Metal Filings In Your Freaking Cereal

This video by Dr. Thomas E. Levy illustrates that the nutrients present in your “enriched” foods may not be as nutritious as you thought. Manufacturers of cereals are allowed to use indigestible iron filings in breakfast cereal. These cereal products can be dangerous for children and all patients with inflammatory diseases.

 

Nutritional Support for Wound Healing

Nutrition plays a crucial role in wound healing. Nutritional status of patients at the time of trauma or surgery influences the biochemical processes necessary for the phases of normal healing to occur. Evidence exists that vitamins A and C, zinc, arginine, glutamine, glucosamine, bromelain, Aloe vera, and Centella asiatica may be beneficial to wounded or surgical patients.

 

Douglas MacKay and Alan L. Miller

Nutritional support for wound healing 
Altern Med Rev 2003; 8 (4): 359-77 

 

ABSTRACT

Healing of wounds, whether from accidental injury or surgical intervention, involves the activity of an intricate network of blood cells, tissue types, cytokines, and growth factors. This results in increased cellular activity, which causes an intensified metabolic demand for nutrients. Nutritional deficiencies can impede wound healing, and several nutritional factors required for wound repair may improve healing time and wound outcome. Vitamin A is required for epithelial and bone formation, cellular differentiation, and immune function. Vitamin C is necessary for collagen formation, proper immune function, and as a tissue antioxidant. Vitamin E is the major lipid-soluble antioxidant in the skin; however, the effect of vitamin E on surgical wounds is inconclusive. Bromelain reduces edema, bruising, pain, and healing time following trauma and surgical procedures. Glucosamine appears to be the rate-limiting substrate for hyaluronic acid production in the wound. Adequate dietary protein is absolutely essential for proper wound healing, and tissue levels of the amino acids arginine and glutamine may influence wound repair and immune function. The botanical medicines Centella asiatica and Aloe vera have been used for decades, both topically and internally, to enhance wound repair, and scientific studies are now beginning to validate efficacy and explore mechanisms of action for these botanicals. To promote wound healing in the shortest time possible, with minimal pain, discomfort, and scarring to the patient, it is important to explore nutritional and botanical influences on wound outcome.

 

Zinc Regulates Communication Between Brain Cells

– Zinc has been found to play a critical role in regulating communication between cells in the brain, possibly governing the formation of memories and controlling the occurrence of epileptic seizures.

A collaborative project between Duke University Medical Center researchers and chemists at the Massachusetts Institute of Technology has been able to watch zinc in action as it regulates communication between neurons in the hippocampus, where learning and memory processes occur – and where disrupted communication may contribute to epilepsy.

“We discovered that zinc is essential to control the efficiency of communication between two critical populations of nerve cells in the hippocampus,” said James McNamara, M.D., senior author and chair of the Department of Neurobiology at Duke. “This addresses a longstanding controversy in the field.”

The study appeared in Neuron Journal online on Sept. 21.

McNamara noted that zinc supplements are commonly sold over the counter to treat several different brain disorders, including depression. It isn’t clear whether these supplements modify zinc content in the brain, or modify the efficiency of communication between these nerve cells. He emphasized that people taking zinc supplements should be cautious, pending needed information on the desired zinc concentrations and how oral supplements affect them.

More than 50 years ago scientists discovered that high concentrations of zinc are contained in a specialized compartment of nerve cells, called vesicles, that package the transmitters which enable nerve cells to communicate. The highest concentrations of brain zinc were found among the neurons of the hippocampus, the center of learning and memory.

Zinc’s presence in these vesicles suggested that zinc played some role in communication between nerve cells, but whether it actually did so remained controversial.

To address this controversy, McNamara and his colleagues at Duke teamed up with Dr. Steve Lippard and colleagues in the Department of Chemistry at the Massachusetts Institute of Technology.

The Lippard team synthesized a novel chemical that bound zinc far more rapidly and selectively than previously available compounds. Use of this chemical let the Duke team rapidly bind the zinc released by nerve cells, taking it out of circulation and preventing enhanced communication.

The Duke team went on to confirm that eliminating zinc from the vesicles of mutant mice also prevented enhanced communication. They also found that increases in the transmitter glutamate seemed to increase zinc-mediated enhancement of communication.

