Bioelectromagnetics

cogreslab said:
R13:

(What evidence do you have that "radio waves cause [AIDS] to happen... and the viruses are somehow transmitting itself through the sexual activity," as you've been quoted as saying?)

This is a complete misquotation, and is in no way representative of the correlation I reported between MW radiation and comparatively high percentages of registered AIDS people in major US cities.
I don't think that poster was that far off the mark, sir. You, however, missed the obviously high correlation between neighborhood bakeries and AIDS. Also, car exhaust and density of pubs.

Your science skills are truly... uh... astonishing.
 
"Field", at 32mV??? ehr, how exactly did you apply that?

A function generator's output was attached to the gold wire. This led into the space above the culture in a sealed phial. The parameters were dialled into the FG. Since it was an electric field there was no need to complete the circuit.
 
Lucianarchy said:
*snip*
Sorry, Garbo, but even if you are uneducated you can still be a scientist. You just have to stick to the scientific methods and if you're arguing against a position the burden of proof is on you.

But, as most others have noticed by now, we are not arguing against a position, we are arguing against a claim. A claim made by Mr. Coghill. Which puts the burden of evidence on him.

Amongst us sceptics

:id:

it is the rigeur that you must provide credible evidence, sources and references.

Actually often, sound logic will do. But, the onus of proof is on Mr. Coghill.


As Mr Coghill has done. It is the way of things.

And this whole thing is about our refutations of the evidence that Mr. Coghill has provided in support of his claims (and asking for the evidence he has NOT provided ;)).

Uhh, Luci, I suppose all this is a bit over your head, and really, Mr. Coghill has all the problems he needs here, even without your "support".

Why don't you go back to predicting the future. You predictions are so much better than your logic. --- And as to your knowledge about electromagnetics, I don't suppose you could tell the difference between a near field and a repeller grid if it bit you in the nose :rolleyes:.

Hans
 
From BB: "You, however, missed the obviously high correlation between neighborhood bakeries and AIDS. Also, car exhaust and density of pubs."

Three UVJs here.

Skeptometer reading 94.
 
Ahh, let me have a try at scoring an UVJ: How aboust the extremely high incidence of AIDS in rural African districts and .... uhh, radio waves? ... no, wait...

Hans
 
cogreslab said:
"Field", at 32mV??? ehr, how exactly did you apply that?

A function generator's output was attached to the gold wire. This led into the space above the culture in a sealed phial. The parameters were dialled into the FG. Since it was an electric field there was no need to complete the circuit.
So, the electrical field was between the lead and ... what?

Hans
 
cogreslab said:
From BB: "You, however, missed the obviously high correlation between neighborhood bakeries and AIDS. Also, car exhaust and density of pubs."

Three UVJs here.

Skeptometer reading 94.

You deny a high correlation between neighborhood bakery density and AIDS? You deny a high correlation between car exhaust and AIDS?
 
cogreslab said:
To Bouncer Bull (sorry, Bill): You said:


I have addressed the more serious point about how the cancer may be transferred in a previous post, to which as of now there has been no contradiction: the carcinogen will block the ox phos pathway in response to which the cell up/down regulates the cell's gene expression so as to shift to glycolysis as a means of survival (remember all cancer cells are still alive, even though aberrant).

Carcinogens don't block this pathway, you have insufficinet evidence to make this claim.

Mitosis at that point will reproduce the transformed cells, which will continue (as in metastasis) even without any further carcinogenic action.
STOP - how can cell division reproduce transformed cells unless the cells DNA has been in some way altered ?

until a superior dehydrogenator such as parabenzoquinone arrives to correct the problem (if it ever does) and thereby restore oxidative phosphorylation.

We see this in our lab using PBLs and conducting a glucose oxidase and hexokinase assay (these Sigma Diagnostic kits are available easily for would be replicators) before and after administering the quinone, which shows a slow down in the uptake of glucose after the administration. (we have not published this yet, but will probably present initially at a conference in London in September).

