directly done by cis acting elements on the plasmid, but relies on a compatible host strain.

Are you sure that they refer to genome hybridization and not e.g. 16S similarity?

one has to keep in mind that the term evolution in different contexts mean different things. In biology, it refers to the change of allele frequencies over time. As such, it does not cover the rise of self-replicating molecules. In the strictest sense, it does not even cover all self-replicating molecules per se as the narrow definition is tied to DNA-based replicating systems (including all known life forms and mobile genetic elements). Again, one could try to broaden the definition, but the correct context has to be given.

Yes. What about coffee?

AFAIK regulations stipulate that natural products are extracts from natural sources. However, salt and sugar are generally not regulated. Regulation-wise it may be a grey area. Outside of regulatory rules, they would be considered artificial, though.

Good point about not using the autoclave alone.

Modifying bacteria in order to make them more susceptible to bacteriocidal agents is pretty much working backwards. And yes, getting rid of spores is even tricky with physical means (including being safe from viruses. A number of bacteriophages are pretty resilient, too (just ask a lab with a P1 infestation). Though usually not as much as spores.One could have spores with phages added to the mix though. In any case, use of viruses is impractical overall.

Cap, foil or something similar similar is usually needed to maintain sterility of the tubes once you take them out. Do not close them off airtight, though.

1) If you prepare things for immediate measurement, they easily water soluble (but not stable if stored in it). Ideally you should use the same buffer as you are going to use for your real sample for Bradford. 2) If 4.12g are 20,000 U how much g corresponds to 1U? You should use a buffer that ensure DNAseI activity. A common one is Tris pH 7.6 with MgCl2 and CaCl2 (2.5 and 0.5 mM if I recall correctly). For storage, however Tris with 50% glycerol and CaCl2 is generally used.

I have not read the paper, however based on the description above it appears that synaptic plasticity appears to be affected (as e.g. by establishing persistent LTP or suchalikes) rather than cell viability. The latter of which would be, to my knowledge, rather unusual.

Nature has its ups and downs. I would consider it mainly a bio journal, though. At least much in it is not rigorous enough for pure bio, but have some sexy stuff (often interdisciplinary) to sell it. I assume due to its format, about any discipline has something to complain about Nature (or, for that matter, Science). Formats of papers (whether it includes a long or short intro, discussion or not, numbering, etc.) are outlined by each journal, so that is usually the first thing to check. However, it is impossible to write a decent paper without knowing the background of the topic (and thus knowing what is the novel aspect of ones own work).

I see your point. In the end, it depends on how the lecture was set up. If I have e.g. discussed the principles of, say, an analytical method in class, I like to evaluate how well students have understood it by giving them a paper that inserts a little twist on the method. What I want to see is whether they understood the principles well enough to explain what the twist does. Or, lacking that, at least figure out that there was a difference and at least try to figure out what it does. Direct and specific questions will be answered, of course. However questions on the level of "I do not understand, gimme all the material so I can understand it" without any specifications are frowned upon. I do not think that most here mean that "you have to do it on your own" equals no assistance whatsoever. However, I see my main role as a guide, not as a spoon feeder.

QFT Many important things have already been mentioned. Regarding undergrad talks: it is rare that a great polished talk is expected. In fact, at the undergrad level talks are often used as a means to gauge the level of understanding as well as ability to fill knowledge gaps of the student. The form and style are also often discussed, but (depending on the prof, of course) rarely the centerpiece of it. Almost all first talks are (from a style viewpoint) bad. And this is OK, and it forms the basis for improvement. Not understanding the material on a basic level is something different, though.

It is not a problem of number, but the ability of the virus to successfully infect a bacterium. If it is resistant throwing a whole lot at them won't do much. Also if the bacterium is confined to a location it is easier to kill it with unspecific disinfection methods.

In cases when you deal with diverse range of expertise another approach could work, if you have enough time. Essentially give the bare minimum needed to understand the concept, then declare that you are going to give more in-depth info for those interested (so that those without expertise are prepared), summarize the gist again, and move to the next topic. By stating easily, going into depth and rising back again one can provide the depth without frustrating the non-experts too much, while satisfying the experts (which, depending on the format of the talk, may actually otherwise interrupt the talk).

Viruses can kill bacteria, but almost inevitably there will be resistant bacteria. It is good for destroying e.g. a monoclonal lab culture (which are all genetically identical). But destroying a wild-type population is very unlikely to happen.

Well let us interpret the curves in more detail. First, in order to differentiate between the two alleles I presume that different primers were used. That alone will result in differences in amplfiication efficency and thus render a direct comparison between orange and blue irrelevant. I.e. you generally can only compare CTs of orange to orange (one set of primers) and blue to blue (the other set) without further normalization. However, one tricky bit is determining the threshold, i.e. where you determine the CT. Note that in your two plots the indicated threshold would result in very close CTs, however in plot 2 the absolute signal in the blue curve is much lower. The shape of the blue curve in plot 2 indicates that the efficiency of the PCR is very low. One key element here is the threshold. It should be: 1) way over the background noise of the initial cycles to ensure detections and 2) be in the exponential part of the amplification curve Looking at plot 2 it appears to me that the threshold is very close to the initial noise (i.e. early amplification cycles where there should be no meaningful signal) and the exponential part is hardly visible. Based on that I would conclude that the threshold has to be higher and no proper CT can be derived from the blue curve. In other words, the curve appears not to be indicative of a proper product. The observed signal could be easily background (again, note the hump at the beginning) or unspecific amplification. Either the sample contained no blue allele, or the PCR simply failed for technical reasons. To be certain I would have to see the actual values, of course. The melting curve could give hints whether unspecific amplification may have occurred. Of course, the PCR could simply be super-inefficient for the blue primer pair, but looking at blue in plot 1 reveals that the curve can look very similar to the orange one (assuming in plot 1 the same sample was used). So based on the curve shape and assuming the PCRs worked fine, my assessment would be sample1: heterocygote, sample 2: homocygote. Note that the CT did not play a role (provided it is not something like cycle 30 or above, depending on the polymerase).

Bottom line, molecular rhythms have (surprise!) inherent variability that can adapt to external stimuli.

You have to understand that these circadian clocks are not precise. One single cycle has individual-to individual variation, as well as day-to-day variation. 24h is just the approximate for the diurnal cycle. The studies that analyzed human behavior found anything between 23-27h cycles, with an average close to 25.