A good friend of ours is an English teacher who paints in her spare time. We have a number of her works hanging in our house. The artwork above is a photo of one of her paintings done when facing south from our tent sites where our families camp together each summer holidays.
Her art group is having a presentation in a month or so with the theme: absence/presence. She suggested that I could write a song based on the theme and play it at the opening. This is what I came up with.
As always, all comments and constructive criticism welcome.
NIce crisp guitar chords at the start. Relaxed vocal. Evocative lyrics. Good variety in the structure of the song. The "you and your guitar" simplicity works well for this song. Excellent work, my friend! You'll need a few copies of "A Lucky Man" with you at the opening after you sing this!
Thanks, Philip. I can imagine this number coming up OK with a grander arrangement, and perhaps I will do that anyway for this year's CD :-), but the solo acoustic path beckoned and that fits in with my goal for the year of making sure that every song I post, I still feel comfortable singing round the campfire. I appreciate your support and friendship. Talk soon, Peter.
Thanks for having a listen, Ramona. Glad you enjoyed it. Take care, Peter.
nice one peter. i always like a c - fmaj7 trip. good honest vocal....one take wonder.
The old C - Fmaj7 trick eh, Chief. That's the third time I've fallen for that this month :-) Thanks for dropping by, Julian. One take - all care, no responsibility... Talk soon, Peter.
This is the perfect recording to display what an impressive talent you are. Great song! Strong and accurate guitar accompaniment! Excellent vocal! Clear crisp recording! And you're doing it on a guitar you built with your own two hands! Inspiring!
Thanks for the kind words Andrew. You are too kind. Really, you are too kind :-) It is satisfying to be able to sing a song you have written using a guitar you have made, though. I appreciate your unstinting support. Take care, Peter.
You pull it off very nicely and the lyrics really paint a picture.
Thanks, Jay. Me and my guitar/s have been been keeping ourselves entertained for many years now. It is a great way to pass a few hours/months/decades... :-) I appreciate your comments. Regards, Peter.
Thanks, Neil. The open mic feel is what I was hoping to present so it is good you thought it worked out OK. Kind regards, Peter.
i do like the Peter unplugged sound. just voice/instrument is always good to hear. words appear to fit the occasion perfectly. will some one videotape the show? if so, you should upload some clips for us.
Hi Sam. Thanks. I do most of my singing unplugged and I wanted to see what you guys thought. Glad to see it seems to come across OK. I will see what we can come up re video. Our painter friend seems happy with the song. I appreciate your support. Take care, Peter.
70's AM folk rock is my desert island genre, i never get tired of it. this has that same vibe. i like it. those are good old comfortable chords too. enjoyed.
Thanks, Craig. My genre, too. As you can tell :-) There are some chord combinations that just sit together nicely. The C - Fmaj7 combo is one such beast. Glad you liked it. Take care, Peter.
Thanks, Chris. In this situation I will probably be just providing background music most of the time whilst people walk around and look at the artwork, so background talk will be inevitable. Hammers... there's a thought :-) Glad you liked it. Rant accepted. Regards, Peter.
Thank you, Patty. So glad you liked it. Regards, Peter.
Thanks, John. My friend, the artist, is very pleased. Let's hope others think so as well. I appreciate your comments. Take care, Peter.
good grief, there is no end to your talent! this is fabulous sir!
Thanks, Karen. There are many talented people round here, yourself included. I am just happy to be part of it. Kind regards, Peter.
Hi Heidi. Thank you for your kind words. I will probably re-record this with additional instrumentation at some stage. I wanted to make sure the song worked unplugged as well. I appreciate you dropping by. Regards, Peter.
No issues at all with your comment, Heidi. I agree with you that it would come up well with full instrumentation. I was just having a bit of fun with a play on words (to be or not to be...) I really appreciate your comments. Take care, Peter.
Hi Graham. Yes, I am sure there have been quite a few songs with the same title. It seemed to fit this song though, so I went with it. Thanks you for your kind words. I am glad you liked it. Regards, Peter.
The music itself paint pictures! Very nice Pete! Thanks for sharing!
Hi Freddy. Glad you liked this one. I did try to add some colour into the lyrics :-) Talks soon, Peter.
Peter! this is excellent, unplugged, real and really shows your talents as a song writer. I enjoyed this ... something to be said about a capo on an acoustic and you built it? Fantastic.
... and tell your friend she's done a lovely painting.
Thanks, Stan. Solo, unplugged has a warmth and intimacy that you can't beat, and is how I play 95% of the time, so I thought it was fitting to present a song about art and performance in that format. The guitar I made (at a luthier school) is a beautiful thing - all Australian tonewoods - blackwood, bunya pine, huon pine, gidgee, queensland maple. 000 - small with a wonderfully warm and rich tone. Great to fingerpick in the quiet of the morning. I compose most of my songs on it. I will pass on your kind words about her painting to my friend and show her some of your fine work. Take care, Peter.
A Tour de Force of strength and subtlety gracefully presented. Wow.
Thanks, RT. "Strength and subtlety gracefully presented" - very nice words, indeed. I really appreciate them. Take care, Peter.
Thanks, Maurice. There is every chance I will be sitting round in the evening whilst we are camping this summer and singing this song to my family and friends :-) I agree, re the orchestration. I will probably do an orchestrated version as well at some stage. I appreciate you dropping by. Take care, Peter.
I didn't know that Peter! It sure sounds nice.
Hi Neil. Yes, I made the guitar at Thomas Lloyd Guitars, in Melbourne. It was a fantastic course! I am glad you liked the song and the format. Love the US accent... Talk soon, Peter.
Really enjoyed this piece mate.
Your friend's work looks amazing with the beautiful colours and use of light.
Hey, Gerald. Thanks for dropping by. I am glad you liked the song. I will pass on your kind comments about our friend's painting to her. Take care, mate. Regards, Peter.
Live Crowd! And Loving It!
Play and sing this my friend. Between you and Gad it sounds like the Vox is on this week. Yeah Peter kick those lyrics out and your licks are seriously Guitting it here baby. Love it my man. Late 60's early 70's progressive going on here baby!
Thanks for the kind words, Ricky. "The Vox is on this week" LOL. Glad to see I just snuck out of the 60's :-) Take care, Peter.
Thanks for dropping in, SH. Glad you liked the lyrics of this one. I appreciate your kind words. Take care, Peter.
man, you could easly play the coffee house circuit. great performance peter!
Thanks for the supportive comments, Vic. I might be able to cadge a free coffee if I'm lucky. Take care, Peter.
Thanks Shadowman. I am used to playing at events where the music is a secondary focus, so I don't get too fussed about people talking (but hopefully listening with one ear) at the same time. Glad you liked it. Regards, Peter.
You have mine. Best of luck with the show.
Thanks, Les. It is nice if there is a smattering of applause at the end :-) Kind regards, Peter.
Peter, such a great concept and as always, performed crisply. The lyric and melody are both very well conceived, and your vocal is nice. I like it in this intimate state, but could easily hear this in full band form. Great song!
Thanks, Chris. Glad you liked the stripped back approach. I will also probably produce a version in band form as well. I appreciate your support. Regards, Peter.
I love the sound of an acoustic capoed up like that. A nice homage for your friend, and you definitely hit the theme square in the bullseye.
Thanks, Dave. Yes, the capo was critical for the key that I wanted to sing the song in but also to allow the hammer ons and pull off that I wanted on the chords. They give the guitar great versatility. Take care, Peter.
& solid work all around. & in one take at that, makes it all the more impressive. good luck on the upcoming presentation!
Thanks for dropping by for a listen. I appreciate your comments. Take care, Peter.
Very nice! Easy to listen to. Much enjoyed! Thanks.
Thanks, Carrie. Easy listening is my style. I am glad you enjoyed it. Kind regards, Peter.
really nice chord sequence, I love major 7th chords. A great song Peter and nice lyrics. I do like acoustic numbers and to hear you singing and playing guitar is a perfect combination.
Thanks for dropping by, Bob. I agree re major 7ths. Nice open, ringing sound. I appreciate your continued support of my music. Take care, Peter.
Beautiful song. Great playing man.
Not really much more to add to that.. it's just good.
Thanks, Reverend. I am glad you liked this stripped back post. Take care, Peter.
Peter how this has a sense of how Don Mclean did tribute to Van Go.
But you really seem to have a tremendous conviction for this artist. I assume the painting is of the artist involved, she seems so good!
Terrific tribute indeed! Love the audience feeling in this tune as well. Enjoyed the singing, sounds very pro folk and the strumming to me show great feeling as well as of course the vocal!
Thanks for the detailed, supportive comments, Bill. The artist is a very good friend of ours and she does do some terrific paintings. I appreciate you dropping by for a listen. Take care, Peter.
Thanks, Harald. I appreciate you dropping by for a listen. Regards, Peter.
arrangement, really enjoyed all the little additions to fill out the tune.
Thanks for finding time to have a listen to this one, J. Glad you enjoyed it. Take care, Peter.