Which can be explained without resorting to unprove theories of carcinogenesis



In my view this is a better explanation than the traditional multistage explanation for carcinogenesis, which leaves out the vital steps re metabolic change. These are the steps which Szent Gyorgii added in around 1960, but which William Koch had deduced and proven in clinical practice in the first decades of the 20thC.

and your view is not supported by the evidence

Yes, I said in clinical practice:

The cancer mortality figures for Detroit 1920 to 1929 show a 23 percent fall, in a decade where every other major US city was recording increases of up to 32 percent in annual cancer mortality. Koch's quinone-based reagents were the principal cancer treatment modality in Detroit at that time.

Ok show the evidence for the last claim please.


Simply put a cell will make its protein based on the genetic coding for that protein in its DNA. If Mr Coghills theory is correct and cancer is a result of a metabolic process, then every carcinogenic cell would have to have been exposed to a carcinogen. This clearly is not the case. Therefore a genetic element is involved. Mr Coghill has not answered questions as to how this can occur in his theory. You have the situation where every cancer cell has an altered metabolism and mutated genetic state. Mr Coghill maintains it is the metabolic state that causes the genetic damage, but crucially has no mechanism for this and ignores questions about it.

As this is the point that Mr Coghill has run out of references and ideas, and cannot answer the questions i predict more unsubstantiated assertions and repetition of previous comments.


Lets have a new link every post, for this post we have:

http://www.nci.nih.gov/cancerinfo/genetic-testing-breast

Yes there is a G e n e t i c risk for breast Cancer.

BRCA 1 and 2 are the genes that have been identified.

You're putting the cart infront of the horse Mr selective answering Coghill.
 
The change of an oncogene from normal to cancerous function can be caused by a simple point mutation in the sequence of a gene. For example, a change in the ras oncogene, located on human chromosome 11, from guanine to cytosine is frequently associated with bladder cancer. This simple change results in glycine at amino acid #12 being substituted with a valine. This dramatically changes the function of the G-protein encoded by the ras gene. Normally, the protein cycles from an inactive to active state by change the bound GDP to GTP. The mutation does not allow the release of GTP, and the protein is continuously active. Because the signal delivered by the ras oncoprotein is continuously delivered, the cell continues to grow and divide. This unabated growth leads to the bladder cancer.


http://www.ndsu.nodak.edu/instruct/mcclean/plsc431/cellcycle/cellcycl5.htm
 
From BB to cogreslab: "Your science skills are truly... uh... astonishing".

Well this was really a UVJ too, but we have seen enough evidence on this thread to suspect he may be able to confirm it with references as to the good quality of my science and argument. So I'll let him off that one.
 
Prag pointed to:

"The change of an oncogene from normal to cancerous function can be caused by a simple point mutation in the sequence of a gene. For example, a change in the ras oncogene, located on human chromosome 11, from guanine to cytosine is frequently associated with bladder cancer. This simple change results in glycine at amino acid #12 being substituted with a valine. This dramatically changes the function of the G-protein encoded by the ras gene. Normally, the protein cycles from an inactive to active state by change the bound GDP to GTP. The mutation does not allow the release of GTP, and the protein is continuously active. Because the signal delivered by the ras oncoprotein is continuously delivered, the cell continues to grow and divide. This unabated growth leads to the bladder cancer.


To which I respond:

Bioelectromagnetics. 1992;13(2):111-8.


Transcription in Drosophila melanogaster salivary gland cells is altered following exposure to low-frequency electromagnetic fields: analysis of chromosome 3R.

Goodman R, Weisbrot D, Uluc A, Henderson A.

Columbia University Health Sciences, Hunter College, City University of New York.

Abstrract: The use of the transcription autoradiographic method permits identification of nascent RNA chains directly on identifiable regions of Drosophila salivary gland chromosomes. Changes in transcriptional activity at 13 defined regions of the right arm of chromosome 3 (3R) were observed following 20-min exposures of salivary glands to five different extremely low frequency (ELF) electromagnetic (EM) fields. Changes in translational patterns were also induced by the ELF EM fields in exposed cells. Differences included an increase in over-all polypeptide synthesis as well as in the number of polypeptides resolved in cells exposed to EM fields.

