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Ok, this is long, but interesting (I think).
I was cautious about using copper supplements because I read that diabetics can have high levels of copper. I wrote Dr. Loren Pickart, a biochemist & leading reseacher on copper peptides. He has given me permission to post this.
There is a great deal of confusion in this area. 30 years ago, it was thought that copper caused many diseases. But by the 1990s, it was found that copper supplements would cure or correct many of these diseases. Plasma copper and ceruloplasmin were used to determine copper levels but were not useful because they are increased by inflammation and disease, and may be falsely high.
Also, may studies use free copper ion and not peptide or protein bound copper. For example, free copper oxidizes low density lipoproteins. GHK-copper blocks the oxidation of low density lipoproteins. There is essential no free ionic copper in the human body. It is all bound the GHK or proteins.
As for diabetes, additional supplemental copper reduces many of the biochemical problems associated with diabetes like excessive tissue oxidation and protein damaging glycations.
Metabolism. 2008 Sep;57(9):1253-61.Oxidative stress in Cohen diabetic rat model by high-sucrose, low-copper diet: inducing pancreatic damage and diabetes.Ryu S, Ornoy A, Samuni A, Zangen S, Kohen R.
Department of Anatomy and Cell Biology, Laboratory of Teratology, Hebrew University-Hadassah Medical School, Jerusalem 91120, Israel.
Increased oxidative stress contributes to the development and progression of both types of diabetes mellitus (DM) and its complications. In the Cohen diabetic (CD) rats, a known genetic model of nutritionally induced type 2 DM, a high-sucrose, low-copper diet (HSD) induces within 4 weeks DM in the sensitive (CDs) rats but not in the resistant (CDr) rats. To assess the possible involvement of oxidative stress in the induction of DM, we studied the effect of HSD on the tissue levels of antioxidants and the extent of oxidative injuries in these animals in comparison with the regular outbred strain of nondiabetic Sabra rats. The specific aims were to investigate, at the onset of HSD-induced DM, (1) the extent of oxidative injury, as reflected by levels of malondialdehyde and protein carbonyl groups; (2) the overall antioxidant capacities to cope with increased oxidative stress; and (3) the modification of oxidative damage biomarkers in various tissues of CDr, CDs, and Sabra rats. Female CDs, CDr, and Sabra rats were fed regular diet or HSD for 4 to 5 weeks; and several parameters of oxidative injuries and antioxidant levels were determined. Changes in the levels of nonenzymatic low-molecular weight antioxidants (LMWAs) were measured by cyclic voltammetry and oxygen radical absorbance capacity. The activities of the antioxidant enzymes superoxide dismutase and catalase were measured. Oxidative damage was evaluated by measuring lipid peroxidation and protein oxidation. (1) In all animals fed HSD, the levels of LMWAs were decreased in most organs, although not plasma. (2) A significant difference was consistently found in antioxidant enzymes' activities in the pancreas of HSD-fed CDs rats, but not in other tissues. (3) The activities of superoxide dismutase and catalase and the levels of malondialdehyde and protein carbonyl group increased, whereas the levels of LMWAs decreased, in the pancreas of HSD-fed CDs rats. In the CD rats that develop DM when fed HSD, the pancreas showed susceptibility to oxidative stress-induced injuries. Thus, enhanced oxidative stress seems to play a role in the pathogenesis of DM in this strain.
Environ Health Perspect. 2007 July; 115(7): A341–A342.
Copper Deficiency, Lead, and ParaoxonaseLeslie M. KlevayUniversity of North Dakota, School of Medicine and Health Sciences, Grand Forks, North Dakota, E-mail: firstname.lastname@example.com
Li et al. (2006) measured paraoxonase 1 (PON1) in workers and found an inverse association between lead exposure and enzyme activity. This observation compliments some epidemiology and related experiments with animals, because low paraoxonase activity is associated with diabetes mellitus, familial hypercholesterolemia, ischemic heart disease, and metabolic syndrome (Klevay 2004). Paraoxonase, although studied most extensively because of its ability to detoxify organophosphate insecticides (James 2006; van Himbergen et al. 2006), has drawn increasing attention because it hydrolyzes homocysteine thiolactone, a vascular toxin that inhibits copper enzymes (Klevay 2006).Lead intoxication has many manifestations (Fischbein 1998), lesser-known of which is induction of copper deficiency (Klauder and Petering 1977). Rats deficient in copper have an approximately 28% decrease in paraoxonase activity (Klevay 2004). These observations are consonant with the decrease in superoxide dismutase (SOD) associated with occupational exposure to lead (Ito et al. 1985) because this enzyme also depends on adequate copper nutriture for activity (Linder and Goode 1980; Owen 1981). Thus, SOD is an index of copper nutriture in humans (Uauy et al. 1985).Li et al. (2006) stated that "the mechanism by which heavy metals inhibit serum PON1 activity is still not clear." It seems likely that lead interferes with copper utilization in the workers, leading to low copper nutritional status (Li et al. 2006). Low copper status has been related to a large variety of adverse cardiovascular phenomena in both animals and people; in this context, the most important are hypercholesterolemia, hypertension, and impaired oxidative defense (Klevay 2000, 2002).
Are there unpublished copper data on the workers, or can they be reexamined to test this copper hypothesis? Plasma copper and ceruloplasmin are not likely to be useful because they are increased by inflammation (Pepys 1996) and may be falsely high. Extracellular SOD may be helpful because it is sensitive to low copper status (Johnson et al. 2005), and low values have been associated with atherosclerosis in humans (Landmesser et al. 2000; Wang et al. 1998).
from http://www.acemagnetics.com/ed...bracelets-aging.html
Can Copper Status Affect Aging?Author/s: Judy Mcbride
Agricultural ResearchAugust, 1999
Could a marginal intake of the essential element copper contribute to the aging process? ARS physiologist Jack T. Saari thinks that's a strong possibility--based on rat studies, along with a good bit of indirect evidence.
Saari and a colleague, chemist Gwen Dahlen, at the Grand Forks Human Nutrition Research Center in North Dakota wanted to see if copper deficiency spurs sugar molecules to attach to proteins. The process--nonenzymatic glycosylation, or protein glycation for short--is a spontaneous binding of sugar to protein without the aid of enzymes. It is thought to cause much of the tissue damage in people with diabetes. And it increases in all of us as we age, Saari says.
Tiny sugar molecules attached to a huge protein molecule may be likened to fleas on a dog. But the attached sugars can be more than annoying; they can be deadly to the protein. That's because their free ends tend to hook up to other proteins or other sites on the same protein, forming cross-links. These cross-links bend the protein out of shape so that it no longer functions properly. The useless protein soon gets degraded and hauled off for recycling or disposal.
In the early 1980s, Saari's colleague, Leslie M. Klevay, M.D., reported that copper-deficient rats had glycated hemoglobin--the oxygen-carrying molecule in red blood cells. Klevay heads the Mineral Nutrient Requirements Unit at Grand Forks.
Saari says this and more recent indirect evidence led him to look for a connection between copper deficiency and protein glycation.
Two pieces of indirect evidence come from studies at ARS' Beltsville (Maryland) Human Nutrition Research Center, as well as Saari's laboratory. Rats fed copper-deficient diets have high blood sugar, says Saari. This raises the odds for glycation.
"Their condition is like type-II diabetes," says Meira Fields, who conducted the Beltsville studies. Unlike Saari, Fields finds that the copper-deficient rats exhibit high blood sugar only when their diets are high in sugar--either fructose or sucrose. This sugar-laden diet also causes the rats to secrete less insulin, she says, which is needed to move sugar out of the blood and into the cells to serve as fuel.
What's more, Fields' studies have repeatedly shown that rats suffer the most tissue damage from this diet when the sugar is fructose. Saari notes that in the test tube, fructose is a better glycator than glucose.Two more pieces of indirect evidence come from Saari's own studies. He reduced the symptoms of copper deficiency--such as an enlarged heart--by two different treatments. First, he fed the rats only a portion of the food they would normally eat. This kept blood glucose levels low, he says, reducing the chance of glycation. Second, he treated the rats with a chemical--aminoguanidine--known to block advanced glycation or cross-linking of sugars. And it worked.
Fractured Proteins
Armed with this evidence, Saari and Dahlen designed a study to look directly for increases in protein glycation. The results bore out their suspicions. Both the early and advanced stages of protein glycation increased significantly in the rats fed a copper-deficient diet.
One sensitive indicator of advanced glycation is a measure of the proteins that it has rendered ineffective. This indicator was at least six times higher in the copper-deficient rats. It was nearly undetectable in the control rats, he says, noting that Dahlen made this very delicate analysis possible by refining an existing analytical method. They published their findings in the April 1999 issue of the Journal of Nutritional Biochemistry.
Treating the rats with aminoguanidine did not reduce cross-linking in this study as it did in the earlier one, says Saari, probably because the dosage was too low. So he and Dahlen did a follow-up Study using a higher dosage. The earliest results available at this writing are showing a reduction in glycation caused by copper deficiency.
Copper Intake Lags
Humans consume more copper than rats do. But the average copper content of diets in the United States, Canada, Great Britain, and Belgium still falls below the U.S.-suggested intake range of 1.5 to 3 milligrams per day.