A review of Gary Jackson's Syndrome X Theory about psoriasis.
For over four years, Gary Jackson (aka Evetsm or Steve M) has become more and more convinced of a strong link between psoriasis and "Syndrome X." Late in the Summer of 2000, he created a web site describing the evidence he's gathered,and the conclusions he's made. This article is a point-by-point rebuttal of the arguments Jackson makes.
From the very first sentence on Jackson's web page, it is obvious that there are definition and evidence problems. Jackson claims that psoriasis is a "skin plaque disease," which does little but trivialize it. Psoriasis is most likely a complex disease of the immune system, with a probable genetic basis. There are five main types of psoriasis, but Jackson fails to make any distinctions.
Nowhere does Jackson give us a hint as to what other conditions might be considered "diseases of Syndrome X." And in no place does he ever hint at what is cause and what is effect. Reaven often cites the "diseases of Western civilization" (high blood pressure and cardiovascular disease) as the "effects" of Syndrome X. Polycystic ovarian syndrome may also now be considered an "effect." And all of these metabolic disturbances can be traced back to insulin resistance (IR) and compensatory hyperinsulinemia (CHI).
Jackson claims that just the concommitant risk factors are "sufficient" to show that psoriasis is a "disease ofSyndrome X," but I doubt very much that Reaven would feel the same way. Reaven himself has shown, for example, that smoking can induce IR, and therefore Syndrome X metabolic disturbances. Smoking, according to Jackson, would then have to be considered a "disease of Syndrome X" since smoking is correlated with many of the Syndrome X risk factors. The absurd implication behind the language Jackson uses is that by treating the insulin resistance, a person should stop smoking! If Jackson were more clear about his own definitions of Syndrome X and its diseases, this rebuttal might not have been necessary.
Jackson's definition also suffers from the fact that he fails to cite Reaven at all. Reaven is widely published and is often refered to as the expert on Syndrome X, its causes and its consequents. Jackson chooses to cite a French review of the literature and a study from a single Micronesian island to support his definition. The abstract of the French review gives a decent, but short definition largely matching Reaven's.
Jackson's grammatically-bizarre assertion that only three out of the five main markers need to be present to show that a person has Syndrome X is completely unsupported by the abstracts he's provided, and appears to contradict Reaven's work.
Of course, Jackson's evidence follows his definition. He shows that a few of the metabolic disturbances associated with Syndrome X exist more often in psoriatics than in the general population. However, the way he's written it, "In psoriasis there has been shown to be an endogenous hyperinsulinism, with insulin resistance and hypertriglyceridemia with dislipidemia in statistically significantly elevated values above normal," would make one think that this is true for all people with psoriasis. It isn't, and some of his own citations bear this out.
What does Jackson show us, specifically, as evidence? Given his style, it isn't possible to say very quickly. He presents his conclusions, then follows with a list of links to Medline abstracts. He expects that, given these abstracts (and through personal communications with him, it's obvious that he's only ever read the abstracts of these articles, never the full text) we'll draw the same conclusions that he has. Here, I look at each abstract, and describe what it says to me. I will do so chronologically, since it's important in this discussion to remember that Reaven's "breakthrough" in Syndrome X research happened in 1988.
1976 — Pfahl, et al show that "major endogenous hypertriglyceridaemia" is found in 39% of psoriasis patients (although how many patients were studied is unknown — due to rounding, 39% could mean a sample size as small as 18 patients). "This study would tend to integrate psoriasis into the category of the metabolic diseases, coinciding with the notion of troubles with glucose metabolism in psoriatics," the abstract says, "since it is now accepted that [80%] of [people with this abnormality] are pre-diabetic." What did "pre-diabetic" mean in 1976? The abstract doesn't say. If it means, 12 years later, that they've got Syndrome X, then, well, 80% of 39% is 31.2%, or well within the "1 out of 3 or 4" people in the general population with Syndrome X as stated by Reaven. We also don't know anything about the study participants. For example, were they all French? Jackson, as we will see, has a penchant for generalizing from tiny and/or specializied samples to the global psoriatic population.
1976 — Meynadier and Guilhou publish a review of all sorts of interesting metabolic changes in psoriasis. The abstract contains not a single number or percentage. I'm fairly certain Jackson includes this review solely for its mention of Syndrome X markers, but there's so much more in it that's also interesting and has little to do, directly, with Syndrome X. Systems other than insulin/glucose are hypothesized as perhaps being responsible for all the changes noted.
1977 — Pelfini, Jucci, Fratino et al publish "preliminary results" which "seem to indicate" that psoriatics are insulin-resistant. The abstract doesn't mention sample size, or degree of resistance at all.
1979 — Pelfini, Jucci, and Fratino, again, with a few new authors, publish the results of a study they did to figure out which kind of insulinogenic index best suits their desire to demonstrate the relationship between hyperinsulinemia and the diseases they have studied. This particular citation, on Jackson's part, is worthless, as the abstract itself shows nothing in the way of new or different evidence from the study above.
1980 — Wach et al publish a paper describing normal glucose levels with hyperinsulinemia in psoriatics after glucose loading — a classic sign of insulin resistance — but conclude that a connection between psoriasis and diabetes "must be denied." Given the date, it is quite possible that the authors simply did not know that chronic IR can lead to type-II diabetes. There is no information in this abstract about sample sizes.
1987 — Valquist et al show that in 20 middle-aged men, possible markers for occlusive vascular disease exist, and that the levels are correlated with psoriasis severity. To me, the wording suggests that the authors believe that the psoriasis drives the levels of triglycerides. Jackson would likely suggest the opposite is true.
1988 — Neugebauer and Weber publish a study on yohimbine treatment, which reduces the secretion of insulin, in 59 psoriatics. The abstract appears to say that perhaps 88% of psoriatics are hyperinsulinemic, but without reading the full paper, it isn't possible to say for sure. What really strikes me about this study, though,is that it appears that no thought is given to the effects of lowering insulin levels. If psoriatics have high levels due to IR, then reducing insulin secretion should make the patients hyperglycemic, and long-term treatment with yohimbine would then lead to serious type-II diabetes. Dangerous stuff, given what we know now.
1989 — Rakhmatov says that 49 of 64 psoriatics (77%) are hyperinsulinemic, and states that the level of hyperinsulinism depends on the severity of psoriasis. Again, as with the Valquist study above, the abstract implies that the metabolic disturbances are caused by psoriasis, rather than the other way around.
1989 — Abramovich publishes something titled "The clinical significance of dislipidemia in psoriasis patients." Medline has no abstract for this, but Jackson cites it anyway, even though it is highly unlikely that he has read the full article. For all we know, Abramovich might say that there is no clinical significance. This citation, therefore, is absolutely worthless as support for Jackson's point.
1994 — Offidani et al publish an article describing increased lipid peroxidation — in vitro, in the presence of copper sulphate — of lipoproteins from psoriatics, and how this might suggest an increased risk for atherosclerosis. How this study methodology supports the Syndrome X hypothesis at all, I have no idea (since increased lipid peroxidation in the presence of copper sulphate isn't something I've seen Reaven describe as a common condition in Syndrome X) and Jackson doesn't say, either. In short, this is another worthless study.
So, from Jackson's own evidence (and considering the limitations of Medline abstracts), what can we safely conclude? One, that IR appears to be present in more psoriatics than in the general population. Two, that low- and very-low-density lipoprotein profiles in psoriatics may match that expected in Syndrome X. And three, that high triglyceride levels might also be present. Given the lack of concrete numbers in many of Jackson's citations, along with the fact that not one of the studies appear to have been double-blinded, or even had a large (100 plus) sample size, jumping to further conclusions would be inadvisable.
What can we not conclude? That psoriasis is caused by IR or any other Syndrome X metabolic disturbance. Two of his abstracts imply the opposite by saying that Syndrome X marker levels are dependent upon psoriasis severity, and not theother way around.
Jackson's second "test" of his hypothesis deals with the expression of the gene for the creation of peroxisome proliferator-activated receptors (PPARs) amongst various cell types, and drugs which activate one particular kind of PPAR (PPAR-gamma), the thiazolidinediones (TZDs). Jackson believes that since TZDs have an insulin-sensitizing effect, and are clinically effective in both IR and psoriasis, that psoriasis must be due to IR. This is naïve, as I've pointed out to him on several occasions, since many drugs have more than one biological effect (aspirin, thalidomide, etc).
Coincidentally, PPAR-gamma mRNA is also down-regulated in IR states, according to Itoh et al. Hydrogen peroxide and tumor necrosis factor alpha can both suppress expression of the PPAR-gamma gene. The authors show that TZDs can recover "TNF-alpha-induced down regulation of PPAR-gamma mRNA expression." Their abstract doesn't mention whether or not PPAR-alpha is likewise affected, but as per Rivier et al, it too is down-regulated in psoriasis.
So, why are two PPARs down-regulated in psoriatic skin? Jackson doesn't say, but it appears he assumes that it is due to IR and nothing else. He does not explain why this IR state does not often affect 100% of the keratinocytes (full-body psoriasis is fairly rare). He is talking about systemic IR, after all, and Rivier et al don't specify any particular body part (such as elbow skin) in their abstract.
However, one piece of evidence that Jackson has pointedly overlooked is the TNF-alpha aspect. TNF-alpha is a potent pro-inflammatory cytokine, abundant in psoriatic skin. It seems obvious that TNF-alpha-induced down-regulation of PPAR genes can be explained quite easily by the inflammation which is a characteristic of psoriasis.
Jackson's other evidence, that one particular TZD improves psoriasis, and that TZDs have a whole host of varying actions in different metabolic pathways, does very little to support his point of view, and in some instances, contradicts it.
Based on the postulation of thiazolidinediones activity as a useful tool to identify diseases of SyndromeX, psoriasis must be seen to be a disease of Syndrome X.
Since "postulate" means "to assume without proof," Jackson's conclusion is that we must see psoriasis as a disease of Syndrome X based on nothing more than an assumption.
Jackson's third point is that other diseases of Syndrome X are found more often in psoriatics than in the general population. To follow his other apparent lines of argument, we should take these findings as meaning that Syndrome X causes psoriasis. However, he once again neglects cause-and-effect entirely, since obesity, according to Reaven, is not caused by insulin resistance. Obesity, especially abdominal obesity, is a recognized cause of IR.
So, given that psoriatics tend to weigh more, smoke more, and drink more than the general population, is it any wonder that there is increased risk of IR, and thus Syndrome X?
Also, for the sake of the argument, let's say that psoriasis is caused by IR, and the reason we see lots of obesity among psoriatics is because the IR caused by obesity in turn causes the psoriasis. Again, the question of why the psoriasis often only affects small patches of skin becomes paramount. Why would systemic IR due to obesity affect only a few square inches of skin? Are the keratinocytes so vastly different millimeters apart? On the other hand, what makes scalp skin and elbow skin so similar that psoriasis frequently appears first in those locations? Jackson may or may not have even thought of these questions.
Jackson's fourth point is that psoriatic mothers tend to have babies with a higher birth weight than other mothers, which fits right in with the "thrifty genotype" hypothesis. Of course, since IR can be induced by environmental factors alone (Reaven only claims that 50% of the IR picture can be attributed to genetics), then there's ample reason to believe that a mother who is IR for any reason during the course of pregnancy could give birth to a heavier baby (since if the baby is not IR, then the increased insulin coming across the placenta will have a fat-storing effect on the developing child).
Jackson then, in a "footnote," responds to Ed Anderson's page responding to Jackson's newsgroup posts. Jackson begins badly by claiming that Anderson believes there is "no substance" to the hypothesis, which as far as I can tell, is simply untrue and nothing more than a straw-man attack. Anderson clearly feels, as I do, that there is evidence, but it's neither very strong nor all in Jackson's favor.
Jackson begins with the coincidence of the two diseases. While Jackson's own evidence shows that there is a higher incidence of type-II diabetes among psoriatics, the opposite claim, that there's a lot of psoriasis among diabetics, is not strongly in evidence — especially as the American Diabetes Association fails to mention psoriasis as a possibility among its list of dermatological diseases that can occur in uncontrolled diabetes. This says quite a lot, actually, but Jackson has ignored it.
Even more unfortunate for Jackson, he chose to cite Bernstein once again, as he's done several times on the psoriasis newsgroup. Jackson has letters from two of Bernstein's patients who say that Bernstein claims that 100% of the diabetics he sees have psoriasis. The letters themselves, however, paint a very different story: we hear of Bernstein claiming that "dry skin patches" or lines in the fingernails are psoriasis. Were this actually the case, I'd hazard a guess that psoriasis incidence would jump to 50% or more of the general population, considering the booming business in sales of moisturizing products. A friend of mine frequently applies moisturizer to his hands (more than twice a day) because they become dry and annoying. It would appear that Bernstein would claim that he has psoriasis.
Such a "diagnosis" is patently absurd given the tremendous volume of medical literature on psoriasis. It shows that either Bernstein has some sort of diagnostic bias towards psoriasis, or that he's never heard of a differential diagnosis. That Jackson continues to cite Bernstein as a reliable source of psoriasis information, despite repeated entreaties to stop doing so in the face of this absurdity, demonstrates that Jackson has a dogmatic desire to show a linkage between the two diseases, rather than, as he's stated publicly, a desire to promote the truth.
Second, Jackson attempts to tackle an apparent contradiction to his theory. If, as is widely known, psoriasis often clears up during pregnancy, and pregnancy can lead to IR (gestational diabetes), doesn't that mean that IR cannot cause psoriasis, since in pregnancy-induced IR, psoriasis should get worse, not better? Jackson tries to answer this concern with some new research into corticosteroids and IR, but fails to interpret the studies he cites correctly.[27,28] He also tosses in some blatantly incorrect guesswork about possible similarities between insulin and steroid feedback loops in the endocrine system. It's been known for quite some time that steroids can induce insulin resistance, Bjorntorp and Rosmond are doing little more than suggesting that a genetic susceptibility exists in men for the HPA axis to go haywire and produce chronically-high amounts of corticosteroids — thus inducing IR. Not, as Jackson seems to think, for there to be some sort of "cortisol resistance" akin to IR. The researchers clearly state that the faulty receptors are central to the feedback loop (whereas the fault in IR is widespread throughout the body's muscles and fat). In other words, only the hypothalamus need be "broken" (and thus "reading" a lower level of steroids than actually exists in the blood) for overproduction of steroids to occur. Jackson says, "There is strong evidence that in Syndrome X the cortisol feedback loop is damaged," again confusing cause and effect, since his own references on this point state that Syndrome X exists because of an abnormal cortisol feedback loop.
And while Jackson agrees with Anderson that "immune system factors are present during pregnancy," he then disagrees that they are present at other times. This single sentence appears to show that Jackson would completely deny what is widely recognized about psoriasis: that it is, at all times, an immune-mediated disease. Inflammation is an immune response. Steroid treatment of psoriasis inhibits the inflammation, thus clearing up psoriasis, but in large doses (usually only orally-administered) can actually induce IR.
Finally, Jackson prejudiciously dismisses another potential problem for his theory with a bunch of questions for which he largely knows the answers already. In populations with high level of IR, such as Native Americans, there is also a very low rate of psoriasis. Jackson pleads ignorance on this point, as he has for over two years despite repeatedly being shown the evidence. He's even cited some of the answers to his own questions in the past. He knows quite well that Native Americans in general have a very high incidence of IR and the disturbances of Syndrome X — and has pointed out the Pima Indians as an example, with their 50% rate of type-II diabetes.
