Patrick S

I don't think so. Legname et al is only study I know of where synthetic prions were administered, and in that study they were injected.

I loved the cake, but for anyone who doesn't like combining lemon with chocolate, just leave out the lemon cream disc, and you'll have a wonderful chocolate mousse cake. One problem I had with was with the mousse. As I understand the recipe, it directs you to whip 1.75 cups of cream to medium peaks, and chill until ready to use. This is to be folded into 10ozs of chocolate that has been melted and cooled to 114F. The problem is that if you combine chilled whipped cream with warm chocolate, the chocolate starts to sieze up and you can hardly combine them. So what I did was warm the cream+chocolate over a double boiler just enough to get them combined, chilled it, then whipped it a bit.

Great-looking pain au chocolat, Ling!

Looks really beautiful. Considering it slumps, how do you keep the edge so even? I assume you are filling the shell with rice/beans/pie weights? I have a slumpy but delicious tart dough recipe that contains ground walnuts (I sometimes substitute hazelnuts), and the directions suggest letting it slump just a bit over the edge of the pan. I find it tends to "cut itself off" over the edge of the pan and drop in quickly-congealing blobs on the bottom of the oven (That's just Lurch getting his share, I figure,) and the result is a fairly even edge; but it's messy. ← I use pennies as pie weights, set over parchment. What I did with that crust was unroll the crust over the tart pan, press it in, and roll off the excess with a rolling pin. I guess what is really happening is the tart shell is shrinking rather than slumping. I'll try your suggestion next time and see how it works.

Interestingly, a similar relationship was found for Kuru. Members of the Fore with the MM genotype at Codon 129 of the PRNP gene appear to have had a much shorter latency period, and to have progressed more rapidly to death than those with MV or VV genotypes. Thus, the cases that occurred in children were mostly in people with MM, whereas cases that occurred in older adults were mostly in people with MV or VV. It remains to be seen whether vCJD will fully develop in humans with MV or VV genotypes, but it is, I suppose, sadly possible that it just has a very long latency period in these people, and the first cases will appear in years to come. It's also significant to point out that Kuru killed over 1100 people between 1957 and 1968, according to the Wikipedia article, whereas vCJD has claimed something like 150 lives. Regarding the state of the debate over vCJD today, I think its fair to say that there is little disagreement as to whether there is some type of infectious agent in cows with BSE that causes vCJD in humans. The debate that has occurred has been mostly about the nature of the infectious agent itself, specifically whether or not it possesses any nucleic acids (e.g. RNA or DNA). There is plenty of evidence that, taken together, convinces me that TSEs are indeed transmitted by an infectious agent that it protein-only, and does not contain any nucleic acids. For instance, you can take a sample of brain homogenate from a BSE infected cow, expose it to chemicals that normally decompose nucleic acids, yet the homogenate retains infectivity. There have also been a couple of papers over the past couple of years that seem to provide fairly strong support for the protein-only position. Legname et al (2004) induced "BSE" in mice using purified proteins generated by transgenic bacteria that were engineered to produce PrP. Link Legname et al, 2004. Synthetic mammalian prions, Science 305:673-6.

I finally made the Riviera from the first Desserts book. I've been wanting to make this for a long time. My version of the cake consists of, from top to bottom, flourless chocolate cake, chocolate mousse, more cake, thin layer or mousse, thin layer of lemon cream, more mousse, another layer of cake, and some cocoa powder.

Here's what the pound cake looks like. Several days later, and its still great stuff. Sweet, dense, vanilla goodness.