Klevay, a physician, pulled together data from the chemical analyses of 849 diets in the four countries. He says they show that 61 percent contained less than 1.5 mg of copper daily, and nearly a third of the diets provided less than 1 mg.
"That's in the range that has proved insufficient for both men and women in controlled dietary experiments," he says.
Vegetarian diets had more copper than nonvegetarian diets. That's because nuts, seeds, mushrooms, whole grains, and legumes--such as soybeans, peas, chickpeas, lentils, and peanuts--are good sources of the mineral. The richest sources of copper are animal--oysters, crabs, and liver--which are not common in the daily diet.
Estimated copper intake in the United States, based on USDA's latest nationwide food consumption survey, averages 1.2 mg/day for all individuals--below the 1.5 mg suggested minimum. The estimates show men averaging just the minimum 1.5 mg/day, while women average only 1 mg/day.
Saari speculates that years of eating a diet low in the mineral may be a factor contributing to the age-related decline in tissue function from increasing protein glycation.
"It's a low-grade phenomenon," he says. "It's not like diabetes where blood glucose stays high after an overnight fast." Instead, he says, blood glucose peaks higher than normal after a meal--increasing glycation--but it doesn't stick around. "The only way you know this increase is happening is through a glucose tolerance test or a test of glycated hemoglobin."
The early stage of glycation--when the sugar first attaches to the protein--is reversible. As blood sugar drops, the sugar can detach. Once the cross-links are formed, however, they don't come apart, Saari says. So far, he has looked only at glycation of hemoglobin and serum proteins. But it can also happen to structural proteins that form tissues.
Copper and Oxidation
The most accepted theory of aging holds that it results from cumulative damage to tissues by oxygen free radicals. These radicals are generated during normal metabolism and delivered by environmental pollution. Saari says his thesis fits hand in glove with the oxidation theory because glycation appears to increase oxidation.
According to reports in the diabetes literature, both free and attached sugar molecules can convert the benign oxygen molecule into a free radical. What's more, glycated proteins are more vulnerable to oxidation.
Copper is important to the body's defense against oxidation through a copper-containing enzyme--superoxide dismutase, or SOD. Saari notes that SOD activity reportedly decreases with aging, while oxidative damage increases.
Over the long term, a low copper intake could plausibly weaken this inherent antioxidant defense, slightly elevate blood sugar, and increase attachment of sugar to proteins--all of which tend to increase oxidative damage.
This research is part of Human Nutrition Requirements, Food Composition, and Intake, an ARS National Program described at http://www.nps.ars.usda. gov/programs/appvs.htm.
Jack T. Saari and Leslie M. Klevay are at the USDA-ARS Grand Forks Human Nutrition Research Center, P O. Box 9034, University Station, Grand Forks, ND 58202; phone (701) 795-8353, fax (701) 795-8395, e-mail jsaari@gfhnrc. ars.usda.gov.
Copper's Protective and Anti-Aging Actions
Copper is an essential metal and the intake of copper at reasonable levels should improve your health. The generally recommended dosages per day of copper range from 1 to 3 milligrams daily, however, recent human studies suggest that 4 to 7 milligrams of supplemental copper daily might greatly reduce the rates of some degenerative diseases.
Copper deficiency in animals causes increased cellular oxidation, increased cancer, increased cardiovascular risk, more atherosclerosis, higher LDL-cholesterol, decreased HDL-cholesterol, more lipid oxidation, aortic aneurysms, osteoarthritis, rheumatoid arthritis, osteoporosis, chronic conditions involving bone and connective tissue, brain defects in newborn, obesity, graying of hair, increased sensitivity to pain and lower brain enkephalins, accelerated development of Alzheimer's disease, obesity, and reproductive problems. See more below.
In humans, copper deficiency is associated with all of the above plus depression, impaired brain function, and general fatigue.
Some copper recommendations are based on the recommended zinc dietary levels, and maintaining what these nutritionists feels is a proper zinc to copper ratio. Other recent studies in humans found that supplementation with 3 to 6 milligrams of copper daily had positive actions such as reducing damaging cellular oxidation and lowering cholesterol and LDL levels, while increasing HDL levels. See more below.
Metabolically Active Copper
In the body, copper moves between cuprous (copper 1 or Cu 1+) form and the cupric (copper 2 or Cu 2+) form. The majority of the body's copper is in the Copper 2 form. The copper type that induces tissue regeneration and skin repair is copper 2. Copper 2 is also what is called the body's copper called is called "metabolically active copper".
Only a very small fraction, less that 1% of the body's copper, is called metabolically active copper and this fraction is exchanged between the various tissues of the body as needed. This metabolically active fraction is bound to either amino acids, peptides, or proteins. This fraction is high in healthy people but diminishes in persons with inflammatory diseases such as arthritis.
Most of the body's copper is bound into proteins where it plays an important role in biological activities such as anti-oxidant effects, energy generation, tissue regeneration and so forth.
Confusion Over Blood Copper and Disease States
Blood serum copper is about 5% metabolically active copper; the other 95% being in the anti-oxidant protein ceruloplasmin. During many diseases and stress conditions, the body increases ceruloplasmin levels as a protective anti-oxidant mechanism. Because metabolically active copper is technically difficult to measure, most studies of copper and disease states reported only the total blood serum copper. This has caused much confusion and often has led to false conclusions as to the role of copper in disease states.
For example, total blood plasma copper is elevated in diseases such as cancer, heart disease, and arthritis but this increase is due to increased ceruloplasmin in the blood. Some misinformed persons have interpreted this increase in blood copper to indicate that high copper causes these conditions and diseases. But when copper supplements are given to animals or humans, the additional dietary copper has been found to lower carcinogenesis and tumor growth, inhibit the development of cardiovascular problems, and reverse many arthritic effects. See more below.
Should Dietary Copper Intake be Raised to Reduce Major Diseases?
Some experts on copper are of the opinion that copper intake should be raised. Copper deficiency diseases are virtually the same as the pattern of major diseases in the USA. This suggests that some of these diseases may be partially due to inadequate copper in our diet.
Copper toxicity is a rarity and most experts consider a daily intake of 10 milligrams to be safe. However, since copper and zinc compete for uptake in the body, a high copper intake reduces zinc absorption, and, conversely, a high zinc intake reduces copper uptake. Thus, a balance should be maintained between these to metals. Most commonly, nutritionists recommend a ratio of 7 parts by weight zinc to one part copper.
There Are No Adequate Studies on Toxic Levels of Copper in Water
This is how the toxic level of copper in water was determined. A group of nurses had a party after which a number became ill. It was felt that the illness may have been due to the water they used. The water was analyzed and had a high level of copper. So this amount of copper in the water was divided by 4 and called the toxic level of copper in water. Whether the copper in the water caused the illness is still unknown.
When excess copper is ingested, within a range of 10 to 25 milligrams per day, the superfluous copper is excreted by the liver into the bile and copper balance is maintained.
The one condition where copper intake must be restricted is Wilson's disease, a rare genetic condition that affects 1,600 persons in the USA.
Anti-oxidant Actions of Copper and Dietary Intake
The copper-containing protein, copper,zinc-superoxide dismutase (or CuZnSOD) is the primary anti-oxidant defense in the human body. Higher levels of CuZnSOD are a primary factor in longer lifespans in animals.
However, because copper 2 is usually in short supply in the human body, CuZnSOD has only about 50% of its needed copper (zinc supplies are usually adequate), and this markedly reduces CuZnSOD's anti-oxidant powers and is another reason why more dietary copper would be beneficial. Harris (Department of Biochemistry and Biophysics, Texas A&M University) pointed out that while copper,zinc superoxide dismutase requires two, copper and zinc, only copper, seems to regulate the expression of functional anti-oxidant activity. Restricting dietary copper quickly impairs the catalytic function CuZnSOD in numerous tissues. However, when diets are supplemented with copper, the CuZnSOD activity is quickly restored. (Harris ED, J Nutr, 1992, pp 636-40)
Under some biochemical circumstances, such as after traumatic tissue injury, copper (as well as other metals) can reverse its normal anti-oxidant role and cause damaging cellular oxidation. This has led some benighted amateur nutritionists to propose restricting dietary copper to reduce damaging oxidation in the body. But, controlled animals studies have found the opposite to be true: a reduced copper intake actually increases deleterious cellular oxidation and promotes a wide variety of the types of degenerative diseases associated with aging. On the other hand, a higher dietary copper intake in animals reduces overall damaging cellular oxidation.
It is true that there are damaging oxidative reaction in the human body. What is the answer to reduce destructive oxidation? First, do not worry too much about metal intake. People living in certain high mountain valleys of the world such as the Hunza area of Pakistan, the Vilcabamba area of Equador, the Caucasus of Georgia, Northwest Tibet, and Titicaca region in the Peruvian Andes, eat very different diets but all drink water with a very high mineral content (hard water from glaciers) but the lifespan and health of the elderly in these regions is exceptional high. In contrast, regions with low mineral water (soft water) are characterized by high rates of cancer and heart disease.
One analysis of drinking water in the Hunza valley found a zinc to copper ratio of 1.8. This far lower than the normally recommended ratio of 7.0 and also suggests a higher intake of copper might be beneficial.
Daily Fruit Juice Reduces Lipid Peroxidation by 75%Also, to reduce damaging cellular oxidation in your body, use other anti-oxidants such as coenzyme-Q10, alpha lipoic acid, vitamin E isomers, and melatonin. These help protect the polyunsaturated fats in cellular membranes.
