text:
Why It Pays to File for Bankruptcy: A Critical Look at Incentives Under U.S. Bankruptcy Laws and A Proposal for Change
AbstractThis article rst examines the economic justication for having a personal bankruptcy procedure at all. I argue that it is economically worthwhile to have a bankruptcy pro- cedure, but that costs rise more quickly than benets as the exemption level increases.
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Bibliographic InfoPaper provided by Michigan - Center for Research on Economic & Social Theory in its series Papers with number 98-02.
Length: 37 pages
Date of creation: 1998
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Handle: RePEc:fth:michet:98-02
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Postal: UNIVERSITY OF MICHIGAN, DEPARTMENT OF ECONOMICS CENTER FOR RESEARCH ON ECONOMIC AND SOCIAL THEORY, ANN ARBOR MICHIGAN U.S.A.
Related researchKeywords: BANKRUPTCY ; DECISION MAKING;
Find related papers by JEL classification:
- G30 - Financial Economics - - Corporate Finance and Governance - - - General
- G33 - Financial Economics - - Corporate Finance and Governance - - - Bankruptcy; Liquidation
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- Lin, Emily Y. & White, Michelle J., 2001. "Bankruptcy and the Market for Mortgage and Home Improvement Loans," Journal of Urban Economics, Elsevier, vol. 50(1), pages 138-162, July.
- Henry, Ruby, 2013. "Business, Bankruptcy, and Beliefs: The Financial Demise of NBA Stars," IZA Discussion Papers 7238, Institute for the Study of Labor (IZA).
- Yannis Georgellis & Howard J. Wall, 2006.
"Entrepreneurship and the policy environment,"
Federal Reserve Bank of St. Louis, issue Mar, pages 95-112.
- Yannis Georgellis & Howard J. Wall, 2004. "Entrepreneurship and the policy environment," Working Papers 2002-019, Federal Reserve Bank of St. Louis.
- Krueger, Dirk & Perri, Fabrizio, 2011.
"Public versus private risk sharing,"
Journal of Economic Theory,
Elsevier, vol. 146(3), pages 920-956, May.
- Krueger, Dirk & Perri, Fabrizio, 2010. "Public versus Private Risk Sharing," CEPR Discussion Papers 7625, C.E.P.R. Discussion Papers.
- Dirk Krueger & Fabrizio Perri, 2009. "Public versus Private Risk Sharing," NBER Working Papers 15582, National Bureau of Economic Research, Inc.
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FAQ: Is ID just a religious or theological concept?
The Long Answer:
This article adapted from our "Religious and Scientific Affiliations Page" and from our article "Intelligent Design Theory, and the Relationship between Science and Religion.
Introduction When discussing the subject of "origins" (i.e. the question "How did we get here?", people often make both religious and scientific claims. Additionally, people have many different views on the proper relationship between science and religion. The purpose of this FAQ is to discuss the nature of science, the nature of religion, and the relationship of science and religion. The article will show how intelligent design theory is science, and not religion, and that while many proponents of intelligent design have religious beliefs, this affect neither the quality of the science of intelligent design nor does it negate the secular, scientific basis of the theory of intelligent design.
What is science?
"Science is a particular way of knowing about the world." So says the National Academy of Science in its Teaching about Evolution and the Nature of Science.1; see also ref. 2 A primary goal of science is to understand nature, where "understanding" means "relating one natural phenomena to another and recognizing the causes and effects of phenomena."1 Progress in science consists of the development of better explanations for the causes of natural phenomena.1
Although there is no "demarcation" definition of science agreed upon by all philosophers of science,3 many scientists and philosophers have suggested that scientific explanations are:
1. Based upon results obtained through observations and experiments that can be substantiated by other scientists.1,2
2. Subject to testing because scientists can observe the natural world to see if the explanation holds up.4, 5
3. Falsifiable, in the sense that some type of observations could conceivably count against the theory.4, 5
4. "Tentative," meaning that they are not held absolutely but are held subject to state of the evidence.1
As the National Academy of Sciences explains, observations (often via experimentation) are fundamental to science:
The Scientific Method:
As seen at left, scientific understanding begins with observations. Scientists then make a hypothesis to explain those observations. The hypothesis should make predictions which can be tested via experiments.17 If the predictions of the hypothesis are verified, it is concluded that the hypothesis is supported by the scientific data. That conclusion is an observation in-and-of itself, which can form the basis for further hypotheses, experiments, and conclusions. In this way, scientific knowledge builds upon itself:
Thus, scientific knowledge is at its heart based upon observations and experiments. Another way of putting it is that science is based upon empirical data.
What is religion?
Religion is another way of "knowing about" the natural world. While science bases all statements upon observations, religion bases many of its statements upon faith or divine revelation. The main difference between religion and science is that only religion has a component of faith. Faith statements are not ultimately based upon the observable, and are not tentative, nor testable nor falsifiable through the scientific method, but are believed to be true for reasons that go beyond empirically observable evidence--often because of divine revelation.
Because religion has faith, religious beliefs are held absolutely, and faith may maintain religious beliefs if there is an absence of confirming evidence. Scientific beliefs are said to be "tentative," for nothing in science is absolutely proven; scientific claims are only said to be "supported to a given degree by the evidence." Only religious beliefs are "dogmatic" in the sense that they are claimed to be absolutely known to be completely true.
Religious claims are not necessarily any less valid than scientific claims. Some religious beliefs may even be testable and/or supportable by "empirical data." For example, one could envision empirical evidence for the resurrection of Christ. Jesus himself did not teach that the Christian faith is blind, as he helps his disciple Thomas who doubted that Jesus had really risen from the dead:
(John 20:27, NIV)
(John 20:29, NIV)
Do Science and Religion Overlap?
When talking about the question, "How did we get here?" (i.e. origins) both science and religion speak. An accurate model of science and religion must recognize that fact:
Science and religion are both different "ways of knowing" can be different ways of knowing about the same thing: origins. Science knows things through the scientific method. Religion knows things through faith and divine revelation. Science approaches the subject of origins through the scientific method. Religion approaches the subject of origins from faith and divine revelation:
Is Intelligent Design Theory Science or Religion?
Intelligent design is an answer to the question, "How did we get here?" If understanding in science is to "recogniz[e] the causes and effects of phenomena"1 and scientific progress "consists of the development of better explanations for the causes of natural phenomena"1 then if certain natural objects were caused by intelligent design, then it would increase scientific understanding would science would undergo progress to discover that fact. Yet, a common question about intelligent design is if it is a "religious" or "theological" concept or if it is a scientific theory. Part of the confusion stems from the fact that one can answer the question "How did we get here?" with "Life was intelligently designed" by using both scientific methods or the methods of religion:
Before one can understand why intelligent design theory is science, and not religion, one needs to understand how intelligent design theory works, and why it is based off of the scientific method, and not faith or divine revelation. The following is a description of the logical steps one takes to infer that an object was designed through intelligent design theory:
In this description, only the scientific method, via observations of the natural world, is used to conclude that life was designed. There is no appeal to the supernatural, and no reliance upon faith or divine revelation (including any religious text). Intelligent design thus uses none of the "methods" of religion in makings its claims.
However, it should be noted that many religions may teach that life was intelligently designed. While intelligent design theory makes claims about the natural world which are consistent with these religious claims, intelligent design theory is science not because of the claims it makes, but because of how it makes those claims. Remember, science is a "way of knowing"--not a set of things which can be known. If a conclusion may be arrived at through the scientific method, even if some religious faith or divine revelation is coincidentally teaching that same conclusion, it is scientific.
In determining if something is science or religion, what matters is not the claim you are making, but how and on what basis you are making the claim. What you 'know,' or what your claims are about, do not determine whether those claims are religious or scientific. Rather, it is the 'way,' or means by which one makes those claims that makes them religious or scientific. Intelligent design theory is a purely scientific way of arriving at the conclusion that life was designed, even if that conclusion may also be reached via religious means.
