Patrick S

Now, I know Wendy said to use my best judgement, but I'm also the same person that has no idea how many that 5 lb. roast is going to feed in the end either. I'm clueless when it comes to knowing how much a pile of ingredients is going to end up as. And toffee is certainly not something I would want to be messing around with while I'm searching for a pan to put it in. Also, I've tried the above brownie recipe in a regular 12x9 pan, and it didn't work! Does anyone have the answer to the above question? I'm sure it's a simple answer and I've just made a baking ignoramous out of myself! ← Without seeing the recipe, it won't be possible to answer that question. Most brownie recipes call for 8-9" square or a 13x9" pan. If you tell us what the recipe calls for, we can determine the volume of the ingredients and tell you which pan would be best. When you tried the recipe in the 12x9, what do you mean that it didnt work? Did it overflow the pan, was it thin as a pancake, did it not set?

You mean there is a way to feed yourself without killing living things?

Good luck quitting, but do you think that keeping a cigarette nearby and readily accessible is a good idea? I quit cold-turkey after 13 years of pack-a-day smoking, and knowing that I would have to drive to the store for cigarettes was actually helpful. It would have been way too tempting to have had one in the trunk.

Thanks so much for the compliments, Ling and filipe! I hope you'll be taking your camera with you to Paris, filipe! Regarding the Plasir, I made some thinner chocolate sheets and reassembled some of them, and it was even better. The sheets should really be just a smear on the acetate, IMHO. If they are too thick, they obscure the other textures. If they are really thin, you get all the textures recognizably -- the chewy dacqouise with crunchy hazelnuts, the "fudgy" Nutella and ganache, another bit of crunch from the chocolate, and a smooth creaminess from the milk chocolate whipped cream. I had some time after work today, and some good light, so I tried to get a better shot of the Riviera. I ended up getting one I like better.

I also looked a little yesterday to see what evidence there might be for Ebringer's theory that the bacterium Acinetobacter calcoaceticus causes BSE/vCJD. The answer appears to be "none whatsoever." According to the first return from a Google search, Acinetobacter calcoaceticus is an opportunistic pathogen that is "ubiquitous in nature", and is "present as normal flora of the skin and throat of human beings." That's a problem for Ebringer: one of the most salient facts about BSE/vCJD is the very limited geographic distribution of these diseases (almost exclusively occuring in the UK). Why would a bacterium that is ubiquitous in nature cause disease in virtually exclusively in cows and humans in the UK? And why would the prevalence of these diseases appear to rise and fall in response to circumstances (like the ban on certain kinds of cattle feed) that have nothing to do with the bacteria?

They shouldn't be able to. The issue with the studies I've seen that use those deomposing chemicals is that they then inject the end result into mice that are predisposed to get mouse-vCJD or what ever it's called. ← Huh? Maybe you could specify which studies are you looking at, Fat Guy, because the work I was referring to was done using scrapie prions, not BSE prions, on normal sheep, not mice genetically engineered to overexpress PrP. I don't know if these experiments were repeated with BSE prions (probably, I'll look), but the point still stands: there are infectious agents that cause spongiform encephalopathy that are not destroyed chemical and physical insults that scramble nucleic acids and destroy all known viruses and bacteria. ← As an example of this type of experiment, Safar et al (2005) subjected brain material from infected golden hamsters first to a purification process that, among other things, uses benzonase incubation. Benzonase is an enzyme that basically, chops up nucleic acid sequences into sequences smaller than ~20 bases. After purification, the material was subjected to strong UV radiation, at a wavelength (254nm) that breaks apart nucleic acids. The material was then innoculated in normal golden hamsters, and sure enough, still caused the disease. Towards the end of the article, Safar et al (2005) give some interesting commentary on the history of prions and the search for nucleic acids associated with them: Safar et al, 2005. Search for a Prion-Specific Nucleic Acid. Journal of Virology 79, 10796-10806.

Half the reviews really do read like that.

I tried that back in Jan 05, and also loved it. IIRC, Fernwood loved it too. If you want to make it more dense, maybe you could just leave the whites unbeaten, or use less whites?

Here is my attempt at the Plasir. I followed the recipe in the book, with the following exceptions: 1) I used some caramel ganache that I already had stored, 2) I substituted almonds for hazelnuts in the dacquoise, so it was an almong dacquoise with toasted hazelnut halves rather than a hazelnut dacquoise with toasted hazelnut halves, and 3) I made them as 4" rounds rather than 2x4" rectangles. One thing I will do differently next time is try harder to make the chocolate sheets as thin as possible. I was afraid of getting them too thin, so I ended up having some of them too thick.