Copper May Reduce Some Cancers
The Center for Disease Control states that "Copper has not been shown to cause cancer in people or animals". The International Agency for Research on Cancer has determined that copper is not classifiable as to human carcinogenicity. Added copper complexes reduce spontaneous colon cancer in rats and, when administered to tumor-bearing rats, slow the rate of tumor growth. In cell culture, copper complexes cause some types of cancer cells to revert to non-cancerous growth patterns.
In 1912, cancer patients in Germany were treated for facial epithelioma with a a blend of copper chloride and lecithin with some success. In 1913, researchers at at the University of Liverpool reported injections of a copper salt degenerated carcinomas transplanted into mice.
John R. J. Sorenson (University of Arkansas for Medical Sciences, College of Pharmacy) and colleagues treated rats with solid tumors with various copper complexes (such as copper salicylate) with SOD activity and this decreased tumor growth and increased survival rates in rats. These copper complexes did not kill cancer cells but often caused them to revert to the growth patterns of normal (differentiated) cells. (Sorenson, Prog Med Chem 1989; 26: 506-507) Sorenson also found that numerous copper complexes with SOD activity prevented or retarded the spontaneous development of cancers in mice and possessed anticancer, anti-carcinogenic, and anti-mutagenic effects both in vitro and in vivo. (Sorenson (ed.), Biology of Copper Complexes. Humana Press, Clifton, NJ. 1987)
The serum level of copper is often elevated in animals and humans with cancer (Inutsuka and Araki, Cancer 1978; 42: 626; Willingham and Sorenson, Tr Elem Med 1986; 3: 139-140.) It appears that this elevation of serum copper that occurs as a part of the body's response to the cancer, rather than its cause. Most tumor cells have decreased CuZnSOD activity compared to normal cells, and it has been suggested that the elevation in serum copper is a physiological response designed to activate CuZnSOD or other copper enzymes in cancer cells to inhibit their growth. (Oberley and Buettner, Cancer Res 1979; 39: 1141).
Colon cancer is the second most deadly cancer in the USA. When rats were fed low copper diets, they had a higher incidence of carcinogen-induced colon cancers compared with rats fed a high copper diet. (DiSilvestro, Greenson, Liao, Proc Soc Exp Biol Med 1992; 201: 94-99).
Also, APC is a gene known to suppress the formation of tumors and this gene is altered early on during colon cancer development. Familial adenomatous polyposis is a disease that has been linked to mutation changes in the APC gene. Individuals possessing these mutations develop numerous intestinal polyps (precancerous lesions) at an early age. A species of mice (Min or multiple intestinal neoplasia) have a mutation similar to the human gene (APC) that causes intestinal polyps and colon cancer. A study reported in 2001 by nutritionist Cindy D. Davis at the Human Nutrition Research Center (Grand Forks, N.D.) found that, when Min mice were fed a copper deficient diet (20% of normal level), they developed a significantly higher small intestine tumor incidence and a significantly higher small intestine tumor mass than mice fed adequate dietary copper. The low copper also decreased the expression of various protein kinase C isozymes, a series of proteins involved in the signal transduction pathway within the cell, thus upsetting normal cell regulation. Dr. Davis says these results have implications because 80% of the people in the USA do not ingest adequate amounts of copper.
Another study of copper deficiency in animals by Narayanan, Fitch and Levenson found that copper stimulates the production of the tumor-suppressor protein p53. This protein inhibits the growth of tumors in the body. (Narayanan, Fitch and Levenson, Dept. of Nutrition, Florida State U., Tallahassee, FL in The Journal of Nutrition, May 2001)
Copper and Cardiovascular Disease
Humans and animal studies demonstrate that copper deficiency increases the plasma cholesterol and LDL-cholesterol while decreasing HDL-cholesterol, thus increasing the cardiovascular disease risk. (Klevay, Inman, Johnson, et al, Metabolism 1984; 33: 1112-1118. Klevay, Med Hypothesis 1987; 24: 111-119; Klevay, Med Hypothesis 1987; 24: 111-119).
Klevay theorized that a metabolic imbalance between zinc and copper, but more a copper deficiency than zinc excess, is a major factor in the genesis of coronary heart disease. (Klevay, Lack of a recommended dietary allowance for copper may be hazardous to your health. Journal of the American College of Nutrition. 1998; volume 17: pages 322-326) Other investigators found that copper complexes also can minimize damage to the aorta and heart muscle following myocardial infarction.
Severe copper deficiency results in heart abnormalities and damage (cardiomyopathy) in some animals. (Institute of Medicine. Dietary reference intakes for vitamin A, vitamin K, boron, chromium, copper, iodine, iron, manganese, molybdenum, nickel, silicon, vanadium, and zinc. Washington, D.C.: National Academy Press. 2001: pages 7-1-27)
A multicenter placebo-controlled study found copper supplementation with 3 or 6 mg/day increased the resistance of red blood cells to damaging oxidation indicating that relatively high intakes of copper do not increase the susceptibility of LDL or red blood cells to oxidation. (Rock, et al. The effect of copper supplementation on red blood cell oxidizability and plasma antioxidants in middle-aged healthy volunteers. Free Radical Biology and Medicine. 2000; volume 28: pages 324-329; Turley, et al. Copper supplementation in humans does not affect the susceptibility of low density lipoprotein to in vitro induced oxidation. Free Radical Biology and Medicine. 2000; volume 29: pages 1129-1134)
Rats on a copper deficient diet had a decrease in aortic integrity that produces eventual aneurysm. (Greene, et al, J Surg Res 1987; 42: 503-512)
Immune System Function
A medical publication in 1867 reported that, during the cholera epidemics in Paris of 1832, 1849 and 1852, copper workers did not develop cholera. Another observation was that persons with Menke's disease died from frequent and severe infections due to an inadequate immune response. Menke's is an inherited disease causing defective copper absorption and severe copper deficiency. (Percival, Copper and Immunity. American Journal of Clinical Nutrition. 1998; volume 67: pages 1064S-1068S; Failla and Hopkins, Is low copper status immunosuppressive? Nutrition Reviews. 1998; volume 56: pages S59-S64)
Studies with animals demonstrated that animals deficient in copper had an increased susceptibility to bacterial pathogens such as Salmonella and Listeria. (Bala and Failla, Proc Natl Acad Sci USA 1992; 89: 6794-6797) A study of 11 infants with copper deficiency found that the ability of their white blood cells to engulf pathogens increased after one month of copper supplementation (Heresi, et al. Phagocytosis and immunoglobulin levels in hypocupremic children. Nutrition Research. 1985; volume 5: pages 1327-1334) A study of adult men on a low-copper diet (0.66 mg copper/day for 24 days , then 0.38 mg/day for another 40 days) showed a decreased ability of mononuclear cells to respond to antigens. (Kelley, et al. Effects of low-copper diets on human immune response. American Journal of Clinical Nutrition. 1995; volume 62: pages 412-6.) Abnormally low numbers of white blood cells is a clinical indicator of copper deficiency in humans and functioning of macrophages decreases in even marginally copper deficient rats . (Babu and M.L. Failla, J Nutr 1990; 120: 1700-1709)
Some studies have suggested that immune function and neutrophil activity is more sensitive to low dietary copper than standard measures of copper status. Immune impairment can be detected by one week after the start of a diet low or marginal in copper; conversely, the addition of adequate copper rapidly reverses the immune suppression within one week. Copper deficiency also reduced DNA synthesis in activated T-cells but this is also quickly reversible after copper supplementation. (Bala and Failla, Proc Natl Acad Sci USA 1992; 89: 6794-6797)
It has been suggested that, because the immune system is very sensitive the changes in the body's copper status, it may be possible to set a scientific RDA (Recommended Daily Allowance) for copper by giving persons graded amounts of dietary copper and then determining the optimal copper dosage for optimal immune function. (Babu and Failla, J Nutr 1990; 120: 1700-1709)
Copper, Inflammation, and Arthritis
Studies of rheumatoid arthritis and copper exemplify the paradoxes that have so confused research on copper and its effects on various diseases.
In 1885, the French physician, Luton, used copper acetate to treat arthritic patients. He made a salve of hog's lard and 30% neutral copper acetate for application to the skin over affected joints. He also had his patients take pills containing 10 mg. of copper acetate per day.
In 1939, the German physician, Werner Hangarter, wrote that Finnish copper miners remained free of arthritis while they worked in the mining industry. This was notable since rheumatism was widespread in Finland. This finding led Finnish medical researchers to treat patients with a mixture of copper chloride and sodium salicylate. They reported treatment successes in patients suffering from rheumatic fever, rheumatoid arthritis, neck and back problems, and sciatica.
Between 1940 and 1970, studies of persons with rheumatoid arthritis found them to have higher than normal serum copper levels. Similar results were found in other various inflammatory diseases in man and animals. (Lewis, Agents and Actions 1984; 15: 513-519) Yet, in seeming contradiction, copper complexes were successfully used in the treatment of numerous conditions characterized by arthritic changes and inflammation. (Sorenson and Hangarter, Inflammation 1977; 2: 217-238). But this use of copper complexes was superseded by the development of anti-inflammatory steroids and aspirin-like nonsteroidal anti-inflammatory drugs in the treatment of these conditions.
