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Lincoln Park Cultural Center
2045 N. Lincoln Park West Chicago, Illinois 60614
(312) 742-7726
Fee: Free
Age Range: Any
Soldiers are coming home from long and controversial wars. Some are healthy, some are wounded, some carry deep psychological traumas. For some, integrating into civilian society can be difficult and painful. This workshop performance of "Unraveling Veterans" seeks to relieve these traumas by working with veterans to tell their stories through dance.
Storytelling Workshop to follow performance.
The completed project will premiere at the National Veterans Art Museum at 3pm and 8pm on May 31st, June 7th and 14th 2014. All performances are free and open to the public.
Directed by Jack RyanWritten by Ellyzabeth Adler and Jack RyanChoreographed by Ellyzabeth Adler, Jack Ryan and Cast
Cast: Christopher Young, Alex St. John, Matthew Webb, Isaac Samelson, Maren Rosenberg, Jack Ryan, Lauren Parets, Lisa Leszczewicz, Shane Rhodes, Ellyzabeth Adler, McKenna Liesman
If you or someone you know is in interested in telling your story or getting involved please contact us at: email@example.com
About CDEChicago Danztheatre Ensemble challenges, engages and inspires audiences both onstage and in the classroom, through innovative, multidisciplinary storytelling in the genre of Tanztheatre, which unites all art media and to achieve an all-embracing, radical change in humankind. As an Ensemble, we collaboratively create thought-provoking arts performances and educational outreach programs incorporating elements of theatre, music, movement, visual arts and literary text. We are dedicated to "performance with a purpose. www.danztheatre.org
CDE is in residence through the Chicago Park District's Arts Parnter in Residence Program, which unites artists and communities in Chicago's parks.
About Team Red, White and BlueTeam RWB is transforming the way that America supports its veterans when they return from combat. We are creating communities of veterans, their families, and American citizens that enjoy authentic interaction through physical and social activities and events all across the country. Our chapters and communities deliver consistent, local opportunities for veterans and the community to connect through physical and social activity. They host weekly fitness activities, monthly social events, and participate in local races and events together. These programs are at the core of Team RWB?s mission. Join the team at http://teamrwb.org/get-involved/join-the-team
Support for "Unraveling Veterans" provided by the Boeing Foundation with additional support from the Richard H. Driehaus Foundation, the Illinois Arts Council, the Gaylord and Dorothy Donnelley Foundation, as well as many private and individual donors.