Understanding the Identity of the Designer:
The scientific theory of intelligent design cannot name the identity of the designer, but only detects the past occurrence of intelligent design in the natural world. Intelligent design theory cannot name the designer because it works off the assumption that all designers in general create a certain type of information when they act. While we can detect that type of information in the natural world to infer intelligent design, finding that type of information does not give us any more information about the designer other than that the designer intelligently designed the object in question. Consider the following diagram:
In this diagram, many types of intelligent agents could produce identical objects with high levels of CSI. Intelligent design theory can only find the object containing high levels of CSI and works backwards. While it can detect that the object was designed, it cannot discriminate what kind of designer designed the object, nor determine any specific properties about the designer, other than that it was an intelligent agent. All intelligent design theory can infer is that the object was designed. Intelligent design, as a scientific theory cannot identify the identity of the designer.
Not identifying the designer is not a cop-out nor does it stem from an unwillingness to be honest about motivations. It results solely from the pure empirical limitations of scientific investigation:
Common Arguments Against the Scientific Nature of Intelligent Design: Motivations and Religious Affiliations
It has been argued by many critics of intelligent design theory that ID is religion because of the religious affiliations of many groups or individuals promoting intelligent design theory, or because of the nature of the subject. Many have argued that because many theists promote intelligent design theory, it must be a religious concept. However, to attribute characteristics to something just because those affiliated with it have certain characteristics is to commit what is known as the genetic fallacy or to make what is called an ad hominem argument. Neither of these are valid lines of argumentation.
The "genetic fallacy" occurs when one judges an idea based on its past or its origin. In reality the origin or history of an idea is irrelevant to its present properties. It does not follow that because some proponents of intelligent design are religious, that therefore intelligent design theory must be a religious concept.
An ad hominem argument criticizes a person rather than an argument. To criticize a person because they are religious, or have religious motivations, does not therefore mean that their claims (such as intelligent design) are unscientific. Religious motivations are irrelevant to determining if an idea is scientific or scientifically true. Many famous scientists, such as Kepler and Newton, used their religious beliefs to justify their belief that God created an ordered and rationally comprehendible universe. Their religiously motivated scientific claims were confirmed, leading to hundreds of years of fruitful scientific progress.
Even if these fallacious arguments were true, there are still intelligent design organizations with no religious affiliation. The International Society for Complexity, Information, and Design (ISCID), founded by William Dembski in 2001, is a professional research society that investigates the purely empirical scientific methods for detecting intelligent design. There are individuals with a wide variety of religious and metaphysical beliefs who see merit to intelligent design theory and are fellows of ISCID. ISCID has no religious requirements for membership.
Religions Premises vs. Religious Implications:
Since both science and religion speak about the subject of origins, science can often agree with some religious claims. In these instances a genuinely scientific theory--not built upon religious premises--may have religious implications. A theory is scientific if it has scientific premises--and is not based upon religious premises. However, the fact that a theory has scientific premises does not mean it cannot have religious implications.
Many have seen the scientific theory of evolution as having religious implications. Stephen Jay Gould wrote that evolution has very particular religious implications for humanity:
But what about quotes from ID proponents talking about ID as if it were religion?
Some people amass quotes from intelligent design proponents where they are talking about intelligent design as if it is merely a religious concept. Various quotes are often given trying to show that ID proponents are merely making religious arguments in favor of intelligent design. William Dembski, a mathematician and philosopher who has written on intelligent design from both a religious and a scientific perspective, says the following on this matter:
"For more than a century we have heard that scientific progress has made Christian belief obsolete. Given the cultural prestige of science, this claim has prevented many from considering the Christian faith. If intelligent design theory exposes the inadequacy of materialistic explanations in the natural sciences, it will deflate this assertion, and could contribute to a renewal of Christian belief in the twenty-first century. This would be its most significant apologetic contribution." (Jay Wesley Richards, Signs of Intelligence: Understanding Intelligent Design edited by William A. Dembski and James M. Kushiner)
"Although intelligent design fits comfortably with a belief in God, it doesn't require it, because the scientific theory doesn't tell you who the designer is. While most people - including myself - will think the designer is God, some people might think that the designer was a space alien or something odd like that." (Michael Behe, Pittsburgh Post-Gazette, 02/08/01)
"The objective [of the Wedge Strategy] is to convince people that Darwinism is inherently atheistic, thus shifting the debate from creationism vs. evolution to the existence of God vs. the non-existence of God. From there people are introduced to 'the truth' of the Bible and then 'the question of sin' and finally 'introduced to Jesus.'" (Phillip Johnson, "Missionary Man", Church & State, April 1999)
"He [Reverend Sun Myung Moon] frequently criticized Darwin's theory that living things originated without God's purposeful, creative activity... (Jonathan Wells, "Why I Went for a Second Ph.D.", 1996, [www.tparents.org/Library/Unification/Talks/Wells/DARWIN.htm])
To see the charges made against intelligent design in action, consider these two charges from the ID-critical book, Creationism's From Trojan Horse (pg. 273):
[ ]
"Phillip Johnson made it crystal clear that ID is creationism: "The idea of divine creation, which is what I'm talking about, [is] that there is an intelligence behind life." (Creationisms Trojan Horse, by Paul R. Gross and Barbara Forrest, pg. 273, 274)
If ID critics are going to use quotes like these to prove that ID is creationism, religion, or theology, then they have a very weak case indeed. Because both religion and science can speak to intelligent design, one has to ask how one knows that life is designed. ID as a scientific theory does not know that life is designed because of divine revelation, and indeed it does not come to the conclusion that life was supernaturally designed. It can only tell you that life was designed, and nothing more. This scientific theory of intelligent design is what ID proponents would like to see scientists consider, and perhaps one day schools to teach. But religious investigations of the implications of intelligent design theory are not appropriate for science.
1. Teaching About Evolution And The Nature of Science (National Academy of Press, 1998).
2. Science and Creationism, A View from the National Academy of Sciences, 2nd Edition (National Academy Press, 1999).
3. Many philosophers of science reject "demarcation arguments" between science and non-science. See "The Demise of the Demarcation Problem" by Larry Lauden in But Is It Science?, edited by Michael Ruse (1988).
4. Popper, K., Conjectures and Refutations, p. 257 (1963).
5. Ayala, F. J., "Biological Evolution: Natural Selection or Random Walk?," American Scientist, 62:700 (1974).
6. Mark 12:30, NIV; emphasis added.
7. 1 Thessalonians 5:21, NIV.
8. Dembski, W. A., Eugenie Scott and the NCSE: Darwin's Predictable Defenders.
9. Gould, S. J., "So Cleverly Kind an Animal," in Ever Since Darwin: Reflections in Natural History, p.267 (1991, reprint).
10. Provine, W. B., "Evolution: Free will and punishment and meaning in life," http://fp.bio.utk.edu/darwin/1998/provine_abstract.html.
11. Dawkins, R., The Blind Watchmaker, p.6 (1986).
12. Simpson, G. G., The Meaning of Evolution, (1967) p. 345.
13. Miller, K. and Levine, R., Biology (1995).
14. 1995 Statement of the National Association of Biology Teachers.
15. Gould, S. J. in "The Meaning of Life," Life Magazine, pg. 84 (Dec. 1988).
16. Graham, B., in The Meaning of Life, by David Friend and the editors of Life Magazine, pg. 104 (1991).
17. Experimentation acts as the workhorse for the scientific method. Experimentation allows us to isolate a particular object of interest, usually referred to as a variable. Experimenters do a comparison between their variable group or condition with the control or normal group or condition. In other words, theyll often run two experiments one with the variable and one without. Then, they compare the two results to see if there are differences. If the differences match what the expectations are (i.e. the hypothesis), then the hypothesis is said to have experimental support. One thing that is crucial in experimentation is to try to limit experimenter bias that is, that the person doing the study may skew their results to be more favorable to their particular outcome. Limiting the effect of this observer/experimenter bias can be accomplished in one of two ways: 1) through double blind experiments, and 2) through repetition by independent scientists. Double blind experiments are often done with medical drugs. In these kinds of experiments, not only is the patient unsure if they are getting the actual drug (i.e. the variable), but so is the doctor administering the pill/shot/etc. This is one way to help ensure honesty in the results. But, repeatable experiments are often used as well, sometimes in conjunction with the former. Once a particular experiment is run and the methods and results of the experiment are shared with others, the other groups can run the same experiment to see if they get the same results. Consistent results between independent groups adds to the validity of the first groups findings. These are the ways that the scientific method allows a means of checks-and-balances to make sure there is no horsing around with the data going on in the experiments. You dont want to pay money to take a new drug only to find out that, in reality, it had no appreciable affect to treat whatever it is youre taking it for that defeats the purpose.