Interestingly, the nerve cells in which the high concentrations of zinc reside are critical for a particular type of memory formation. Excessive enhancement of communication by the zinc-containing nerve cells occurs in epileptic animals and may worsen the severity of the epilepsy.

“Carefully controlling zinc’s regulation of communication between these nerve cells is critical to both formation of memories and perhaps to occurrence of epileptic seizures,” McNamara said.

McNamara also noted that the scientific collaboration between the Duke and MIT scientists was critical to the success of this work. The availability of the novel chemical provided a critical tool that allowed the neuroscientists to unravel the puzzle.

 

Reference

Pan E, Zhang X, Huang Z, Krezel A, Zhao M, Tinberg CE, Lippard SJ, McNamara JO. Vesicular Zinc Promotes Presynaptic and Inhibits Postsynaptic Long-Term Potentiation of Mossy Fiber-CA3 Synapse. Neuron 2011; 71 (6): 1116-1 126.

 

Link Between Parkinson’s Disease And Manganese Poisoning

The Yeast PARK9 protein (Ypk9) is localized to the vacuole membrane. Shown are yeast cells expressing Ypk9 fused to the green fluorescent protein.

A connection between genetic and environmental causes of Parkinson’s disease has been discovered by a research team led by Aaron D. Gitler, PhD, Assistant Professor in the Department of Cell and Developmental Biology at the University of Pennsylvania School of Medicine. Gitler and colleagues found in 2009 a genetic interaction between two Parkinson’s disease genes (alpha-synuclein and PARK9) and determined that the PARK9 protein can protect cells from manganese poisoning, which is an environmental risk factor for a Parkinson’s disease-like syndrome.

Manganism, or manganese poisoning, is prevalent in such occupations as mining, welding, and steel manufacturing. It is caused by exposure to excessive levels of the metal manganese, which attacks the central nervous system, producing motor and dementia symptoms that resemble Parkinson’s disease.

In Parkinson’s patients, the alpha-synuclein protein normally found in the brain misfolds, forming clumps. Yeast cells, the model system in which Gitler studies disease proteins, also form clumps and die when this protein is expressed at high levels. These are the same yeast cells that bakers and brewers use to make bread, beer, and wine.

As a postdoctoral fellow at the Whitehead Institute in Cambridge, Massachusetts, Gitler and colleagues started looking for genes that could prevent the cell death caused by mis-folded alpha-synuclein in yeast. Eventually they found a few genes to test in animal models and some were able to protect neurons from the toxic effects of alpha-synuclein. “One of the genes that we found was a previously uncharacterized yeast gene called YOR291W. No one knew what it did back in 2006,” he recalls.

Yeast PARK9 gene (YPK9) helps protect cells from manganese toxicity. Yeast cells missing the YPK9 gene (ypk9) grow normally under standard conditions (- Mn2+) but are much more sensitive to manganese (+ Mn2+) than wild-type (WT) cells.

In the meantime, researchers in Europe published studies about a family that had an early-onset form of a type of Parkinson’s disease caused by mutations in the PARK9 gene. “When I read about this study, I wondered what the closest yeast gene was to the human PARK9 gene and it turned out to be YOR291W,” explains Gitler. “It was one of the genes that could rescue alpha-synuclein toxicity from our yeast screen. That was the big Eureka! and completely unexpected. It suggested that Parkinson’s disease genes could interact with each other in previously unexpected ways.”

Because of its similarity to the human PARK9 gene, Gitler and colleagues renamed the yeast gene to YPK9 (which stands for Yeast PARK9). Researchers at Purdue University and The University of Alabama teamed up with Gitler and his colleagues to show that the PARK9 gene could also protect neurons from alpha-synuclein’s toxic effects.

Next, the team set out to find the function of YPK9. Study co-first author, postdoctoral fellow Alessandra Chesi, PhD, discovered that YPK9 encodes a metal transporter protein. “Its sequence looks like other proteins that we know transport metals,” says Chesi.

She deleted the YPK9 gene from yeast and the cells were fine. Then she exposed YPK9-deficient yeast cells to an excess of different metals — zinc, copper, manganese, iron, etc. — to determine which metal it might transport. Of all the metals Chesi tested, she found that in the presence of manganese, the YPK9-deficient yeast did not grow as well. They were hypersensitive to manganese.