Subsequent researchers examined this paradoxical role of copper, and they concluded that increase in serum copper is a physiological response to inflammation, rather than a cause of inflammation. (Sorenson, J Pharm Pharmac 1977; 2: 450-452) The rise in serum copper is due to an elevation of the protein ceruloplasmin in serum, but ceruloplasmin has strong anti-inflammatory activity and tends to counteract the inflammatory state. (Frieden, Clin Physiol Biochem 1986; 4: 11-19) Further research established that copper deficiency increased the severity of experimentally-induced inflammation. (Sorenson and Kishore, Tr Elem Med 1984; 1: 93)
Professor John R. J. Sorenson (University of Arkansas for Medical Sciences, College of Pharmacy) has led the scientific work on the use of copper complexes to treat patients with arthritic and other chronic degenerative diseases. He has found that the copper complexes of over 140 anti-inflammatory agents, such as aspirin and ibuprofen, for example, to be far more active than these compounds without copper. Copper aspirinate has been shown to be more effective in the treatment of rheumatoid arthritis than aspirin alone. It also has been shown to prevent or even cure the ulceration of the stomach often associated with aspirin therapy. Sorenson has reviewed a wide variety of of copper complexes that have potent anti-inflammatory activity when administered to humans or animals; his review is 110 pages long and with a bibliography of 736 references. (Sorenson, Prog Med Chem 1989; 26: 437-568)
Copper and Osteoporosis
200 years ago, the German physician Rademacher established that copper supplements speeded the healing of broken bones in patients. (Dollwet and Sorenson, Tr Elem in Med 1985; 2: 80) In the years that have followed, compelling evidence has established a vital role for copper in the biosynthesis of bone and connective tissues and their maintenance.
Inadequate dietary copper causes osteoporosis in numerous animal species and humans. (Dollwet and Sorenson, Biol Tr Elem Res 1988; 18: 39-48) Copper deficiency is associated with scoliosis, skeletal abnormalities, and increased susceptibility to fractures. (Worthington and Shambaugh, J Manipulative Physiol Ther 1993; 16: 169-173) Danks. Copper Deficiency in Humans. In: "Biological Roles of Copper." CIBA Foundation Symposium-79. Exerpta Medica, Amsterdam, 1980. p. 209) Inadequate dietary copper lowers bone calcium levels. (Strause, P. Hegenauer, R.C. Saltman, et al, J Nutr 1986; 116: 135)
One study of elderly persons found a decreased loss of bone mineral density from the lumbar spine after copper supplementation of 3 milligram daily for 2 years (Conlan, et al. Serum copper levels in elderly patients with femoral neck fractures. Age and Aging. 1990; volume 19: pages 212-214)
Healthy adult males on a low copper intake of 0.7 milligrams daily for 6 weeks exhibited an increased rate of bone resorption (breakdown). (Baker. et al. Effect of dietary copper intakes on biochemical markers of bone metabolism in healthy adult males. European Journal of Clinical Nutrition. 1999; volume 53: pages 408-412)
Copper and DHEA
DHEA (dehydroepiandrosterone) is a key hormone that produces mainly secondary hormones and counter's the damaging actions of cortisol during stress. It is widely used as a dietary supplement to help prevent deleterious changes with age. Klevay and Christopherson found that copper deficiency in rats decreased DHEA in serum by approximately 50%. The authors suggest that eating a diet higher in copper will increase the DHEA level in the body. (Klevay and Christopherson, Society Of Experimental Biological Medicine Proceedings, 1999)
Copper and Pregnancy
In the 1930's at a sheep station in Western Australia many newborn lambs were uncoordinated, had difficulty standing, and died. Later, it was determined that the pregnant sheep were pastured on land that produced grass with a very low copper content. This herbage did not provide enough copper for normal development of the lambs' nervous system and the brain.
Recent research at the USDA's Grand Forks Human Nutrition Research Center found that even marginal copper deficiency in pregnant rats produces brain damage and neurological defects in their offspring. The newborn rats have structural abnormalities in the areas of the brain involved in learning and memory and responsible for coordination and movement. These produced further behavioral changes and the young rats lack the normal "startle" reflex to unexpected noises. This deficit permanently affected the young rats and could not be correct by diets higher in copper.
During pregnancy, a sufficient copper intake is essential for normal neurological development of the fetus. Tom Johnson, Ph.D., lead author of the study said "A reserve of copper is built up in the liver during fetal development that helps satisfy the requirement of the newborn for copper. Thus, adequate copper intake during pregnancy is important to ensure the fetus acquires sufficient copper to fill this reserve. However, for the health of the mother, she should have a copper intake of 1.5-3.0 mg/d postpartum and during lactation."
Small deficits in dietary copper produce substantial changes in fetal brain enzymes. Protein kinase C (PKC) is a copper-dependent enzyme that is crucial in the development of the nervous system. The PKC levels were measured in the brains of rat pups whose mothers had been fed a copper-deficient diet during and for a few weeks after pregnancy. The diet was defined as 1 mcg/d for one group and 2 mcg/d for a second group of rats (one third of the recommended copper), while the control group received sufficient dietary copper. While PKC levels rose in all the rat groups during the three weeks after birth, the increase was only half as much in the group whose moms got 1 mcg/d, and 25% less in the 2mcg/d group. Moreover, at 2 mcg/d, one form of PKC was off by 50% in the cerebellum, which happens to be the control center for motor function and muscle coordination.
Another study from the University of California at Davis reported that that copper deficiency during pregnancy can result in "Numerous gross structural and biochemical abnormalities," which seem to arise as the copper deficiency reduces free radical defense mechanisms, connective tissue metabolism and energy production. The same researchers found that copper is better absorbed from breast milk than from infant formula. (Lonnerdal B., Copper nutrition during infancy and childhood. Am J Clin Nutr 1998 May;67(5 Suppl):1046S-1053S.)
Pregnant women (and others) can obtain copper from supplements and seafood, oysters, liver, nuts and seeds, beans, whole-grained bread, cocoa, chocolate.
Anticonvulsant Activities of Copper Complexes
The brain contains more copper than any other organ of the body except the liver, where copper is stored for use elsewhere. This fact suggests that copper plays a role in brain functions. With reports of seizures in animals and humans following the protracted consumption of copper-deficient diets, it was reasoned that copper has a role to play in the prevention of seizures. It was subsequently discovered that organic compounds that are not themselves anti-convulsants exhibit anticonvulsant activity when complexed with copper. Further, it was found that copper complexes of all anti-epileptic drugs are more effective and less toxic than their parent drugs. ( J.R.J. Sorenson, Prog Med Chem 1989; 26: 437-568.)


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Question about Toshiba TEC B-472 Thermal Label Printer
I keep getting the Rewind Full error, though i don't have any labels bunched up and the sensors are all clear from paper. I can't make it clear and restart. The spool thing, from what i can tell, is empty and there is nothing blocking it. I have had this error once before, and I dumped the memory. It won't dump the memory right now, i can't make it. Which buttons do you hold when you turn it on? How do i just get rid of the error and print my labels. Please help me with what ever you can.
Posted by ben3305 on
There is either is misalignement of the sensors or one of them is out of order. If you still have problems just unplug the big Green cable on the rewinder board. Switch off and on should do the trick
Posted on Sep 04, 2009
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For a Free Consultation Call Baltimore, Maryland Workers Compensation Attorney Mr. Rodabaugh today at +1 (410) 937-1659 OR Email
Mr. Rodabaugh has numerous offices and meeting locations in Baltimore and throughout the state of Maryland. In home consultations are available. For some injured workers the ability to travel is limited. Mr. Rodabaugh is able to meet them at their homes or somewhere more convenient.
What is included in the free consultation?
Who is the best Baltimore workers compensation attorney?
What does a Maryland workers compensation attorney do?
Know your rights and let Mr. Rodabaugh make sure you get them.
Get answers to workers comp questions here.
WE DO IN HOME CONSULTS and
WE CAN MEET ANYWHERE IN THE STATE if mutually agreeable!
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For years Mr. Rodabaugh has practiced law only in workers compensation and personal injury. Focusing on this area of law allows him to stay up to date on changes in the law and provide the legal representation that injured employees need in an attorney. Mr. Rodabaugh knows that every situation is unique and that is why he approaches each and every workers compensation case with a different plan of action. Because he handles Maryland workers compensation cases every day he very rarely faces situations that he has not dealt with in the past and can craft solutions accordingly.
Sometimes there is no choice but to take immediate action at the Baltimore Workers Compensation Commission: file for sanctions, request penalties, or file for a hearing! Other times a single phone call from Mr. Rodabaugh to the workmans comp adjuster will do the trick.
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Attorney Andrew Rodabaugh was born and raised in Baltimore County and has continued residing in Maryland throughout his life. He attended Dulaney High School and began his legal studies at Stevenson University (formerly Villa Julie). The Paralegal Studies Program at Villa Julie provided Mr Rodabaugh the foundation and practical legal knowledge which many practicing attorneys do not possess today. Mr. Rodabaugh graduated from Villa Julie with Honors. From Villa Julie Mr. Rodabaugh was admitted to the University of Baltimore School of Law where he focused his studies on personal injury and workers' compensation. From their he began his career as a Baltimore Workers Compensation Attorney.