No. A stand mixer will make some jobs much easier (like breads or marshmallows), but most things you can do with a very inexpensive hand mixer, or even by hand.

In summation, there is believed to be some risk of leeching carcinogens, and of course any food product being porous and absorbent coming in direct contact with PVC could be risky. And as ascertained in the article, heating the PVC will definitely release carcinogens. I think it'd be better just to not risk it. ← There's only one problem with your analysis -- rigid PVC pipe, the type that would be used for cake and mousse rings and water pipes, does not contain plasticizing phtalates. These are only used in soft plastics made with PVC.

Can you show a single example of tranmission of spongiform encephalopathy via eating beef? ← If by 'beef' you mean the muscle tissue of cows, then I'll repeat what I said above: I don't think beef per se is responsible for the transmission of BSE or vCJD. Rather it is the presence of small amounts of high-risk materials (e.g. nervous system tissue, intestines, lymph nodes, spleen) that sometimes works its way in to the beef during processing. If beef per se was infectious, we really would expect an enormous number of vCJD cases in the UK, rather than the 150-ish so far noted. Now, if the question is can I show case of spongiform encephalopathy transmission via those materials, the answer is absolutely, just check out the references I've already provided.

They shouldn't be able to. The issue with the studies I've seen that use those deomposing chemicals is that they then inject the end result into mice that are predisposed to get mouse-vCJD or what ever it's called. ← Huh? Maybe you could specify which studies are you looking at, Fat Guy, because the work I was referring to was done using scrapie prions, not BSE prions, on normal sheep, not mice genetically engineered to overexpress PrP. I don't know if these experiments were repeated with BSE prions (probably, I'll look), but the point still stands: there are infectious agents that cause spongiform encephalopathy that are not destroyed chemical and physical insults that scramble nucleic acids and destroy all known viruses and bacteria.

I'm not positing anything. I'm a writer not a medical researcher. So I can only answer your question by giving examples of what real researchers have posited. For example, Alan Ebringer, professor of immunology at King's College London, posited that vCJD, BSE, etc. could be autoimmune diseases or similar to autoimmune diseases and that the damage could be caused by the body's reaction to an infectious agent. Specifically, the agent he identified was Acinetobacter calcoaceticus. He found that cows with BSE also had high levels of the antibodies that attack Acinetobacter, and that these same antibodies might attack brain cells. So he theorized that "Prions are not infectious particles. Instead they are the breakdown products of damaged nervous tissue." ← I'm not a writer or a medical researcher either, or even a college graduate for that matter, but a couple of obvious questions about this theory leap to mind immediately. First, is Acinetobacter calcoaceticus limited to, or enormously more prevalent in the UK compared to surrounding countries? Second, and this one is really obvious, do cows given doses of Acinetobacter calcoaceticus develop BSE?

Well, anyone who has even a passing familiarity with the history of science will recognize immediately that just about every single well-established theory today was originally thought to be counterintuitive. As it turns out, the universe is very, very weird. Geocentrism was weird. Germ theory of disease is weird. Genetics is weird. Plate tectonics is weird. General relativity is weird, and certainly science-fictiony. Quantum mechanics is weird. Stellar mechanics is weird. The expansion of the universe is weird. If you'll pardon me for saying so, I don't find the fact that Fat Guy or any other person finds the prion theory "weird" to be a strike against it. See what I mean? If you think that protein folding and protein misfolding is "science-fictiony," you might want to read an introductory text on molecular biology. Its a fairly well-understood phenomenon and is fundamental to all sorts of cellular processes. And if you think that inert infectious agents sound science-fictiony, I'm puzzled as to why you would think viruses are any less so. Just like prions, they are inert until they can interact with other biological materials. You continue to imply that little or no effort has been devoted to finding a bacterium or virus associated with BSE/vCJD. Not only is this simply incorrect, you have yet to explain how a virus or bacterium could survive treatment with nucleic-acid decomposing chemicals. Maybe there is a good explanation and I just haven't heard of it. If so, I'd love to hear about it. ETA: Fat Guy's saying that prion theory sounds weird and science-fictiony reminded me of a quote, but it took me a minute to recall what it was. It was this quote from Richard Dawkins: ""Never say, and never take seriously anyone who says, 'I cannot believe that so-and-so could have evolved by gradual selection.' I have dubbed this kind of fallacy 'the Argument from Personal Incredulity.' Time and again, it has proven the prelude to an intellectual banana-skin experience." Richard Dawkins - River out of Eden