In the past, Jackson has also dismissed this point based on the fact that concommitance of Syndrome X diseases is unpredictable, but he obviously feels it's okay to use disease concommitance in making his main argument. All we hear from Jackson on this question is side-stepping, stonewalling, and self-contradiction — he has no answer.
· Jackson uses a unique definition of Syndrome X, and doesn't bother with the real meaning of Syndrome X at all. The best spin anyone could put on this is that all he is attempting to do is show that there is a risk of cardiovascular disease with psoriasis, but he fails to ever state his ultimate intent in any way. It has been clear, through communicating with Jackson, that he believes that IR causes psoriasis, and thus fixing the IR should also fix the psoriasis — he's shown this belief by repeatedly suggesting that an IR-reducing diet should help reduce psoriasis symptoms. He has no evidence of this whatsoever.
· Jackson's evidence of metabolic abnormalities in psoriasis is actually fairly scant and not highly controlled. The fact that he relies on interpretations of short abstracts — guessing as to what the researchers mean — leaves much to be desired.
· Both the disease concommitance data and the heavier-birth-weight data is far from compelling when psoriatics live with risk factors for IR, possibly as a consequence of having psoriasis.
· Jackson's attempts to answer Anderson's criticisms of the Syndrome X hypothesis are based on number games, guesswork which appears to contradict the intent of some researchers, and a deft ability to avoid answering at all. His "answers" are completely meaningless.
Overall, Jackson fails to even postulate a mechanism whereby IR might induce psoriasis. No other "diseases of SyndromeX" are mediated by the immune system. Not one. No other disease or metabolic disturbance caused by IR appears to be inflammatory in nature. Jackson fails to state what would, in light of these facts, make psoriasis so different from other inflammatory or immune-mediated diseases that it should be included among the other diseases of Syndrome X, while the rest should not.
On the other hand, Jackson fails to mention why he believes anyone should be interested in knowing that psoriasisis a disease of Syndrome X. Giving him the benefit of a doubt for a moment, if it is because he'd like to make psoriatics aware that there is a risk of heart disease, high blood pressure, polycystic ovarian syndrome, and, in extreme cases, type-II diabetes associated with psoriasis, he could do so with just a few good references to the facts that we tend to be fat smokers and drinkers who don't exercise, and that all of these are recognized risk factors for IR and Syndrome X.
However, all the fuss in his article, along with his communications in the psoriasis newsgroup really indicate that he believes that psoriasis is caused by IR, and that an IR-reducing diet or other lifestyle modifications aimed at eliminating this silent killer will have a beneficial effect on our psoriasis symptoms (but not Jackson's — he doesn't have psoriasis). He provides no evidence that Reaven's dietary suggestions, or losing weight, or quitting smoking or drinking, or getting more exercise will have any effect on psoriasis at all. If psoriasis is caused by IR, then all five should be statistically correlated with a reduction in psoriasis symptoms, and Jackson should be highlighting such evidence as conclusive.
Jackson announced an update to his page (in response to this page) on the Newsgroup, in a fairly nasty message. His update is little but a list of misunderstandings, to put it mildly.
DaveW has made claims that there is no substance to this IR-psoriasis hypothesis.
This is simply untrue, and Jackson knows it's not true, because I've told him so, many times. The evidence shows a correlation between IR and psoriasis, there's no dispute over that. What I've attempted to show is that Jackson's evidence (and his interpretation of that evidence) does not support jumping to the conclusion that psoriasis is a disease caused by IR and CHI, which is what his page, and his newsgroup posts, either imply or state outright.
Jackson is quite incorrect about what he thinks my "key arguments" are, as should be obvious by what he picks to summarize.
a) "Jackson also neglects to offer any evidence whatsoever to support his assertion that psoriasis "tends to first appear after the late teens in most people"." Davew then says in the next sentence that "Although it is a true statement"....I guess if he knows it is true I don't need to supply the evidence.
When critiquing Jackson's page, I was unaware that he meant it only for me to read. Since I read it with the idea in mind that he was presenting his ideas to the world, every claim should be backed up with supporting evidence for those who aren't as knowledgable about the subject.
b) "There are five main types of psoriasis, but Jackson fails to make any distinctions"." Not one study that speaks of psoriasis and any factors of Syndrome X makes this distinction either.
If I believed for one moment that Jackson had read the studies he cites, instead of just the abstracts (which are summaries that don't specify all the details), then I might believe this. Jackson's "rebuttal" of this point is simply ludicrous in light of the fact that he relies on the abstracts.
Does this invalidate all of the studies and all other studies that mention psoriasis without typing ? This would leave us with very few psoriasis studies of any sort.
Of course it doesn't invalidate the studies. My statement that Jackson makes no distinction is simply to point out the fact that he is making broad generalizations, and since he doesn't appear to read full articles, he's doing so from very little data.
c) Davew says that I don't use Reaven's definition of syndrome X : "Syndrome X is a cluster of metabolic risk factors for heart disease"." Well, Davew, what are "includes the simultaneous presence of hypertension, dyslipidemia, abnormal glucose metabolism and insulin resistance and hyperinsulinemia" if not risk factors for heart disease ?
When has psoriasis been considered to be a metabolic disease? Also, as I pointed out above, Jackson makes no claims about cause-and-effect. He's never come right out and said, "psoriasis increases the risk of heart disease," for example. Without showing how psoriasis adds to the risk of heart disease, calling it a "disease of Syndrome X" makes no sense. And if the basis for calling it such is simply disease concomitance, then why psoriasis is linked to other diseases like it is becomes of the utmost importance. Jackson has shown little interest in "why?" however.
And as I have already shown, obesity is not caused by Syndrome X, but is a cause of Syndrome X. According to Reaven, the claims that insulin resistance makes a person obese (or just makes it more difficult to lose weight) are "Not True!" If both the causes and effects of IR and CHI are "diseases of Syndrome X," it makes the term almost meaningless.
e) "Smoking, according to Jackson, would then have to be considered a "disease of Syndrome X". No, smoking may contribute to the cause of diseases of Syndrome X. It is an external input that exerts influence on IR and other factors in Syndrome X.
But if it fits the "definition" that Jackson puts forth ("includes the simultaneous presence of hypertension, dyslipidemia, abnormal glucose metabolism and insulin resistance and hyperinsulinemia"), then why isn't smoking a "disease of Syndrome X?" This is an example of why it is a poor definition.
f)"In psoriasis there has been shown to be an endogenous hyperinsulinism, with insulin resistance and hypertriglyceridemia with dislipidemia in statistically significantly elevated values above normal," would make one think that this is true for all people with psoriasis. It isn't, and some of his own citations bear this out." Statistical observations NEVER include the word ALL, they contain only statistical significance. That is why they are called statistical observations.
This response misses my point. Jackson's own citations show that some psoriatics do not show significantly elevated values of these conditions. Also, his citations point these things out independently of one another, for the most part, so his use of the words "with" and "and" are inappropriate.
g)DaveW claims that all 11 studies that I cite that make statements connecting psoriasis with insulin resistance are wrong.
This statement is a perfect example of how Jackson fails to understand what I write. I never claimed that even one of those studies was "wrong," and I challenge Jackson to point to any sentence I've ever written on this subject that says that. In fact, I believe that for the most part, they are as "correct" as they could be at the times and conditions under which they were completed. What I think is "wrong" is Jackson's interpretations of those study abstracts, and the conclusions he jumps to because of those interpretations.
First the fact that there are at least 11 studies linking psoriasis and insulin is in itself significant.
Second all his critisizms are of the statistical methods employed. The correctness of statistical methods used are implied in the the concluding statements in the abstract, since in order to make those statements the statistical criteria must have been met and reviewed before publishing.
Absolutely. But meeting some sort of statistical criteria does not mean that the data itself is any good. Small studies with no blinding can show "statistically significant" results quite easily without being correct, and still be published in major medical journals. Otherwise, there would be no need for further testing. Jackson's insistence that peer reviewers are somehow god-like in their ability to sort truth from falsehood is absurd, given the number of published studies which have turned out to be wrong upon further investigation.
Davew, , [sic] who admits to having not a single day of math statistical training. . .
When did I ever admit to any such thing? It's not true, why would I "admit" to a lie?
. . .show us the statistical math explaining why all those studies have the wrong conclusion or are insignificant.
See above. Jackson's challenge here is for me to prove what he and I both know to be wrong. It's absurd.
h) "Jackson believes that since TZDs have an insulin-sensitizing effect, and are clinically effective in both IR and psoriasis, that psoriasis must be due to IR. This is naive". This is a postulate, made in two published papers, one review pulished in the NEJM, and are entirely reasonable and they are not my own. The TDZs are proposed as tools to show that a disease is likely to be a disease of Syndrome X and is merely one data point among many in my postulate.
Again, Jackson is obviously unaware of what the word "postulate" means. That he calls his own ideas "postulates," when he certainly is backing them up with evidence, just proves my point. From the book review Jackson cites: "The availability of thiazolidinediones that act directly to reduce insulin resistance may prove the most rapid route to defining unambiguously the role of insulin resistance in the pathophysiology of the diverse disorders to which it has been linked." Emphasis mine, as it means that taking the use of this "tool" as a given is unreasonable.
i)"This is to be expected, since psoriatic keratinocytes don't differentiate much at all". What does this mean ? I'm sure that they don't differentiate. They probably don't even discriminate or pontificate.
This illustrates Jackson's lack of basic medical knowledge about psoriasis.
j)"However, he once again neglects cause-and-effect entirely, since obesity, according to Reaven, is not caused by insulin resistance.23 Obesity, especially abdominal obesity, is a recognized cause of IR." Davew keeps seeing IR and psoriasis, or IR and any diseases of Syndrome X, in a simplistic cause and effect unidirectional relationship. This mechanism is not linear with one factor strictly proceeding the other, rather, it is an example of the positive feedback loop in effect, where cause and effect are interchangeable and are self-reinforcing.
Interchangeable?!? Jackson fails to see here that some things are, indeed, recognized as causes of the abnormalities in the insulin/glucose feedback loop, and that those abnormalities cause other conditions, without feeding back into the root problem(s). To see the whole gamut of conditions as a whole slew of interconnected feedback loops is to make the term "Syndrome X" meaningless. Jackson also fails to provide any evidence that cause-and-effect are truly interchangeable. For example, evidence that supports the contention that insulin resistance is caused by hypertension, or dyslipidemia, or a heart attack, or any evidence that obesity is caused by insulin resistance.
Jackson apparently hasn't read this in detail. Neel provides evidence that Syndrome X diseases are probably not due to the same genetic disorder. Even then, the Thrifty Genotype Hypothesis is just one of many root causes of insulin resistance, but it seems that Jackson believes it is the main cause. The Mercola article Jackson cites here shows that, perhaps, a Thrifty Gene can explain 33% of the occurances of the diseases under study. It's quite obvious that physical activity and obesity play a large role in causing insulin resistance, with or without any Thrifty Gene.
and more recently by its refinement, the cortisol hypothesis.
I dealt with this study he cited in response to Ed Anderson above. Jackson appears to think that this is a "refinement" to the Thrifty Gene hypothesis, when all it really is, is another, different, feedback loop which can induce insulin resistance, with its own genetic basis.
In conclusion, until Davew understands the difference between a linear, uni-directional, cause and effect and the interchangeable cause and effects of a positively disturbed feedback control loop, he will always search in vain for IR as an absolute cause or effect of diseases of Syndrome X.
Considering that I am not searching for IR as an asolute cause or effect of anything, the above is absurd. Just another example of Jackson putting his own words in my mouth.
Understanding the Thrifty-Genotype hypothesis will help him grasp how this feedback control loop is originally disturbed and what people are likely to be susceptible.
I already know this, and more, as should be obvious from the above.
Second, until Davew stops thinking in absolutes and starts thinking statistically and probabilistically, and until he graps the implications of the phrase "statistical significance", he will forever believe that I have to be either completely wrong or completely correct.
Again, Jackson is inventing beliefs for me, and nothing more. Right now, I believe he is only a little bit correct, but mostly wrong. For example, he's completely wrong in thinking that I think only in absolutes.
I won't go into the rest of his document, because based on the spuriousness of what he has already said, the rest is moot.
To conclude this update, I believe it's fairly obvious that Jackson doesn't know or understand what my "key arguments" are, even after years of open and honest discussion, and is therefore making "conclusions" about my position without a full comprehension of my points. This "rebuttal" of his is little but falsehoods, straw men, and more of the same willful ignorance that Jackson has used throughout the years. It does nothing to either support his own argument or discredit mine.
On February 26, I wrote in the Newsgroup about how a couple of Jackson's own citations seem to state that insulin-resistance markers are driven by the severity of psoriasis, and not the other way around. I wrote about this in the main article, above, as well. Thirteen days later, Jackson replied with another wave of his "feedback" magic wand, and seemed to think that would suffice for an explanation.
So, I made a comment that such an idea seemed to indicate a rather different attitude from previous discussions, in which Jackson had soundly ridiculed the idea that psoriasis could, in any way, cause insulin resistance. I also asked for any evidence he might have of the feedback loop he mentioned.
As far as I know, it isn't. The proper scientific/skeptical viewpoint of the Syndrome X link to psoriasis is that until more information and evidence is gathered, the current evidence cannot support, on its own, the conclusion that psoriasis is caused by insulin resistance, or that it is "a disease of Syndrome X." Even Reaven seemed uninterested in the question (but perhaps only for practical reasons).
If I "obviously believe" anything, it's that Jackson has jumped to conclusions. I certainly do not believe that psoriasis "initiates all this." It seems, to me at least, that Jackson finds it necessary to exaggerate my beliefs (or even fabricate them) in order to attack them. This is a classic straw man — instead of responding to what I actually say, Jackson is making mincemeat of oversimplified or overblown positions which I do not hold. While this makes it much easier on him, it does absolutely nothing to refute my arguments.
Also, I haven't been asking "wrong questions," I've simply been asking questions which Jackson refuses to answer. Given his tendency to not read what I write, it seems likely that he is not even aware of most of the questions I've asked him over the years.
But Jackson continues, stating a couple of "FACTS" which, as I've already shown in the main article, above, aren't so much "facts," but are instead misleading, context-free abbreviations of actual facts. Jackson appears to be comfortable throwing away "the big picture" in favor of making arguments based on half-truths, but I'm not. Since I've already dealt with these two "facts" (see the main article, above), I won't bother doing so again here.
These 2 facts say that psoriasis is LIKELY to be a disease of Syndrome X.