Other FAQs:
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subset: commoncrawl


text:
|Sabres claw back to tie it in second
|02.09.10 at 8:49 pm ET
It was a wild first five minutes of the second period in Buffalo. The Sabres came out with more aggression than they showed in the first which was immediately evident when their captain, Craig Rivet, decided it was time to throw down with Bruins enforcer Shawn Thornton at 2:54. The fight started at the same time that a penalty whistle was blown to send Bruins forward Milan Lucic to the box for a hooking call. The Sabres were then given a golden chance to get back into the game when Steve Begin took a holding penalty 54-seconds later to give Buffalo 1:08 of 5-on-3 hockey at 3:46.
The Sabres would not need all of it to get on the board. At 4:35 Buffalo center Derek Roy found himself in the middle slot facing down Tuukka Rask with time and space. Roy let go a wily wrist shot that beat Rask glove side to cut the Bruins lead to 2-1.
Boston got its first chance on the power play when Paul Gaustad tried to throw down with Zdeno Chara at 9:52. The towering Bruins captain cannot fight though because he tore most of the ligaments in his pinky the first time the Bruins played in Buffalo on Nov. 20. The finger looks pretty ugly as it is bent at a 90-degree angle and Chara has to wear a split on it during practice and games. Per NHL rules, a player cannot fight with any outside material on his hands, hence Chara cannot fight for fear of a suspension or injuring the finger more seriously than it already is. Gaustad went to the box for a two-minute unsportsmanlike yet the Bruins could not break down Ryan Miller's door.
With the Sabres putting steady pressure on the Bruins through the period, Boston's best chance came near the 18:30 mark when the puck got loose in the crease in front of Ryan Miller. Boston forward Mark Recchi dove for it but it was cleared and skipped through the neutral zone off the center wall to defenseman Tyler Myers. Bruins defenseman Adam McQuaid missed on the loose puck and Myers picked it up and let go of a sneaky wrist shot that surprised Rask on his glove side the Buffalo tied the game at two at 18:35.
Shots through second period (total):
Bruins — 11 (22).
Sabres — 14 (31).
|Bruins cannot catch a break
|02.06.10 at 5:08 pm ET
When things are going bad there is a no such thing as catching a break. Sometimes the break catches you.
The Bruins were skating to what was looking like a 2-1 win against Vancouver on Saturday afternoon when Canucks defenseman Sami Salo broke his stick trying to send a blast on Bruins goaltender Tuukka Rask. The puck idled off the shot and was over-skated in a clearing attempt by Milan Lucic before Tanner Glass came in and found it in the high slot to send it back on Rask. Vancouver forward Pavol Demitra was in the perfect place to redirect it with the shaft of his stick to tie the game at two. Vancouver went on to win in a shootout.
"Bad luck, story of my season, [expletive deleted], nothing can go right. What can you do?" Lucic said.
Rask saw the play develop in front of him but the odd deflection was enough to get it passed him in his second straight start and second straight shootout loss.
"I saw it, I saw it," Rask said. "But the guy tipped it in front of me and you can't just stand there and wait for the tip. I try to be square for the puck and he just happened to make kind of a weird tip and he tipped it over my shoulder. That's the kind of luck we haven't gotten in the past couple of games. Just got to stick with it, and it's coming."
It is those type of plays that are really starting to wear on the Bruins patience. For three straight games Boston has played well only to see a seemingly innocuous play turn into the deciding factor in the game. On Thursday it was the Matt Hunwick's penalty that led to the first on Montreal's two goals in the final minutes of the second period that turned the game around. On Tuesday against the Capitals it was Blake Wheeler and David Krejci not being able to get the puck past Jose Theodore on a wide-open net and then watch as Washington comes storming back minutes later. Good games by the Bruins are turning into losses on a dime.
"It is disheartening. You guys watched that last goal. A guy breaks his stick, [Lucic] should be off on a break away, 2-on-1, and it just kind of flubs through his legs and skate and the guy turns and fires it away," Savard said. "It is not even a clean tip, it hits his shaft and skips up in the top corner. It is just disheartening, like I said. We go through overtime trying to get the win but no break."
The Bruins were good in the third period against Vancouver. They did not sit back and wait to lose the game, they were active in trying to put a third goal passed Luongo. The Canuck stoned them which allowed his team enough of an opportunity to catch the break that the Bruins have not been able to in their 10 game skid.
"I still thought we played well in the third with that 2-1 lead and then that mistake and that turned into a goal and that is the end of it," coach Claude Julien said. "I really thought that we were playing well enough in the third that we could have won that game 2-1. When [Lucic] over-skated that puck and they just threw it at the net, those are the type of things where you say 'you've got to be kidding me, give me a break here' . . . right now it is just the way it is."
So it is. The Bruins 10th straight loss turned on a broken stick, a breakaway that wasn't and a tip off the shaft of Demitra's stick. With all the breaks, it is a wonder that the Bruins cannot catch one. That is just how things work when a team is in the skids.
|Rask: 'Don't know to cry or laugh'
|02.04.10 at 11:47 pm ET
Perhaps it was complete frustration of it all that inspired Bruins goalie Tuukka Rask to sum up the current state of affairs for the Bruins after firing 47 shots on net and scoring twice in a 3-2 shootout loss to Montreal, extending their futility streak to nine games.
"I don't know to cry or laugh here because I think we pretty much dominated the whole game," Rask said of his teammates who outshot Montreal, 47-25.
"Good chances and their goalie plays an unbelievable game. Going into shootout, I wanted to win so bad, make that save."
Neither team seemed destined to score after two scoreless rounds to open the shootout. But then Brian Gionta beat Rask up top with a backhander. And when Marc Savard failed on his attempt, the ninth straight 'L' was in the books.
"Their guy happened to beat me there and we took the loss," Rask said. "At least we get a point so it's something."
|Recchi strikes for first period lead
|at 7:45 pm ET
Neither the Bruins nor the Canadiens looked sharp in the early minutes of the first period at TD Garden. Boston had a couple power play opportunities in period when Brian Gionta went to the box at the :46 mark for hooking and then again when Jaroslav Spacek took an interference call at 9:13. The Bruins tied-17th ranked power play unit could not muster much against Habs goaltender Jaroslav Halak or the Montreal defense.
Boston looked a little tight in the early going and had trouble in making crisp passes out of its defensive zone. The Canadiens were up to the challenge though as they looked equally inept at sustaining offensive pressure and only managed to put five shots on Tuukka Rask.
As the period wore on, Boston was able to start asserting itself more and the defense clamped down and the offense started to put pucks on Halak.
Montreal continued to rack up penalty minutes and it eventually cost it a goal at 15:48 when Andre Markov went to the box for a delay of game. The Bruins set up their power play offense and Derek Morris was able to move the defense by sliding down the right wing before cycling back up to Dennis Wideman at the point. Wideman had plenty of time and space and released a slap shot towards the goal that deflected of Mark Recchi past Halak for the 1-0 lead.
First period shots:
Boston - 15
Montreal – 5
|Canadiens set to invade TD Garden
|at 1:27 pm ET
If there was ever a game for the Bruins to get back to their winning ways, Thursday night against archrival Montreal Canadiens would be it. Boston has fallen from fifth to 12th in the Eastern Conference standings during its eight game losing streak and has watched division opponents like the Habs leapfrog them in the standings.
Over the past three games the Bruins have played with good energy and decent emotion but have not seen the results on the scoreboard. The team has not had a positive seminal moment during the season, a game that defines the squad and sets the pace for winning hockey. With the Canadiens in town and all the fanfare that comes along with them, Thursday could be a good time to turn things around.
"There is a lot of history in it, the crowd always gets into it. It is kind of cool when they have all those Montreal Canadiens fans in the crowd. It always gets us excited every time we play these guys," Milan Lucic said.
Yes, there is history between these two Original Six hockey clubs, but recent history between the players on each roster is not worth much going into Thurday's contest. Last year Boston and Montreal hooked up for a memorable, fight filled battle in the Bruins last home game of the regular season and tensions and between the two were high during the Boston's three game, first round sweep in the playoffs. Yet, significant agitators on last year's Habs roster such as Mike Komisarek (Toronto), Saku Koivu (Anaheim), Georges Laraque (released late January) and Andrei Kostitsyn (knee injury, out till after Olympics) are not around as are several players from last year's Bruins roster. Hence, there are not many hard feelings carried over between the players going into Thursday's contest.