“This was astonishing, because it was known for years that welders and miners that inhale manganese get a Parkinson’s-like disease called manganese poisoning,” says Chesi. “The specific neurons that are lost in the miners are from the globus pallidus, a brain motor center. The European parkinsonism patients with the PARK9 mutation also lose neurons in this region.”

Gitler then found that the protein made by YPK9, the yeast gene equivalent of PARK9, is localized to the vacuole membrane in the yeast cell. Vacuoles are inner cell components that wall off toxic substances for later disposal. “Our hypothesis is that the vacuole, a bag in the cell that captures toxins, is sitting there and taking in manganese and sequestering it for detoxification, keeping it away from other cell organelles,” explains Gitler. “But, having a mutation in the PARK9 gene causes problems for this process in yeast and possibly in humans”.

 

Related Articles

Guilarte TR. Manganese and Parkinson’s disease: a critical review and new findings. Environ Health Perspect 2010;118 (8): 1071-80.

Gitler AD, Chesi A, Geddie ML, Strathearn KE, Hamamichi S, Hill KJ, et al. Alpha-synuclein is part of a diverse and highly conserved interaction network that includes PARK9 and manganese toxicity. Nat Genet.2009; 41 (3): 308-15.

Aschner M, Erikson KM, Herrero Hernández E, Tjalkens R. Manganese and its role in Parkinson’s disease: from transport to neuropathology. Neuromolecular Med 2009; 11 (4): 252-66.

 

Manganese In Drinking Water: Study Suggests Adverse Effects On Children’s Intellectual Abilities

A team of researchers recently completed a study showing that children exposed to high concentrations of manganese in drinking water performed worse on tests of intellectual functioning than children with lower exposures.

A team of researchers led by Maryse Bouchard, adjunct professor at the Center for Interdisciplinary Research in Biology, Health, Environment and Society (CINBIOSE) of the Université du Québec à Montréal and a researcher at Sainte-Justine University Hospital, and Donna Mergler, professor emerita in the Department of Biological Sciences and a member of CINBIOSE, recently completed a study showing that children exposed to high concentrations of manganese in drinking water performed worse on tests of intellectual functioning than children with lower exposures. Their results are published in the prestigious scientific journal Environmental Health Perspectives, in an article entitled “Intellectual Impairment in School-Age Children Exposed to Manganese from Drinking Water”.

Manganese: toxic in the workplace but harmless in water?
The neurotoxic effects of manganese exposure in the workplace are well known. This metal is naturally occurring in soil and in certain conditions is present in groundwater. In several regions of Quebec and Canada and in other parts of the world, the groundwater contains naturally high levels of manganese. Does it pose a danger? What effect might it have on children’s health? This is the first study to focus on the potential risks of exposure to manganese in drinking water in North America.

The study, carried out by researchers at the Université du Québec à Montréal, the Université de Montréal and the École Polytechnique de Montréal, examined 362 Quebec children, between the ages of 6 and 13, living in homes supplied by with groundwater (individual or public wells). For each child, the researchers measured the concentration of manganese in tap water from their home, as well as iron, copper, lead, zinc, arsenic, magnesium and calcium. The amount of manganese from both tap water and food was estimated from a questionnaire. Finally, each child was assessed with a battery of tests assessing cognition, motor skills, and behaviour.

Lead author Maryse Bouchard explains, “We found significant deficits in the intelligence quotient (IQ) of children exposed to higher concentration of manganese in drinking water. Yet, manganese concentrations were well below current guidelines.” The average IQ of children whose tap water was in the upper 20% of manganese concentration was 6 points below children whose water contained little or no manganese. The analyses of the association between manganese in tap water and children’s IQ took into account various factors such as family income, maternal intelligence, maternal education, and the presence of other metals in the water. For co-author Donna Mergler, “This is a very marked effect; few environmental contaminants have shown such a strong correlation with intellectual ability.” The authors state that the amount of manganese present in food showed no relationship to the children’s IQ.

What next?
So what can be done about it? Some of the municipalities where the study was conducted have already installed a filtration system that removes manganese from the water. According to one of the other co-authors of the study, Benoit Barbeau, NSERC Industrial Chair in Drinking Water at the École Polytechnique de Montréal, “A viable alternative solution is home use of filtering pitchers that contain a mixture of resins and activated carbon. Such devices can reduce the concentration of manganese by 60% to100% depending on filter use and the characteristics of the water.”