Work History
Like many of his clients, Mr. Rodabaugh started off working in hard labor. This is what sets him apart from other Baltimore Maryland Workers Compensation attorneys. He worked as a refrigeration pipe fitter for the better part of a decade. This is where he learned to appreciate the risks of work injury to which so many hardworking and loyal employees expose themselves. He has had multiple jobs in the maintenance industry as well which help him understand what the injured worker is truly going through.
Mr. Rodabaugh was able to obtain a law clerk position at Cohen & Dwin P.A. while he studied at the University of Baltimore before becoming a licensed attorney. His first associate position was with the Baltimore County Office of Law as an Assistant Baltimore County Attorney in the workers compensation department. It is there where he began his legal career and gained priceless experience in Maryland Workers' Compensation Law. He now practices in Baltimore with Cohen & Dwin and represents clients from all walks of life when they are injured on the job. Whether you are a construction worker from La Plata, a bus driver from Baltimore, police officer in Cambridge, or secretary in Cumberland, Baltimore Workers Compensation Attorney Andrew M. Rodabaugh is able to help.
Mr. Rodabaugh regularly attends hearings before the Maryland Workers Compensation Commission. He handles workers compensation cases before the various state Circuit Courts and the Court of Special Appeals.
Family Life
Mr. Rodabaugh now lives in the Parkville/ Towson area with his daughter, wife, two dogs, and one ornery cat.


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"This was an exciting game because both teams are so evenly matched," UW coach Dean Duerst said. "I'm happy that our team was able to accomplish so much in such a tight game."
The Badgers will remain in South Bend, Ind., for the tournament's second round, where they will face national No. 4 seed Notre Dame (20-1-1) Sunday at noon. The Irish dispatched of Eastern Illinois 4-0 Friday.
The loss to UW was just the second of they year for the Flyers' (20-2) who had won a nation-best 20 consecutive games.
Wisconsin remained a perfect 11-0 in non-conference matches this season and improved to 16-5-1 overall.
Vermeulen, a first-team All-Big Ten selection this year, almost netted UW's regulation goal but Dayton's Jen Simonetti inadvertently converted Vermeulen's free kick for an own-goal, which gave UW a 1-0 lead at 58:05.
Atlantic 10 Offensive Player of the Year Reba Sedlacek was held to just one shot, while Simonetti had none. The latter, though, redeemed herself for the own goal three minutes later when Tesha Kozlowski capitalized on her free kick to tie the match.
Wisconsin sophomore midfielder Kara Kabellis had a game-high six shots, including three (all on goal) in the first half, in helping Wisconsin advance to the second round for the third time in five years.
Each team took 11 shots, and the stalemate continued until sophomore midfielder/forward Allison Preiss set up Vermeulen for her third game-winning goal of the season and team-leading 12th goal of the year overall.


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When do I receive my race pack?
Race Packs will be sent out before the race, more information will be posted nearer the event day. The pack will include your t-shirt, timing chip, sponsor form and race number.
Will there be photography on the day?
The Rennie Grove team will be taking photos on the day, and Sussex Sport Photography will be taking photos of runners as they cross the finish line. For more information click here.
Do I have to raise sponsorship?
Rennie Grove Hospice Care relies on the generosity of the local community to fund around 85% of our £7.2 million annual costs, and fundraising events such as the Herts 10k are hugely important in helping us to reach this target. This year we are challenging all runners to raise £50. If everyone does this we can raise enough to cover the cost of four nurses for a year. Please note this event is to raise money for Rennie Grove Hospice Care only.
Can you give advice on how to raise sponsorship?
Yes, please see the Raising Money page for more information or email the Fundraising Team on email@example.com.
How does Gift Aid work?
Anyone giving sponsorship money who is a UK tax payer, should tick the gift aid box on your sponsorship form. This makes the donation worth more; an extra 25p for every £1 pledged.
What is the minimum age to take part?
All participants of the Herts 10K must be 12 years old or over on the day of the event to take part. Participants who are under 18 must have consent from a parent or guardian to take part. All participants under 18 must be accompanied by an adult on the route and must provide emergency contact details of another adult.
Is there parking available?
There will be no parking at Rothamsted Research. However there will be parking at the following places:
- Harpenden train station has kindly agreed to runners parking in the east car park free of charge. Please download and print a copy of the parking permit to leave on the dashboard for identification.
- Harpenden town centre. Please allow at least 15 minutes walking time to get to the START/FINISH line from Harpenden town centre.
- Sun Lane car park is free on a Sunday. Turn right at the roundabout as you head out of the town towards Luton – this holds around 75 cars.
- Amenbury Lane – Parking is available on the road which the leisure centre is situated on.
Where is the start and finish point?
Rothamsted Research, Harpenden, AL5 2JQ.
What are the details of the route?
Please click here to download the route map (PDF).
Are there any first aid points on the course?
Yes. GB-EMS will be located at the start/finish area and will also be on route.
Is there somewhere to leave my bag?
Yes there will be a bag drop area, but items are left at the owner's risk.
How can I sign up to be a volunteer at the HERTS 10K?
We are looking for volunteers on the day and to help with preparation for the event. Please email us at firstname.lastname@example.com. We would love to have you on board!


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The Guidelines view self-regulation as a foundation of development because children's emerging ability or inability to self-regulate directly impacts growth in the four developmental domains. Self-regulation refers to how children take in information from both their bodies and their environment, and how they respond to that information.[1]
Self-regulation also refers to children's emerging ability to regulate or control their attention, thoughts, emotions and behaviors. Since self-regulation includes how children cope with situations that produce either change or stress, children who have a difficult time managing stressors may not be able to reach a calm state where growth and learning can occur, even with the help of their caregiver. Therefore it is important that caregivers pay attention to children's self-regulation skills and help them learn how to regulate their emotions, thoughts, and behaviors. Just as with development in other domains, children's self-regulation capacities progress as they develop, and heavily rely on sensitive and nurturing relationships with caregivers.
Children's capacity to self-regulate in the first three years is not fully developed. Children's development accommodates for this maturing ability by relying on caregivers to act as the external regulators, or co-regulators.[2] Central to the development of healthy self-regulation is children learning to read their bodies' signals. At first, caregivers are the ones who respond to these signals. For example, when young children feel hunger, they must depend on their caregivers to recognize their cues and appropriately meet that need. If there is a loud noise that is causing the child to feel stressed and overwhelmed, the caregiver must modify the environment for that child to regain a calm state. Children rely on attentive caregivers to read their cues and meet their needs. Children's needs include everything from maintaining a normal body temperature to managing their physiology and behavior, and learning to soothe themselves. As they develop children also depend on their caregivers to help them manage emotions and behavior, and build attention.[3]
Self-regulation is a lifelong process that depends on children's social and cultural contexts, and the child and caregiver relationship. Cultures differ in both the physical and emotional expectations they have of young children and how they respond to children's behaviors and signals. Therefore, how children react and what they do about feelings or occurrences will differ depending on their unique experiences.
When caregivers properly meet children's needs in a consistent manner, they help them feel safe, content, and organized. After having these needs met over and over, children learn that feelings of stress or discomfort will quickly pass, building their internal capacity to respond to these feelings and become less reactive and impulsive. As young children learn to read and respond appropriately to their own cues, they become capable of managing their own self-regulatory processes. "This transition from external regulation to self-regulation is one of the most important tasks of growing up."[4] In the following sub-sections, the four types of self-regulation are further explained. Additionally, the concepts of self-regulation are integrated throughout the Guidelines.
IEL is providing access to a PDF of the full 170-page printed version of the Guidelines:
This webinar provides a short overview of the Illinois Early Learning Guidelines for Children Birth to Age Three. It also provides a tour of the resources available on the Illinois Early Learning Project website that can support the use of the guidelines in practice and at home.
Find resources related to the Illinois Early Learning Birth to 3 Guidelines:
The opinions, resources, and referrals provided on the IEL Web site are intended for informational purposes only and are not intended to take the place of medical or legal advice, or of other appropriate services. We encourage you to seek direct local assistance from a qualified professional if necessary before taking action.
The content of the IEL Web site does not necessarily reflect the views or policies of the Illinois Early Learning Project, the University of Illinois at Urbana-Champaign, or the Illinois State Board of Education; nor does the mention of trade names, commercial products, or organizations imply endorsement by the Illinois Early Learning Project, the University of Illinois at Urbana-Champaign, or the Illinois State Board of Education.


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Friday, August 31, 2007
Needed a break
I've also been needing a break from the steady diet of Beethoven, Strauss and Wagner I've been on. I swerved hard in Verdi's direction and I've been going through Nabucco. It's the 21st century - there should be no guilt on the part of a German music lover who partakes of the sunnier delights from south of the Alps. Right? (And I did listen to the first 25 numbers of the St. Matthew Passion before bed last night so I've redeemed myself.)
I had been planning on doing a post on a comment I heard on TV from a soprano back in the 90s. It must have been during a Met telecast. During an intermission, she said that the role of Susanna in Le nozze di Figaro was longer than Brünnhilde's in the Ring. I'd thought since then that that must be wrong. Reading Michael Kennedy's Master Musicians series book on Strauss last week really motivated me because he claimed that Och's role was the second only to Susanna's in length. That was it - I was going to find out how many bars we're talking about here.