Jackson continues to imply that insulin resistance causes psoriasis, without stating it outright. If that's not his intent, then all this talk of psoriasis being a "disease of Syndrome X" is meaningless. Why? Because if you remove both the cause (insulin resistance) and the effect (heart attacks — as he does, below), then all you're left with is a label which carries with it no suggestions for prevention, treatment, or consequences. Since this would mean that six years of his posts to the newsgroup — presenting evidence, arguing his case, etc. — would have been worthless, medically, I cannot accept that the implication isn't there. This is further backed up by another newsgroup post of his, which I will get to in a few paragraphs.
So, what does it mean if psoriasis is a disease caused by insulin resistance? It means that we should be able to treat the disease by controlling that resistance, possibly even through a careful diet and exercise, without drugs, messy ointments, or the like. There is no good evidence that this is the case. It would be wonderful if there were.
Don't get your pyramid head into a knot wondering if psoriasis causes heart disease. It may, it may not. It does not further the argument that psoriasis is a disease of syndrome X. It is a non sequiter. [sic] It is beside the point. It is superfluous.
The funny thing about this is that the whole heart attack angle, while definitely important, is really beside my main point. That Jackson wastes so much time on calling it a waste of time, time he could have better spent answering the other issues both in my main article and the first update, says quite a bit about him. He is once again stonewalling on the really central questions, and appears to be purposefully evading all attempts at reaching an understanding.
Its the definition, stupid !
And the fact that he is, again, stooping to base insults strongly suggests that he really has no good response to any of the important points.
Now let us not disrupt this group with this crud !
This was the last sentence of that newsgroup post. Jackson was unable to follow his own suggestion, however, and just a few hours later, before I had a chance to reply, he posted another message, which begins by listing a bunch of studies which show that a specific type of fat is a probable cause of insulin resistance. I can only guess that he's done this because he thinks I don't believe this is true. If so (and I don't know of any other reason why he would do such a thing), then he is, of course, wrong, but since he doesn't read what I write, he wouldn't know.
Once again, Jackson shows how easy it is to get confused by all these articles. Regardless of the good evidence he's been shown (and has shown himself) that insulin resistance can be caused by a number of things, what does he claim? He claims that "visceral adipose tissue […] is the cause of insulin resistance" (emphasis mine). This is not a conclusion supported by the evidence he provides.
For example, one of the citations he provides (Peng and Gao, 2000) states, "The abdominal subcutaneous adipose tissue of type II diabetic patients, as visceral adipose tissues, contributes to their insulin resistance" (emaphasis mine, again). Not "causes," but "contributes to." Another, Lebovitz, 2001, relates three distinct possible causes of insulin resistance.
Psoriatics are often overweight. Psoriasis improves with weight loss.
you claim, is NOT likely the cause of IR.
I don't believe I've ever once claimed that psoriasis lesions were a "likely" cause of insulin resistance. I presented the idea as a possibility. There is evidence that the inflammation of psoriasis can contribute to insulin resistance (through tumor necrosis factor alpha), but that's irrelevant to this point: Jackson is once again inventing claims for me. Claims with which I do not agree. This is just more evidence that Jackson does not understand my objections. Or, if he does understand, then he's doing nothing but constructing more straw men to attack.
I'll spell it out, once again, in terms related to the above argument: nothing that Jackson has shown or argued to date makes it likely that insulin resistance is the cause of psoriasis. The very fact that psoriatics tend to be obese is, to me, the likely cause of the increased prevalence of insulin resistance among us. The fact that we tend to smoke and drink more than the general population also contribute to the findings of insulin resistance. Apply Occam's Razor, and the idea that insulin resistance causes psoriasis is sliced into tiny pieces.
Psoriasis improves with weight loss.
is completely unsubstantiated. There has been no good evidence of this presented in the medical literature, and no scientific evidence whatsoever (of any quality), since, at the latest, 1969. At least, I have yet to find any, and I've been looking for more than two years. One would think that if the claim were true, it'd be widely publicized. It isn't. I don't know where (or even if) Jackson has found evidence for this statement, but it's not the first time he's made it. Repeated requests for citations supporting the idea that psoriasis improves with weight loss were met with no response. Once again, we can see that Jackson is uninterested in trying to find out what the truth of the psoriasis/IR relationship is, but instead uses a fabrication to support what appears to be a flimsy position.
Maybe you will take that rubbish off the internet now ?
I'll leave it to the reader to decide who is publishing rubbish. And, even if Jackson is correct, since his own writings on the Internet lack rigor and support, I'll be leaving this page up for at least as long as he leaves his up, or changes it to provide better information.
Then, the next day, again ignoring his own suggestion that we avoid "disrupting this group," Jackson posted another abstract which shows, yet again (this is getting tiresome), that psoriasis is correlated with the metabolic disturbances of Syndrome X (Rocha-Pereira et al, 2001). While we know this already, this study is perhaps the best of the bunch that Jackson has presented.
But, again (and I know this also is getting tiring), Jackson's reason for posting this abstract, and making a big "stink" over it, is most likely because he refuses to believe that I believe that psoriasis is, indeed, correlated with Syndrome X abnormalities. My only point since putting up this page has been that none of the evidence presented so far, not even this latest study, shows any sort of cause-and-effect relationship, but it's clear that Jackson thinks that insulin resistance causes psoriasis. Otherwise, why spend so much time and effort?
Concluding this update, it's clear that Jackson is answering questions I no longer ask, and haven't asked in quite a long time. I guess now I'll wait to see which single sentence he chooses to reply to next. I hope he'll surprise me, by presenting something new, relevant, and perhaps even compelling, but I won't be holding my breath.
I was wrong. Jackson didn't reply to a single sentence of my latest update, he didn't bother to reply to the update at all. Instead, Jackson is further disrupting the Newsgroup (as he said we shouldn't) with posts about how visceral fat causes insulin resistance and how visceral fat is a source of tumor necrosis factor alpha (TNFa).
We know these things already. This is old, boring stuff.
That Jackson chooses to bring up a post of mine from September of 2000 shows that he's completely confused about who's arguing what today. It appears, however, by his insistence on this connection to adipose tissue, that he still believes that "visceral triglycerides" are "uniquely necessary for the existance of TNF." If Jackson wants to roll the clock backwards 19 months, I'm game (especially since he is so very incorrect on that point).
TNF is produced primarily by macrophages, however it has also been demonstrated to be synthesized and secreted by adipose tissue.
T-lymphocytes and macrophages were the predominant inflammatory cells [found in psoriasis lesions].
We also know that the T-lymphocytes are capable of producing TNFa, from Austin, et al (1999). And Lange, et al (1998) showed that even keratinocytes (skin cells) are capable of producing TNFa (presumably in order to begin an inflammatory immune response to a threat, or perceived threat). In light of this evidence, Jackon's old position on the source of TNFa is simply ludicrous.
Thus, adipose TNF-alpha and ASP seem to be important autocrine factors that inhibit and stimulate triglyceride storage in the adipocyte, respectively.
In fact, only 5-6% of insulin sensitivity variation is explained by circulating levels of TNF-alpha. Rather, the action of TNF is local (i.e., autocrine or paracrine), shown through studies of explanted SAT, in which the higher the level of TNF-alpha, the more inhibition of insulin-stimulated glucose transport into the adipocytes was seen.
The above two quotes confirm what I learned when I first began researching TNFa in relation to psoriasis. Insulin forces adipocytes (fat cells) to take in glucose, and store it as triglycerides. When the fat cells get too fat, they begin producing TNFa in order to force themselves to become insulin resistant, and thus stop or slow intake and storage of glucose. After all, the "auto" part of "autocrine" in the above quotes means "self." This is a nifty feedback loop, but has very few implications for the disease progress seen in psoriasis, since TNFa is produced on its own, locally to psoriasis plaques. It also does little to foster overall insulin resistance, which is mostly a function of skeletal muscle.
Psoriasis lesions probably produce much less TNFa than fat cells. But, any TNFa produced by the immunological processes in a psoriasis lesion which happen to get to the general blood flow can, indeed, contribute to insulin resistance in adipose tissue. How much this contributes is not known. Several studies have found no correlation between blood levels of TNFa and severity of psoriasis, but these appear to be contradicted by later studies. Also, Ljungqvist, et al (1998?) claim that any major injury, including surgery, induces insulin resistance. Injury invariably involves inflammation, as does psoriasis.
Until further research is done, the TNFa aspect of psoriasis is a dead end as far as insulin resistance is concerned. There's not enough evidence to show that TNFa produced in psoriasis plaques causes significant insulin resistance (although theoretically it can exacerbate insulin resistance, and thus Syndrome X). And while blood-borne TNFa produced by adipose tissue can conceivably exacerbate psoriasis, there doesn't appear to be any evidence whatsoever that it is involved in the pathogenesis of the disease.
Morton's demon was a demon who sat at the gate of my sensory input apparatus and if and when he saw supportive evidence coming in, he opened the gate. But if he saw contradictory data coming in, he closed the gate. In this way, the demon allowed me to believe that I was right and to avoid any nasty contradictory data.
…Morton's demon makes it possible for a person to have his own set of private facts which others are not privy to, allowing the [victim] to construct a theory which is perfectly supported by the facts which the demon lets through the gate. And since these are the only facts known to the victim, he feels in his heart that he has explained everything. Indeed, the demon makes people feel morally superior and more knowledgeable than others.
Jackson's insistence that I keep this page on the web "for posterity" is a clear indication he thinks I am just plain wrong about everything I write. That he refuses to read and understand what I write shows that Morton's Demon is working up a sweat in his head. In short, at this point in time (while the demon is functioning), Jackson appears to be beyond reason. An open, honest discussion with him is an exercise in futility, regardless of his previously-stated desire for such a debate.
Davew, you are right, not only is their [sic] little evidence that psoriasis produces TNF that causes IR, there is NO evidence.
That's part of the reason why this avenue of thought is, currently, a dead end. Jackson doesn't appear to agree that the other part of the TNF scenario is also a dead end.
There is? Where? What evidence is there that the TNFa which induces inflammation in wounds comes from adipocytes? This would mean that injury-induced insulin resistance follows a convoluted pathway: wound occurs, something signals from the wound to the adipocytes that the wound occured, the adipocytes respond by dumping out lots of TNFa, which would somehow preferrentially induce inflammation at the wound site. Jackson has yet to show what the "something" and the "somehow" are.
In the skin, TNFa gene expression occurs in the epidermis within minutes after either physical disruption (UV irradiation, burns, wounding) or application of chemical sensitizers or irritants. The function of TNFa in allergic and irritant contact dermatitis is similar to its role in other organ systems and involves regulation of immune and inflammatory processes. An additional role for TNFa in the skin is to provide a signal for Langerhan's cell migration from the epidermis to the draining lymph node, an event required for induction of an immune response. Similar to other organ systems, diminished responses to contact allergens and irritants are observed in the skin of mice rendered deficient in TNFa responses either through genetic alterations or administration of neutralizing agents.
It's important to note that Luster is talking about cells in the skin expressing the gene for the manufacture of TNFa, and not about the general levels of TNFa itself (which Jackson could otherwise claim comes from fat). The only conclusion a reasonable person can draw is that TNFa is created in the skin itself, at the start of an immune and inflammtory response. And, in contrast to Jackson's postulates, Luster fails to mention adipocytes or adipose tissue (visceral or otherwise) at all in an otherwise highly informative editorial.
Well, 5 to 6% of the variation in insulin resistance can be explained by serum TNFa levels. Since visceral adipose tissue appears to be the primary source of free-floating, serum TNFa, then one might conclude that only 5-6% of the variation in IR can be explained by variations in total visceral adipose tissue.
Systemic inflammation, yes, as shown by Jonkers, et al (2002). But what about the massive, localized inflammation of psoriasis? After all, people who are insulin resistant aren't walking around as red as lobsters from the inflammation, are they? Is a chronic blush often found in type-II diabetics? Where is the mechanism through which visceral adipocytes trigger the tremendous immune response seen in psoriatic skin, local to the plaques, and absent from skin just millimeters away?
Again, systemic inflammation. I haven't seen any evidence that localized inflammation, from wounds or other immune-system processes, is any less severe in lean people than in fat people. Jackson will need to provide such evidence in order to make this point valid in relation to psoriasis.
Again, there is no "concrete, iron cast evidence" that this is true. See above, in the March 14, 2002 update. Jackson must either show this to be the case, or stop using this made-up "fact" in his arguments.
AND using drugs that specifically act on adipose to reduce IR clears psoriasis.
The TZDs again. The fact that TZDs have many different effects on human biology is ignored by Jackson, as shown above, in the main article. See also Pershadsingh, et al (1998) for a host of possible mechanisms through which TZDs can have direct effects on the disease process of psoriasis, independent of their effects on insulin resistance.
You see the pathway of action ? They do not act directly on the inflammation (psoriasis etc) they act on the fat to clear the psoriasis. ie the source of the mediators of inflammation is in the fat.
I see a convoluted and bizarre pathway of action. A much more direct pathway of action for TZDs in psoriasis is that they up-regulate the gene for PPAR-gamma receptors of keratinocytes in the skin (which is down-regulated by TNFa generated by macrophages, T-cells, and keratinocytes in the skin), thus allowing the skin cells to differentiate properly. This action of improving keratinocyte differentiation is also key to the action of Dovonex, so this method of treatment is not without precedent.
If psoriasis inflammation produced IR then clearing IR cannot clear psoriasis !
The implication here is clear: Jackson believes that clearing insulin resistance does clear psoriasis. Since that is, in effect, what Jackson is trying to prove, his argument has become circular. Using the conclusion one wishes to reach as an assumption in the argument you present (in order to reach that conclusion) is simply bad logic.
You cannot clear a cause by clearing the effect.
This is simply irrelevant, since the premise is logically flawed.
Jackson goes on to quote two papers, neither of which mention psoriasis, but instead talk about one of the many effects of TZDs. He is simply blinding himself to simpler explanations which cover much more of the available data, than just the tiny, select sub-set of facts and fabrications he's looking at.
Ad Hominem: calling me "stupid," a "taskmaster," etc.
Nothing Jackson has shown indicates anything other than that Syndrome X and psoriasis are independent conditions which can complicate each other through interactions of TNFa (and perhaps other cytokines). A similarity in risk factors easily explains their comorbidity.
Jackson postulates no mechanism through which insulin resistance might cause psoriasis (which involes many biological changes other than inflammation). His hypothesis makes no testable predictions which aren't already assumed to be true by him (the hypothesis cannot, with Jackson's apparent point of view, be falsified). This is amatuer-level pseudo-science — easily-detectable "baloney" — illustrated also by the fact that of all the studies (well, abstracts) showing a correlation between Syndrome X metabolic changes and psoriasis, not a single professional researcher (who's medical knowledge is far beyond either Jackson's or my own) even hints that psoriasis might be caused by insulin resistance.
This page created on 20010423, and last modified on 20100509.


