CharonY

This is kind of off topic, but this is actually quite an interesting point. The problem is, of course that without extensive studies it is hard to figure out if a treatment really cures cancer, or whether it was just an isolated event in the lab. Of course patients with terminal cancer are prime candidates for the early rounds for clinicals as in principle they can only benefit from it. In addition, the routine timeline for clinical trials is around 6-8 years. So 50 years would probably include the discovery of a substance with yet unknown function. In fact I heard of examples of the identification of proteins that were identified around 40 years ago and are now undergoing phase II trials...

And for those that do not- welcome to the club

I think you are confusing who wants what. The companies are not per se interested in creating certain behaviors with their drugs. This is between the doctor and the patient to decide. They do provide pharmaceuticals that have demonstrated to influence conditions/diseases/whatever in a certain way that patients/doctors may find to be an improvement compared to their current condition. What precisely the drug causes is what clinical trials are for. In the given test population the reactions are monitored and communicated to the FDA who will then approve (or not) whether the given medication will be useful in treating a given condition (that is the short of it, anyway). One should also note that no medication works precisely in a given way. Organisms are terribly complicated systems and there can and will be several effects associated with any given medication. The trials are there to find out what, on average they may be. However individual differences can lead to unforeseeable results. Medicine is not deterministic and it cannot guarantee precisely the desired result. However, any medication has to be shown that in most cases improvements will be seen. In future there is the vision for individualized therapies in which omics data will be used to assess, for each person, whether any given medication may or may not be effective. But this is just a vision right now. But to answer the initial question: I cannot see how providing medication does, in any way interfere with patient's rights. Of course a doctor can misinform a patient, maybe even due to incitement by pharma companies, but that is a different matter altogether.

Let's blindfold the communicator, mix up the letters on the touchscreen and try again.

That is what I get roughly, too. Show the calculations. Also did you consider that you only used a part of each dilution (i.e. that your sample is even more diluted by a factor)?

What does gelatin consist of?

Very, actually. Just two pointers Salmonella as mentioned above and Clostridium. Read up on both.

Well, I have grown plants on nutrient medium with agar. The agar plates are whitish translucent and you can see the plant pretty well in it. The plants probably do not really benefit from the agar itself, but it allows you to solidify the nutrient solution.

Actually I would not necessarily call them equations, precisely as it conjures mathematical equations, but rather mechanistic models. Laws in sciences tend to be very specific models that can be described mathematically precisely because they are so well defined. However they do describe physical relationships rather than mathematical ones. Most constants used throughout physics and chemistry are based on empirical studies and have no direct relationship from purely mathematically derived relations. They just behave and scale in a way that can be described mathematically.

The very basic information is the order of the bases. It can refer to regions (or loci) that are coding for RNA but it may also apply to regulatory regions that are not transcribed. Nothing tells the bases how they are ordered per se, one strand just gets replicated complementary to the existing one. I.e. there is no higher ordering mechanism.

I assume that you are supposed only to count plates which have between 25-250 colonies. If there are more counting them may be considered tricky (though actually quite feasible). The other reason may be that, if you look at the numbers, there was obviously some kind of mistake between 10-4 and 10-5 dilutions. Yes, you count the colonies for each plate and then calculated back based on the dilution on how many were initially in one ml. In theory you would also want to give average and standard deviation but with two data points it is not very informative.

The description of the experiment is missing (what is being measured with what means). That being said it appears to me that only a description of what the differences between the enzymes might be is asked (what does the Km and Kcat tell you, describe the differences). Without knowing what experiment that is I can only guess but I think this should be sufficient. Especially as those abbreviations generally are not helpful in identifying them nor do I think that the sequence will help you in any way.

There is some weird use of amplification here. Once inserted the plasmid may or may not be replicated in a given cell. If the gene product is not the desired one, generally a different strategy (e.g. different vector) has to be employed. Amplification generally for PCR reactions of particular DNA sequences which does not make sense in this context. Again, you amplify the gene you want to clone, put it into the vector, then into the cell. There is no need for further amplification unless you want to verify the gene inside a given cell. Generally integration occurs via homologous recombination. If there are sequence similarities between vector and chromosome (regardless of whether it was in the cloned fragment or the somewhere else on the vector) it can integrate as a whole into it. Depending on whether a second event occurs the whole plasmid or parts of it can be integrated. Additionally the plasmid can be lost again with, or without the exchange of the homologous region. The rate of the event depends on the similarity and the length of the respective sequence. There are several counter-selection methods out there. It works by disrupting a given gene due to the successful integration of a fragment into the MCS. In other words, the loss of the function of the counter selective gene, you can determine which of those which have been selected for the presence of the plasmid also have an insert. It does, of course not tell you whether it is the correct fragment so that you would have to make a another analysis (usually analytical PCR , sometimes with digestion or Southern). Fusing the fragment in question with another functional gene is more cumbersome and then you have the problem that you still have to verify if your fusion-construct is correct. This kind of defies the convenience that you get from the standard cloning vectors. Counter selection can be based on the classic blue-white selection or what many have, based on suicide genes. That is, genes without a disruption of the gene (i.e. with an insertion of a desired fragment) will die under selective conditions. So by including the selective properties of the vector only those cells survive that a) have the vector (e.g. selected by AB resistance) as well as a disruption in the suicide gene by a cloned fragment.