I dug out the Figaro score and got to work. I'd decided to count every measure in which a note for Susanna appears - i.e. including pick-ups. The recitatives didn't contribute as much as I thought they would. But that Act II finale really is a monster. Something like 650 measures for her in that one. My grand total ended up being roughly 1680. I then turned to Walküre and started counting.
The task was pretty tedious by this point and I realized that my supposition is that whoever first asserted this couldn't count. (Or maybe it was that I was the first person dumb enough to sit down and count these things out.) I couldn't face finishing the Ring, let alone plouging through Rosenkavalier. I gave up. For now, I'm content to let the assertion stand. Susanna is the longest opera role ever in the world.
Part III of Album Cover Follies is coming this weekend. I thought it was going to be a one-time deal, but it turns out you can pretty much make fun of any album cover...
Wednesday, August 22, 2007
Greatest Classical CD Covers EVER, Part II
Now THIS is a production of Carmen I'd like to see! A totally nude beauty gets pawed by Mumenschantz? Leave the kids at home when you go to play this CD! Oooh Nellie!
|Annette Dasch - Armida
This looks like the cover of a CD you get along with the free sample of Fructis that comes in the mail. I don't know how her voice is but I'm sure her hair smells great.
|Elgar - The Collector's Edition
I'm never going to England again. Not while the ghost of Elgar haunts the English countryside. I'll bet this is some spooky-ass music. Hopefully all of Elgar's pieces for theremin are included in this collection.
|Lang Lang - Beethoven: Piano Concertos 1 & 4
Looks like Lang just spent the afternoon shopping and is pissed because he just realized he forgot all his shopping bags on the subway. Tough luck there, Mr. Metrosexual. I hope he didn't forget his iPhone as well.
|Max Emanuel Cencic - Rossini: Opera Arias & Overtures
God, this guy is funny on those Ricky Gervais podcasts. The thing about the bee having the heart attack? When he gets angry about that poisonous frog? Classic stuff. I didn't know he could sing.
|Artemis Quartet - Schumann and Brahms Quintets
These hipsters sure are proud of their glowing cupboard doors. If you look at their legs, they're spelling out something, kinda like the Village People spelling out "YMCA". I think these guys are spelling out "YOINT".
|Leonard Bernstein - West Side Story
What the hell's so goddamn funny, Len? You make a 20th century update to a beloved love story and you do nothing but giggle? Well I hope nothing bad ever happens to you, sir.
|Strauss - Complete Works for Wind Ensemble
This picture is a mindbending paradox. Old Strauss is conducting Young Strauss in heaven while Young Strauss himself conducts? If you buy this, you'll just stare at the cover, get more and more violently confused and pretty soon you're shaking and the CD self-destructs like a Mission: Impossible cassette and you won't even get to listen to it.
|Mozart - Cosi
You didn't know Cosi fan tutte was a dystopian nightmare? The best part of the opera is when THX-1138 and RMK-5930 exchange their unisex jumpsuits and totally confuse their assigned breeding partners and it's the time of the month where they are allowed to engage in the reproductive act with the females so there are hijinx galore. In the end, everyone, even the cynical cyborg UNI-MOPH, learns a little something about life.
Tuesday, August 21, 2007
Another Masterclass
Liz and I watched another masterclass from the Barenboim on Beethoven set. This time it was the first movement of the Appassionata with Lang Lang. After Lang plays, and Barenboim gets the requisite compliments out of the way, the constructive criticism starts. Barenboim says he'd like to hear a better grasp of the structure of the piece from Lang. Now, the classes are taped before an audience and they're always in the background. A few of them brought scores with them, the nerds. One of the nerds can be seen scribbling this piece of advice down. What did he write? "Grasp of structure = good"? "Lang doesn't know what he's doing"? Good thing he brought the notepad.
In another class, Barenboim (who plays all the sonatas from memory) has a question about one of Beethoven's performance markings and asks to take a look at one of the nerd's scores. Of course, they've brought some jive, unreliable edition instead of a proper urtext edition. Barenboim notes it but doesn't wipe his butt with the score which is what he should have done.
One of the best parts of the class was Barenboim's advice about one note. He said that Lang should create the illusion of a crescendo on the note and then played the passage in question. Sure enough, the effect was there. One of the audience members asked how he did it. Barenboim said that if he told it wouldn't be an illusion anymore. He then told an anecdote about meeting Horowitz who gave him a memorable piece of performance advice: "You must have will." Barenboim then apologized for not fully answering the question but that sure sounds like the full answer to me. Hope the nerds got that one down.
(Why the hostility to the nerds? Self-revulsion because I identify with them? NO. LEAVE ME ALONE.)
Monday, August 20, 2007
New Verdi Letter
Wednesday, August 15, 2007
Greatest Classical CD Covers EVER?
Every once in a while, I'll come across a classical CD whose cover will burn itself into my memory forever. Here are a few...
|Mendelssohn - Elijah
I remember cracking up the first time I saw this cover. He's supposed to look like he's imploring a higher power but instead looks dubious about a lighting rig used during the photo shoot. Actually, it looks more like he's trying to work out a square root in his head. Plus, the stage beard looks good at 50 or 100 feet but looks pretty weak this close up. I will not be purchasing this recording.
|Rossini - Il barbiere di Siviglia
Domingo looks like a total spaz here. I'd dump a chamber pot on a goon like this if he came around to senerenade me with a look like that on his puss. I may purchase this recording if it is reissued with a different cover. It should not feature Domingo cutting hair.
|Johann Strauss - Famous Works
I'm sure this is a wonderful Johann Strauss DVD. Only have one misgiving about it: they've slapped a picture of RICHARD Strauss on the cover. It inspires confidence. Close enough, guys. God knows what you'd get if you actually played this thing. Episodes of McMillan & Wife? An instructional video for your new LG washing machine? There's literally no way to know.
|Richard Wagner - Parsifal: An Orchestral Quest
Robert Mapplethorpe is apparently a Wagnerian. I'm glad this isn't the cover of a recording I'd have the slightest interest in. I'd feel real uncomfortable with this cover nestling next to my other Parsifals.
RICHARD Strauss - Salome
I wouldn't feel too comfortable having this cover sniffing around my collection either. It looks like the funniest outtake from the photo session that got out and is passed around in the underground opera scene. Don't even think about the number of people that had to be involved in putting the cover together and that none of them raised the red flag. I know of someone who ordered in a copy of this recording and paid more to get the previous cover.
|Placido Domingo - Granada: The Greatest Hits (aka "THE HAT")Wow. I'm thinking when some assistant pulled that mother out of the tickle trunk that that would have been the time to put your foot down, Placido. You wouldn't see Daniel Barenboim in a crazy hat like that!
|Bruckner - Symphonies
Aw, Christ.
|Lara St. John - Bach - Works for Violin Solo
I was all ready to make jokes about how inappropriate this cover was. What, with her state of undress and apparent age 'n all. "So you want to take a picture of a topless 12 year-old and slap it on the cover? Run with it!" But after some quick research, I found that St. John herself wrote a reply to a review in the Edmonton Journal of all things in which she states she was 24 when the picture was taken. She only looks 12. So it's okay then.
|RICHARD Strauss - Zarathustra/Don Joan/Rosenkavalier Suite (Maazel)
This is the greatest cover of anything ever. I want gloves to make my hands look like Space Hands like that. There's no way an orchestra would miss a downbeat if Maazel had mitts like that. But surely the only misstep in this cover is the space hands, right?
|RICHARD Strauss - Zarathustra/Don Joan/Rosenkavalier Suite (Maazel)
Wrong! If anything, this one is even more distressing. Why are his hands doing that? We notice even more the psychotic look on his face. Physical assault looks like one of his more benign intentions.
I love how someone at the record company realized how crazy the Space Hands were and reissued the recording without them. But now instead of looking like Timothy Leary, Maazel looks like Charles Manson.
Click here for the complete (ongoing) series...
Tuesday, August 14, 2007
Edmonton Opera
The Edmonton Opera has a history page with a number of interesting items:
- Not only was Kathleen Battle here in the 90s, but so was Joan Sutherland, Kiri Te Kenawa and Cecilia Bartoli. What was I doing when Dame Kiri came to town that I didn't go? Playing with pogs?
- Marilyn Horne, Jose Carreras, and Anna Moffo all sang here.
- Beverly Sills sang here three different times.
- 1976 Bohème with Teresa Stratas?!?!
Something obviously happened around 1980 because these superstar bookings stopped (excepting the recital series mentioned above). I went to a number of productions in the 90s and things have actually gone even further downhill since then. I actually saw works like Britten's Rape of Lucretia or Strauss's Ariadne here and I'm thinking that would never happen now. (I guess they lost a ton of money in the 90s.) Liz and I had been subscribers for a few years recently, but after a brutally bad Barber of Seville, I think that's it for subscriptions. Especially with the Met HD broadcasts at movie theatres. After the Edmonton fiasco, we went and saw Bartlett Sher's Met production of Barber in the theatre and it was fantastic. With 8 Met presentations in the theatre next season, it's no contest.
To be fair, I did enjoy one Edmonton production - the Turandot from a few years ago, the highlight of which was Sally Dibblee's Liu. It was the best singing I've ever heard here... Except for Kathleen Battle, of course, if I could remember it.