In Quebec, where the study was conducted, manganese is not on the list of inorganic substances in the Ministry of Sustainable Development, Environment and Parks Regulation respecting the quality of drinking water. “Because of the common occurrence of this metal in drinking water and the observed effects at low concentrations, we believe that national and international guidelines for safe manganese in water should be revisited.” the authors conclude.

 

Reference

Bouchard MF, Sauvé S, Barbeau B, Legrand M, Brodeur M-È, Bouffard T, et al. 2010. Intellectual Impairment in School-Age Children Exposed to Manganese from Drinking Water. Environ Health Perspect :-. doi:10.1289/ehp.1002321.

 

FDA: Fluoride Supplements Never Found Safe Or Effective

Sodium fluoride supplements “have not been found by FDA to be safe or effective,” according to the US National Library of Medicine’s (NLM) website, reports the New York State Coalition Opposed to Fluoridation, Inc. (NYSCOF).

Routinely prescribed to children in non-water-fluoridated communities, sometimes even in fluoridated areas, sodium fluoride drops, lozenges and “vitamins” are meant to reduce tooth decay.

Before testing was required, sodium fluoride ingestion slipped into common usage without FDA approval. Now, the FDA is cracking down on unapproved drugs such as sodium fluoride (1).

The following warning – “Note: This Drug Has Not Been Found by FDA to be Safe and Effective” – is newly included with sodium fluoride drug information meant for ingestion (2).

Fluoride supplement­s deliver no benefits to primary teeth but increase dental fluorosis risk – white spotted, yellow, brown and/or pitted teeth, according to a 2008 Journal of the American Dental Association systematic review (3),

In fact, “In non-fluoridated communities, the use of fluoride supplements during the first 6 years of life is associated with a significant increase in the risk of developing dental fluorosis,” concludes a meta-analysis in Community Dentistry and Oral Epidemiology (2/99) (4).

“It is therefore concluded that the risks of using supplements in infants and young children outweigh the benefits…fluoride supplements should no longer be used for young children in North America,” writes Burt (Fall 1999 Journal of Public Health Dentistry” (5).

Further, Belgium stopped selling fluoride supplements in 2002 because documentation revealed that fluoride can cause physical and neurological harm with little evidence of decay reduction (6).

According to the NLM, fluoride’s side effects could include (7):
· staining of teeth · unusual increase in saliva · salty or soapy taste · stomach pain · upset stomach · vomiting ·diarrhea · rash · weakness · tremor · seizures

The FDA asks that fluoride drug side effects, including dental fluorosis, be reported at http://www.fda.gov/Safety/MedWatch or 1-800-332-1088.

Freedom of choice governs fluoride supplements but not water fluoridation. Even in small doses injected into drinking water supplies, fluoride can have serious side effects especially to the brain, thyroid, kidney patients and babies (8 a, b, c, d).

“We urge parents to deeply research fluoride supplements and fluoride varnish before dosing their children,” says attorney Paul Beeber, NYSCOF President.

“We also urge everyone to contact their legislators and do what it takes to stop the unnecessary force-feeding of fluoride chemicals into their bodies via the public water supplies,” says Beeber.

New York City Council Members have introduced such legislation. “NYC residents must show their support by contacting their Council member to support this bill,” says Beeber. For more info: http://tinyurl.com/NYCfluoridation

 

How Fluoride Supplements Came To Be Used

The first human-health fluoride experiment began in 1945 when sodium fluoride was poured into Newburgh, NY’s, water supply to learn if fluoride would harm children.

Pre-schoolers, adults and sick children were excluded from examination. Even with this research flaw, after ten years, Newburgh’s school-children had more anemia, cortical bone defects and early puberty than never-fluoridated nearby Kingston, NY (9). Brain, thyroid effects and cancer rates weren’t considered.

Despite these failures, officials prematurely claimed the Kingston/Newburgh study proved water fluoridation was safe and, therefore, assumed fluoride supplements were safe also.

Contact: Paul Beeber, JD, nyscof@aol.com
http://www.fluoridation.webs.com
http://www.FluorideAction.Net

SOURCE: NYS Coalition Opposed to Fluoridation, Inc.