This is an early study, but since then there are many more to confirm the transcriptional and translational effects of ELF EM fields on gene expression. Harder science indeed.
 
Transcription in Drosophila melanogaster salivary gland cells is altered following exposure to low-frequency electromagnetic fields: analysis of chromosome 3R.

So if this is verfied then its showing an effect on transcription ? Doesn't this rather contradict your carcinogenesis theory ?



Link for the post:

Somatic Mutation of p53 Leads to Estrogen Receptor {alpha}-Positive and -Negative Mouse Mammary Tumors with High Frequency of Metastasis.

http://www.ncbi.nlm.nih.gov/entrez/...ve&db=pubmed&dopt=Abstract&list_uids=15150107

Full article available as well. Title says it all really. (p53 is a classic is it not Mr Coghill)
 
As this is the point that Mr Coghill has run out of references and ideas, and cannot answer the questions i predict more unsubstantiated assertions and repetition of previous comments.


Sorry, PJ: my subsequent post quoting Goodman et al., 1992 has proved you wrong.

Skeptometer reading now 93.
 
No PJ. I included non ionising radiation within my definition of a carcinogen (as does IARC now), and explained the idea that this could occur through mitochondrial membrane depolarisation.
 
Pragmatist wrote:

Oh, and why on your paper that I quoted, which is an article written by YOU, does it say DRS Tamara Galonja-Coghill and Roger Coghill? I mean why is DRS in PLURAL? I don't know about your wife (and don't care), but what doctorate do YOU hold?

Actually, the title doesn't seem to be warranted in either case.

It's a woo woo thing. They just can't help themselves. They're so enamored of the instant credibility that such titles seem to lend that they just can't resist the temptation to tack them on when they think no one is looking.
 
cogreslab said:
No PJ. I included non ionising radiation within my definition of a carcinogen (as does IARC now), and explained the idea that this could occur through mitochondrial membrane depolarisation.

You missed my point, which i might add is almost irrelevant anyway, but is the one you decided to pick up on.

Reversibility of oncogene-induced cancer.

http://www.ncbi.nlm.nih.gov/entrez/...ve&db=pubmed&dopt=Abstract&list_uids=15108803



Role of the c-myc proto-oncogene in the proliferation of hereditary gingival fibromatosis fibroblasts.

http://www.ncbi.nlm.nih.gov/entrez/...ve&db=pubmed&dopt=Abstract&list_uids=15088873

?
 
cogreslab said:
Prag pointed to:

"The

snip

This is an early study, but since then there are many more to confirm the transcriptional and translational effects of ELF EM fields on gene expression. Harder science indeed.


You're getting confused Mr Coghill, you arguing with me about cancer, trying to show that it is not caused by genetic defects in certain genes. To whit demonstrating that ELF EM fields can cause genetic damage (if it is indeed true) hardly supports your cause does it now?


The role of ras genes in the neoplasmic transformation in animals.
http://www.ncbi.nlm.nih.gov/entrez/...ve&db=pubmed&dopt=Abstract&list_uids=15061485
 
cogreslab said:
From BB to cogreslab: "Your science skills are truly... uh... astonishing".

Well this was really a UVJ too, but we have seen enough evidence on this thread to suspect he may be able to confirm it with references as to the good quality of my science and argument. So I'll let him off that one.
What we see evidence for we'll leave to the gentle readers, sir. Meanwhile, how about you deal with the original question, sir. You reported a correlation between radio and TV transmissions and AIDS in major U.S. cities. So what? As has been pointed out, high AIDS rates exist in relatively broadcast-free areas of Africa. And as has been pointed out, AIDS also correlates with density of bakeries, pubs and car emissions.

That you miss the import of those points is quite telling.
 

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