First thing is to determine what kind of microorganisms are supposed to grow on the plates you used. This will limit the overall possibilities. The problem with fungi is that they tend to be a tad unspecific if grown on bacterial media. The diameter is itself not diagnostic as they continue to grow, of course. To put in other words, if the medium is highly selective and if what you have was a bacterium then the colony morphology itself could provide good hints on what possibly could be there, but if it is a fungus and the medium is just a full medium I am not sure how the teacher can expect proper identification without further analyzes. And btw. fungi tend to be a bit more unspecific in their habitats (or so it appeared to me). It is quite possible that the fungi were growing due to some contamination (i.e. they were not actively growing on chicken). And if the medium is highly selective it is possible that you won't get anything grown from chicken (I assume it is not a live one). And only now do I realize that actually two people have asked the same question.

So it is better that the limits are defined by the insurance companies?

What precisely do you have trouble understanding?

jimmy, it is not quite correct to say that the carriers of the genes are not important. The gene-centered view just sees them as vehicles. As such it almost mean the opposite of If you are good at surviving as an organism then the genes also survive.. The reason for the gene-centric view is that organisms exhibit behaviour that are precisely contraproductive for survival. But they are important for successful procreation. From the viewpoint of an organism this behaviour is bad for survival. From the viewpoint of the gene, it precisely allow its survival. The survival of the gene, that is. And rather not try to divine the meaning from pioneer's post. Last time I tried I my eyes started bleeding and I messed up an important experiment.

If the ion concentration on both sides are equal there is not gradient through which the molecules would move. If a gradient is made by pumps the molecules would diffuse freely from higher to lower concentrated areas. This can be harnessed by specialized proteins. And just btw. proton pumps have also been found to play a role in regulating the membrane potential.

I do not see how the one follows from the other.

Do artificial cat brains dream about computer mice?

Emotions come in if one is on the receiving end, I presume. Say, you got cancer and a 100k treatment will be denied as studies suggest that it will prolong your life for only a week or so. Or if a DNA screening shows that you got an allel which makes you unresponsive to said 100k treatment. Logically one could say that it does not make sense, but if one is desperate it is much harder to do so.

I am sorry, but I do not get the point of this post. In health care there are of course cost-benefit studies that are often a basis for standard policies. One of the problems with the cost, of course, are end-of life treatments. I recall that the majority of health care costs are generated (obviously), and it is here where most cost-benefit analyzes turn ugly. For instance, there are certain treatments that go for around 10-100 k per treatment cycle but on average only prolong life for around 2 weeks or so. Question is whether such treatments should be denied or not. Similar questions arise for certain screening approaches. Recent studies for instance show that PSA screening for prostate cancer do not increase life expectancy (but increase overtreatment). And I have heard similar for mammographies. But in the end, for a number of treatments such studies are there. Arguably there are not enough due to the cost involved in performing them (oops yet another cost factor)...

First one is the major point although the last sentence is incorrect. The -10 to -35 region is the sigma factor binding site which does not equal the promoter region. The second is not a real issue. The mRNA of eukaryotes are also only transcribed by one polymerase species. The important bit is that each polymerase needs specific factors in order to interact with specific promoters. The thirds is also a good point. The fourth less so. The slight differences in some bacteria compared to animals may result in translation error but it does not necessary abolish the protein synthesis. However, the points mentioned above will be prohibitive for proper transcription so that translation would not occur in the first place. If we assume that those problems are corrected there are even more problems during the protein synthesis parts.

Iron-fisted dictatorship, provided the fist is mine.

Underlining is used instead of italicizing for handwritten , but not for typed notes. Unless you got an old typewriter that does not do italics. To be absolutely correct however it would be Genus sp. as sp. is only an abbreviated placeholder and not a species name.