Sunday, August 12, 2007
Strauss on Sirius III: The Voyage Home
I was looking at the booklet that came with the Böhm recording. There's a note in it in which he claims the cuts he uses were sanctioned by the composer. Not surprised that he claims this since it's the only possible justification for making cuts. It could be that Strauss said something to Böhm but it could also simply be Strauss's refusal to go to war over cuts being taken as a sanction. (I doubt he approved of the butchery that Die Frau ohne Schatten was/is subjected to and he did make that famous dry comment about a conductor forgetting to make a couple more cuts to Act III of Rosenkavalier - the concluding Trio and Duet.) Böhm also says that Strauss conducted the work with cuts in the last 20 years of his life. In the 30s Strauss suddenly decided that Elektra had too much fat and needed some trimming? In any case, he made no changes to the published score which for me is a definitive gesture. He didn't, so to me, the cuts still = bad.
Friday, August 10, 2007
Classical Downloads
Thursday, August 9, 2007
Mission Accomplished
Update: Liz couldn't resist commenting on this.
Wednesday, August 8, 2007
And while you're waiting for that, check out the 50 CD set of Schubert works for $80. Or what about the 22 CD set of Stravinsky conducting Stravinsky for $43?
Hear the clarity and definition!
But what is the price of inferior audio quality? Can poor audio touch the heart as deeply as better sound? John Meyer, who designs and builds some of the world's best speakers at his Meyer Sound Labs in Berkeley, doesn't think so.
Um, of course a hawker of overpriced speakers is going to think this. But really - we can't respond as strongly to a mono recording as to a stereo one? I think Elisabeth Schwarzkopf singing Strauss's Four Last Songs would turn me into a blubbering wreck regardless if I'm listening on a $50K system or on my iPod, stereo or mono.
Seems to me that when we listen to poorer-fidelity music, we make the adjustment pretty quickly and don't really notice the sound quality after a few minutes. The range of acceptable sound quality is pretty wide.
Plus, weren't these same types complaining when CDs came out and how the compromise in sound quality was unacceptable there, too?
Tuesday, August 7, 2007
Today's Anna Netrebko Picture
I was not at all surprised to see that John Derbyshire was all over this a few months ago...
(At no point was this post going to be called "Anna Get Your Gun.")
What's a word stronger than "asinine"?
And as that devout Wagnerian Michael Portillo pertinently asked in a New Statesman article a couple of years ago, why is it that a love of Wagner is so often taken to signal right-wing, antisemitic tendencies when a love of Richard Strauss, at least on occasion a Nazi sympathiser, signals only the height of good taste?
The part of the question about Strauss is the stupidest thing I've read in the last 14 months. The single biggest feature of the history of Strauss reception is the attempt by fellow composers, critics and academics "of good taste" to write off most if not all of his works as kitsch (Schoenberg, Stravinsky, Joseph Kerman in Opera as Drama, etc. etc. etc.). There is no other composer who is accused of bad taste as often as Strauss.
I'm sure Stephen Pettitt meant to get us thinking when he quoted a "provocative" question posed by a "devout Wagnerian" but instead has presented us with a funhouse mirror of stupidity. Every angle reveals something new.
I'm off to put my head in ice water.
During Lunch
Plus, I saw a guy who had a mullet that was humbling in its magnificence.
Saturday, August 4, 2007
Back to Rutherford
I ended up taking out a volume from the Neue Bach Ausgabe (the one with the Johannisfest cantatas) and Bruckner's Fifth Symphony (the edition edited by Nowak).
Would Sobeys Have Vöslauer?
I'm surprised I haven't posted a video or picture of Anna Netrebko yet... Here she is singing the Flower Duet from Lakmé with Elina Garanca.
And here's one of her Vöslauer Mineral Water commercials.
Thursday, August 2, 2007
The iPod Decision
I was finding that making a decision about what to listen to was getting more difficult as more and more stuff appeared on the iPod. I finally realized that I could make a few decisions to focus what was on there a little better. I can have everything ripped and stored in one place at home and walk around with a subset of that. Do I need all the Haydn symphonies and string quartets at the same time? During the day, are the chances I'll listen to a given work all equal? These kinds of questions made me realize that limiting my choice would help diversify the listening as well as save space. So only Symphonies 1-8 and the Op. 20 quartets are on the iPod today. Only one recording of Parsifal (the 1951 Knappertsbusch), only a few volumes of the Beethoven edition, one Don Carlos, only the live King Crimson stuff from 1972-74, only the 1963-68 stuff by Miles Davis, etc.
This has helped. My July listening has been a little more diverse with me hearing a few things for the first time. This kind of approach is probably pretty obvious to a normal person but to a mildly obsessive completist it's a revelation.
(Okay, fine, there are 7 Rings currently on the iPod - most of them were downloaded from the Yahoo opera share group. So sue me. What, I have to have only one of every single thing? Who made you boss of my iPod?)


text:
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text:
Hebrew Israelite
Posted in the African-American Forum
United States
#68182 Jun 24, 2013
Your book as astro-mythology.If you are thinking and got your logic cap on, then you will know, that the Age of Taurus proceeds the Age of Aries, as the Ages go backwards,that's why the age of Jesus was the age of the Fish/Pisces,and we are now at the Age of Aquarius.
So why is Abraham in Genesis, and Moses in Exodus, but the Age of Taurus is before the age of Aries?
Abraham, is told to go to the mountain, where he is to sacrifice his Son Isaac, his God was testing his faith/ loyalty The Ram who in Egypt symbolizes Ausar/Osiris the Father of Heru/ Horus, this was Abraham recognizing the New Age of Aries, which symbolized War(hence the sacrafice of the Ram).
On mount sanai remember they just left Egypt,and the calf symbolized, Het-Heru the Apis bull.The bull was prominent because the zodiac age was the Age of Taurus, and Moses being the scholar and wiseman, knew that this was an age that was on the way out
United States
#68183 Jun 24, 2013
Aderibigbes date corresponds to that of the Hyksos invasion of Egypt 2000-1500BC. On the possible eastern origin of the Yorubas
The the Nubians were descended or colonized by the Egyptians, the Ijebu, and by extension, all Yoruba customs, derived from the Egyptian. Many traditional Yorubas have always claimed Egypt as their place of original abode, and that their monarchical tradition derives from the Egyptians. Apostle Atigbiofor Atsuliaghan, a high priest of Umale-Okun, and a direct descendant of Orunmila, claimed that the Yorubas left Egypt as a result of a big war that engulfed the whole of Egypt.. He said the Egyptian remnants settled in various places, two important places being Ode Itsekiri and Ile-Ife.Chief O.N Rewane says Oral tradition has it also that when the Yorubas came from South of Egypt they did not go straight to where they now occupy. They settled at Illushi, some at Asaba area Ebu, Olukumi Ukwunzu while some settled at Ode-Itsekir The modern dynasty of ancient kemetic/egyptian kings such as Akufu(not Khufu),King Tutu Ankoma(not Tutankhamun) is the Akuapem Dynasty that can be found today in the Eastern Region of Ghana,west africa. o called European experts do not know the Ancient Egyptian story because they are not familiar with African tribal names. They do not have the linguistic and cultural backgrounds to identify Egyptian names and have simply transposed the African names of people and places in Ancient Egyptian history into European languages to make it possible for them to claim expertise
Cape Town, South Africa
#68184 Jun 24, 2013
The found the real skulls of indigenous Canaanites in Egypt and guess what??? They were Caucasian! So those so-called ancients were darkened!
Cape Town, South Africa
#68185 Jun 24, 2013
But you all are mixed. Ethiopians are mixed even Glim will tell you that!
Cape Town, South Africa
#68186 Jun 24, 2013
Yorubas also claim to be of Israelite descent although they havent got a drop of Middle Eastern DNA! They probably have not a drop of Egyptian DNA either!
Since: May 13
Location hidden
#68187 Jun 24, 2013
Dam! thats Easy READ this!
Tacitus: Agricola Book 1 [10]
. The geography and inhabitants of Britain, already described by many writers, I will speak of, not that my research and ability may be compared with theirs, but because the country was then for the first time thoroughly subdued. And so matters, which as being still not accurately known my predecessors embellished with their eloquence, shall now be related on the evidence of facts.
Britain, the largest of the islands which Roman geography includes, is so situated that it faces Germany on the east, Spain on the west; on the south it is even within sight of Gaul; its northern extremities, which have no shores opposite to them, are beaten by the waves of a vast open sea"
So you can READ can't you well he had to be there in order to write the geography of the land. and also a lot of romans wrote on this land and described the people.
See this is your FALSE comment "that he personally saw and studied my ancestors the Silures'
Silures are your forefathers? So I guess that you are ABORIGINE cause all the early inhabitants of Europe from north to south were brown skin ABORIGINES NOT any white originated out of Europe none.
here this is what the Gauls or silures, celts looked like when they fought your real forefathers the White Roman killers
Ludovisi Battle Sarcophagus: Battle of Romans and Barbarians(gauls)
These are Gauls:
Ludovisi Sarcophagus detail. Head of barbarian in battle from front of Sarcophagus - 1
Ludovisi Sarcophagus detail. Head of barbarian in battle from front of Sarcophagus - 2
These are The Barbarians (Gauls) Ludovisi Battle Sarcophagus
1. http://farm4.staticflickr.com/3565/3499101028...