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Debate and discussion of any biological questions not pertaining to a particular topic.
Moderator: BioTeam
4 posts • Page 1 of 1
Even very moderate drinking during pregnancy appears to cause subtle but long-lasting damage to the baby, according to a study released yesterday, adding hard and daunting data to recent research that backs the old precautionary advice to abstain.
The study, published in the journal Alcoholism: Clinical and Experimental Research, found significant learning deficits in the grown offspring of rats that had consumed low levels of alcohol during pregnancy. Those findings in rats followed a study published last month that found that children of mothers who drank, even lightly, during pregnancy grow up measurably smaller than the children of teetotalers.
"What the data shows is that something equivalent to probably one-and-a-half drinks a day produces increased risk that there could be subtle brain damage which may not become apparent until a child is older," said Daniel Savage, chair-man of the Department of Neuroscience at the University of New Mexico Medical School and lead author of the rat study.
Federal health officials estimate that of the 4 million American women who get pregnant each year, more than half a million continue to drink: about 120,000 in the moderate-to-heavy range of seven or more drinks per week, and 400,000 in the light-to-moderate range;
So, a woman orders a jumbo strawberry margarita at my workplace, but from studies in biology alcohol can harm an unborn child.
What are the problems in this situation? (if any) who are the affected parties, Possible options open to you including:
- bring the customer her drink
- refuse to serve the customer alcohol
- ask the bartender to make this drink without alcohol
- show the warning label to the customer – other
what would be the best option?
Re: FINDINGS GROW THAT ALCOHOL HARMS FETUS
Is this a real thing or some hypothetical where there is very little science going.
What happens if your manager forces you to serve the customer, you going to give up your job over it? Probably not right
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University Marketing and Communications plans and implements integrated marketing communications strategies to enhance UMSL's overall brand awareness, institutional reputation and student recruitment.
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The Implausible Engines of Evolution
Discussion of everything related to the Theory of Evolution.
Moderator: BioTeam
The Implausible Engines of Evolution
I was reading my textbook's chapter on evolution (Miller) and found that evolution had several different types of engines which it runs by. I was looking at the various mechanisms, and I had some questions and doubts. I thoroughly disagree with evolution on account of several holes in the theory, but I have been repeatedly told that i am "dumb", "uneducated", that I "don't know what I'm talking about", and wrong. However, not one evolutionist has bothered to answer my questions or clear any misconceptions I might have. Answering to my statements rather than a cop-out would be much more productive. I would appreciate if I could get some REAL answers accompanied with SOLID evidence, not porous conjecture. I would also like to know the specifics of how evolution explains HOW these engines work.
Mutations, as stated by the book, are mostly lethal. However, evolution is predicated upon the random possibility that those mutations are positive. Evolution sais that most aren't, and there are the rare few that are not. Add to this the random chance of a beneficial mutation, and this becomes highly implausible. Even if by chance there was a beneficial mutation, it is only passed down if both mates have the mistake in DNA. A mutation is not a trait that can be passed down, but it is a mistake in DNA that randomly occurs and has a very low possibility of ever being a beneficial mutation.
I was reading the Miller book, and it had the same conclusion about evolution which I had deduced from a long time ago without reading the book: the genetic information has to already be present in order for it to appear in the population. Often, favorable genes are recessive (f), and the other unfavorable gene is dominant (F). If this is so, wouldn't the statistics presented by the punnet square only allow 25% to have the favored gene (ff), and 50% to be carriers of that gene (Ff). I understand from the book that 100% can have the favorable recessive gene if 2 that are ff mate, but that would be a miracle generation because of the small chance of them meeting. Also, if ff and ff mate, then 4 ff offspring are produced. The 4 offspring have to mate with other genes, Ff and FF (preferably Ff) in order to maintain genetic diversity and eliminate a "kissing cousins" situation. This need to mate with others also prevents differential reproductivity and keeps the population of favorable genes (ff) proportional to the population to other genes (Ff and FF).
The book states that this is competition between 2 species, thus causing the two to adapt to each other and strengthen each other's genes. My question is WHERE does the genetic information come from? As previously stated, the book sais that the information has to be there PREVIOUSLY. And if there previously, did it have those adaptations when that species had first appeared? I think no because the adaptation is a genetic response to a threat, environment, etc. Therefore, how could it have those adaptations when the species was never threatened? Also, if the individual never had this adaptation, and the adaptation was never present in the population, how can it appear as genetic information when the threat begins? Wouldn't the individual perish rather than adapt? By then, it has no adaptation. Also, how do individuals who have never encountered this threat able to adapt to it, especially since the threat which has not been adapted to kills individuals that it comes in contact with. Despite these obstacles, how is this possible?
4)Evolutionary Divergence
The book tells me that this creates specialist species, which result from generalist species. The book's example of this is the variety of honeycreepers. However, where is the fossil of the common ancestor? Also, one example by which evolution is founded are the finches on Galapagos island. Assuming they have been there for quite some millions of years, or several hundred thousand, why has a common ancestor fossil not been found on Galapagos island? Also, according to the book, the genetic information has to be previously present. All the genetic information for each finch's dietary preference, color, type of beak, etc must all be in the ancestor. Therefore, the ancestor should be able to lay eggs, each with a different type of finch because all of the genetic information is present in the ancestor and each type of finch is simply a genetic trait that determines the different finch in each egg based on dominant or recessive traits. Otherwise, how can one finch, without the traits for different finches in its DNA, possibly produce different kinds of finches? Continuing on this deduction: If all finches are from the same ancestor, and all finch types are traits, they should also be able to mate with each other and produce different finches already present in genes from the ancestor. However, this is not observed in the natural world at all. Am i wrong in this? I have simply deduced from information in the book what is necessary for evolution to be true. However, these things are not observed in the natural world. If not be these devices and very slim possibilities are not how evolution developed the finch, please elaborate.
-facts, observed events, plausible explanations, and solid evidence
I am sorry but you certainly seem to have misunderstood a whole lot of things, and maybe it is no wonder if evolution seems implausible to you. I do not have time to cover all aspects of your post now, but I'll start with a few and maybe someone else adds to them.
1) Firstly, you say that the mutation must be present in both mates in order to be passed on to following generations, but that is incorrect. If only one of the mates has the mutation, the mutated allele can be passed on to the offspring (the offspring is heterozygote for the given gene). Depending on the mutation, one allele may or may not have an effect on its own. But as generations pass and if the mutation prevails in the population, the chances are that two heterozygotes mate, possibly producing a homozygous offspring and the full effect of the mutation can be seen.
Depending on the usefulness of the given mutation against the organism's environment, the mutation may be deleted (severely debilitating mutation), it may prevail as a heterozygote (no obvious harm or benefit), or it will increase in numbers (beneficial as heterozygous or as homozygous). In certain environments even a "bad" mutation can do well, a famous example of this would be the association of malaria and sickle cell aenemia.
2) There is no such association that favourable mutations would be recessive and unfavourable ones dominant. Quite to the contrary, unfavourable genes can prevail in the population as recessive forms in heterozygous carriers even if it were lethal in homozygous form. If the same allele was dominant, it would always be lethal and so it would eliminate itself from the gene pool. If the mutated allele was not lethal but still unfavourable, it would anyway lessen the chances of its carrier's survival and thus would likely be removed from the gene pool of become very rare in the course of time.
3) I do not think I quite understood your question here. However, in coevolution the same rules apply as in "normal" evolution: random mutations give traits, good or bad or neutral, to their carriers. If there is a change in the environment (and there always is some change, or pressure), one of those mutations is likely to have some effect on its carrier's survival chances. In coevolution, however, the mutations in one species reflect to the other species as well, improving or decreasing its fitness as well.
4) Briefly: the finches can acquire new genetic material from mutations. But this need not be the case. For example, if the finches carry a gene or genes that determine how long their bill will become (similar to humans' genes for height, for example), there are finches of different bill lengths in the population, just like there are humans of different height - pretty much in a Gaussian way. Now, if on one island most of the finches' food would require a long bill to reach to, the long-billed ones would do well, mate with one another and produce more long-billed finches. If on the other island the food the finches eat would require a robust and short bill, the opposite would happen. In due time, there would be two types of quite different finches. The same idea is used when humans create different breeds of animals. This was perhaps a bit simplified example, but hope you get the idea.
And what comes to the fossil of the first common ancestor - this is one of the forever questions in evolution. Despite dozens of fossils of common ancestors that have been discovered for several species, this question always pops up. It is worth remembering that the different developmental phases of species is often very challenging to identify from fossils alone and thus often only the most obvious cases can be identified with certainty. Furthermore, the fossil record is and always will be incomplete, because, for example, many regions that once were land now remain deep under the sea, and that could just as well be the only place when this much sought for common ancestor used to live.
Hope my answers helped to cover some of your questions, and I hope I did not make many mistakes myself when trying to explain things. Perhaps others can continue from this and point out if I managed to include errors in my text.
Over & out.
Even a terrible seeming thing such as cancer-proneness can be retained. When they find it has been retained in more than one
way ( finding within an organism, the ability to go genetically cancerous by more than the one pathway) it shows the importance of something related to that apparently very deleterious effect, which is producing a net positive.
1)You wrote "even a 'bad' mutation can do well, a famous example of this would be the association of malaria and sickle cell aenemia."
I wonder if you could explain this as a positive association. I do not know of this information. Also, a bad mutation turning out to be good is rare and hardly observed in the natural world, especially when it comes to multi-cellular organisms. Also, keep in mind that most mutations are lethal, and thus they do not continue. The probability of a mutation being positive is also extremely low and very close to impossible, and has not been shown or observed to increase at the passage of time. Also, the probability of positive mutations does not increase the more mutations occur in a population.
2)I could indeed be wrong in saying that mutated genes are recessive. I did say that this was an assumption, although, it was more a deductive reason for why mutations do not dominate. However, I would like to know where it has been observed that mutations are dominant (my thing with evolution is that evolution has not been observed in the environment or replicated in the environment- I will post on "Life in a Tube" in the near future).
However, consider the probability of a mutation, then the probability of that mutation being beneficial, then 2 in that population of the same generation and of different sexes and with the same matching, beneficial mutation, and then consider the probability that they will meet and mate with each other. This is so far fetched to the point of simple impossibility.
3)Since when has a mutation in one species been observed, which is not unlikely to occur, and then even more unlikely to be positive? The probability of a positive mutation does not increase the more mutations occur in a population, and it does not increase with time. The problem with coevolution is that a mutation in one species does not provoke a genetic mistake, which must be beneficial, in another species, especially because genetics is not dictated or altered by the environment or other species. An organism's genetic make up does not change just because of a competing species or a predator or geological separation. It is a mistake, nothing more nothing less, with the extreme unlikelihood of being positive. The chromosome is not aware of surroundings. The chromosome is not a living thing. It does not change or make a random mistake that will somehow turn into a positive "adaptation".
4)Yes, evolution sais that if 2 finches in the same area feed on 2 different things, and one island has the food for one and the other island the food for the other, each of the finches will not be able to stay on the other island. This one portion of this science is excepted and observed. Not to belittle evolution, but obviously, if a species does not have food in one area, then it will not survive there. This would ring true regardless of evolution. What I am debating is the repeatedly stated "fact" of evolution that sais that 2 finches come from one finch. This common ancestor, evolutionary divergence, and genetic drift from genetic mistakes is very near impossible.
Crucible: I can see that cancer proneness can continue. However, cancer proneness is not a beneficial mutation (if it is a mutation). It is a harmful genetic trait. Imagine the possibility of a positive mutation. This is very near impossible.
Biohazard & Crucible: I encourage both of you to stay around the evolution string and look for more of my topics. I will be posting on several issues. I promised "Life in a Tube" to Biohazard, so I think I will start there. I enjoy the conversation and difference of opinion and appreciate the debate. Although, in all honesty, I am a Christian and would like to see the facts considered, and to see evolutionists move off of this theory. However, this is the only time I will include religion in the discussion. I will talk about facts etc etc. However, if you wish to discuss religion, message me. My next topic title is "Flaws of Life in a Tube". It will be much shorter than this piece, I can assure you.
-facts, observed events, plausible explanations, and solid evidence
Correction: this is not the only time I will mention religion. I will soon enough want to hear what you all have to say on the Bible, creationism, etc. But first, I will be posting a myriad of proofs against evolution.
-facts, observed events, plausible explanations, and solid evidence
Sickle cell anemia is disease, where haemoglobin is mutated in one amino acid and this causes bad-shaped red blood cells and that makes another problems. It is even lethal when homozygous. However, it is beneficial when one gets sick by malaria, because the malaria somehow cannot reproduce (see this and futher). That's the reason, why there are so many heterozygotes in the sub-saharian Africa (however, the homozygoty is still lethal).
Just take into account, that during each replication, you get about 3 mutations per your genome. With this it's much higher chance to get something beneficial, isn't it?
Moreover, you must consider, that recently we are adapted to our environment and everything, but in the origin, the enzymes and proteins were not that much adapted, so the chance that they will be improved was much higher.
yeah, it's common to assume things which are good for us
Take it the other way. Imagine there is a mutation and it is not lethal. Such individual is even able to reproduce having several offspring.Thus in the next generation there will be several individuals with the same mutation, right? If they will be able to reproduce again, the mutation will spread. And so on and so on. The level of the mutation will fluctuate, but it may rise slowly. Due to several mechanism, it can disappear or even become dominant version (in the means of representation, not domination/recessivity). Anyway, after few generations, there can easily be two individuals mating who both posses the same mutation.
However, I don't see the link to topic; how it matters.
Are you sure?
Cis or trans? That's what matters.
Jackbean: I would appreciate if you could explain our adaptation to the environment. And yes, that statistic on the frequency of the occurrence of mutations may be true. However, each mutation is an individual case, unaffected by the other. Its not like its there are 10 possibilities and one good, and as each mutation occurs, the bad options are striked until eventually the good is chosen. For each mutation, there is a extremely probability of a lethal or neutral mutation, and then the next impossible for a good mutation. The possibility does not increase with each mutation.
Hmm. Yes it is. I should look that up and research that. There should be a definite scientific fact that sais that all or most mutations are either dominant or recessive. By the way you post that comment, you attribute assumptions and a lack of truth to my personality. If I was truly morally incorrect, I would have argued with you and never admitted to the fact that I assumed that based on deductive reasoning.
3) The level of mutation will not increase. While there are those who produce the mutated gene in the next generation, there are the majority who are producing the regular gene. The growth between the two is proportional. There is no differential reproduction. Also, this mutation must be positive. This is near to impossible. Each mutation is an individual event unaffected by the other, and the probability of beneficial mutation does not increase with each mutation.
-facts, observed events, plausible explanations, and solid evidence
The current organisms are adapted to the enviroment, where they live, no matter, whether you think they evolved into such adaptation or whether they were created, right? Think about the animals in desert, who need to deal with high temperature and high water loss, or how different birds are adapted to different food sources.
Let's assume, the evolution is right for a moment. In such a case, they were not adapted like this, but they were noobs in survival in particular enviroment. Thus, the probability of beneficial mutations was much higher. However, after milions of years of evolution, they are perfectly adapted and the chance to get something even more beneficial is still lower and lower.
I didn't understand much to the rest of the first paragraph.
You're wrong. That would be true, if the population was growing, but if it's size is stable, then the number of offspring will be approx. the same each year (or generation). Thus the mutation must spread. Of course, it can be eliminated fastly, but it can also become fastly dominant. That depends on several factors, which you knew better, if you studied the mechanism of evolution better.
Cis or trans? That's what matters.
1)You said "In such a case, they were not adapted like this, but they were noobs in survival in particular enviroment. Thus, the probability of beneficial mutations was much higher."
This is the simple reality of a organism that is in an environment that it is not suited to live in, such as a canary in the desert: the organism will die. Period. An organism not suited for an environment will not reproduce, and it will not be concerned with finding a mate. An organism in the desert will not know how to find water and will not have the genetic information suited to retaining water. Thus it will die.
A threat to an organisms life does not bring about the greater possibility of a mutation. Threats towards an organism has no direct effect in altering an organism's genetic traits.
2)Keep in mind that the mutation must be positive. This is a near impossibility. It does not occur in nature. If adaptations are mutations, then this means that adaptations we see today in nature should be present in one generation, disappear the next, and then reappear. And if not successive generations, then over several generations. However, this has never been observed in the natural world.
-facts, observed events, plausible explanations, and solid evidence
1) you're taking it little bit too extreme. The evolution is not such big jumper. If the animal cannot survive, than you will have, surprisingly, no evolution. But living organisms are much versatile and have broad spectrum of livable environments.
2) you're still assuming, that the probability of positive mutation is near zero. However, as I tried to explain you, it's not that true.
Cis or trans? That's what matters.
Answer this question: are most mutations neutral or lethal?
The answer is yes, as according to Miller AP Environmental Science Book. (Chapter 5 is on evolution)
Then, if most are lethal or neutral, can the possibility of a positive mutation be not near impossible? The fact of the matter is that the probability of a positive, beneficial mutation is near impossible. If this is not so, then why does it take million of years for the theory of evolution to unfold?
The probability of a beneficial mutation is near impossible. In fact, so near, that it is impossible, thus making the engine for evolution an impossibility and the theory of evolution an impossibility.
I do not know if you have looked at my reply on the digestive system evolution, but I will relate to you something of the same. The theory of evolution sais that "life comes from life", and a prokaryotic cell, which is alive, can come from the randomly accomplished organization of chemicals, which is not alive. A complex, alive, functioning system cannot come from basic chemicals which are not alive. Chemical are not alive and thinking, and cannot start as complex chemicals arrange themselves into more complex chemicals (this is called the chemical revolution), and then the complex chemicals arrange themselves into a complex, single cell, which is the simplest form of life. And then more complex forms come from simpler forms of life. If any normal person were to use their common sense, they can clearly see this is an impossibility (you may say that I do not know how evolution works, but we have previously discussed mutations and their impossibility).
-facts, observed events, plausible explanations, and solid evidence
You seem to be underestimating the number of DNA replications occuring in the nature. Let us assume that one mutation in a billion is beneficial (just a random number for the sake of example). In terms of probability it is near impossible. But there are billions and billions germline cells produced by all organisms every hour. And since virtually every new cell has several mutations, you can calculate that among a myriad bad or neutral mutations, there will be huge amount of potentially good ones as well. Heck, a single ejaculate from a human male contains some 500 million candidates for a beneficial mutation. Of course, there is a long way to go to fertilization and a healthy baby that can benefit from their mutation. But unlike harmful mutations that get usually aborted in the early pregnancy, neutral or beneficial mutations have much higher chance to survive. Thus, even though the rate of such obviously beneficial mutations among people or animals is low, it is still a lot higher that you seem to think.
Let us take quite an extreme example of a situation where you are almost guaranteed to stumble upon a beneficial mutation: HIV and antiretroviral treatment. HIV is an single-strand RNA virus, which means it is very prone for mutations because of its lack of proof-reading enzyme activity due to one strand only and due to its RNA genome. Now, since it is prone to mutations, you would expect that many new HIV viruses have bad mutations in them and do not survive. And that is correct: big portion of all new HIV particles are inactivated and "sterile" because of the deleterious mutations. Despite this, they hide inside immune cells, where they undergo replications constantly, millions and millions of them during the course of time. And since they are under pressure from antiretroviral drugs, at the very moment there is a mutation that helps to fight the drug, that particular viral strand takes over and the disease starts to progress. If the patient is treated with only one antiretroviral drug, the virus with a beneficial, protective mutation will emerge within months - practically always. Even with the most sophisticated combination treatments there will eventually be a mutant that is resistant to all the drugs. The chances for this are so small that it can take decades to happen, but usually it will happen nonetheless.
If you do not accept HIV as a model organism since it is a virus (thus bordering the line of living vs. non-living), we can take some other similar example, such as Mycobacterium tuberculosis, which is famous for developing multiple drug resistances in the course of time if it is under selective pressure of antimicrobial drugs. Surely, many other bacteria do the same, just do not get confused with plasmid-mediated resistance here, which is not caused directly by a mutation within the bacterial genome. Furthermore, some higher organisms develop similar resistances, e.g. pest insects targeted by pesticides. However, the "higher" the organism and longer the life cycle, the longer it takes for the beneficial mutation to emerge and enrich in the population.
The examples are many and there for everybody to look upon, you just have to remove your blindfold for a minute and let yourself see them.
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Formaggio Kitchen BBQ: A Labor of Love
During BBQ season here at the shop (March-October), when I work in the bakery on Saturdays, I get the benefit of Eric's company for a brief while in the morning as he puts the finishing touches on his BBQ. Saturdays find him baking off cornbread, roasting the chickens and finishing off ribs. As I go through the process of making cinnamon bread, I observe the different stages he goes through – the testing of the golden cornbread studded with colorful peppers, the brushing of the chickens with his BBQ sauce and the final glazing of the ribs with that same sauce.
The half chickens begin their journey on Friday when they are split and marinated in a special rub. On Saturday morning, Eric roasts them for about 45 minutes, bastes them in their own juice and, as he says, "gives them a sauce bath." Once they are out on the sidewalk, customers have the option of another "sauce bath" before their chicken goes on the grill for the grand finale. As Eric points out, the basting process helps to crisp the skin while the layering of the BBQ sauce allows for a delicious development of flavor.
Rib preparation starts on Thursdays when they go in the smoker. On Fridays, the ribs are cooked "slow and low" for about 3 ½ hours. On Saturdays, the ribs go in the oven when they also get a good "sauce bath."
Eric does a variety of pulled meats: pork, lamb, beef and spicy chicken. Preparation of these meats also begins on Thursdays when the fat of the meats is scored and Eric's special rub is applied. The beef gets the addition of a good slathering of mustard while the chicken gets some additional fennel and cayenne (where the "spicy" comes from!). The pork, lamb and beef are then smoked on a large Weber grill over apple wood chips that have been soaked in apple juice. The meats get about 2 ½ hours of smoke with frequent rotating in order to ensure even cooking.
On Friday, all of the pulled meats go back on the grill, this time for cooking, at 7am. They cook for about 10 hours. The chicken gets slightly different treatment – in addition to getting the rub, it is also soaked overnight in beer for some extra flavor. On Friday, the chicken goes into our hot smoker indoors and spends about 4 hours there before a brief stint in the oven where they are crisped up and finished off. After cooking, Eric tells me that the pork pretty much falls off the bone. The beef too falls off the bone but, occasionally, Eric trims the fat a bit. The chicken is bone-in and is trickier to "pull." The lamb too can be quite labor intensive and often requires a fair amount of time bone picking. Once the meats are pulled, they are put in their respective pots for the grill and they all get a bit of sauce, salt and pepper. The lamb gets the addition of some smashed cloves and rosemary. All of the pulled meat sandwiches are put on Iggy's ciabatta squares.
What about the sides? Eric does a delicious apple-raisin slaw that is tossed with a lemon Dijon vinaigrette. His baked beans are also popular, studded with pieces of bacon and immersed in a molasses based sauce. Occasionally, Tripp makes his scrumptious pickled eggs and we also have McClure's pickles (and occasionally housemade pickles!) available on the side.
Eric's chili-lime corn is roasted in the oven and then rolled in chili-lime butter before going on the grill. This style of corn on the cob is called "elote" – a street food in Mexico, you can usually choose from a selection of butter rubs and then top your corn with Queso Fresco. Here at Formaggio, we have grated Ricotta Salata available to top your corn!
The hot dog line-up: Niman Ranch Fearless Franks are a regular request as they are a quarter pound all-beef nitrate-free dog. One of the most popular dogs, however, is the Pearl in the Hole, a creation of former grillmaster, Kurt. The Pearl is a half pound Pearl Kountry Klub hotdog (made in Randolph, MA).
Another all-beef dog, it gets grilled and put into a hollowed-out half of an Iggy's baguette. Then, it is up to you to slather on the toppings of your choice from the condiment bar which has ketchup, relish, sauerkraut, chopped onions, hot peppers and three types of mustard. BBQ sauce is available for you on request! In addition to the beef dogs and, courtesy of our house charcutière, Julie, we usually have a variety of housemade sausages available – occasionally she does hot dogs too! Hot dogs come on B&R Artisan brioche rolls.
Later in the summer, Eric starts grilling lamejun. Lamejun is an Armenian flatbread spread with a ground meat, garlic and parsley paste. We do not make the lamejun in house but source them from Eastern Lamejun Bakers in Belmont. However, we do the grilling and provide a tomato salsa (similar to pico de gallo) to top the sandwich. Some customers also like to add one or more of the pulled meats to their lamejun!
Eric is a man of many talents – he is at home working in all areas of the shop: cheese, produce and the bakery – and it seems to me that he can fix almost anything. His passion for excellence and quality work is evident in everything he does and it is particularly evident to me when I see him working on the BBQ. The BBQ takes a great deal of hard work and involves three full days of preparation. To do it well every week for six months out of the year, you have to love what you do and, judging by how his BBQ tastes, Eric definitely loves what he does! If you are reading this and have yet to taste the result of his hard work, get yourself over here on a Saturday sometime between March and October. BBQ starts at 11am and they 'cue 'til they're through (i.e. until about 3pm or the BBQ runs out)!
We recently did a survey on Twitter, asking folks what their favorite BBQ item was… No one thing led the pack. Instead, the results were all over the board with shout-outs for the pulled lamb and the Pearl in the Hole, among others. The pulled lamb and the pulled pork were my usual go-to BBQ items – sometimes one, sometimes the other, sometimes mixed – and, yes, always with onions and BBQ sauce. Generally, I would get them straight up, figuring the bread took up too much valuable real estate in my stomach, preferring to allot that space to the meaty goodness. Towards the end of the 2009 season, however, I got out to the curb-side too late and the pulled meats had all sold out… As a result, I decided to try the chicken – slathered with BBQ sauce. Of course. I often shy away from chicken – perhaps the upshot of too much bland institutional food in school? However, I should have known better when it comes to Eric's cooking. The chicken is now my standard order and, if I take it home at the end of the day, I tote along a container of BBQ sauce too. If I have extra sauce, it does not go to waste – I told Eric that his slogan for the sauce should be: "it makes everything better!" I mean that, literally and figuratively.
Formaggio Kitchen BBQ: every Saturday from 11am (March – October). For the menu, click here.