There were about 2,260 acres of residential land and property for sale in South Carolina's Williamsburg County based on recent Land And Farm data, making it the most common type of land for sale in Williamsburg County. The combined market value of farms, ranches and other land for sale was $14 million. The average size of residential land and property for sale in Williamsburg County was 40 acres, which is much bigger than the average size of residential land and property for sale throughout the rest of South Carolina. Browse all residential property and land for sale in Williamsburg County to find residential land and properties that suit your lifestyle needs, from existing residential homes and estates to land ready for future residential-property development. You can also browse more residential land and other rural acreage for sale throughout South Carolina on Land And Farm. Williamsburg County is in South Carolina's Pee DeE region. Williamsburg County is one of the ten biggest counties in the state. To find more land for sale in South Carolina, sign up for our South Carolina land-for-sale email alerts to be notified when new listings matching your search criteria come onto the market in Williamsburg County. You can also search Land And Farm to find land brokers and agents in South Carolina who specialize in selling land, rural acreage and other recreational property in regions throughout South Carolina, including land for sale in Williamsburg County.
5.7 AC Long Branch Rd.
3045 I M Graham Rd.


text:
Author - David Van Biema
My real-life Da Vinci Code moment
(RNS) — Three years ago I discovered a strange diagram written into an ancient monastic book. (Commentary)
Opinion • wp-export
The Green family's other collection
(RNS) — While the Museum of the Bible is trying to sort out the origins of its holdings after a U.S. government lawsuit over the 'unlawful importation' of...
News • Was Blind, But Now I See
So, how Jewish was Modigliani?
NEW YORK (RNS) — The Jewish Museum exhibit would be a must-see for Modigliani lovers even if it had no thesis, but it also delves deeply into identity...
'Portrait of a Bride' tells the story of a market in Jewish art
NEW YORK (RNS) Isidor Kaufmann got rich selling paintings of Hasidic Jews to assimilated Jews. Today, Hasidic Jews are snapping up his works.
Marvelous miniatures give up some — but not all — their treasures
NEW YORK (RNS) This is a story about a mysterious artist, his glorious art, a failed royal marriage and virtual-reality goggles. And, oh yes, faith preserved...
An eerie echo in 'Silence'
(RNS) Despite their very different attitudes toward faith, 'Silence' and 'Life of Galileo' offer striking parallels.
A partnership with Martin Scorsese gives this openly evangelical artist wider exposure
(RNS) Were it not for his outspoken Christianity, Makoto Fujimura would belong to the international art elite.
Met show celebrates Jerusalem as house of mirrors
NEW YORK (RNS) The show's true spectacle is aggregate: dozens of compelling objects and images interacting, fighting, influencing and being influenced by one...
Culture • News • Was Blind, But Now I See
Alfonse Borysewicz's lonely struggle gives Catholic art a modern face
(RNS) His paintings are all about faith; at the same time, they speak fluently and powerfully in the language and palette of contemporary art.
Arts & Media • Culture • Faith • News • Was Blind, But Now I See
Tobi Kahn's soulful art is for Jews — and non-Jews too
(RNS) The New York artist is one of the best-known and least easily compartmentalized contemporary fine artists doing faith-based work.