2. These are The Barbarians (Gauls) Ludovisi Battle Sarcophagus
These are romans
These Are Romans
1.http://farm3.static.flickr.c om/2713/4197205312_19d00b42e4. jpg
Head Of a Roman legionary Ludovisi Sarcophagus
notice the BIG difference between the two people
The romans look like modern day white people the gauls look like modern day ABORIGINAL people.
here is a description by another roman historian named Ammianus Marcellinus
Ammianus Marcellinus: XII. Of the manners of the Gauls.
Nearly all the Gauls are of a lofty stature, fair, and of RUDDY complexion; terrible from the sternness of their eyes, very quarrelsome, and of great pride and insolence. A whole troop of foreigners would not be able to withstand a single Gaul if he called his wife to his assistance, who is usually very strong, and with blue eyes; especially when, swelling her neck, gnashing her teeth, and brandishing her SALLOW arms of enormous size, she begins to strike blows mingled with kicks, as if they were so many missiles sent from the string of a catapult.
Ammianus Marcellinus said that the skin color of the Gauls was RUDDY and SALLOW those words discribes the color of Brown or a dark color example
Online Etymology Dictionary
type in the words on the Etymology dictionary the Words Ruddy and Sallow mean thus:
1.Ruddy complexion - Ruddy (also called florid) is a reddish-rosy crimson colour, closer to red than to rose. A brownish shade of ruddy called ruddy brown
2.SALLOW - "dusky, dark" (related to sol "dark, dirty")
In other words The Gauls Skin Complextion ranged from Dark Reddish Brown Skin to a Light Brown Skin tone.
Cape Town, South Africa
#68188 Jun 24, 2013
Josephus never ever mentioned any Israelites ever! He only mentioned the Hyksos who he said were Hebrews from Canaan. He was a Jew and Caucasian so why would he say the Hebrews/Hyksos were black?
He looks completely Jewish and no one can mistake him for anything else:
Cape Town, South Africa
#68189 Jun 24, 2013
They all look snow white to me! I think you just want to tease Jeff lol
Since: May 13
Location hidden
#68190 Jun 24, 2013
To prove that you are a Hater of the original people and to prove that YOU are the Edomite I will address this in front of EVERYBODY that you will lie mis direct mis quote and change the quotes just to fit your JEALOUS mind.
Your comment " every humans skin turns brownish/blackish after they die" WRONG!
This condradicts YOUR BULL,They are called Tarim mummies, these ARE THE ONLY WHITE SKIN MUMMIES EVER TO BE FOUND their skin is NOT BROWN nor BLACK
Tarim mummies
those are PRESERVED WHITE SKIN EDOMITE MUMMIES they Represent the MODERN WHITE RACE those are YOUR people these people are NOT.
SCYTHIAN SALT MAN Front Head of Salt Man 1 on display at National Museum of Iran in Tehran
The ancient sycthians WERE NOT YOUR RACE
you are a fool! these two people are from different races YOU PINK FAGGOT Jeff
Since: Jan 12
Location hidden
#68191 Jun 24, 2013
LOL Af,
Let's make this easy for you... ok?
If Josephus say that 1 million ISRAELITES fled into Africa, what do you think happened to them?
Go back to JACOB taking his sons and family that were 70 something souls into Africa EGYPT, shall we?
They became the majority of the population in a couple hundred years living in Egypt (and no doubt migrating even then to other parts of the continent freely and as rulers).
Wouldn't then if 1 million went into Africa become billions over more than a thousand years?
Come on, son. Give it up. Don't let death take you before you bow down and confess TRUTH.
Since: Jan 12
Location hidden
#68192 Jun 24, 2013
Sorry, but pale skin was a sign of sin.
The CREATOR makes it abundantly clear throughout prophecy that HIS People are those that HE FORMED FROM THE BEGINNING. AND that HE, THe CREATOR change not!
Why would you even fathom that HE would bring something to the Ancestors/Fathers that look nothing like them. That pale skin will scare the Ancient Fathers.
Johannesburg, South Africa
#68193 Jun 24, 2013
One million is far too many! I still believe the Hyksos were the Israelites. According to Josephus, the Egyptians kicked them out and they went to Jerusalem. Yes Im sure there are West Africans with Middle Eastern DNA but I think its more than likely came from North Africans.
Johannesburg, South Africa
#68194 Jun 24, 2013
Most African Americans have European DNA as do most North Africans. I think one of Ms Unfazed ancestors was probably a very white hairy neanderthal looking man! Where does it say all white people are sinners and only black people are going to heaven? The ancient Hebrews were Caucasians and look just like their descendants the Samaritans!
Since: Jan 12
Location hidden
#68195 Jun 24, 2013
It's hard for you to accept. It pains you to come to the realization that you all new comers. Who have been fed lies and took on the identity of the TRUE PEOPLE of the BOOK. The TRUE Descendants of ISRAEL/JACOB and killed, destroyed, enslaved them.
Its hard for you to come to terms with the TRUTH that you all the the Enemies of THE CREATOR and took part in fulfilling the curses and abominantions on the PEOPLE that belong to THE CREATOR.
That is all.
It's not too late for you to repent and do the right thing. Will your proud heart and arrogance be your stumbling block?
Since: Jan 12
Location hidden
#68196 Jun 24, 2013
Another desperate lie, Af?
MOST African Americans DO NOT have Euro Dna. Try again.
You would be hard pressed to find about 25 percent of the population of African Americans with Euro Dna. Its only about 25% that have admixture. Go figure.
So how do you get out of that as "Most African Americans have European DNA" ?
Even out of that, it's not Euro, but an admixture of others. The rest of the population is still black, mixed with black. Or straight pure.
Stop buying into the latest propaganda because you all are losing the fight.
White people ain't that fertile. Hell, you all can't produce nowadays with your own kind without science helping you all along.
Back to Euro dna... You meant to say, Blacks already have that dna, they are the progenitors. Don't forget that. It's whites that have black blood running through their veins. Or they'd be extinct.
Which the less they have, the more lacking in existance they are becoming. Fade to ......
Since: Jan 12
Location hidden
#68197 Jun 24, 2013
As for Glimmer and the rest of you bedlamites that are quick to claw onto the caucasoid or caucazoid or caucaroid bs...
You are just admitting that you are from the caucus mountains.
Ain't no Caucus nothing INDIGENOUS to the continent of Africa.
Since: Jan 12
Location hidden
#68198 Jun 24, 2013
* Yes, I am using double negatives into my grammar. Intentionally.
Cape Town, South Africa
#68199 Jun 24, 2013
Well I dont know about white people not being fertile. Ultra Orthodox Jews in Israel are having 7,8,9 children per couple and will rule Israel in the near future! I dont believe this lie that whites are infertile. I just think they use contraceptives. This story whites are going extinct is also rubbish. If every white person (in the US) had a child with every black person, there would still be millions of whites that didnt have children with a black person. Throughout history, the smaller population is always swallowed up by the larger population. The only reason why AA people havent become extinct is because of racism but more and more people of different races are getting together so I think into the future AA people will become extinct! I dont know where you get this idea that Jews and whites are evil and are going to get punished. Its more than likely Jesus was Caucasian because the Jews at the time of Jesus were Caucasian. Skull analysis has proved that! The Samaritans were also around at the time of Jesus and they were most definitely not black!
Since: May 13
Location hidden
#68200 Jun 24, 2013
No! I am NOT TEASING YOU NOR JEFF I AM CLOWNING YOU and JEFF for your lies
I did not know that pink people are called ABORIGINAL when did this HAPPEN?
THESE are ABORIGINAL men here on the Ludovisi Battle Sarcophagus artifact.
Ludovisi Sarcophagus detail. Head of barbarian in battle from front of Sarcophagus
That Gaul looks just like these ABORIGINAL PEOPLE
I have more lets compare African and Jeff lets see more gauls and compare them to modern day aboriginal people who are not considered "BLACK"
This is a Gaul
These are Aboriginal men
the gaul people
aboriginal people
now compare these aboriginal people and Gauls to the modern day White man and romans
White Roman soilders
Head Of a Roman legionary Ludovisi Sarcophagus
He is "PINK" with classic white features
modern day "pink" PEOPLE
see that pink man looks just like a ancient Roman and the Gaul looks like a modern day ABORIGINAL man
Go home pink boys. You LOST! I am Tired of you pink people heckling us
Lying on history
mis quoting people on this thread on PURPOSE
Distorting FACTS
Pulling FAKE artifacts
Never answering any questions
Getting mad when we show you TRUE historical accounts then you try to down play it
then you will pull something FAKE
NO ONE on thread likes you nor do they talk to you So this is the LAST time I reply to non historical STUPID, HILLBILLIES,
Since: Jan 12
Location hidden
#68201 Jun 24, 2013
Read your bible, Af,
Everything I say about punishment is about those according to scripture. Those THAT SCRIPTURE says exactly who the Enemies of THE CREATOR are.
The descendants of those people are the same people that you claim are jews. Add it up.
So, I'm only typing and posting what the scripture that you avoid recognizing reveals. TRUTH.
Don't be mad at the messenger.
Your whole purpose here it s to deny the TRUTH and spread lies and propaganda. Trying to turn your lies into Truth, Black into white, wrongs and evils into good.
That is all you do.
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