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helicopter charter in Winter Haven, FL
Maximo Air21299 US Highway 27, Lake Wales, FL map
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City of Playford
About the community profile
Demographic change across Australia is recorded by the Australian Bureau of Statistics (ABS) in the Census collections every five years. Population experts, .id(opens a new window), analyse and convert these raw figures into stories of place to inform council staff, community groups, investors, business, students and the general public.
The City of Playford Community Profile provides demographic analysis for the City and its suburbs based on results from the 2016, 2011, 2006, 2001, 1996 and 1991 Censuses of Population and Housing. The profile is updated with population estimates when the Australian Bureau of Statistics (ABS) releases new figures such as the annual Estimated Resident Population (ERP).
Suburb boundaries and Census questions change over time, but .id manages the data to ensure that there is an accurate time series provided for the current geographic boundaries. You can read more about this in the Geography Notes section.
Results for the City of Playford include population, age structure, ethnicity, ancestry, religion, income, qualifications, occupations, employment, unemployment, disability, disadvantage, volunteering, childcare, family structure, household structure, housing tenure, mortgage and rental payments, and the size and type of the dwellings people live in.
The Community Profile presents this information in clear maps, tables and charts with concise factual commentary to answer three important questions:
- What are the characteristics of the people who live here?
- How are they changing?
- How do they compare to other areas?
This provides the basis for making evidence-based decisions about how to provide services for the community as it changes.
You can be confident about the quality of the information as it is derived from Australian Bureau of Statistics data, analysed and presented by population experts and funded by the City of Playford.