redpajama_set_name: RedPajamaCommonCrawl


text:
Soldier treats
Sgt. gets a surprise from Buckskin Elementary
By Angela Shepherd - For The Times-Gazette
Sgt. Austin DePugh from Chillicothe is pictured with the candy the received after it was donated by Buckskin Elementary students.
Buckskin Elementary students each year donate some of their Halloween candy to send overseas to American soldiers far from home. This year, one of their boxes made it to a local soldier and his platoon in the Middle East.
Candy shared by Buckskin Elementary students has made its way to a soldier far from home, but whose hometown is not far from the school in South Salem.
The importance of sharing, caring for others, and giving back to the community is something that Buckskin staff have long tried to instill in students, and one of those ways is to give students the opportunity to share their candy from Halloween trick or treating with folks who are far from home and serving in the military.
The school has done this for years, collecting the candy in a box set up outside principal Michael Shumate's office. He said the kids are always very generous with sharing their candy. They are never sure where the candy ends up, only that it goes to soldiers. He said they have always thought it would be neat if it ended up with someone from the area that had at least heard of Buckskin Elementary.
This year, the kids donated enough candy to fill three boxes to ship off to soldiers. According to teacher Lynda Cottrill, "That would appear to be the end of the story." But it is not.
Cottrill said the story continued when a Buckskin parent received a message from a friend saying that a local soldier and his platoon had a box of candy from Buckskin Elementary. That local soldier is Sgt. Austin DePugh from Chillicothe.
The message relayed to Cottrill was that when the box arrived, it came with the announcement, "Special delivery from Buckskin Elementary." DePugh responded with, "We have one of those back home." Then it was learned that the package was, indeed, from Ohio. DePugh "was in disbelief," Cottrill said.
Despite the seemingly impossible odds, the box of Halloween candy donated by Buckskin students to bring a bit of joy to someone far from home had made it thousands of miles away to the Middle East and into the company of someone who grew up in the area.
"This heartwarming story has touched every heart that has heard it,"Cottrill said. "How a simple act of kindness from a group of kids and staff could make a positive impact on soldiers all those miles away. No act of kindness is too small! Thank you Austin and your fellow soldiers for your service and dedication to our country and the sacrifices you make for us."
Shumate is retiring this school year, but he hopes that the incoming principal will continue this tradition. He also challenges other school districts and organizations to join in the effort of supporting every small act of kindness.
Angela Shepherd is a correspondent for the Greenfield Exempted Village School District.
https://www.timesgazette.com/wp-content/uploads/sites/33/2022/12/web1_soldier-pic-1.jpgSgt. Austin DePugh from Chillicothe is pictured with the candy the received after it was donated by Buckskin Elementary students. Submitted photo
https://www.timesgazette.com/wp-content/uploads/sites/33/2022/12/web1_Soldier-pic-2.jpgBuckskin Elementary students each year donate some of their Halloween candy to send overseas to American soldiers far from home. This year, one of their boxes made it to a local soldier and his platoon in the Middle East. Submitted photo
By Angela Shepherd
For The Times-Gazette
Hi! A visitor to our site felt the following article might be of interest to you: Soldier treats. Here is a link to that story: https://www.timesgazette.com/news/71132/soldier-treats


text:
443: Remorse
What can you do on a rainy day when you are cooped up with a restless alien who is in deep trouble with a third member of your household? The alien is nattily attired man of maybe 23 who looks like he just left a fraternity party at some expensive private college. The third member is my wife.
"I have no recollection of doing it." he said. He was lounging on a couch drinking a beer.
"You say you didn't break her priceless heirloom practicing your golf putt?"
"Isn't that what I just said?"
"No," I think you said you didn't have a recollection of doing it."
"There you go," he said. "If I had done something that thoughtless, I would have remembered it. I have a photographic memory you know."
"You always remember?"
"Like the time you used her grandmother's photograph to practice with your air rifle?"
"That's ridiculous. I'm not going to honor that hypothetical question with the truth."
While he seemed to be considering whether that sentence had turned out he way he intended, I broke in. "I seem to remember that's what she claimed."
"That was a long time ago and I hadn't been here but a short time."
"That excuses things?"
"Falloonians like to experiment when they first arrive on your planet. I was just having fun. Inipurtseeastrms will be Inipurtseeastrms. You can't blame them for that. You would never allow us membership on your planet if you didn't allow us a lane at sea that is a regularly used route for vessels. I am a man, after all."
"I think," I said, "that we allow you a good deal of 'leeway' as you tried to put it, man or no man."
"Then you understand I was just trying to learn Earthiness by having a little fun."
Earthiness? I would have to remember that. "Mischief is okay if you are just having fun?"
"I think so. Don't you?"
"Were you just having fun when you sold her battery-powered drill to the junk man?"
"Women aren't supposed to have those kinds of things. They are supposed to have feminine things that keep them in the kitchen and bedroom. Your country would run a lot smoother if they did."
"If I were you I wouldn't let her hear you say that. She still remembers the time you and Rodney used her best colander to pan for gold in Bayou Meto."
"A little adventure never hurt anyone. Why is she so sensitive?"
"I don't know. Why don't you return the ZZ Top CD you stole from her and ask her then?"
"It was someone else who did that. I have a witness."
"And who might that be?"
"My counterpoint in Mississippi. He could vouch for me."
"Why doesn't he?"
"He had to return to Falloonia for a, uh, … conference. Yeah, a conference. But he definitely saw that it was someone else."
"And who might that have been?"
"How should I know?" He sat up and looked at me with as serious a face as I've ever seen on him.
"Look," he said.
Men, our biggest fear in America
today is gang warfare. - C.W.
"Us men got to stick together."
"And if we don't?"
"And if we don't, it's going to be hell to pay. What if Mrs. Big Dope forms a gang?"
"A gang of what?"
"Other pissed-off women."
"Pretty soon, they'd be wanting to speak out loud in church."
"You don't even go to church."
"I heard one of those guys on TV say it, so it must be true."
"You believe TV preachers?"
"When they say things I can profit from."
"I can tell you something you can profit from."
"Don't bother," he said. "Mrs. Big Dope has given me three things already. I'm supposed to master them within three days or else."
"Or else what?"
"She didn't say, but it sounded bad."
"And what were those three things?"
"Repentance, reflection, and remorse. She said they might, just might, lead to a fourth 'R' if I tried hard."
"And that would the fourth be?"
"Redemption," he said, "but that's going to cost me a bundle."
Don't Get Me Started
Enjoy these at all? If so, order Big Dope's Book at Wattensaw Press, Amazon, or other book sellers. It will make him so happy. Also, click on an ad. It earns him a little and costs the advertiser, sort of a win-win.
Labels: American Politics, conservatives, politics, women's rights
444. Power
442. Guilt
441. Suspicion
440. Respect


With over 70 years experience manufacturing customised stainless steel sinks, basins, benches and architectural products, Britex have a reputation for innovation in stainless steel fabrication.
Britex are frequently used by architechs and designers to provide unique, purpose-built stainless steel sink for modern kitchens, that meet exact size, style and specifications.
Using a skilled team of trades people and designers, Britex work closely with customers to ensure that their customised stainless steel sinks blend seamlessly into the surrounds of the kitchen and are incorporated in a complimentary way.
Britex sinks are available nationwide.