"I wish [there was carry over] but they have kind of revamped their lineup so a lot of those guys who we had the big rivalries with in the last three years are gone. I would not mind creating new ones, I suppose," Bruins enforcer Shawn Thornton said. "We don't like each other, we haven't for years. I think it will be a fun game to play in, I think everybody will be up for it. So, I hope we will turn it around, yeah."
The Bruins roster turmoil has had some effect on their goal output recently as they strive for chemistry on newly formed lines with the roster turnover or players returning from injury. As players such as Marco Sturm and Marc Savard get their health and timing back, the hope is that Boston can start generating more goals and find a way to win some games.
"We have not helped ourselves either with all the different line combinations but we are not the only team going through that and we are not going to make excuses but we have not had the same lines," coach Claude Julien said. "The chemistry with injuries and the lines, it is a challenge and kind of have to fight through that and hopefully as we are getting a little healthier hopefully that comes back."
At the same time, the Bruins goaltenders would do the rest of the team a big favor if they could completely shutdown an opposing team. Tuukka Rask was the first goalie off the ice after Thursday's morning skate and will likely get the start against the Canadiens. He said that both him and Tim Thomas are always approach games with the notion that the goaltender might be able to steal a win for the team.
"We got to have that state of mind before every game. The past few games have been like that, we can't let in any weak goals. We approach games that way that we are going to steal them and hopefully it is going to happen soon," Rask said. "We really feel that we have been playing better and better here just without the results but I am trying to get the win here today."
10 Bruins forwards participated in the morning skate with Mark Recchi, Savard, Sturm and Michael Ryder the missing men. On the blue line Boston had six skaters with Andrew Ference taking the ice and Dennis Wideman absent. Ference has missed the last 12 games with a groin injury. Mark Stuart will still be sidelined with a broken finger he sustained against the Kings last Saturday and is expected to be out until after the Olympics at the very least. It remains doubtful that Ference will play against the Canadiens which probably means that Adam McQuaid and Wideman will be on the rink when the puck drops barring a last minute change of plans.
|Savard shooting for next week, Sturm out again
|01.21.10 at 12:06 pm ET
Here are the notes from the morning skate at TD Garden.
– The Bruins recalled 24-year-old Drew Larman from Providence, which means that Marco Sturm, Steve Begin and Byron Bitz all will once again be unavailable for Boston Thursday evening when the B's take on Columbus at TD Garden. None of the three forwards participated in the morning skate. Coach Claude Julien would not describe Bitz or Begin's injuries because they could "be back at any time" and doing so would be a "liability." Sturm left practice yesterday to prevent a setback with the leg injury he has been dealing with in the past week.
"He didn't set himself back he just felt that he wasn't ready so he pulled himself off before he set himself back," Julien said.
There are no smoke and mirrors with the Bruins injury situation right now as the players who took part in the morning skate will be the ones to take the ice tonight.
"What you saw out there is what we got," Julien said. "I don't think there are any secrets there. We have got our 20 guys and that is what we will run with."
– Marc Savard spoke the the media after the skate and said that he expects to be back in the lineup next Friday on the road against Buffalo. He sustained a Grade 2 partial MCL tear against Chicago 28-seconds into the first period on January 7th. Today was the second day that he has skated and he has been wearing a big brace on during his workouts.
"When I am actually out there and doing stuff and skating I am not thinking about it but when I stop I think about it for a bit. But, besides for that it feels pretty normal," Savard said.
"Hopefully I am better for all of this and I finish strong," Savard said. "I was out there today and I felt pretty good. I said 'maybe I can come back Sunday?' But that is not the case. I have got to watch it and make sure, you don't want to come back on Sunday and hurt it again and be losing my mind. I am just going to work through it and have a good skate tomorrow and go from there."
– Tuukka Rask was the first goaltender off the ice which probably means that he will get the start tonight against the Blue Jackets.
|Turn up the volume: Chiarelli on Rask
|11.05.09 at 7:16 pm ET
Bruins general manager Peter Chiarelli addressed the media prior to Thursday's game with Montreal and explained why the club decided to sign goaltender Tuukka Rask to a two-year contract extension through the 2011-12 season.
Chiarelli said they have seen steady improvement from Rask since they drafted him from Finland.
Chiarelli said veteran Tim Thomas is still the team's No. 1 and a great role model for the 22-year-old Rask.
Chiarelli explained the origin and motivation of the Rask contract talks.
More from the team release below:
Rask has appeared in nine NHL games in his career - all with the Bruins – and has registered a 5-2-2 record, 2.43 Goals Against Average, .917 save percentage and two shutouts. He has played in four games this year for the Bruins and has posted a 2-1-1 record, 2.41 GAA and .920 save percentage. He is coming off a 2-0 shutout win of the Edmonton Oilers in his last start on October 31.
Rask made his NHL debut for the Bruins on November 20, 2007 against the Toronto Maple Leafs and recorded his first NHL victory in that game. He spent the majority of the last two seasons in the American Hockey League with the Providence Bruins where he had a 60-33-6 record and five shutouts in 102 appearances. He opened the season on an NHL roster for the first time in his career this year.
The 6′2′', 171-pound native of Savolinna, Finland played two seasons in the Finnish Elite League before coming to North America in 2007 and he has represented Team Finland in three World Junior Championships.
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PHILADELPHIA -- Outfielder Bobby Abreu has signed a minor league contract with the Philadelphia Phillies and will be invited to spring training.
The 39-year-old Abreu was a two-time All-Star with the Phillies in 2004-05. He was traded to the New York Yankees in 2006 and didn't play in the majors last year.
Abreu could fill Philadelphia's need for a left-handed hitter off the bench. He hit .322 in 50 games in the Venezuelan Winter League in 2013.
Abreu has 2,437 career hits, 287 home runs, 1,349 RBIs and 399 stolen bases over 17 seasons with Houston, the Phillies, Yankees, Los Angeles Angels and Dodgers. He ranks 22nd in baseball history in walks (1,456) and 23rd in doubles (565).
Keep up with the latest on Canada's national programs from the governing body for amateur baseball in Canada.
Baseball Canada Website
Scott MacArthur, Richard Griffin & Gregor Chisholm discuss quiet trade deadline for the Blue Jays, struggling rotation & potential Biogenesis fallout.
Scott MacArthur & Toronto Star's Richard Griffin preview the trade deadline, Blue Jays' needs & being on Boston as Jon Lester rumours ramp up.
LA Angels infielder, John McDonald joined Blue Lunch to discuss his career from the time he left Toronto to the present.


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Can Israel trust the United States when it comes to Iran?
"Even if Barack Obama is truly the pro-Israel president his Jewish supporters claim he is, the [Lyndon] Johnson precedent tells us that it may not matter. Like Johnson, Obama presides over a nation wary of another military adventure, especially in the Middle East. According to Israeli press reports, Netanyahu intends to ask Obama to state—beyond the vaue formulation that all options are on the table—that the U.S. will use military force if Iran is about to go nuclear. But few here expect Obama to make that policy explicit."
—Yossi Klein Halevi, "Can Israel trust the United States when it comes to Iran?"
Photo courtesy of Getty Images.
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Now browsing: Hometown News > Fishing > Henry Caimatto
Offshore, we started the week with great fishing from 30 feet out. We had Dolphin, Sails, Kings and Cobia.
If there were too many boats in one location, all you had to do was go deeper to next color line and you were back in the fish. And there were lots of fish.
Anglers reported as many as six to eight on Sails and more Dolphin than you could want. Trolling or using the live bait the fish were eating, and most of the Dolphin were gaffers and the Sails were everywhere. It was very busy fishing.
Cobia fishing was a little different. They follow the sharks, so if you did get one on and you were not fast enough, the sharks had their way with your catch. Talked with several anglers that just gave up, because they felt like they were just feeding the men in gray suits.
But as the week progressed so did the seas, which built to eight feet and kept many weekend anglers just looking and saying, "We should have gone yesterday."
Looking at pictures of the St. Lucie Inlet at the points the rock jetties, I saw they were covered by waves, which were not a good idea.