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CES slideshow: Next big (or little) things
21 comments
LAS VEGAS Gary Shapiro, poobah of the Consumer Electronics Association, likes to call International CES "the greatest show on earth." With more than 150,000 people in attendance here this week, hes certainly entitled to a measure of grandiosity. Its the only show on the planet that brings together a decidely eclectic audience drawn from the consumer electronics, mobile, PC, healthcare, semiconductor and software industries.
And a lot of bloggers.
What follows is a sample of both the small and big things we found on the CES show floor that might well alter the consumer electronics landscape in 2013.
Ground Zero for consumer electronics.


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Ask the Expert: Fertilization Strategies for Success: Dec. 12, 2017
Learn how to do more with less when it comes to your fertilization services. Join the live Ask the Expert event hosted by Koch Turf & Ornamental: Dec. 12, 12-2 p.m. ET in the Fertilizer Application forum .
600 gallon Finn Hydroseeder in Ct.
Discussion in 'Marketplace' started by Planet Landscaping, Sep 19, 2006.


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Health officials hit back at e-cig claims
Health professionals say more research is needed to prove using e-cigarettes is a good way to quit smoking.
Aust women in biggest heart death danger
According to new health figures, Australian women are far less likely to survive a heart attack than men.
Sunscreen protection not total, says study
Research says high factor sunscreen can't be relied on to protect against the deadliest skin cancer form.
Men feel more emotion than women, study finds
A British study using skin electrodes has found men experience greater levels of emotion than women.
Protein in diet 'cuts stroke risk'
High protein diets may protect against stroke, especially if they contain a lot of fish, scientists say.
Too much driving 'is bad for you'
Driving too much is bad for your health, according to a study of 40-thousand middle-aged Australians.
'Big rise' in suicides during recession
Researchers say the financial crisis may have led to thousands of suicides in Europe and North America.
GM mosquitoes a new malaria weapon
Biologists have devised a new weapon against malaria by genetically engineering mosquitoes.
Bariatric surgery tops diabetes study
Stomach-shrinking bariatric surgery beats other forms of treatment in bringing about remission of diabetes.
Junk food ads target sports kids
Junk food advertising at community clubs is undermining the benefits of children's sport, a study says.
Phones in pockets may harm male fertility
Men who keep phones in their pockets could be inadvertently damaging their chances of becoming a father.
Tomato pill 'good for heart health'
A daily 'tomato pill' can improve the functioning of blood vessels in patients with heart disease.
Study shows gaps in heart attack treatment
Aust, NZ hospitals are failing to take simple steps needed to prevent repeat heart attacks among survivors.
Fears hair dyes contain carcinogens
Scientists have called for more research into hair dyes to assess whether they contain a harmful substance.
A third 'have borderline diabetes' in UK
More than a third of adults in England have borderline diabetes, new research suggests.


