Copper

[Kathy]

Nervenarzt. 2008 Apr;79(4):421-425.

[Copper deficiency as a treatable cause of myelopathy.][Article in German]


Jung A, Marziniak M.
Klinik und Poliklinik für Neurologie, Universitätsklinikum Münster, Albert-Schweitzer-Straße 33, 48149, Münster, Deutschland.

Copper deficiency myelopathy is an important and treatable differential diagnosis of vitamin B12 deficiency, of degenerative diseases presenting with the cardinal sign ataxia, and less often of motor neuron diseases. We report a 30-year-old female who presented with progressive gait disorder and sensory disturbances in her feet. Neurological examination showed tetraparesis with spastic ataxia. Laboratory investigations showed malabsorption, anemia, and leukopenia. Further extensive diagnostic investigations revealed copper deficiency due to malabsorption as the probable cause of the neurological deterioration. After oral copper substitution was started, the progression of her neurological symptoms could be stopped.

PMID: 18274721

sounds alot like polioencephalomalacia or PEM

sounds alot like the research of some doctors who treat autism with daily B12 injections and diet

Here is a study showing that when measuring blood copper levels, we should be looking at plasma copper levels not just serum copper levels. There is a significant difference. Molybdenum soil levels influenced copper levels.

Vet Rec. 2008 Feb 23;162(8):237-40.
Relationships between the concentrations of trichloroacetic acid-soluble copper and caeruloplasmin in the serum of cattle from areas with different soil concentrations of molybdenum.

Suttle NF.
Moredun Foundation, Pentland Science Park, Penicuik, Midlothian EH26 0PZ, UK.

The concentrations of trichloroacetic acid (tca)-soluble copper and caeruloplasmin were determined in 345 serum samples taken from cattle in March 1998 by eight Scottish Agricultural College veterinary disease surveillance centres serving areas with soils ranging from being 'high' in molybdenum (Thurso) to 'low' (Perth and St Boswells). The mean concentrations varied significantly between the centres, with Thurso having the lowest values for both variables. There were strong linear regressions (r>0.8) between caeruloplasmin and tca-soluble copper for each centre but no significant differences in slope or intercept between the areas with the highest and lowest soil molybdenum, and the pooled regression accounted for 88 per cent of the variation. The distribution of the ratios of caeruloplasmin to tca-soluble copper, unlike those of the individual variables, was not normal, and 70 per cent of the values fell within 10 per cent of the mean ratio of 20.3 mg/micromol and close to the 22 mg/micromol copper expected in pure caeruloplasmin. Low ratios were generally associated with low tca-soluble copper. Ratios above 24 were found in 8 per cent of the samples and were probably attributable to acute-phase reactions and the non-specificity of the assay for caeruloplasmin.

PMID: 18296665

PLoS Biol. 2008 Apr 15;6(4):e100

Host PrP Glycosylation: A Major Factor Determining the Outcome of Prion Infection.

Tuzi NL, Cancellotti E, Baybutt H, Blackford L, Bradford B, Plinston C, Coghill A, Hart P, Piccardo P, Barron RM, Manson JC.

The expression of the prion protein (PrP) is essential for transmissible spongiform encephalopathy (TSE) or prion diseases to occur, but the underlying mechanism of infection remains unresolved. To address the hypothesis that glycosylation of host PrP is a major factor influencing TSE infection, we have inoculated gene-targeted transgenic mice that have restricted N-linked glycosylation of PrP with three TSE strains. We have uniquely demonstrated that mice expressing only unglycosylated PrP can sustain a TSE infection, despite altered cellular location of the host PrP. Moreover we have shown that brain material from mice infected with TSE that have only unglycosylated PrP(Sc) is capable of transmitting infection to wild-type mice, demonstrating that glycosylation of PrP is not essential for establishing infection within a host or for transmitting TSE infectivity to a new host. We have further dissected the requirement of each glycosylation site and have shown that different TSE strains have dramatically different requirements for each of the glycosylation sites of host PrP, and moreover, we have shown that the host PrP has a major role in determining the glycosylation state of de novo generated PrP(Sc).

PMID: 18416605

Evidence that the healthy copper loaded PrPC is not capable of being converted to PrPSc. Demonstrates that the unglycosolated prion protein within the cell, manufactured by the cell, is affected in such a manner as it is unable to attach to the cell membrane and attach copper to it via the glyco anchor - and draw the necessary copper into the cell. Loss of function, lack of intake of copper into the cell, and bluidup of the unglycosolated (copper deficient) full length protein. If other metals, like manganese attach to the prion, it becomes non-functional.


Go figure, copper-oxides are capable of inactivating HIV -1 virus.
I wonder if they have ever characterized the elements found in the HIV virus particles??

Antimicrob Agents Chemother. 2008 Feb;52(2):518-25. Epub 2007 Dec 10. Links
Deactivation of human immunodeficiency virus type 1 in medium by copper oxide-containing filters.

Borkow G, Lara HH, Covington CY, Nyamathi A, Gabbay J.
Ruth Ben-Ari Institute of Clinical Immunology, Kaplan Medical Center, Hebrew University Hadassah Medical School, Rehovot 76100, Israel. [email protected]

Human immunodeficiency virus type 1 (HIV-1) can be transmitted through breast-feeding and through contaminated blood donations. Copper has potent biocidal properties and has been found to inactivate HIV-1 infectivity. The objective of this study was to determine the capacity of copper-based filters to inactivate HIV-1 in culture media. Medium spiked with high titers of HIV-1 was exposed to copper oxide powder or copper oxide-impregnated fibers or passed through copper-based filters, and the infectious viral titers before and after treatment were determined. Cell-free and cell-associated HIV-1 infectivity was inhibited when exposed to copper oxide in a dose-dependent manner, without cytotoxicity at the active antiviral copper concentrations. Similar dose-dependent inhibition occurred when HIV-1 was exposed to copper-impregnated fibers. Filtration of HIV-1 through filters containing the copper powder or copper-impregnated fibers resulted in viral deactivation of all 12 wild-type or drug-resistant laboratory or clinical, macrophage-tropic and T-cell-tropic, clade A, B, or C, HIV-1 isolates tested. Viral inactivation was not strain specific. Thus, a novel means to inactivate HIV-1 in medium has been developed. This inexpensive methodology may significantly reduce HIV-1 transmission from "mother to child" and/or through blood donations if proven to be effective in breast milk or plasma and safe for use. The successful application of this technology may impact HIV-1 transmission, especially in developing countries where HIV-1 is rampant.

PMID: 18070974