Because the gels are (or were during the relevant time period) made from cattle byproducts. People were getting cattle byproducts into their systems in many ways, not just by eating beef. So even if it's true that BSE can jump the species barrier and cause vCJD it's not clear that eating beef is the method of transmission (and it almost surely wasn't in the case of the vegetarians who got it). ← Thank you for the clarification. First, let me point out that there is no doubt whatsoever that the agent that causes BSE in cows can "jump the species barrier" and cause spongiform encephalopathy in other species. You appear to be conceding this point, so forgive me if I beat a dead horse, but I do want to make this clear. For ethical reasons you cannot take material from a BSE-positive cow and feed it to a human, but you can literally take a little bit of brain from a BSE cow, feed it to primates in a single oral dose, and see the primate develop vCJD-like spongiform encephalopathy a few years later. This has been shown with macaques (Lasmezas et al, 2005) and lemurs (Bons et al, 1999) and other species. And further, these animals not only develop spongiform encephalopathy, they develop spongiform encephalopathies that are basically identical to vCJD but different from other spongiform encephalopathies such as scrapies (e.g. Collinge et al, 1996; Hill et al, 1997; Bruce et al, 1997). Even more compelling is the study by Scott et al (1999). As I said above, you can't give a healthy human a dose of brain from a BSE cow. But what you can do, and what Scott et al did do, is take brain from a deceased human that died of vCJD, and brain from a cow that had BSE, administer both materials to genetically identical mice, and compare the effects. When they did this, they found that "The incubation times (approx 250 days), neuropathology, and disease-causing PrP isoforms in Tg(BoPrP)Prnp0/0 mice inoculated with nvCJD and BSE brain extracts were indistinguishable." Second, if gels were contaminated with the BSE agent, wouldn't western blots detect this? If so, were is the evidence for this? It is estimated that hundreds of thousands of BSE positive cows entered the food chain in the UK, now where is the evidence that the BSE agent entered the pharmaceutical chain? Can you show a single example of tranmission of spongiform encephalopathy via a pharmaceutical gel? It may well be the case that some of the vCJD cases were spread by a mode other than food, I'm just curious to see what the evidence is for this. For the record, let me clarify that I don't think that steaks were responsible for transmitting the BSE agent to humans. I would think it much more likely that ground beef with bits of high-risk materials is much more likely. Third, obviously you are right that someone who hasn't eat beef can't have been exposed to the BSE agent by beef. I've only read about one vegetarian who developed vCJD, and this person is said to have worked for years in a pet shop that sold feed made with higher-risk cow materials, and thus almost certainly could have been orally exposed to the BSE agent, perhaps by inhaling small feed particles. Further, there are at least a couple of cases where the vCJD agent appears to have been transmitted person to person by blood. So, I agree with you that eating beef is not necessarily the only mode of transmission. Again, where is the evidence? What kind of a bacterium could be so good at evading detection? How could even the bacterium's nucleic acids be so good at evading detection? As I already pointed out, we know that you can take the material from a BSE infected cow, subject it to chemical or physical insults that are known to decompose nucleic acids, and yet the the material retains its infectivity. How is that consistent with a bacterium being the causal agent? I have read that you can take the original infectious material from a cow, purify it until nothing is detectable but the PrP-res, and it is still infectious.