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Quick Facts
- 41 years of experience
- Speaks English
- University of Iowa
- 1 specialty
- 8 expertise
- 2 board certifications
- 2 hospital affiliations
- 1 location
Type 2 Diabetes
Type 2 diabetes is a chronic disease in which your body is unable to maintain a normal blood sugar (glucose) level.
Care Guides
- Birth Control Facts about birth control to help decide which type is right for you.
- Type 2 Diabetes Basic facts about type 2 diabetes & risk factors to be aware of.
- COPD The facts about chronic obstructive pulmonary disease (COPD).
- Diabetic Macular Edema Facts about diabetic macular edema, including the different types.
- Flu Facts about influenza (flu), including symptoms and vaccines.
- GERD Get the facts about gastroesophageal reflux disease (GERD).
- Lupus Get the facts about lupus, including symptoms, risk factors, and the different types.
- Menopause Facts about menopause, including the stages, symptoms, and types.
- Ulcerative Colitis Facts about ulcerative colitis, including causes, signs and symptoms.
- View All Care Guides Prepare for your next visit with our extensive library of Care Guides
About Dr. Allan Sill
Dr. Allan Sill, MD is a Doctor primarily located in Eau Claire, WI. He has 41 years of experience. His specialties include Internal Medicine. Dr. Sill is affiliated with Luther Hospital Mayo Health System and St Lukes Hospital. He speaks English.
1400 Bellinger St
Eau Claire, WI 54703
Get Directions
Dr. Allan Sill has the following 1 specialty
- Internal Medicine
An internist is a physician who focuses on the diagnosis and treatment of conditions that affect the adult population—both acute and chronic.
These doctors are often who adults see as their primary physicians because they treat a broad...
8 Expertise
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Dr. Allan Sill is similar to the following 3 Doctors near Eau Claire, WI.
Dr. Gina Adel
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Dr. Mohan Sengodan
Hospitalist, Internal Medicine
Eau Claire, WI 0 mi13
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Watch These Cats Running Into Things — Daily Distraction
[onescreen item="5031866″]
Cats vs. mirrors: the battle rages on.
We suppose it could be confusing, but a lot of these cats are grown-up cats—by now you'd think they'd recognize that other cat who keeps doing the making the exact same movements they're making. As for the kittens, it's just a part of growing up. Cherish these moments, cat owners, and yes, it's okay to laugh. Grown-up humans have just as much trouble navigating this dangerous, confusing world.
The Daily Distraction is your Internet break from reality. Whether you're eating lunch at your desk or avoiding high school exes on Facebook, you might just laugh, say "aaahhh" or not believe what you just watched.


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Death Notice for Oct. 24, 2013
Gazette staff
Thursday, October 24, 2013
David O. Oberg, 69, Edgerton, died Monday at UW Hospital, Madison. Services will be at 1 p.m. Friday at Ehlert Funeral Home and Cremation Services, Edgerton. Visitation will be from 11 a.m. until the time of services Friday at the funeral home.


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Search for clues, synonyms, words, anagrams or if you already have some letters enter the letters here using a question mark or full-stop in place of any you don't know (e.g. "cros...rd" or "he?p")
If you have a moment, please use the voting buttons (green and red arrows) near the top of the page to let us know if we're helping with this clue. We try to review as many of these votes as possible to make sure we have the right answers. If you would like to suggest a new answer (or even a completely new clue) please feel free to use the contact page.


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Hatco S-18 Description
Imperial Electric Booster Water Heaters Model S18 208v / 1pH, 18kW
The Hatco Imperial Electric Booster Water Heater combines quality construction and rugged dependability to provide up to 573 GPH (2169 LPH) of sanitizing rinse water. Storage capacity is 16 gallons(60 liters).
- Features
- Castone lined tank with a 10-year limited warranty.
- Features include a temperature/pressure relief valve and gauges, a high-temperature limit control, indicator light, on-off switch, and allow-water cut-off to prevent element burnout due to a low water condition.
- Features include a temperature / pressure relief valve, a pressure reducing valve, two temperature / pressure gauges, a high-temperature limit control, pilot indicator light, on-off switch, and a low-water cut-off to prevent element burnout due to low water condition.
- Each Booster has a built-in heat trap and fiberglass insulation to minimize heat loss.
- Hatco electric booster heaters are factory pre-plumbed and pre-wired with calibrated immersion thermostat and high-temperature limit switch.
- A stainless steel front panel and powder-coated silver-gray hammer-tone body is standard on all Imperial models.
For items shipping from our warehouse in Tennessee we are required to collect sales tax for orders shipped to or billed to addresses within Tennessee. For Hatco items shipping direct from the Hatco warehouse we are required to collect sales tax for orders shipped to California, Florida, Louisiana, Michigan or Wisconsin. Sales tax will show on your online invoice on only the Tennessee addresses and will be added before your credit card is charged for the other states.
Consult the product specification sheet for options or other voltages that may be available at additional cost.
To obtain pricing for optional accessories and/or voltages, please use the feedback form below, contact customer service at 800-541-8683, or use our .
Imperial Booster Heater, electric, 16-gallon storage capacity, 18KW, stainless steel front, custom fittings & Castone tank. 208V, 18 kw, 1ph. NOTE: Water supply in excess of 3.0 grains of hardness per gallon (GPG) must be treated and softened before being used; water containing over 3.0 GPG will decrease the efficiency and reduce the operating life of the unit. Please be advised that product failure caused by liming or sediment buildup is covered under warranty ONLY with proper usage of Hatco water treatment system.
*The warranty will not be honored for residential or non-commercial use of any Commercial Equipment.
Hatco S-18 SpecificationsPDF Spec Sheet
|40F Recovery
|181 gph
|70F Recovery
|103 gph
|Water Booster Heaters
|Width (in)


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Music roundup for Oct. 31-Nov. 6, 2013
Ricky Skaggs and Bruce Hornsby at 8 p.m. Friday, Nov. 1, Potawatomi Bingo and Casino, Northern Lights Theater, 1721 W. Canal St., Milwaukee. Kentucky Thunder also performs. Tickets: $55-$65. Call Ticketmaster at 1-800-745-3000.
Bluegrass star Ricky Skaggs and versatile pianist, singer and songwriter Bruce Hornsby will reunite Friday for a show of original tunes from both performers and a few covers of hit songs redone in bluegrass fashion.
In 2007 the pair released the album "Ricky Skaggs & Bruce Hornsby," which reached No. 1 on Billboard's bluegrass chart. The album features reworkings of Hornsby originals as bluegrass tunes, along with traditional songs and a Skaggs original.
This year, Skaggs and Hornsby released their second album together, the live recording "Cluck Ol' Hen." It's been placed in the bluegrass category for this year's Grammy Awards vote.
The pair first worked together in the early 1990s when both appeared on the Nitty Gritty Dirt Band's "Will the Circle Be Unbroken Vol. 2" album.
Since then, Hornsby and Skaggs have teamed up for several tours.
The reception they received was not always positive. Traditional bluegrass purists don't like people messing with their music, but Skaggs said playing with Hornsby stretches the boundaries of what he and his band, Kentucky Thunder, can do on stage.
"He's such a great musician," Skaggs said in a telephone interview. "He has a real love for tradition, but he loves a good gumbo, too. So you never know when he might throw in some Professor Longhair or Leon Russell into traditional bluegrass. I love that, too."
Skaggs' bluegrass roots go back to his childhood, when he performed with Bill Monroe and appeared on Lester Flatt and Earl Scruggs' television show. In his late teens, he became a member of Ralph Stanley's Clinch Mountain Boys. He later joined Emmy Lou Harris' band.
Hornsby broke onto the national music scene in the 1980s with such hits as "Long Valley Road" and "That's Just the Way It Is."
His more recent forays into bluegrass are part of a larger journey that takes him into the worlds of jazz, jam-band rock and the music he creates with his own band, the Noisemakers. He has toured or collaborated with the Grateful Dead, Bela Fleck and the Flecktones and the jazz bassist Christian McBride and drummer Jack DeJohnette.
Chris Cornell at 8 p.m. Saturday, Nov. 2, Orpheum Theater, 216 State St., Madison. Tickets: $37.50. Call Ticketmaster at 1-800-745-3000.
Chris Cornell rose to fame as the lead singer in the Seattle grunge band Soundgarden. He formed the band in 1984 with friends Kim Thayil and Hiro Yamamoto, with Cornell originally on drums and vocals.
Soundgarden became one of the most successful bands to emerge from Seattle's 1990s grunge scene. But creative differences caused the group to split after the release of its 1996 album, "Down on the Upside."
By 1997, Cornell was working as a solo artist. After leaving Soundgarden, he released the solo studio album "Euphoria Morning." For a self-penned single, "Can't Change Me," he was nominated for best male rock vocal performance at the 2000 Grammy Awards. He also was hired to score music for the film "Mission: Impossible II," crafting the song called "Mission 2000."
After releasing "Euphoria Morning," Cornell joined the remaining members of Rage Against the Machine and formed a new band, Audioslave. He recorded three studio albums with Audioslave before leaving to again work as a solo artist in 2007.
In 2007, Cornell supported Aerosmith on at least two legs of the band's 2007 world tour.
In January 2010, Cornell announced plans for Soundgarden to reform and to headline Lollapalooza 2010. Since then, he has performed both as a member of Soundgarden and as a solo singer and guitarist. He has released four albums as a solo artist, including "Songbook" in 2011.
Stephen Marley at 9 p.m. Saturday, Nov. 2, Barrymore Theatre, 2090 Atwood Ave., Madison. Tickets: $24. Call Ticketmaster at 1-800-745-3000.
Stephen Marley, 41, has reggae royalty in his blood. Born in Wilmington, Del., and raised primarily in Jamaica, he is the son of reggae legend Bob Marley and singer Rita Marley. Stephen Marley also is a five-time Grammy Award winner.
He began singing at age 8, when he took lead vocals on the single "Sugar Pie." He later was part of the reggae group Ziggy Marley & the Melody Makers with three of his siblings. He produced much of his brother Damian Marley's three solo albums, most notably "Welcome to Jamrock" in 2005, and performed on several tracks. He also produced for brother Julian Marley, and he was executive producer and performed on the 1999 Bob Marley mash-up "Chant Down Babylon."
In 2003, Stephen and his brother Damian put together an album under the group name of Marley Boyz.
Stephen Marley's debut album, "Mind Control," was released in March 2007. He won a Grammy for best reggae album in 2012 for his newest work, "Revelation Pt. 1: The Root of Life."
Basia Bulat at 7:30 p.m. Wednesday, Nov. 6, Stoughton Opera House, 381 E. Main St., Stoughton. Tickets: $25. Call 608-877-4400.
Toronto-based singer-songwriter Basia Bulat projects a powerful voice to go with raw emotion on her new album, "Tall Tall Shadow."
The album, released late last month, is the 29-year-old multi-instrumentalist's third full-length album since her debut, "Oh, My Darling," in 2007.
Bulat, who grew up in Ontario and has been compared to a young Joni Mitchell, performs on guitar, autoharp, hammered dulcimer, piano, ukulele and charango, a ukulele-like instrument from South America.
Bulat and her brother, who plays drums and percussion in her band, were raised by a music teaching mother and the sound of "oldies" on the radio. She recorded an independent EP in 2005, and that led to a recording contract with Rough Trade Records.
Several of her songs caught on with college radio in North America and Europe, where Bulat has toured extensively.
She has received lots of critical acclaim over the last five years for her "rare, extraordinary voice" and simple songs that morph into "engrossing accounts of desire and regret."
A review of her new album in the New York Times noted a "sound that nods to Fleetwood Mac and early Joni Mitchell" and described her voice as "warm and honeyed."