I'm not sure of the total fact of that statement, but there is a relation between prions and an open reading frame on Chromosome 20 in humans. ← There is at least one genetic polymorphism that does appear to be associated with increased susceptibility to vCJD. The gene PRNP, which codes for the PrP protein. The PrP protein, of course, is the "prion" protein that is thought to become modified and play the dominant role in transmissable enchephalopathies, so it would make sense that genetic variations in the gene that codes for that protein would be associated with susceptibility. PrP is 145 amino acids long. Each amino acid on the PrP protein is coded for by a group of 3 DNA bases on the PRNP gene called a codon. Codon 129 of the PRNP gene can code for the amino acids methionine or valine. Since each person has two copies of this gene in their genome, any person can have one M and V (heterozygous), M and M (homozygous), or V and V (homozygous). In the general population, what we find is 50% MV, 40% MM, and 10% VV. However, amongst humans with vCJD, all tested have been MM. In 2004, however, it was reported in the Lancet that one person who had contracted vCJD was a MV heterozygote (Peden et al, 2004). This person died of something other than vCJD, and did not have any symptoms of neurolgical disease, but had recieved a blood transfusion from another person who later developed vCJD. Upon his death, tests showed the presence of the mishappen PrP protein in his spleen and one lymph node, but none were detected in his brain. So, maybe this means that heterozygotes get vCJD, but that they have a much longer latency. Or it may mean that the abnormal proteins can't get to the brain and cause vCJD. Nevertheless, it is still significant that no clinical case of vCJD has ever been found in the 60% of the population that is MV or VV. Peden et al, 2004. Preclinical vCJD after blood transfusion in a PNRP Codon 129 heterozygous patient. Lancet 254, pp. 527-529.

I tried your pound cake recipe, Becca. I love it! I halved the recipe to make 1 9x5 loaf. I've been on a vanilla kick lately, so I doubled the amount of vanilla the recipe called for, plus added some tahitiensis vanilla beans. My cake was done in about 53 minutes. I'll try to add some pictures later.

Great-looking desserts, Megan and Klary. I made another tart, the caramel custard tart from The Secrets of Baking. I used the pate sucre recipe from Cook's Illustrated's perfect lemon tart recipe. I like this tart dough pretty well, though it has a habit of slumping down a little when it is blind baked, making the tart a little shallow. My MIL was literally raving about how much she liked this tart. I thought it was delicious too!

Billington's claim could be a little confusing, since all brown sugar is sucrose+cane molasses, in a ratio of 16:1 to 32:1 by volume. The difference is that some brown sugars are made by simply refining raw sugar to the specified sucrose:molasses ratio (16:1 for dark brown and 32:1 for light brown), whereas other brown sugars are made be mixing molasses back into completely refined sucrose. A major difference between these two methods is that if you are mixing refined sucrose with molasses, it doesn't matter if the sucrose comes from beets or from cane.

I use one of those. Only cost me a few bucks and it works great. Unless I want the garlic practically pureed, thats what I always use.

Yes. I've made this recipe for chocolate baklava twice, and think its delicious. The crust was fine, but not really outstanding, IMHO. Overall the tart was delicious. I forgot to point out that I cooked the filling with 3 lemons worth of zest, which I strained out at the end.

My understanding, which may be incorrect, is that any mixture of sweetened milk/cream and eggs is a custard, and pastry cream is just a custard thickened with corn starch.

Last night I made Thomas Keller's lemon tart with pine nut pate sucre. Recipe

You'll always be welcome at my place, sweets. tarteausucre, your cake looks delicious. I love raspberry and chocolate. Ling, you're making me crave pound cake. As much as I like dense, deadly rich cakes, I'm surprised I haven't made more of them.

I often use Cake Bible, or King Arthur Flour weight approximations as well. One thing that gets me is this - RLB has three weights for flour - sifted, dip and sweep, and lightly spooned. How do I know, when a recipe doesn't specify, which one I should take weights for? Should I assume sifted always? ← Well, that's the problem, isn't it? If the recipe doesn't specify, all you can do is guess. I will say this, in the vast majority of recipes I've used where both weight and volume are specified, the weight of AP flour is given as 5oz per cup, which is a dip-and-sweep weight.

Ok, I realize this statement was made over two years ago, but NVNVGirl, if you are still around, would you mind substantiating the claims you make above? I have been unable to find a single documented case of death or respiratory failure resulting from inhalation of emissions from overheated Teflon cookware. So, I find remarkable your claim to have seen "people", plural, on ventilators, plural, as a result "teflon posoning."