Charlotte Simone. | Monday's Child.
Charlotte Simone is a brand that came onto my radar early this year…an Instagram 'like' and 'add' on my feed had me curious as to who/what this brand was about… And it was love at first sight.
Since then the Charlotte Simone brand has exploded onto the scene, lately every magazine I have opened has featured at least one of the stunning pieces.
Worn by Olivia Palermo, Rita Ora & Millie Mackintosh.. to name a few , these Autumn Winter essentials are getting the recognition that they truly deserve!
…Or the all Black version, seen below, from the Official Lookbook.
The 'Popsicle' is also high up there on my wish-list – the playful pop of colour makes this item a great piece in my 'predominantly black' wardrobe – My favourite colour-way being the Orange and black.
photographs used have been taken from Charlotte Simone's Instagram or official website.


PV-Systems exposed to extreme weather and environmental conditions like street lights, navigation buoys, etc., for increased risk for damage in the power electronics. In order to assure reliable battery charge control under such conditions, Phocos developed the CIS encapsulated PV charge controller to prevent corrosion.
The Phocos CIS is an industrial-grade charge controller that is suitable for all practical PV applications. The The Phocos CIS is a high-quality, 4-stage PWM-charging mode is combined with features such as: low-voltage disconnect, flexible load timer functions, and a multi-LED system status display.
The Phocos CIS charge controller features a dual load timer (2L-series) to independently control dual loads. The CIS has no moving parts, switches or buttons. Settings such as battery type, deep discharge thresholds, timers, etc. are made quickly and easily via infrared remote control accessory.
All devices are connected to the controller by supplied lead wires rather than wire terminals. This feature eliminates the risk of damage from external elements like corrosion, dust, water, bugs, chemicals, physical shock, where components make electrical contact to the controller.
Phocos-CIS-N single-load version with negative grounding: available here.


text:
Tobacco Company 'Turns State's Evidence'
By John Schwartz, Saundra Torry
WASHINGTON -- The smallest of the nation's major tobacco companies settled 22 state lawsuits Thursday by admitting that smoking causes cancer and other diseases, that nicotine is addictive and that the industry targets underage smokers -- concessions that could have repercussions for the entire industry.
Liggett Group Inc. also agreed to release thousands of pages of internal documents that could provide damaging evidence in lawsuits still pending against other cigarette makers and to provide Liggett employees to testify as witnesses in those cases.
Minnesota Attorney General Hubert H. Humphrey III compared the Liggett action to "turning state's evidence," and explained, "This is a little like busting a street drug dealer to get at the Colombian drug cartel."
"I believe this is the beginning of the end of this conspiracy of lies and deception," said Arizona Attorney General Grant Woods at a news conference where the agreement was announced. "Someone is finally telling the truth."
Breaking for the second time with the tobacco industry's decades-long united front, Liggett also agreed to beef up the warning labels on its products and pay 25 percent of pretax profits to the states for the next 25 years. The money would be used to help pay for the costs of treating smokers' health problems and for anti-smoking programs, which is what the original lawsuits had sought.
Before the deal was even signed, the other major tobacco companies denounced the agreement and raced to court in Winston-Salem, North Carolina, where they won a court order temporarily blocking Liggett from releasing documents covered by other companies' attorney-client privilege.
Liggett immediately released a handful of documents that it determined were not covered by attorney-client privilege to the attorneys general, and sent the thousands of pages of protected documents to courts around the country hearing the state suits. If a judge determines the documents show that the papers show crimes or fraud had occurred, the legal protections for those papers could be broken.
Attorney General Mike Moore of Mississippi was confident that the North Carolina injunction would not prevent the release of documents to courts in other states. The first state trial begins June 2 in Mississippi.
Moore, who brought the first state suit against the industry in 1994, said the new cache "will be the most incriminating documents in the entire history of tobacco litigation."
The documents also could be used in some 200 other lawsuits filed against cigarette makers by smokers, ex-smokers and people who say they are victims of secondhand smoke.
In addition, federal prosecutors investigating the tobacco industry said they would be taking a close look at the documents as possible evidence of fraud and false statements to Congress and government agencies.
The admission that companies target children could also help the Clinton administration's initiative giving the Food and Drug Administration power to limit youth access to tobacco products, which is currently being challenged in federal court in North Carolina.
Although publicly they have denied any negotiations are under way, Thursday's announcement might increase pressure for a broader settlement that would end all lawsuits against all tobacco companies in exchange for money and agreement to abide by underage smoking regulations.
The other major tobacco companies were quick to denounce the agreement, saying it was part of an ongoing effort by Liggett Chairman Bennett LeBow in his bid to sell Liggett to R.J. Reynolds. "We suspect he is simply brokering this deal in a desperate attempt to force one of the other cigarette manufacturers to take over his financially troubled and failing tobacco interests," Philip Morris, R.J. Reynolds, Brown & Williamson and Lorillard said in a statement.
While Brooke Group Ltd., parent of Liggett, gained 11 percent Thursday, tobacco stocks fell on news of the agreement. Philip Morris was down 5 percent to $115.87 1/2, and RJR Nabisco Holdings lost 2 percent, closing at $31.50.
Tobacco industry analysts, however, said they were unimpressed with the news. "I don't think this settlement is anything earthshaking," said Diana Temple of Salomon Brothers.


text:
package jp.aegif.android.cmis;

import java.util.ArrayList;

import android.app.ListActivity;
import jp.aegif.android.cmis.repo.CmisItemCollection;
import jp.aegif.android.cmis.repo.CmisItemLazy;

public class ListCmisFeedActivitySave extends ListActivity {

	public CmisItemLazy getItem() {
		return item;
	}
	public CmisItemLazy getItemParent() {
		return itemParent;
	}
	public CmisItemCollection getItems() {
		return items;
	}
	public ArrayList<CmisItemLazy> getCurrentStack() {
		return currentStack;
	}
	public ListCmisFeedActivitySave(CmisItemLazy item, CmisItemLazy itemParent, CmisItemCollection items, ArrayList<CmisItemLazy> currentStack) {
		super();
		this.item = item;
		this.itemParent = itemParent;
		this.items = items;
		this.currentStack = currentStack;
	}
	private CmisItemLazy item;
	private CmisItemLazy itemParent;
	private CmisItemCollection items;
	private ArrayList<CmisItemLazy> currentStack =  new ArrayList<CmisItemLazy>();

}

redpajama_set_name: RedPajamaGithub


Searching for words to explain why he remained, then left, his impoverished Dominican Republic village more than a decade after his wife and children legally immigrated to the United States, all Rosendo Mejia could come up with was that someone had to stay to make things better.
Although beautiful, their small town of Brisas del Este, wedged between the ocean and river, had no school, no paved roads and, worst of all, no clean water. As an attorney, he had the know-how and connections to lead the fight for improvements.
After Mr. Mejia finally succeeded in getting a school, paved streets and clean water for his small village, he rejoined his family in New York City in October 2015. He visited his children's George Washington High School for Health Career and Sciences, a community school that receives support services for children and families from Catholic Charities Alianza division, noticed a lack of parental involvement, and two days after his arrival in the United States, volunteered as a parent leader.
To compensate for all their time apart when finally reunited with his family, he used the same focus as a volunteer at his children's community school support program in Washington Heights run by Catholic Charities Alianza division. His activism proved so significant it was covered by press in the Dominican Republic. Meanwhile, his success organizing fellow parents for Alianza proved so significant he was named its first volunteer promoted to staff.
Community schools recognize that students who are hungry, can't see the blackboard, or are missing school regularly face critical obstacles to learning in the classroom. Alianza's soup-to-nuts social service support offers an alternative to the lure of the streets. At least two New York City Police department vans routinely park in front of the school and an NYPD squad car parks on the school lawn.
Mr. Mejia's teenage son and daughter, Rosendo Jr. and Camila, overcome their neighborhood's challenges by participating in Alianza In School Youth programs. There they hone their talents, take advantage of SAT prep classes, visit college campuses and receive support similar to students attending more exclusive schools.
But without parent participation, the program's impact was limited.
When Mr. Mejia began he called a PTA meeting that only 15 parents attended. The next month 40 parents showed up. Then 60. Then 80. He initiated adult education classes including English as a Second language, GED training and computer literacy to help parents provide better for their children. He kicked off a "Parent Walk-Thru" where parents visit their children's classes each month to see what they are studying. And he took on a caseload of 30 students with high absenteeism rates, working with them and their families until their attendance became among the highest in the school.
So extraordinary was his success that Catholic Charities created a paid part-time parent leader position for him.
"He was an asset so we said let's get him on board," says Catholic Charities Alianza Community Schools Director Peter Tinguely.
While now a paid staff member, Mr. Mejia continues to volunteer at his children's school. He is the first to arrive every morning and the last to leave.