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Rays will find enough offense to compete
Though lacking in resources compared to competitors, club will be in the AL East mix
By Hal Bodley / MLB.com
Just about this time each winter, the word about the Tampa Bay Rays is the same: They've lost vital pieces and it'll be hard for them to contend in the rugged American League East.
Then, Spring Training opens in Port Charlotte, Fla., maestro Joe Maddon picks up his baton and makes sweet music. It's been that way for years, and there's no reason to believe it's going to change in 2013.
You can write it down: The Rays will be the sleeper of their division.
Sure, the rejuvenated Toronto Blue Jays are the talk of the offseason. All they have to do to win the division and go to the postseason for the first time since 1993 is show up. They're that good.
And the surprising Baltimore Orioles will be even better than they were in 2012, when they won an AL Wild Card berth, ending years of disappointment at Camden Yards.
The Yankees are the Yankees, and even with all the turmoil in the Bronx, they're still the Yankees. Enough said.
But to suggest the Rays -- who traded pitcher James Shields to Kansas City and lost center fielder B.J. Upton to free agency -- will be weaker is a huge mistake. In fact, I believe they'll be even better than they were last season, when they just missed advancing to the postseason.
Two years ago, there was a mass exodus of premier players, led by Carl Crawford, and yet Tampa Bay staged a miraculous finish to win the 2011 AL Wild Card. Had it not been for a disastrous Sept. 11-18 road trip, when the Rays lost seven of eight games during stops in Baltimore, New York and Boston, Tampa Bay would've been in the postseason for the fourth time in the past four years in 2012.
The Rays still need an impact hitter, but with AL Cy Young Award winner David Price anchoring one of the best pitching staffs in the league, they should be in most of their games. It would be nice if the offense could be more productive, but their young arms make up for that, even without Shields.
"Not just one person needs to step up and fill James Shields' shoes," said Price. "This is a team effort, and it doesn't have to be a pitcher. A position player can go out there and step up and fill his shoes a little bit."
The Rays' offense was 13th in the AL in hits last season, 11th in runs and 12th in OPS. Maddon believes the cycle is changing in the AL, that defense and pitching will dominate in the future throughout the league. He thinks "offense has come back to the pack."
Maddon said that after adding shortstop Yunel Escobar and first baseman James Loney, whose defense overshadows their hitting.
The addition of veteran second baseman Kelly Johnson, who batted just .225 for the Blue Jays last season, means Ben Zobrist will become the everyday right fielder.
"I love the challenge of what we do and how we do it," said Maddon. "We're not going to be able to outhit our mistakes or outhit the other team nightly. We're not going to spend that dough to be that group anyway."
But still, an impact hitter to go with All-Star third baseman Evan Longoria would almost guarantee a trip to the postseason for Tampa Bay. Longoria played in just 74 games last season because of a partially torn left hamstring.
The hitter could be Wil Myers, the key for the Rays in the Shields trade. Tampa Bay fans are excited about the 22-year-old outfielder, considered among the Minor League's best hitters last season. He batted .314 with 37 homers and 109 RBIs while climbing from Double-A Northwest Arkansas to Triple-A Omaha.
Myers has been invited to the Spring Training with the big league club and will get every opportunity to make the team. He's probably in the same category Washington's Bryce Harper was a year ago.
There's no doubt Myers will be at Tropicana Field before too long, but he'll probably open the season at Triple-A Durham. His potential for power and his overall ability should make for a short stay in the Minor Leagues.
"We're much more focused on the process than really what the back of his baseball card will read in a year, two [or] three from now," Rays executive vice president of baseball operations Andrew Friendman said on MLB.com's Hot Stove show.
"We're just keeping an open mind. We're just excited to get a chance to watch him every day and be around him. We'll have a much better feel for where things stand once we really get into that. It's not fair to make declarative statements one way or the other."
Said Maddon: "I've always felt that it should be easier for a young player to make the team when the season is in progress as opposed to out of Spring Training."
Luke Scott, who had a rough season as the DH in 2012, has been re-signed and could be an unexpected piece for the offense. Scott had shoulder surgery just before coming to Tampa Bay and never found his groove. He missed 45 games during two trips to the disabled list and ended with a .229 batting average, just 14 homers and 55 RBIs in 96 games.
Maddon isn't bashful when he says "we'll be good." That's what he'll repeat to his players next week in Port Charlotte, and the bottom line is they'll listen and believe.
Just because the Rays don't have the resources of the other AL East teams shouldn't be an excuse. Or, as Maddon put it: "We might not have everything everybody else has, but that doesn't mean we're not successful. We look at it as an interesting challenge for everybody in the organization. We look at it as something that can bring out the best in everybody in the organization. There's no downside."
And that's why the Rays will be winners again in 2013.
Hal Bodley is the senior correspondent for MLB.com. This story was not subject to the approval of Major League Baseball or its clubs.


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Most popular Automotive DesignLine stories of 2012
3 comments
What caught your interest in 2012?
Stories about electric vehicles, Toyota, teardowns and safety standards, as it turns out! These were the among the most-read by Automotive DesignLine viewers in the past 12 months.
Here's the complete list of the top 10 most popular stories this year:
1. Slideshow: Paris auto show drives electric
In a climate of economic austerity in which European car sales have declined over the past few years, the renewable and other emerging technologies on display during the recent 2012 Paris Motor Show offered a glimmer of hope.
2. How hybrid electric vehicles can pay off
As in previous years, several news reports have questioned and examined the value and future of HEVs. Now, as the U.S. enters the second decade of HEV sales, the question is still examined: Why do people buy a hybrid vehicle?
3. Special Issue: Inside the Toyota Prius: Part 5 - Inverter/converter
The inverter/converter unit (ICU) is the ringmaster of all of the electrical conversion in the Prius.
4. We tear down a Chevy Volt (exclusive videos)
One of the highlights of the year-long Drive for Innovation was tearing apart a brand-new Volt down to the board level.
5. Toyota accelerations revisitedhanging by a (tin) whisker
A NASA paper delivered at the International Tin Whisker Symposium last year reported on tin whisker growth in Toyota accelerator pedal position sensors that, depending on pedal rate of movement, could lead to unintended acceleration.
6. Teardown Report: Chevy Volt's electronic secrets
Sometimes engineers get an assignment that's not only a challenge and a learning experience but just plain fun as well.
7. Fuel injection, ECUs and the pressure of NASCAR racing
NASCAR this season embraced one of the most significant engine-performance changes in the past 50 years: It mandated fuel-injection, throwing over 50 years of carburetor use fondly remembered by engineers and mechanics.
8. How to select effective ESD protection diodes
New generations of portable products are increasingly sensitive to damage from Electrostatic Discharge (ESD) voltage as newer integrated circuit (IC) technologies employ smaller geometries and lower working voltages.
9. How Bluetooth, UWB, and 802.11 stack up on power consumption
Wireless technologies such as Bluetooth, Ultra-wideband (UWB) and WLAN, all make this wireless data transfer viable today, yet each has its own obstacles which makes its use in the mobile market challenging.
10. Functional safety implementations in modern MCUs
Todays automobiles run various safety critical applications like ABS, electronic power steering, air bag sensors, Radar sensing, and other chassis related applications.