It will settle down this week and maybe we can get out this coming week. Let's hope the fish are still with us.
Big rollers also took their toll on the beach, with lots of white water. As the seas settle, Blue Fish and Jacks will keep most people busy as the second rod is looking for the Pompano.
After two or three years of great Pompano fishing, we are still waiting for them to show. Checking last year's reports, the month of March was the busiest for Pompano. Now if the seas will settle and the turbidity leaves the water's edge, maybe we can go the beach and find a few. That is, if the Blues will leave our baits alone.
With the east wind, it has been the east side of the river that is holding attention. There has been excellent Trout biting all week on everything, and live to all types of artificial baits were getting attention.
Three to four feet was the zone for working baits slowly across the bottom. From Middle Cove south to Joe's Point, we had reports of slot Trout to over the slot. One cool thing, the bite time was all day.
Few Blues and Lady Fish in the mix with the occasional Red Fish, but the rods were bent all day. By the bridges, it was Sheep head, Drum, some Blues and a few Macs that kept anglers busy, but the Snook were just not hungry.
Early in the week, Snook were chewing getting ready for the cold. Mother Nature told them when and when not to eat, and they did. There was a lot of fish to look at but hard to get one to eat.
It is warming this week, so get ready. Yes, there were a few Pompano but they were small, so let's hope for this week.
Now if only the wind and swells will settle.
Henry Caimatto is the owner of the Snook Nook Bait and Tackle shop in Jensen Beach.
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10.2. Principal Components Analysis
PCA is a mathematical technique which transforms the original image data, typically highly correlated, to a new set of uncorrelated variables called principal components.These new components are linear combinations of the original image bands and are derived in decreasing order of importance so that, for example, the first principal component accounts for as much as possible of the variation in the original data. Each principal component is called an eigenchannel. The benefits of the technique from a geological standpoint are principally that information not visible in false colour composite images can be highlighted in one of the resulting component images.
There is a high degree of correlation within the Peru images. As a result false colour composite images may not show the full range of information present in the image bands. A method of extracting subtle information within the image, such as Principal Components Analysis, will be of value in analysing this image.
Open a viewer window. Display a true colour composite image, i.e. band 1 assigned to the blue gun, band 2 to the green gun, band 3 to the red gun and a false colour composite (of channels 6,4,2). Produce a sketch map of the area.
To run the Principal Components Analysis program it is necessary to execute a program called Principal Components from the Raster tab,Resolution group and Spectral and Principal Components.
Figure 10.1 - : Prinpal Components window
Use all six input image channels and specify six 8-bit eigenchannel images to be produced (e.g. 1,2,3,4,5,6) in a file. You should also check the boxes for the Eigenvector matrix and Eigenvalues to be displayed in the session log as shown in figure 10.1.
The variance figures for each principal component are shown in the eigenvalue list. These indicate the amount of variation accounted for by each component within the feature space.You will notice that nearly 99% of the information within this feature space is found within the first two principal components (92.1% in channel 1, 6.5% in channel 2). However this does not necessarily mean that the remaining components do not contain any useful information.
Display each component as a greyscale image and examine each eigenchannel in turn. You will discover that one of the components indicates three distinct oval-shaped porphyry copper ore bodies. You may have noticed one of the ore bodies when looking at the true colour composite image, although rather less clearly defined. Add these features to your sketch map.
To determine the area of each of the ore bodies you will need to use the Measure facility from the Home tab,Information group. Define three polygons, one for each ore body. Select square kilometres as the measurement unit.
Additional notes
Figure 10.2 - : Result of Principle Component Analysis - Clockwise PC 1 (Gray Scale 1), PC 2 (Gray Scale 2), PC 3 (Gray Scale 3), PC 4 (Gray Scale 4) , PC 5 (Gray Scale 5) , PC 6 (Gray Scale 6)
The principal components themselves can be explained as follows:
- PC 1 - accounts for general changes in albedo, i.e. the reflectivity of surfaces. The component is derived from all the input bands
- PC 2 - depicts the areas of moisture and the line of the rivers. The component is derived principally from bands 1, 2 and 3 contrasted with band 5.
- PC 3 - picks out the areas of vegetation with the river valleys. The component is dominated by the signal from band 4, the near infrared band, contrasted with band 6.
- PC 4 - contrasts the granites with the vegetation. The component is dominated by band 3 contrasted with bands 1 and 5.
- PC 5 - picks out the porphyry copper ore bodies. The component is derived from band 6 and to a lesser extent band 4 contrasted with bands 5 and 3.
- PC 6 - accounts for the residual noise or redundant information within the scene
The three porphyry copper ore bodies seen in PC 5 have the following approximate areas:
|Ore body 1
|4.5 km2
|Ore body 2
|1.3 km2
|Ore body 3
|1.4 km2
where ore body 1 is at the top left of the image and ore body 3 at the bottom right. Ore body 1 is of a workable size, the other ore bodies are currently sub-economic.
As an additional task you may wish to attempt to derive a geological map using an unsupervised cluster analysis or supervised maximum likelihood classification. In this case it would be sensible to choose three or four of the principal component images. From the properties of the components above it would be best to choose components 5, 4, 2 and possibly 1. Note that this exercise shows another benefit of using Principal Components Analysis, namely the reduction of data without loss of information, prior to classification.


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Holly Gingerella loves her 13-year-old daughter, Alicia, very, very much.
And she knows that Alicia loves her.
And it's that love that makes Gingerella fight every day to save the life of her daughter, who was purportedly beaten by four classmates last year in Woonsocket in a video that ended up on YouTube.
"She went back to school. She probably lasted maybe two weeks. The other girls were still in the school, so I didn't feel like she was safe and the school was doing enough to keep her safe," Gingerella said.
Gingerella left her job and moves to Westerly, where she hoped Alicia would be safe. She enrolled her in school, but the trauma of her daughter being bullied started to come to light.
"Alicia had been cutting herself, had been telling some friends that she was going to hurt herself, had attempted to commit suicide, and her friends brought it to the school, and the school called me," Gingerella said.
She immediately took Alicia to Westerly Hospital for evaluation.
"The mental health people that were brought in decided she needed hospitalization," Gingerella said.
The hospital didn't have the facilities to properly care for Alicia that doctors thought had a severe mental illness. So she was transferred to Butler Hospital in Providence.
"Butler was good because it kept her safe. It was there when she was diagnosed with BDD," Gingerella said.
BDD, or body dysmorphic disorder, was causing Alicia's skewed perception of herself, and in this case, cutting and self-mutilation.
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Foster emerging musical talent.
The University of Colorado Boulder offers piano lessons for youth ages 6 to 17 years old. Through private lessons, youth will learn from experienced instructors from the CU-Boulder College of Music.
The CU Youth Piano Program trains students through weekly private and group lessons. Instructors are experienced teachers from the CU College of Music, and the program is supervised by the CU Piano Pedagogy Chair, Dr. Alejandro Cremaschi. The lessons provide thorough instruction at the highest and most effective pedagogical standards while providing opportunities for fun, motivation, and enjoyment of music.
The group class is intended for beginners in second and third grade without prior piano lessons. Classes will be taught in small groups of up to 8 in the electronic piano laboratory at the College of Music. Classes begin Sept. 5 (no class Sept. 19 and Nov. 28).
$300 semester tuition (13 one-hour meetings). The instructor is Dr. Meredith Mihm.
For more details, visit: http://spot.colorado.edu/~cremasch/Site/Piano_for_Children_at_CU.html
The lessons include developing skills for:
• Classical and popular pieces
• Reading music
• Healthy techniques
• Ear training and music theory
• Performance opportunities
Lessons target children age 6-17. New students will have a diagnostic lesson and parent interview during the first meeting with the instructor to determine their level and needs.


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What are the best restaurants in Delray Beach and its environs?
- b
- Benjamin68 Feb 4, 2007 05:38 AM
My wife and I will be visiting my mother at her Delray Beach retirement community later this month. We would love to know what the best dining options are in the area. We're primarily concerned with great food, and are not looking to visit nostalgia joints or high-end "status spots," unless, of course, they genuinely merit the status. Thanks for your help.
re: rsanders99
A brief 2010 uodate: rsanders99's list remains good. I would add La Cigale (Mediterranean) on Federal Highway between Atlantic and Linton and Caruso in Royal Royal Palm Plaza in Boca (high end Italian like Tramonti). Though many would disagree, I am not wild about Vic & Angelo's on Atlantic in Delray--but the same owner's new American bistro across the street , The Office, is very good.