I missed this yesterday. The first sentence in the above is, at best, highly misleading. The following is cut-and-pasted from what I wrote on another thread, summarizing the EPA's very own draft risk assessment of PFOA: START SELECTION I just got done reading the EPA's draft PFOA risk assessment, and it includes some very interesting information. Regarding studies that have examined the effects of PFOA exposure in humans (as opposed to high-dose rodent experiments), the draft assessment states: It is true that PFOA, like approximately half of all chemicals tested in high-dose feeding studies, is a rodent carcinogen. In particular, high-dose rodent experiments show an increase in liver and pancreatic tumors. However, the draft assessment points out that the mode-of-action [MOA] for these tumors is such that humans are much less susceptible to such effects. For instance, the draft assessment points out that PFOA causes liver tumors in rodents by acting on what are called peroxisome proliferator-activated receptors (PPARs). These are receptors on hepatocytes (liver cells) which, when over-activated, cause the proliferation of certain cellular organelles called peroxisomes. The details are not really important, but what is important is that compounds that cause rodent tumors by a PPAR mode of action do not cause tumors in other species, such as guinea pigs, dogs and primates. One of the reasons may be that human hepatocytes have only 5-10% the PPARs that rodents have. Confirming this, the draft assessment reports that there was It is also interesting to note that, according to this article, the rats that developed the liver tumors were being dosed with PFOA at a concentration 25,000 times higher than what is currently being found in human blood (125ppm versus 5ppb). In sum, not only is it doubtful that PFOA can cause human liver cancers at all, it is clear that humans are ingesting doses many thousand times lower than that which causes liver tumors in the most-susceptible species. The mode of action for rodent pancreatic cancers also casts doubt on the relevance of PFOA to humans. It is thought that the pancrease tumors in the rats is caused by an increase in cholecystokinin (CCK). As with the PPARs, CCK receptors are much lower in humans than rodents, and the "cynomolgus monkey study with PFOA did not demonstrate any compound-related effects on CCK levels." SNIP 4. PFOA is a rodent carcinogen, but the mechanism by which it causes rodent cancers is species-specific and probably not relevant to humans, according to the EPA draft risk assessment. 5. PFOA has not been shown to cause cancer in any non-rodent species. 6. PFOA has only been shown to cause cancer in rodents at doses that are many thousands of times higher than that found in human blood. END SELECTION

Last night I made beignets using the recipe from The Secrets of Baking. Yum. They're great with a little warm honey. I'm excited about the bottom picture -- not because it is a particularly good one (its not --its badly composed and slightly underexposed), but because it is the first decent food photo I've ever taken with a flash. I borrowed an old flash with a swivel head that allowed me to do a "bounce flash". After experimenting with it for a little while and seeing the possibilities, I'm planning on getting a new Sigma flash (two of them actually) for my camera that will finally give me complete control over lighting. The top photo was taken under natural light.

Thanks filipe. Since a picture is worth a thousand words, as they say, demos like this are really invaluable.

Very cool. Such flawless-looking construction. If ony I could make a tart shell as geometrically perfect as the one on that page. . .

I thought about trying that too, but I worried that in the time it would take to measure the temperature your yolks would partially curdle from the contact with the hot syrup. Beranbaum advises you to add a small bit of syrup and beat right away, then to repeat with more syrup. ← What I have in mind is sticking the thermometer probe down into the mixer bowl after the syrup has been added, while the mixer is operating. You wouldn't want to try this if you are using a newer mixer, becasue the probe will get hit with the beater. My mixer, however, is an older model, with stationary beaters and a rotating bowl, so its easy for me to take the temp without stopping the mixer.

It would depend on a number of things, including how warm the yolks are to start with. My understanding is that Salmonella is basically eliminated instantly at 160F, but 145F will give the same result after 3 minutes. If you start with yolks that are heated in a water bath and add a cup of 220F syrup, you're a lot more likely to reach 160F than if you start with yolks right out of the fridge. I don't know how hot neoclassic buttercream gets right after you add the syrup. Next time I make it, I'll note the temp of the yolks, the syrup, and the mixture, and let you know what I find.

I also think that most of the macaron recipes I've tried have been too sweet. Lebovitz's recipe, for instance, has 165g of sugar to 125g almonds/whites/cocoa. Herme's recipe, by contrast, has more almonds/whites/cocoa than it does sugar (250g sugar/265g almond+egg whites+cocoa). The recipe posted by Nicole Kaplan is intermediately sweet, with a ratio of 500g sugar/467g almond+egg whites+cocoa (assuming 30g of cocoa). To put it another way, DL's recipe has a sugar-to-other stuff ratio of 1.32, PH's has a ratio of 0.94, and NK's recipe has a ratio of 1.07. I recommend trying Herme's recipe. Its the first one I tried, its still my favorite, and I think the sweetness level is just right.