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Austin Town Hall Park
5610 W. Lake St. Chicago, Illinois 60644
(773) 287-7658
Fee: FREE
Age Range: Toddlers
Juice box is a free series of cutting edge performances, Juicebox is geared at toddlers but is engaging for the whole family. Kids can sit on the floor, walk around, meet the artists, and sometimes even play with the instruments and puppets. BYO snacks are welcome too!


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Clinical Trial to Assess the Effect of the Change of Efavirenz (EFV) for Lopinavir/Ritonavir (LPV/r) in Lipoatrophy in HIV-infected Patients (LIPOKAL)
This study has been completed.
Juan A. Arnaiz
ClinicalTrials.gov Identifier:
First Posted: September 16, 2009
Last Update Posted: September 18, 2014
Information provided by (Responsible Party):
Juan A. Arnaiz, Hospital Clinic of Barcelona
- Full Text View
- Tabular View
- No Study Results Posted
- Disclaimer
- How to Read a Study Record
Eligible HIV-infected patients with clinically evident lipoatrophy despite treatment with efavirenz and fixed-dose combination of thymidine nucleoside analogues will be informed and asked to enroll in the study; will be randomized (1:1) into two branches, A: EFV + Fixed combinations of analogue tenofovir + emtricitabine.B (experimental): LPV/r + combination of correspondent analogues. The main variable is the evaluation of the absolute change in limb fat mass at 24 months from baseline in both groups.
|HIV Infections Lipoatrophy
|Drug: EFV Drug: LPV/r
|Phase 4
|Study Type:
|Study Design:
|Allocation: Randomized
Intervention Model: Parallel Assignment
Masking: None (Open Label)
Primary Purpose: Treatment
|Official Title:
|CT to Assess the Effect on the Subcutaneous Fat of Change of EFV for LPV/r in HIV-infected Patients Who Developed Lipoatrophy and Remains Despite Treatment With Efavirenz and Fixed-dose Combination of no Thymidine Nucleoside Analogues.
Resource links provided by NLM:
MedlinePlus related topics: HIV/AIDS
Drug Information available for: EfavirenzU.S. FDA Resources
Further study details as provided by Juan A. Arnaiz, Hospital Clinic of Barcelona:
Primary Outcome Measures:
- Absolute change in limb fat mass measured by DEXA. [ Time Frame: 24 months. ]
|Study Start Date:
|October 2009
|Study Completion Date:
|November 2013
|Primary Completion Date:
|November 2013 (Final data collection date for primary outcome measure)
|Assigned Interventions
Active Comparator: EFV and Fixed combinations of analogues
EFV + Fixed combinations of analogue tenofovir + emtricitabine, or abacavir + lamivudine
Drug: EFV
one pill QD VO.
|Experimental: LPV/r and combination of analogues.
Drug: LPV/r
2 pills QD VO
Information from the National Library of Medicine
Choosing to participate in a study is an important personal decision. Talk with your doctor and family members or friends about deciding to join a study. To learn more about this study, you or your doctor may contact the study research staff using the contacts provided below. For general information, Learn About Clinical Studies.
|Ages Eligible for Study:
|18 Years and older (Adult, Senior)
|Sexes Eligible for Study:
|Accepts Healthy Volunteers:
Inclusion Criteria:
- Patients HIV positive > 18 years.
- Patients in treatment with Sustiva(r)+Truvada(r); or Sustiva (r)+Kivexa(r).
- HIV-ARN < 50 copies/mL in the las six months.
- Clinically evident lipoatrophy (moderate or severe).
- Negative pregnancy test.
- Signed informed consent.
Exclusion Criteria:
- Evidence of failure or mutation to therapy with protease inhibitors.
- Patients that can not be treated with LPV/r.
- Mild lipoatrophy.
- History of alcoholism or drug addiction that discourages participation in the study.
- Pregnancy or breastfeeding.
- Documented current or 4 weeks prior opportunistic infection.
- Creatinin clearance < 60mL/min.
- Concomitant use of nephrotoxic drugs or immunosuppressants.
- Actual treatment with systemic corticosteroids, IL-2 or chemotherapy.
- Patients under treatment with other drugs in investigation.
- Acute hepatitis.
- Any other disease that discourages participation.
Contacts and Locations
Information from the National Library of Medicine
To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.
To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT00978237
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT00978237
|Hospital de Bellvitge
|L'Hospitalet de LLobregat, Barcelona, Spain
|Hospital Universitario Central de Asturias
|Asturias, Spain
|Hospital Clínic de Barcelona
|Barcelona, Spain
|Hospital de la Santa Creu i Sant Pau de Barcelona
|Barcelona, Spain
|Hospital Clínico San Carlos
|Madrid, Spain
|Hospital La Fe
|Valencia, Spain
|Hospital Xeral-Cíes
|Vigo, Spain
Sponsors and Collaborators
Juan A. Arnaiz
More Information
Publications automatically indexed to this study by ClinicalTrials.gov Identifier (NCT Number):
Keywords provided by Juan A. Arnaiz, Hospital Clinic of Barcelona:
Additional relevant MeSH terms:
Publications automatically indexed to this study by ClinicalTrials.gov Identifier (NCT Number):
Rojas J, Lonca M, Imaz A, Estrada V, Asensi V, Miralles C, Domingo P, Montero M, del Rio L, Fontdevila J, Perez I, Cruceta A, Gatell JM, Arnedo M, Martínez E. Improvement of lipoatrophy by switching from efavirenz to lopinavir/ritonavir. HIV Med. 2016 May;17(5):340-9. doi: 10.1111/hiv.12314. Epub 2015 Sep 10.
|Responsible Party:
|Juan A. Arnaiz, MD, PhD, Hospital Clinic of Barcelona
|ClinicalTrials.gov Identifier:
|NCT00978237 History of Changes
|Other Study ID Numbers:
|First Submitted:
|September 15, 2009
|First Posted:
|September 16, 2009
|Last Update Posted:
|September 18, 2014
|Last Verified:
|September 2014
Keywords provided by Juan A. Arnaiz, Hospital Clinic of Barcelona:
HIV - Lipoatrophy
treatment experienced
Additional relevant MeSH terms:
HIV Infections
Lentivirus Infections
Retroviridae Infections
RNA Virus Infections
Virus Diseases
Sexually Transmitted Diseases, Viral
Sexually Transmitted Diseases
Immunologic Deficiency Syndromes
Immune System Diseases
Skin Diseases, Metabolic
Skin Diseases
Lipid Metabolism Disorders
Metabolic Diseases
Reverse Transcriptase Inhibitors
Nucleic Acid Synthesis Inhibitors
Enzyme Inhibitors
Molecular Mechanisms of Pharmacological Action
Anti-Retroviral Agents
Antiviral Agents
Anti-Infective Agents
Cytochrome P-450 CYP2C9 Inhibitors
Cytochrome P-450 Enzyme Inhibitors
Cytochrome P-450 CYP2C19 Inhibitors
Cytochrome P-450 CYP2B6 Inducers
Cytochrome P-450 Enzyme Inducers
Cytochrome P-450 CYP3A Inducers


text:
Your Views: You can keep your insurance? Obama lied to Americans
Barack Obama said repeatedly, "If you like your plan, you can keep your plan, period." According to Forbes, Obama knew in 2010 that 93 million Americans could lose their health plans under Obamacare. He knew the public would not stand for losing the plans they liked. So in order to ram his partisan plan through Congress, he deliberately lied, period.
NBC News cited "four sources deeply involved in the Affordable Care Act" as saying that "50 to 75 percent" of people who buy coverage on their own are likely to receive cancellation notices due to Obamacare.
The "grandfather" provision in Obamacare allows people to keep their existing plans if they like them. Subsequent regulations from the Obama administration interpreted that provision so narrowly as to prevent most plans from gaining this protection. In 2010 the Federal Register predicted more than half of employer-sponsored plans would lose their "grandfather status" and get canceled. According to the Congressional Budget Office, 156 million Americans were covered by employer-sponsored insurance in 2013.
Obama's famous lie that "you could keep your plan" was necessary because he knew that previous Democratic attempts at health reform had failed because Americans were happy with the coverage they had and opposed efforts to change the existing system.
Obamacare forces insurers to offer services that most Americans don't need, don't want and won't use, for higher prices. Now Obama is trying to spin the cancellations on the greedy insurance companies. Obama lied again, period.