119 E Atlantic Ave, Delray Beach, FL 33444
re: Benjamin68
These are not in any particular order.
First bit of advice is stay east of I-95. Once you cross over to the western part of Delray Beach the only good food is bagels and novey.
32 East is the best, full stop. Others, it depends on the night and the chef's temperment. I've had a pretty good meal at the Oyster place across from Kilwins most times, but once it was not that great. People rave about Sonoma Cafe, my lamb was sent back twice and then they screwed up the skirt steak. My dinner was banana ice cream at Kilwin's that night. The sushi/asian place three doors down from Kilwin's looked nice as well.
re: rcburli
Go to Bamboo Fire Cafe. They will make ANYTHING and it's VERY reasonable. Otherwise, in that price. range Downtown Delray is not the place.
Bamboo Fire Cafe
Delray Beach, FL 33483, Delray Beach, FL 33483
re: jfood
jfood, I am quite confused with your statement about staying east of I-95. Is it an age thing? Please explain? I see that you must visit Delray from your past posts quite often.
I respect all of your posts but sometimes I get a little confused with what you are saying.
jfoof, What do you think is a reasonable price for one dozen raw oysters at a Palm Beach county restaurant. I a a laywoman and would appreciate you expertise.
I'm just returned from doing the same thing. Hands down, the best meal I had was at The Cuban Cafe, (561) 495-5999, 14400 Military Trl, Delray Beach, FL 33484. Casual and unassuming - the drinks were a little watered, but the food was outstanding! I blogged about the trip in some detail at http://funplayingwithfood.blogspot.co..., but below are a few photos from our Cuban Cafe dinner. My snapper stuffed with shrimp in seafood sauce was just amazing.
re: NancyH
Was the Snapper a filet or whole fish ? In the picture it looks like filet. I have been finding it very difficult getting whole Snapper in the restaurants locally. I see loads of " Snapper Filet" not mentioning what kind of Snapper it is. With all of the articles in the newspapers about substituting of "Snapper" and "Grouper" I have become very wary of these filets, which makes my restaurant dining not as pleasurable as it should . Recently I went to a restaurnt where I had been eating whole Yellow Tail Snapper for years. They said that they had only filets.Upon further inquiry they said they have whole snapper "once in a while". Sounds fishy to me, eh ?
re: albee
Both restaurants served filet of snapper. The Cuban Cafe's version was a huge filet stuffed with wonderfully fresh shrimp (and I can't stand processed shrimp - the smell and taste of sodiumpolytriphosphate mades me want to heave). Though I know the controversy of which you write - the substituting of cheaper or frozen filets for the local ones.
re: smartie
I agree mostly except for Bostons. Bostons has a great location but they put the "barf" in bar food. Best though is Bamboo Fire Cafe.
Bamboo Fire Cafe
Delray Beach, FL 33483, Delray Beach, FL 33483
Dada offers the best food and setting in Delray, Shore Beach Bar is a great spot for proximity to beach, and Black Tip Reef is a great happy hour.
overall the best restaurant on the avenue. the dimly lit bar, mix of jazz + modern classics + constantly updated menu sets it apart from the others. i'm not very interested in the menu for the most part as items are often trendy + contrived, looking good in print but not working well as finished dishes. the bar area is a great place to enjoy a glass of wine or cocktail along with a margharita pizza which is always available. appetizers can be rather small (seared tuna), house made pastas can be very good as well as fresh fish although the presentation is often uninspired. the desserts are really hit + miss. often a unique sorbet or ice cream will be your best best. a door man would be welcome on weekends when the college kids filter in. they should be pushed towards sol kitchen (owned by 32 east). senior hostess can be rude + forgetful. be sure to check back often to let her or the other girls know you are there as they may forget about you. tables in the bar area may be reserved. the owner is there often + is very pleasant + accommodating.
• extremely friendly bar staft (don't forget other customers)
• margharita pizza is always available
• upscale, intimate bar area during the week
• very good dishes, when the ingredients mesh
• servers are a bit robotic at times
• menu item combinations often unsuccessful
• routinely small appetizer portions + weak presentation
• bar staff often too focused on individual customers
• college kids mixing in late night on weekends
re: themaddiner
resto name please?
#1 Is Bamboo Fire Cafe - It's the only place you will be talking about well after your vacation ends. Go here first because it's less expensive (and better) than most. Only place in Delray you can get gourmet food in a casual setting.
#2 Jimmy's Bistro. Best food in Delray -- can be a little stuffy at times. NOT CHEAP!
#3 The Living Room (Boynton Beach) - it's worth the 13 minute drive.
Bamboo Fire Cafe
Delray Beach, FL 33483, Delray Beach, FL 33483
Jimmy's Bistro
9 S Swinton Ave, Delray Beach, FL 33483
There are a lot of options in Delray Beach. I noted a few comments already posted but will add a few ideas.
Here are a few restaurants that I like.
32 East
Blue Anchor British Pub
Bostons on the Beach
Busch's Seafood Restaurant
Cabana Restaurant - Delray
City Oyster
Delray Beach - Gol The Taste of Brazil
J&J Seafood Bar and Grill
Vic & Angelo's Delray
Each of these has a different flair but very good food.
Best Palm Beach Restaurants http://www.bestpalmbeachrestaurants.com is a good reference for Delray Beach Restaurants. I also look on the site at http://www.bestpalmbeachrestaurants.c... to look for good discounts in the area to save a few bucks.
My personal favorite is VIc & Angelo's but that is because I like the style of food the best.
City Oyster
213 East Atlantic Ave, Delray Beach, FL 33444
Blue Anchor British Pub
804 E Atlantic Ave, Delray Beach, FL 33483
Busch's Seafood Restaurant
840 E Atlantic Ave, Delray Beach, FL 33483
re: jfb130
Busch's closed a few months ago


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text: content LE Magazine March 2004 Memory Assessment Early detection of isolated memory deficits in the elderly: the need for more sensitive neuropsychological tests. BACKGROUND: Early detection of cognitive decline in the elderly is important because this may precede progression to Alzheimer's disease. The aim of this study was to see whether sensitive neuropsychological tests could identify pre-clinical cognitive deficits and to characterize the cognitive profile of a subgroup with poor memory. METHODS: A neuropsychological test battery was administered to a community-dwelling sample of 155 elderly volunteers who were screened with CAMCOG at enrolment (mean age 74.7 years). The battery included tests of episodic memory. semantic and working memory, language and processing speed. RESULTS: Episodic memory test scores below 1 S.D. from the cohort mean identified 25 subjects with non-robust memory performance. This group was compared to the remaining 'robust memory' group with a General Linear Model controlling for age, IQ, education, and gender. Test performance was significantly different in all tests for episodic and semantic memory, but not in tests for working memory, processing speed, and language. CANTAB paired associates learning and spatial recognition tests identified the highest percentages of those in the 'non-robust memory group. Processing speed partialled out the age effect on memory performance for the whole cohort, but the 'non-robust memory' group's performance was not associated with age or processing speed. CONCLUSIONS: Sensitive neuropsychological tests can detect performance below the norm in elderly people whose performance on MMSE and CAMCOG tests is well within the normal range. Age-related decline in memory performance in a cohort of the elderly may be largely due to inclusion within the cohort of individuals with undetected pre-clinical Alzheimer's disease or isolated memory impairment. Psychol Med. 2002 Apr;32(3):483-91 Decline in learning ability best predicts future dementia type: the freedom house study. The authors studied longitudinal change in learning efficiency as a predictor of future dementia type among healthy, well-educated, noninstitutionalized elderly retirees. Serial assessments of memory were obtained using the California Verbal Learning Test (CVLT). Latent growth (LG) models were developed from the slopes of the subjects' performance over the first five CVLT learning trials at each of three serial administrations (e.g., cohort inception [i.e., baseline] [CVLT1], 18 months [CVLT2] and 36 months [CVLT3]). The resulting growth curves were incorporated into a higher order LG model representing the dynamic change in learning efficiency over time (DeltaCVLT). DeltaCVLT was used to predict each subject's "dementia type" (i.e., clinical state) at 36 months (e.g., no dementia, Type 1 [Alzheimer type] dementia or Type 2 [non-Alzheimer type] dementia), after adjusting for CVLT1, baseline age, and baseline dementia type. Nonlinear (logarithmic) LG models of CVLT1-CVLT3 and