References

1) “Guidance for FDA Staff and Industry Marketed Unapproved Drugs “
U.S. Department of Health and Human Services, Food and Drug Administration
Center for Drug Evaluation and Research (CDER) June 2006
http://www.fda.gov/downloads/Drugs/GuidanceComplianceRegulatoryInformation/Guidances/UCM070290.pdf

2) http://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?id=20443

3) Fluoride supplements, dental caries and fluorosis: A systematic review
J Am Dent Assoc November 1, 2008 139(11): 1457-1468
http://jada.ada.org/content/139/11/1457.full

4) Community Dent Oral Epidemiol. 1999 Feb, Fluoride supplements and fluorosis: a meta-analysis,” Ismail and Badekar.
http://www.ncbi.nlm.nih.gov/pubmed/10086926

5) “The case for eliminating the use of dietary fluoride supplements
for young children,” Journal of Public Health Dentistry, Fall 1999, by
Burt. http://tinyurl.com/2bnoff

6) http://www.fluoride-journal.com/02-35-3/353-212.pdf

7) http://www.nlm.nih.gov/medlineplus/druginfo/meds/a682727.html

8a) http://www.fluoridealert.org/health/brain/index.html
  b) http://www.fluoridealert.org/health/thyroid/index.html
  c) http://www.fluoridealert.org/health/kidney/
  d) http://www2.fluoridealert.org/Alert/United-States/New-York/Don-t-Feed-Babies-Fluoridated-Water-say-NYS-Health-Officials

9) Newburgh-Kingston caries-fluorine study. XIII. Pediatric findings after ten years.
J Am Dent Assoc. 1956 Mar;52(3):296-306. SCHLESINGER ER, OVERTON DE, CHASE HC, CANTWELL KT.

 

Zinc Lozenges May Shorten the Duration of Colds

Zinc lozenges might be useful as a treatment option for the common cold, according to a meta-analysis published in The Open Respiratory Medicine Journal.  Studies have shown that taking a dose of more than 75 mg of zinc in the form of zinc lozenges per day cut the duration of the common cold by 20 to 42 percent.

 

 

Harri Hemilä
Zinc Lozenges May Shorten the Duration of Colds: A Systematic Review
Breast Cancer Res Treat 2011; 129 (1): 107-16.


ABSTRACT

Background:
A number of controlled trials have examined the effect of zinc lozenges on the common cold but the findings have diverged. The purpose of this study was to examine whether the total daily dose of zinc might explain part of the variation in the results.

Methods:
The Medline, Scopus and Cochrane Central Register of Controlled Trials data bases were searched for placebocontrolled trials examining the effect of zinc lozenges on common cold duration. Two methods were used for analysis: the P-values of the trials were combined by using the Fisher method and the results of the trials were pooled by using the inverse-variance method. Both approaches were used for all the identified trials and separately for the low zinc dose and the high zinc dose trials.

Results:
Thirteen placebo-controlled comparisons have examined the therapeutic effect of zinc lozenges on common coldepisodes of natural origin. Five of the trials used a total daily zinc dose of less than 75 mg and uniformly found no effect. Three trials used zinc acetate in daily doses of over 75 mg, the pooled result indicating a 42% reduction in the duration of colds (95% CI: 35% to 48%). Five trials used zinc salts other than acetate in daily doses of over 75 mg, the pooled result indicating a 20% reduction in the duration of colds (95% CI: 12% to 28%).

Conclusions:
This study shows strong evidence that the zinc lozenge effect on common cold duration is heterogeneous so that benefit is observed with high doses of zinc but not with low doses. The effects of zinc lozenges should be further studied to determine the optimal lozenge compositions and treatment strategies.

 

Iron Rich Foods

Food Sources of Iron ranked by milligrams of iron per standard amount; also calories in the standard amount. (All are  10% of RDA for teen and adult females, which is 18 mg/day.)