text:
UPDATE: Janesville woman found in river pronounced dead
JANESVILLE—A Janesville woman was pronounced dead after being pulled from a frigid Rock River on Sunday morning.
Emergency communications indicated that a couple walking near the Highway 11 bridge saw what they thought was a body at about 10:40 a.m. Sunday.
The Janesville Fire Department and Department of Natural Resources both put boats in the water, and the woman was pulled from the river.
The woman was taken to Mercy Hospital and Trauma Center. She was not immediately pronounced dead.
Janesville police Sgt. Todd Kleisner said Sunday night that the woman's low body temperature gave hope that an attempt to revive her might work.
Chief Deputy Coroner Louis Smit said Sunday night that he did not yet have the name of next of kin, so he could not disclose the woman's name.
Soon after the call about the body in the river, Janesville police received a report of a woman who was distraught and missing.
She had been missing since about 7 a.m., said police Sgt. Brian Vaughn,
After the rescue, police searched river-access points for the woman's car and found it at River's Edge Bowl, 215 S. River St., Janesville.
Kleisner said investigators believe she jumped in the river at that point. They believe she was trying to kill herself.
Last updated: 11:59 am Sunday, December 1, 2013


text:
Evolution of the nervous system
Discussion of everything related to the Theory of Evolution.
Moderator: BioTeam
Evolution of the nervous system
For vertebrates the spinal column and the skull provides great protection from damage. Thinking in evolutionary terms, why does some nerves by-pass this protective system and travel outside of the spinal cord and its protective spinal column?
When a human gets burned on the finger, the nerves in the finger transmit the signal to the spinal cord and then back to the muscles so that the finger can be removed instantly. If nerves did not travel outside the protective spinal cord, the individual would have difficulties to react to some external factors, e.g. getting burned on the finger, thus the likelihood of survival would decrease significantly. It would be difficult for nerves to receive signals from the outside environment if the nerves were protected by hard bone since the nerves cannot reach out to all vital body parts. The nerves outside the spinal cord and the skull are however slightly protected by the myelin, which is made of lipids from protein.
Is my hypothesis correct? If not, please explain the correct theory. Thank you in advance!
You are not technically wrong, but you are referring only to the end of the nerves that are out of the spine. However there are nerves that are completely outside of the spinal cord. Why would they.
There is an example (extreme) and some food for thought about the reason in this dailymotion video. Enjoy:
http://www.dailymotion.com/video/xdm5he ... aryng_tech
Science has proof without any certainty. Creationists have certainty without
any proof. (Ashley Montague)
Re: Evolution of the nervous system
From what I can see of the design of Windows OS, by Dawkins' viewpoint on this matter, I would would have to say that Windows was not designed.
If you take things for medical examination out of context (vis a vis it's development), you could say something has bad design.
It's fallacious reasoning to insist that if a single species can be found with less than optimal arrangements, that it means "no design" or "poor design".
Those are terms relating to a medical viewpoint. Since we do not know the eventual fate of the nerve in question, it's impossible to say "good" or "bad" design.
If perfection is required from the start and at all points, it must mean immortality for every living thing. That is what Dawkins insists creationists show - or else, no design.
Perfection and immortality is what a medical viewpoint would have as a theoretical goal.
Re: Evolution of the nervous system
correction: "Dawkins insists I.D. shows - or else, no design"
Re: Evolution of the nervous system
Does every thread in this forum have to devolve into the same tiresome argument? Shame on you canalon for encouraging Crucible's post. The video you linked to is not relevant to Anna55's question.
To Anna55: imagine what our bodies would be like if all nerves, up to the nerve endings of sensory nerves, were encased in bone.
The inanity of Crucible comments is not relevant to the point. The fact that Dawkins use it as an argument for evolution (not against creation in that vid) is just bonus.
The point is you have here a nerve that is going from the brain to the heart and back outside of the spine. Why it does that (take that convoluted path and bypass some protections at the same time) is explained in the video. And that is extremely relevant to Anna55 point, and much more so than just "all nerve can't be encased in bones" because it demonstrate why neither the vagus nerve nor the recurrent laryngeal nerve, that could both use the protection of the spine do not actually use it. And the reason is the history of the path of that nerve in our ancestors.
Science has proof without any certainty. Creationists have certainty without
any proof. (Ashley Montague)
Please do show what its inane in my comment, if you intend to start throwing crap.
In agreement with Gavin that you opened it up.
Untrue. Check his introductory statement, ending at 21 seconds in. Time for a retraction from you and apology for your sloppiness.
In agreement with you here, that Gavin is wrong - that is why I recapped the angle of the organism's development and history.
Considering how it could have got that way, is the part that confers some useful info.
If, however, you show Dawkins BS ing, it's like Gavin said.
Might I suggest you boys take your differences to PM ?
'Nuff said.-/+
Re: Evolution of the nervous system
I understood Anna55's question to essentially be: why aren't all nerves encased in bone? Dawkin's video was demonstrating an extreme example of bad design, if design had occurred. I doubt that Anna55 got the connection, since I (a biologist) didn't.
you are spouting inanity when you say that
because when it comes to the recurrent laryngeal, all vertebrates have it, and its (not it's) path do not make sense in any of them, except in light of evolution. The extreme case of the Giraffe is a striking example, but the fact that in my human body that nerve travels back from my heart does not make any sense either. As for software programs, you could say that they do actually evolve, as often, only some part of the code is modified, while the part that are working are often just updated to cut programming time (i.e. costs). This is why after some iterations and updates they often end up a bit clunky and massively bigger (remember the good old times when you could have a software on a single floppy disk?).
But I will admit that I was wrong: Dawkins had some comments about ID, you are right, I was wrong.
I did not understand the question like you did. I read it, as " Some nerves are not using the spine at all to travel inside our body, although it would make sense, could that have a reason rooted in evolution?" to which, the answer is obviously that in our ancestors, travelling through the spine would not have made sense, and we have inherited those pathway in spite of massive changes of body plan since those times. And that is because of common descent. If you think about it, this is a much more interesting answer to a much more interesting question. And the opportunity to demonstrate a sound knowledge of evolutionary theory, as opposed to a simplistic idea of encasing nerves in bones. I might be wrong, but as an educator, that would be the kind of question that I would ask to make student think hard and give answers demonstrating a sound knowledge of the subject as well as deep thinking.
Science has proof without any certainty. Creationists have certainty without
any proof. (Ashley Montague)
I do not know, but I know that long nerves are (relatively) slow to transmit information (compare reflexes to centrally processed actions: the latter are measurably slower than the former, even when trained), and that it makes sense to have as many of the higher functions close to one another to work at maximum speed. Similarly, encasing them in bone is a good way to protect the system from outside shocks.I remembered reading that some dinosaurs did have two brains, but it seems that this is an outdated fact that has been refuted, so I will not fantasize about that any more. Another thing might be that for the farthest of our vertebrate ancestor was one with a single nerve ganglia (sp?) and that we have been stuck with that plan since then, has adding one (or more) new brain, would have been too massive a re-engineering project to allow the intermediate forms to have any fitness in the first place. The vertebrate line was already too high on the fitness landscape to be able to go through such a fitness valley successfully. Even though the next peak might have been higher. Too late to change.
Science has proof without any certainty. Creationists have certainty without
any proof. (Ashley Montague)
How is that inanity ? That I said "single" ?
That is not inanity. I am well aware that there are probably uncountable numbers of such examples - though maybe not so striking. The video even mentioned the approx. length of the loop in humans
You simply are not aware of what you are saying. My statement on "single" is in reference to Dawkins' argument, where the argument could just as easily completely rest with providing only a single example, as by resting on 85 such examples or 850 of them or 850,000 of them. He thinks if he shows a medical insufficiency of some type, it shows there is no design. One such "error" from a designer, is enough to make the point. I would agree that if the argument were correct, it would take only a single example.
You do not agree ? Fine, but it's not spouting inane crap , to make the point.
My comment is that Dawkins needs only one example, to make that argument complete. Why be so insulting over that ?
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