DeltaCVLT best fit the data. There was significant variability about both CVLT1 and DeltaCVLT, suggesting subgroups in the sample with significantly different baseline memory function, and different rates of deterioration in learning efficiency. Age, baseline dementia type, and DeltaCVLT made significant independent contributions to final dementia type. CVLT1 did not predict final dementia type independently of the other covariates. These data suggest that baseline memory performance in noninstitutionalized elderly retirees does not predict future dementia type independently of the dynamic rate of change in memory measures. Serial administrations of memory tests may help identify nondemented persons at greater or lesser risk for conversion to frank dementia in the near-term. Exp Aging Res. 2003 Oct-Dec;29(4):385-406 P300 (latency) event-related potential: an accurate predictor of memory impairment. To determine if P300 latency changes precede and correlate with memory and mental status, patients (N=1506 aged 20-100 years) who received medical and psychiatric diagnoses (from 1997 to 2002), were assessed for P300 (N=1496), WMS-III (N=694), and MMSE (N=456). Patient and control groups included, a) normal WMS-III on all 4 subscales (N=36), b) normal WMS-III and MMSE (N=189) with subjective memory/mental status complaints, and c) medical patients with normal WMS-III and no memory complaints (N=205), and d) P300 control group without medical, psychiatric or memory problems for ROC. Patients with impaired/borderline memory had a prolonged P300 latency (P<0.02) compared to age matched non-impaired controls; in patients with normal WMS-III/MMSE, with subjective mild memory/mental status impairment, P300 latency was prolonged compared to controls (P=0.0004). The P300 latency increased by 0.72ms per year (P=7.9x10(-65)) and voltage decreased by 0.03dV per year (P=6.7x10(-10)), and both parameters were linearly correlated with the age of the subjects. Male subjects had an average voltage of 6.1dV and female 6.8dV (P=0.00009). Statistically, prolonged latency began at age range 41-50 (P=0.0002); reduced P300 voltage began at age range 51-60 (P=0.003). WMS-III memory decline for all measures began in females at age range 61-70 (P value at least=0.02) and for males at age range 61-80 (P=0.02). Prolonged P300 latency (P<0.0001) and memory impairment (at least <0.02) were greater for females than males. MMSE memory decline, male and female, began at age range 81-90 (P value of at least 0.00007). In our logistic regression model P300 latency was more predictive of WMS-III impairment than MMSE > 24. In patients whose WMS-III score is impaired < or = 69, or borderline < or = 79 (P at least=0.004), a P300 latency more prolonged than the norm (> or = 300 + 30 + Age) identifies these patients, whereas a MMSE > 24 failed. With the ROC curve, we confirmed that P300 latency could accurately identify borderline/impaired memory. Clin Electroencephalogr. 2003 Jul;34(3):124-39 P300 latency and age: a quadratic regression explains their relationship from age 5 to 85. The use of P300 latency to demonstrate cognitive dysfunction is important. P300 latency decreases with age in children and then increases with age in adults. It has been debated whether the relationship between age and P300 latency is linear or quadratic. If the relationship is linear, then at least two regression equations in opposite directions are required for children and for adults, and perhaps a third for the elderly. This is a report of data from an age-stratified sample of 97 normal individuals ages 5 through 85. The best regression equation is quadratic, using log transformed age, with accurate projection of 95% confidence limits for P300 latency by age. This quadratic regression simplifies the application of P300 latency across the lifespan in the management of disorders affecting cognition, such as Traumatic Brain Injury, Attention Deficit-Hyperactivity Disorder, and Obstructive Sleep Apnea. Clin Electroencephalogr. 1998 Jan;29(1):1-6 A critical discussion of the role of neuroimaging in mild cognitive impairment. OBJECTIVE: In this paper, the current neuroimaging literature is reviewed with regard to characteristic findings in mild cognitive impairment (MCI). Particular attention is drawn to the possible value of neuroimaging modalities in the prediction and early diagnosis of Alzheimer's disease (AD). METHODS: First, the potential contribution of neuroimaging to an early, preclinical diagnosis of degenerative disorders is discussed at the background of our knowledge about the pathogenesis of AD. Second, relevant neuroimaging studies focusing on MCI are explored and summarized. Neuroimaging studies were found through Medline search and by systematically checking through the bibliographies of relevant articles. RESULTS: Structural volumetric magnetic resonance imaging (MRI) and positron emission tomography (PET)/single photon emission tomography (SPECT) are currently the most commonly used neuroimaging modalities in studies focusing on MCI. There were considerable variations in demographical and clinical characteristics across studies. However, significant hippocampal and entorhinal cortex volume reductions were consistently found in subjects with MCI as compared with cognitively unimpaired controls. While hippocampal and entorhinal cortex atrophy in subjects with MCI are also well-established risk factors for the development of AD, these measures cannot be regarded as being of high predictive value in an individual case. Evidence for other typical neuroimaging changes in MCI is still scarce. In PET and SPECT studies, reduced blood flow and/or glucose metabolism in temporoparietal association areas, posterior cingulate and hippocampus were associated with a higher risk of progressive cognitive decline in MCI. In quantitative electroencephalogram (QEEG), low beta, high theta, low alpha and slowed mean frequency were associated with development of dementia. CONCLUSIONS: Existing studies suggest that neuroimaging measures have the potential to become valuable tools in the early diagnosis of AD. To establish their value in routine use, larger studies, preferably with long prospective follow-up are needed. Acta Neurol Scand Suppl. 2003;179:52-76 Effects of alcoholism, anxiety and depression on P300 in women: a pilot study. OBJECTIVE: The present investigation was designed for the purpose of revealing functional brain impairments associated with alcoholism, anxiety and depression. METHOD: The subjects were 56 women, with an average (SD) age of 34.8 (7.3) years. None reported a history of neurological or major medical disorders, or drug abuse. Twenty-nine of the women met DSM-IV lifetime criteria for a diagnosis of alcohol abuse or dependence. Twenty-five women reported mild or higher levels of anxiety, as indexed by a Beck Anxiety Inventory (BAI) score greater than 7. Electroencephalographic activity was recorded while subjects performed a visual ("oddball") selective attention task comprised of rare target, rare nontarget and frequent nontarget stimuli. P300 event-related potentials elicited by the rare target and rare nontarget stimuli were analyzed. RESULTS: The initial analysis was structured as a 2 (alcoholism) by 2 (anxiety) factorial. Analyses revealed no significant effects of alcoholism on P300. However, women reporting a BAI score greater than 7 exhibited significantly smaller P300 amplitudes than their nonanxious counterparts. The P300 decrement remained significant when depression level (Beck Depression Inventory [BDI-II]) and age were entered as covariates. A separate analysis was conducted in which the 56 subjects were classified by alcoholism and depression level (BDI-II score < or =13 vs >13). The analysis revealed no significant P300 differences associated with these factors. CONCLUSIONS: It is hypothesized that anxiety might play a role in mediating or amplifying the P300 decrements that have been attributed to alcoholism and depression in women. Additional and more comprehensive studies are needed to discern the validity of this hypothesis. J Stud Alcohol. 2001 Sep;62(5):571-9 The P300 brain potential is reduced in smokers. RATIONALE: Tobacco smoking is the most prevalent type of substance abuse, yet its biobehavioral etiology is little understood. Identification of differences between smokers and non-smokers on basic characteristics of neurocognitive functioning may help to elucidate the mechanisms of tobacco dependence. OBJECTIVES: This study assessed the relationship between smoking status and the P300 component of event-related potential (ERP) while controlling for potential confounders such as alcoholism, drug abuse, and psychopathology. METHODS: The ERP responses elicited by a visual oddball task were measured at the mid-parietal site in 905 current smokers, 463 ex-smokers, and 979 never smokers. RESULTS: P300 amplitude was significantly lower in current cigarette smokers compared to never-smokers. Ex-smokers did not differ significantly from never-smokers. P300 reduction was also associated with alcoholism, drug dependence, and family density of alcoholism. However, after controlling for smoking, only family density of alcoholism remained a significant predictor of P300 amplitude. CONCLUSIONS: The results indicate a significant effect of smoking status on P300 amplitude, which is additive to family history of alcoholism and suggest that either (1) long-term tobacco smoking may produce a reversible change in brain function, or (2) reduced P300 may be a marker of risk for nicotine dependence. Psychopharmacology (Berl). 