Food, Standard Amount

Iron (mg)

Calories

Clams, canned, drained, 3 oz

23.8

126

Fortified ready-to-eat cereals (various), ~ 1 oz

1.8 -21.1

  54-127

Oysters, eastern, wild, cooked, moist heat, 3 oz

10.2

116

Organ meats (liver, giblets), various, cooked, 3 oz a

5.2-9.9

134-235

Fortified instant cooked cereals (various), 1 packet

4.9-8.1

Varies

Soybeans, mature, cooked, ½ cup

4.4

149

Pumpkin and squash seed kernels, roasted, 1 oz

4.2

148

White beans, canned, ½ cup

3.9

153

Blackstrap molasses, 1 Tbsp

3.5

47

Lentils, cooked, ½ cup

3.3

115

Spinach, cooked from fresh, ½ cup

3.2

21

Beef, chuck, blade roast, lean, cooked, 3 oz

3.1

215

Beef, bottom round, lean, 0″ fat, all grades, cooked, 3 oz

2.8

182

Kidney beans, cooked, ½ cup

2.6

112

Sardines, canned in oil, drained, 3 oz

2.5

177

Beef, rib, lean, ¼” fat, all grades, 3 oz

2.4

195

Chickpeas, cooked, ½ cup

2.4

134

Duck, meat only, roasted, 3 oz

2.3

171

Lamb, shoulder, arm, lean, ¼ ” fat, choice, cooked, 3 oz

2.3

237

Prune juice, ¾ cup

2.3

136

Shrimp, canned, 3 oz

2.3

102

Cowpeas, cooked, ½ cup

2.2

100

Ground beef, 15% fat, cooked, 3 oz

2.2

212

Tomato puree, ½ cup

2.2

48

Lima beans, cooked, ½ cup

2.2

108

Soybeans, green, cooked, ½ cup

2.2

127

Navy beans, cooked, ½ cup

2.1

127

Refried beans, ½ cup

2.1

118

Beef, top sirloin, lean, 0″ fat, all grades, cooked, 3 oz

2.0

156

Tomato paste, ¼ cup

2.0

54

a High in cholesterol.

Source: Nutrient values from Agricultural Research Service (ARS) Nutrient Database for Standard Reference, Release 17. Foods are from ARS single nutrient reports, sorted in descending order by nutrient content in terms of common household measures. Food items and weights in the single nutrient reports are adapted from those in 2002 revision of USDA Home and Garden Bulletin No. 72, Nutritive Value of Foods. Mixed dishes and multiple preparations of the same food item have been omitted from this table.

Copper Folds Protein Into Precursors Of Parkinson’s Plaques

Researchers at North Carolina State University have figured out how copper induces misfolding in the protein associated with Parkinson’s disease, leading to creation of the fibrillar plaques which characterize the disease. This finding has implications for both the study of Parkinson’s progression, as well as for future treatments.

The protein in question, alpha-synuclein, is the major component of fibrillar plaques found in Parkinson’s patients. Researchers had already discovered that certain metals, including copper, could increase the rate of misfolding by binding with the protein, but were unsure of the mechanism by which this binding took place.

“We knew that the copper was interacting with a certain section of the protein, but we didn’t have a model for what was happening on the atomic level,” says Frisco Rose, Ph.D. candidate in physics and lead author of the paper describing the research. “Think of a huge swing set, with kids all swinging and holding hands – that’s the protein. Copper is a kid who wants a swing. There are a number of ways that copper could grab a swing, or bind to the protein, and each of those ways would affect all of the other kids on the swing set differently. We wanted to find the specific binding process that leads to misfolding.”

Rose and NC State colleagues Dr. Miroslav Hodak, research assistant professor of physics, and Dr. Jerzy Bernholc, Drexel Professor of Physics and Director of the Center for High Performance Simulation, developed a series of computer simulations designed to ferret out the most likely binding scenario.

According to Hodak, “We simulated the interactions of hundreds of thousands of atoms, which required multiple hundred thousand CPU-hour runs to study the onset of misfolding and the dynamics of the partially misfolded structures.”

The number of calculations was so large that Hodak and Bernholc had to devise a new method to make it possible for a computer to process them. Only supercomputers like Jaguar, Oak Ridge National Laboratory’s most powerful supercomputer – the most powerful in the United States, in fact – were up to the task. But the simulations finally revealed the binding configuration most likely to result in misfolding.

Their results appeared in the June 14 edition of Nature Scientific Reports.

The researchers hope that their finding will advance our understanding of Parkinson’s, one of the most common – and devastating – neurological diseases. “Understanding the molecular mechanism of Parkinson’s disease should help researchers in developing drugs that treat the disease rather than merely alleviate symptoms,” Bernholc says.
Reference

Rose F, Hodak M, Bernholc J. Mechanism of copper(II)-induced misfolding of Parkinson’s disease protein. Scientific Reports 2011; 1, doi:10.1038/srep00011.