There was little disagreement last week that low-fat diets would reduce heart disease. Of course there was. There have always been plenty of nutrionists arguing that total calories, not proportion of calories from fat, was much more important. This is not the case with the BSE-vCJD theory, where virtually all of the critics of the prion hypothesis agree with the prion proponents that some type of infectious agent in cows with BSE causes vCJD in humans. Having never applied for a grant to study these diseases, I can't comment on the these difficulties. However, I do know that often when people claim that they can't get a grant to study hypothesis X, their failure to get a grant is not due to irrational bias on the part of the money-people, but rather to the fact that there already exists good evidence that the hypothesis is a dead-end, or that other line of research seems like a much better bargain for the money. In the case of BSE, there has in fact been lots of work done trying to find a nucleic acid sequence associated with the disease pathogen, as there must be if it is a virus or a bacterium, and so far it can't be found. I'm perfectly willing to consider these alternative theories, so let's start with some basic observations and see how well the different theories fare. I promise I'll try my best to give your alternate theories evey benefit of the doubt. 1. Brain homogenate can be taken from a BSE-positive cow and injected into primate and other mammals, causing a vCJD like disease. How would, let's say, pharmaceutical gels explain this observation? 2. The strong temporal (allowing for latency period) and geographic association of BSE and vCJD in the UK, and the decline in vCJD in the UK the ban on feeding MBM to cows. Why have virtually all of the vCJD case occurred in the UK? How do pharamaceutical gels explain the observed temporal and geographic paterns better? The study is usually cited as Legname et al because that is easier and more convenient than citing it as Legname, Baskakov, Nguyen, Riesner, Cohen, DeArmond, and Prusiner. That's just standard practice for citing journal articles, and anyone who follows research in this area (or just reads the author list), understands that these researchers have collaborated on many other papers in this field. I'll read the study again tomorrow more closely, but my understanding was that the mice in this study that recieved the control injections developed no signs of disease, while those that recieved the synthetic prions developed disease, that, even more interestingly, the diseased mice could then be used to innoculate and cause that same disease in wild-type mice, who did not overexpress PrP. So, if we accept for the sake of argument that the spongiform encephalopathy seen in the mice given synthetic prions was largely due to those mice overexpressing PrP, how was it transmissable to the wild-type mice? Also, there was another paper published in Cell in 2005 that is significant in this regard. It used wild-type hamsters, not mice that overexpress PrP. I'll include the abstract and maybe we can discuss this some more in a few days. In the meantime, I look forward to seeing you make the case that pharmaceutical gels are playing a causal role in vCJD. Castilla et al. 2005. In Vitro Generation of Infectious Scrapie Proteins. Cell 121, 195-206.

Maybe I am missing something, Patrick, but I am very much under the impression that viruses can be and are cultured. Perhaps there is a semantic misunderstanding? ← If you go back and look at postulate #2, I specified "pure culture." Pure culture refers to " A nutrient medium containing the growth of a single strain of an organism free from other living species or strains." Of course viruses can be cultured, for instance using tissue culture (which is how viruses are usually cultured) or even innoculating a living organism, but not in a pure culture, and I don't imagine that is how Koch understood his own postulate. I haven't read Koch, so I could be wrong, but if he did in fact require growth in a pure culture as his 2nd postulate, then viruses could not fufill that posutulate.

Can anyone point me to the appropriate part of the paper? ← The technique that Legname et al used to change the conformation of the PrP proteins was described in a previous paper by the same group (Baskakov et al, 2002), which is reference (11) in Legname et al. The procedure involves constantly agitating the proteins in a mildly denaturing, 37C solution with a neutral PH. Baskakov et al, 2002. Pathway Complexity of Prion Protein Assembly into Amyloid. Journal of Biological Chemistry 277, 21140-21148.

Of course I don't mind, and the ingredients were: 1C butter/1C sugar/2 eggs/0.5C buttermilk/1.5C flour (mix of AP and cake). I can't recall how much leavening was in the cake, but it wasn't much -- around .25-.50t baking powder.

Lemon pound cake from The Secrets of Baking. Unusual texture. Overly dense. Delicious, but not the best ever.

Do you really have to ask, Alan? I would love to see the process you're using.

Koch himself realized that Koch's Postulates were far from hard and fast rules for establishing that a particular agent causes a particular disease. And in fact, Koch proposed them for the bacterial illness he was studying, not viruses and certainly not prions. Koch's first two postulates were: 1. The organism must be found in all animals suffering from the disease, but not in healthy animals. 2. The organism must be isolated from a diseased animal and grown in pure culture. Regarding (1), Koch himself realized that there can be asymptomatic carriers of a pathogen. "Typhoid Mary" demonstrated this a century ago, while Koch was still alive. Today we know this is true of lots of pathogens, like Cholera, Polio, Hepatitis, Herpes, HTLV, and HIV. This is not surprising, since we now know, as Koch could not, that there are myriad genetic differences between individuals that affect susceptibility to virtually all infectious diseases. Regarding (2), if prions really are protein-only, do not self-replicate, there is no way they can be cultured (i.e. grown in a petri dish on nutrient media). Viruses also can not be cultured.

Here's a link to the article by the Earth Policy Institute mentioned in the article: Bottled Water: Pouring Resources Down the Drain

I don't think the results for breast and colorectal cancer are too surprising, given the inconsistent findings in previous studies examining the relationship between diet and cancer. The findings about heart disease and stroke are much more unexpected. And in support of this, the paper that covered cardiovascular disease did note that "[t]rends toward greater reductions in CHD risk were observed in those with lower intakes of saturated fat or trans fat". On the other hand, given that the study had almost 50,000 participants and 8 years of follow-up, and still found only a statistically insignificant trend towards reduced CHD in those with lower intake of sat and trans fat, it may be that even differences in the types of fats consumed have only a very modest impact on CHD risk.