2000 May;149(4):409-13 Pectin Endogenous galactoside-binding lectins: a new class of functional tumor cell surface molecules related to metastasis. The formation of secondary tumors by circulating cancer cells (blood-borne metastasis) correlates with an increased tendency of the cells to form emboli by aggregation with other tumor cells or with host cells. Although it is evident that cell-cell recognition and adhesion are mediated by cell surface components, the identity of these molecules is only now being unraveled. Over the last decade an increasing number of studies have demonstrated the presence of endogenous carbohydrate-binding proteins on the surface of various normal cells, and it has been proposed that such lectin-like molecules might be involved in intercellular adhesion. We have shown that various tumor cell lines contain endogenous galactose-specific lectins. Lectin activity was detected at the cell surface by the binding of asialofetuin. This glycoprotein also enhanced the aggregation of the tumor cells. After purification by affinity chromatography on immobilized asialofetuin the lectin activity was associated with two proteins of Mr 14,500 and 34,000. By using polyclonal and monoclonal antilectin antibodies in conjunction with various immunologic techniques we have demonstrated that the endogenous lectins are present on the surface of different tumor cells. Quantitation of cell surface lectins by flow cytometric analyses of antilectin antibody binding revealed that among related tumor cells those exhibiting a higher metastatic potential expressed more lectin on their surface. The binding of monoclonal antilectin antibodies to metastatic cells decreased asialofetuin-induced homotypic aggregation in vitro and suppressed the ability of the cells to form lung metastases after intravenous injection in the tail vein of syngeneic mice. These results strongly implicate the tumor cell surface lectins in cell adhesion and metastasis. We propose that such lectins can increase the ability of tumor cells that enter the blood stream to form aggregates with other tumor cells, or to adhere to host cells or the extracellular matrix and thereby increase their metastatic potential. Other contributing components to tumor cell-host cell interactions are cell surface carbohydrate-binding proteins that have been detected on lymphocytes, platelets, macrophages, hepatocytes, and endothelial cells. These lectin-like molecules might recognize and bind carbohydrates expressed on the surface of tumor cells and enhance emboli formation and organ colonization. Cancer Metastasis Rev. 1987;6(3):433-52 Expression of the endogenous galactose-binding protein galectin-3 correlates with the malignant potential of tumors in the central nervous system. BACKGROUND: The 31-kilodalton beta-galactoside-binding protein galectin-3 has been associated with cellular transformation and metastasis. Because neural tissues contain large amounts of glycoconjugates, and endogenous carbohydrate-binding proteins have been described in the human brain, the authors examined the expression of galectin-3 in human brain tumors and metastases to the central nervous system. METHODS: Brain tumors were categorized by the World Health Organization system and galectin-3 expression by immunoperoxidase staining using a quantitative staining score. RESULTS: Glioblastomas (Grade 4 astrocytomas) all stained strongly for galectin-3, whereas low grade astrocytomas (Grade 2) did not express the endogenous lectin. Anaplastic astrocytomas (Grade 3) exhibited intermediate expression. The staining score was significantly associated with tumor grade (P < 0.001). Normal brain tissue and benign tumors did not express galectin-3, whereas metastases to the brain were all positive for galectin-3 expression. Metastases expressed significantly more galectin-3 than the primary tumors from which they were derived (P = 0.003). CONCLUSIONS: Galectin-3 expression correlates with the malignant potential of tumors in the central nervous system. Cancer. 1997 Aug 15;80(4):776-87 Inhibition of spontaneous metastasis in a rat prostate cancer model by oral administration of modified citrus pectin. BACKGROUND: Prostate cancer is the most common cancer diagnosed in U.S. men and remains incurable once it has metastasized. Many stages of the metastatic cascade involve cellular interactions mediated by cell surface components, such as carbohydrate-binding proteins, including galactoside-binding lectins (galectins). Modified citrus pectin (pH-modified), a soluble component of plant fiber derived from citrus fruit, has been shown to interfere with cell-cell interactions mediated by cell surface carbohydrate-binding galectin-3 molecules. PURPOSE: The aim of this study was to determine whether modified citrus pectin, a complex polysaccharide rich in galactosyl residues, could inhibit spontaneous metastasis of prostate adenocarcinoma cells in the rat. METHODS: The ability of modified citrus pectin to inhibit the adhesion of Dunning rat prostate cancer MAT-LyLu cells to rat endothelial cells was measured by 51Cr-labeling. Modified citrus pectin inhibition of MAT-LyLu cell anchorage-independent growth was measured by colony formation in agarose. The presence of galectin-3 in rat MAT-LyLu cells and human prostate carcinoma was demonstrated by immunoblotting and immunohistochemistry. One million MAT-LyLu cells were injected subcutaneously into the hind limb of male Copenhagen rats on day 0. Rats were given 0.0%, 0.01%, 0.1%, or 1.0% (wt/vol) modified citrus pectin continuously in their drinking water (from day 4 until necropsy on day 30). The number of MAT-LyLu tumor colonies in the lungs were counted. RESULTS: Compared with 15 or 16 control rats that had lung metastases on day 30, seven of 14 rats in the 0.1% and nine of 16 rats in the 1.0% modified citrus-pectin group had statistically significant (two-sided; P < .03 and P < .001, respectively) reductions in lung metastases. The lungs of the 1.0% modified citrus pectin-treated rats had significantly (two-sided; P < .05) fewer metastatic colonies than control groups (9 colonies +/- 4 [mean +/- SE] in the control group compared with 1 colony +/- 1 in the treated group). Modified citrus pectin had no effect on the growth of the primary tumors. In vitro, modified citrus pectin inhibited MAT-LyLu cell adhesion to rat endothelial cells in a time- and dose-dependent manner as well as their colony formation in semisolid medium. CONCLUSIONS: We present a novel therapy in which oral intake of modified citrus pectin acts as a potent inhibitor of spontaneous prostate carcinoma metastasis in the Copenhagen rat. IMPLICATIONS: Further investigations are warranted to determine the following: 1) the role of galectin-3 in normal and cancerous prostate tissues and 2) the ability of modified citrus pectin to inhibit human prostate metastasis in nude mice. J Natl Cancer Inst. 1995 Mar 1;87(5):348-53 Modified citrus pectin (MCP) increases the prostate-specific antigen doubling time in men with prostate cancer: a phase II pilot study. This trial investigated the tolerability and effect of modified citrus pectin (Pecta-Sol®) in 13 men with prostate cancer and biochemical prostate-specific antigen (PSA) failure after localized treatment, that is, radical prostatectomy, radiation, or cryosurgery. A total of 13 men were evaluated for tolerability and 10 for efficacy. Changes in the prostate-specific antigen doubling time (PSADT) of the 10 men were the primary end point in the study. We found that the PSADT increased (P-value<0.05) in seven (70%) of 10 men after taking MCP for 12 months compared to before taking MCP. This study suggests that MCP may lengthen the PSADT in men with recurrent prostate cancer. Prostate Cancer Prostatic Dis. 2003;6(4):301-4 Page12


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Chicago City VS. Suburbs Craft Beer THROWDOWN
Alright...this could get ugly. We are honored, and a little scared, to host the first ever City vs. Suburbs competition in CCBW history (as far as we know). Half our taps will go to the city (Revolution, Half Acre, and Begyle) and half will go to the 'burbs (Solemn Oath, Buckledown, and Two Brothers). We will be rotating through some super-rare offerings from the 6 participants throughout the week. Make repeated visits to make sure you're getting a taste of everything. Throughout the week, brewers and reps from the participants will be swinging by to greet guests, buy some pints, distribute some merch, etc.. Tweet your favorite(s) using the hashtag #SMGBeerVote, as we will be crowning a winner (or winners) on the 24th.
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Kapha skin tends to become oily with enlarged pores. This translates into skin outbreak and acne. A Kapha person generally has Normal – Oily skin and has thick, shiny hair.
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