text:
Airtel Bangladesh Limited
Airtel Bangladesh Limited is one of the leading mobile service providers in Bangladesh. Its previous name was 'Warid Telecom' owned by the UAE-based Abu Dhabi Group, and launched in May 10, 2007. In January 2010, Indian renowned Company named Bharti Airtel Limited, a leading telecommunications services provider in the world, bought out 70% share of 'Warid Telecom'. Meanwhile, the name 'Warid Telecom' change to 'Airtel Bangladesh'. In March 2013, Warid Telecom sold its rest of share (30%) to Bharti Airtel Holdings Singapore Pte Ltd, a concern company of Bharti Group. As a result, its whole management and other functions are controlled by this Company.
After being bought the majority share, Bharti Airtel investment 300 million US dollars, an Indian company's largest investment in Bangladesh, to rapidly expand its mobile service operations in the Country. Airtel Bangladesh sets an aim to be "the most loved brand, enriching the lives of millions" by 2015. Since its launch, Airtel has rapidly gained exalted popularity through its innovative mobile services in Bangladesh. On 8 September 2013, Airtel Bangladesh Ltd bought 5 MHz 3G spectrum from Bangladesh Telecommunication Regulatory Commission (BTRC) by giving 1.25 million US$.
The Products provided, but no limited, by Airtel Bangladesh are Telephony, EDGE (Enhanced Data for Global Evolution), GSM, HSDPA (High-Speed Downlink Packet Access), 3G and more. In addition to these, Airtel also provides lots of outstanding packages for its Prepaid & Post-paid users. In order to provide best services, Airtel Bangladesh has been including lots of innovative advantages for its users.
Banani Model Town:
House 34, Road 19/A
G. P.O. Box 3016
Fax: 02 – 8951786
Email: customerservice@bd.airtel.com
Call Helpline:
786 from Airtel Number
016-78600786 from Non Airtel Number
Website: www.bd.airtel.com
Grameenphone Ltd.
Bangladesh Telecommunication Regulatory Commission (BTRC)
BASIS Softexpo
Bangladesh Association of Software and Information Services (BASIS)
Internet Service Providers Association Bangladesh (ISPAB)
NReach-Net (Pvt.) Ltd


text:
Tamkeen Fund and Al Rasheed Street
by claud39 on Sun Mar 17, 2019 6:10 am
An international organization has recently issued a report that places Baghdad as the worst city to live in compared to the capitals of the world.
I was bothered by this news, whether the standards adopted in the classification are accurate, real or inaccurate, or carrying an agenda to show our capital is the worst.
Baghdad, Rashid, Baghdad, peace, Baghdad Kadhimin and the great Imam and Abdul Qadir Kilani and Rassafi and Jamil Sedqi Zuhawi and Jawahery and Qabnji and Yusuf Omar and cafe Shabandar and Umm Kulthum cafe and Mutanabi Street and the first skyscraper and the highest in Baghdad building Rafidain Bank.
Is it reasonable and logical? To allow the honor of our beloved capital Baghdad to be shamed and allow organizations that claim to be international organizations to harm our capital. Why are the good people? We accept, hear and watch every day what is happening to our Baghdad from neglect and obliterating the heritage of Baghdad and its cultural symbols without shaking us and motivating us to respond to their reports and standards with practical steps to restore the legacy, heritage, civilization and excellence.
It was also returned to 20 squares in Baghdad earlier this year by banks and under the supervision and follow-up of the Central Bank and the Association of Iraqi private banks.
In order to achieve this quickly, we propose that we choose Al-Rashid Street, which represents the Baghdadi and the Iraqi people as a legacy and an eternal cultural symbol, and that the original and good people of Baghdad, especially businessmen, private banks, the Association of Banks, civil society organizations, artists and plasticians, engineers and under the leadership of the Central Bank of Iraq As community initiatives that restore the cultural and heritage heritage of the present world by reviving its heart Rasheed Street.
I invite the government and the Secretariat of Baghdad to announce a competition and not a tender for the most beautiful designs to return Al-Rasheed Street to Al-Qah in 1965. We want to return to the street its heritage buildings, Shanashila, Hafez al-Qadi, Shatt al-Arab Casino, Brazilian coffee, Amo Elias Restaurant, To a heritage museum of Baghdad and to turn the street, which was acquired by the emergency professions and manual carriages to a street with a single track to enter only modern cars with specific models and to allocate Fridays and Saturdays to the heritage and commercial markets and Baghdadi industries, Cars, as is the case in most of the capitals of the world during the holidays, and this, if achieved requires the cooperation of all Iraqis and Baghdadis in particular to be Rashid Street is (the capital of good Baghdad beloved) and invite the owners of international reports to visit them before they put it as the worst city to live in the world.
* Economic and banking consultant


text:
Carroll ist eine Stadt (mit dem Status "City") und Verwaltungssitz des Carroll County im US-amerikanischen Bundesstaat Iowa. Das U.S. Census Bureau hat bei der Volkszählung 2020 eine Einwohnerzahl von 10.321 ermittelt.

Geografie
Carroll liegt im mittleren Westen Iowas am Middle Raccoon River, der über den Raccoon River und den Des Moines River zum Stromgebiet des Mississippi gehört.

Die geografischen Koordinaten von Carroll sind 42°03′57″ nördlicher Breite und 94°52′01″ westlicher Länge. Das Stadtgebiet erstreckt sich über eine Fläche von 14,74 km².

Nachbarorte von Carroll sind Auburn (21,2 km nördlich), Lidderdale (13,3 km nordöstlich), Lanesboro (27,3 km in der gleichen Richtung), Glidden (12,2 km östlich), Willey (13,1 km südsüdöstlich), Dedham (21,3 km in der gleichen Richtung), Templeton (23,3 km südsüdwestlich), Halbur (14,7 km südwestlich), Arcadia (16,4 km westlich), Westside (20,1 km in der gleichen Richtung) und Breda (20,4 km nordwestlich).

Die nächstgelegenen größeren Städte sind die Twin Cities in Minnesota (Minneapolis und Saint Paul) (445 km nordnordöstlich), Rochester (390 km nordöstlich), Cedar Rapids (270 km östlich), Iowas Hauptstadt Des Moines (150 km südöstlich), Kansas City in Missouri (371 km südlich), Nebraskas größte Stadt Omaha (170 km südwestlich), Sioux City (165 km westnordwestlich) und South Dakotas größte Stadt Sioux Falls (303 km nordwestlich).

Verkehr

Im Zentrum von Carroll kreuzen die U.S. Highways 30 und 71. Alle weiteren Straßen sind untergeordnete Landstraßen, teils unbefestigte Fahrwege sowie innerörtliche Verbindungsstraßen.

In West-Ost-Richtung verläuft eine Eisenbahnlinie für den Frachtverkehr der früheren Chicago and North Western Railway durch das Stadtgebiet, die heute von der Union Pacific Railroad (UP) betrieben wird.

Durch Carroll verläuft in entlang des Middle Racoon River auf der Trasse einer ehemaligen Eisenbahnstrecke mit dem Sauk Rail Trail ein Rail Trail für Wanderer und Radfahrer.

Mit dem Arthur N. Neu Airport befindet sich 9 km ostsüdöstlich ein kleiner Flugplatz. Der nächste Verkehrsflughafen ist der Des Moines International Airport (156 km südöstlich).

Geschichte
Die heutige Stadt wurde im Jahr 1867 inmitten einer vorwiegend landwirtschaftlich genutzten Region an einer Eisenbahnstrecke der damaligen Chicago and North Western Railway gegründet. Den Namen erhielt der Ort wie auch das County nach Charles Carroll aus Maryland, einem der Gründerväter der USA. Im Jahr 1869 wurde Carroll als selbstständige Kommune inkorporiert. Im gleichen Jahr wurde die Countyverwaltung in das zentral im Carroll County gelegene Carroll verlegt.

Bevölkerung
Nach der Volkszählung im Jahr 2010 lebten in Carroll 10.103 Menschen in 4357 Haushalten. Die Bevölkerungsdichte betrug 685,4 Einwohner pro Quadratkilometer. In den 4357 Haushalten lebten statistisch je 2,25 Personen.

Ethnisch betrachtet setzte sich die Bevölkerung zusammen aus 96,0 Prozent Weißen, 0,5 Prozent Afroamerikanern, 0,1 Prozent amerikanischen Ureinwohnern, 0,7 Prozent Asiaten sowie 1,5 Prozent aus anderen ethnischen Gruppen; 1,3 Prozent stammten von zwei oder mehr Ethnien ab. Unabhängig von der ethnischen Zugehörigkeit waren 2,4 Prozent der Bevölkerung spanischer oder lateinamerikanischer Abstammung.

23,9 Prozent der Bevölkerung waren unter 18 Jahre alt, 56,4 Prozent waren zwischen 18 und 64 und 19,7 Prozent waren 65 Jahre oder älter. 52,9 Prozent der Bevölkerung waren weiblich.

Das mittlere jährliche Einkommen eines Haushalts lag bei 44.591 USD. Das Pro-Kopf-Einkommen betrug 24.927 USD. 12,0 Prozent der Einwohner lebten unterhalb der Armutsgrenze.

Persönlichkeiten
 Frank Henry Greteman (1907–1987), Bischof von Sioux City (1970–1983), war 1950 bis 1965 Pfarrer in Carroll
 Orlando H. Manning (1847–1909), 12. Vizegouverneur von Iowa (1882–1885), begann seine Karriere als Anwalt in Carroll
 Arthur A. Neu (1933–2015), 40. Vizegouverneur von Iowa (1973–1979) und Bürgermeister von Carroll (1982–1985), geboren und aufgewachsen in Carroll
 Nick Nurse (* 1967), Basketballtrainer, geboren in Carroll

Einzelnachweise

Weblinks

 Offizielle Website
 Handelskammer von Carroll
 city-data.com - Carroll, Iowa

County Seat in Iowa
Charles Carroll als Namensgeber
Gemeindegründung 1867

redpajama_set_name: RedPajamaWikipedia


Mercedes driver outpaces teammate and F1 championship leader Nico Rosberg as track temperature reaches 55C.
Lewis Hamilton started his Hungarian Grand Prix weekend as he intended to continue, leading both of Friday's free practice sessions with championship-leading Mercedes teammate Nico Rosberg behind.
The winner of the last two Hungarian Grands Prix lapped the Hungaroring circuit outside Budapest with a best time of one minute 25.814 seconds in the morning and 1:24.482 in the afternoon.
Rosberg was second fastest in both, 0.183 and 0.238 slower than the 2008 champion in the sessions with track temperatures rising to a sweltering 55 degrees Celsius after lunch.
Ferrari's Kimi Raikkonen and Fernando Alonso were the closest to the dominant duo, who have won nine out of 10 races so far between them, in the morning with third and fourth places respectively on the timesheets.
However Red Bull's quadruple champion Sebastian Vettel, who has never won in Hungary, was third fastest in the second practice with Alonso fourth.
Hamilton is 14 points adrift of Rosberg, despite having won five races to the German's four, but has a far better record in Hungary.