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Oxycholesterol big cardiovascular threat – Cholesterol not dangerous at all
Oxycholesterol big cardiovascular threat – Cholesterol not dangerous at all
Saturday, August 22, 2009
Oxycholesterol problem?
Oxycholesterol is much more dangerous than previously assumed, said Chinese scientists at the 238th National Meeting of the American Chemical Society. They found evidence of Oxycholesterol’s devastating effects on bloodvessel elasticity, amongst other negative effects on the cardiovascular system.
Oxycholesterol has been known for over 100 years – it comes into existence by heating ordinary Cholesterol. Oxygen from the air binds to the Cholesterol and forms Oxycholesterol. When you fry a steak, for example, the heated fat in the meat binds with the oxygen in the air to form Oxycholesterol.
“Oxycholesterol boosts total Cholesterol levels and promotes Arteriosclerosis” said study leader Zhen-Yu Chen, Ph.D., of Chinese University of Hong Kong. This hardening of the arteries is most pronounced with Oxycholesterol, they found in tests on hamsters – an often-used substitute for humans. Fried and processed food, particularly fast-food, contains high quantities of Oxycholesterol. Avoiding these foods and eating a diet that is rich in antioxidants, such as fresh fruits and vegetables, could help reduce its levels in the body, according to the researchers.
Food manufacturers have been deliberately adding Oxycholesterol to the food they sell, because they give an addictive flavor. Such Oxycholesterols are partially hydrogenated vegetable oils and trans-fatty acids. For some reason, Western scientists have neglected research into the overall Cholesterol-raising powers of this substance and focused on cell-damaging properties of Oxycholesterol and Arteriosclerosis instead.
In this interesting new study, Dr. Chen’s group measured the effects of a diet high in Oxycholesterol. Blood Cholesterol in hamsters fed Oxycholesterol rose up to 22 percent more than hamsters eating ordinary non-oxidized Cholesterol. The Oxycholesterol group showed greater deposition of Cholesterol in the lining of their arteries and a tendency to develop larger deposits of it. These fatty deposits, called atherosclerotic plaques, increase the risk for stroke and heart attack.
Chen said that the most important finding concluded that Oxycholesterol had undesirable effects on artery function. It reduced their elasticity, impairing their ability to expand and carry more blood. That expansion could be beneficial in the sense that it would allow more blood to flow through arteries that are partially blocked by plaques, potentially reducing the risk that a clot will form and cause a heart attack or stroke.
These Oxycholesterols, a group of Cholesterol compounds that contain extra oxygen atoms were found to be highly toxic and highly effective in producing arteriosclerosis. They were surprised to find that highly purified Cholesterol, free of all traces of Oxycholesterol by being protected from the oxygen of air, does not injure mammalian arteries. In the original research that found ordinary Cholesterol to be toxic to the cardiovascular system, it is unlikely that precautions were taken to prevent the exposure of the Cholesterol they were using from Oxygen. Thus, almost certainly, they were merely demonstrating that Oxycholesterol contaminants, rather than Cholesterol itself, were producing Arteriosclerosis in their lab animals.
These highly damaging Oxycholesterols are found in foods in which Cholesterol is subjected to heating and exposure to the Oxygen of the air during either cooking, food processing or food preservation. Such foods include dried milk powder, dried egg yolk and foods fried in heated oils. The Oxycholesterol in these foods is absorbed into the blood after digestion and then becomes concentrated in the low density lipoprotein faction of the blood plasma. When lipoproteins are taken up by arterial wall cells, the Cholesterol oxides that are released lead to damage to artery wall cells and tissues, ultimately causing Arteriosclerosis.
Recent epidemiological studies, particularly one from Cambridge, have suggested that vitamin E supplements of 800 IE/day reduce by about 70% the risk of coronary artery thrombosis in patients with pre-existent Angina pectoris. Vitamin E is a powerful fat soluble anti-oxidant vitamin that acts by modifying the reactions of low density lipoprotein with oxygen, thus preventing the formation of Oxycholesterols. There is compelling evidence that a trace of a contaminant constituent associated with fat and Cholesterol is actually capable of producing Arteriosclerosis.
There will certainly be resistance to the demise of the Cholesterol theory. This will come from manufacturers of low -Cholesterol foods but also from the pharmaceutical companies that have been anticipating highly profitable products from the sale of patentable Cholesterol-lowering medicines. In contrast, B-complex vitamins are very cheap, unpatentable and therefore offer no opportunity of profits to anyone.
This Chinese research shows us again that reducing non-oxidized Cholesterol in the diet will not produce any major benefit, as has been shown already in many other studies. Vitamin E and possibly other antioxidants like vitamins A and C and the trace mineral Selenium should counteract the formation of Oxycholesterols.
20091005
Pancreatic Cancer Chemotherapy Resistance
Researchers Find Drug That Reverses Resistance To Chemotherapy In Pancreatic Cancer
Main Category: Pancreatic Cancer
Also Included In: Radiology / Nuclear Medicine
http://www.medicalnewstoday.com/articles/165293.php
For the first time researchers have shown that by inhibiting the action of an enzyme called TAK-1, it is possible to make pancreatic cancer cells sensitive to chemotherapy, opening the way for the development of a new drug to treat the disease.
Dr Davide Melisi told Europe's largest cancer congress, ECCO 15 - ESMO 34 [1], in Berlin, that resistance to chemotherapy was the greatest challenge to treating pancreatic cancer.
"Pancreatic cancer is an incurable malignancy, resistant to every anti-cancer treatment. Targeting TAK-1 could be a strategy to revert this resistance, increasing the efficacy of chemotherapy," said Dr Melisi, who until the start of September was a Fellow at the M.D. Anderson Center in Houston (Texas, USA); he has now moved to a staff position at the National Cancer Institute in Naples (Italy). "During the past few years we have been studying the role played by a cytokine or regulatory protein called Transforming Growth Factor beta (TGFbeta) in the development of pancreatic cancer. Recently we focused our attention on a unique enzyme activated by TGFbeta, TAK-1, as a mediator for this extreme drug resistance."
Dr Melisi and his colleagues investigated the expression of TAK-1 (TGFbeta-Activated Kinase-1) in pancreatic cell lines and developed a drug that was capable of inhibiting TAK-1. They tested the activity of the TAK-1 inhibitor on its own and in combination with the anti-cancer drugs gemcitabine, oxaliplatin and SN-38 (a metabolite of the anti-cancer drug irinotecan) in cell lines, and the activity of the TAK-1 inhibitor combined with gemcitabine against pancreatic cancer in mice.
"The use of this TAK-1 inhibitor increased the sensitivity of pancreatic cells to all three chemotherapeutic drugs. By combining it with classic anti-cancer drugs, we were able to use doses of drugs up to 70 times lower in comparison with the control to kill the same number of cancer cells. In mice, we were able to reduce significantly the tumour volume, to prolong the mice survival, and to reduce the toxicity by combining the TAK-1 inhibitor with very low doses of a classic chemotherapeutic drug, gemcitabine, that would have been ineffective otherwise," said Dr Melisi.
The use of gemcitabine on its own against the cancer in mice was ineffective because of the drug resistant nature of the disease. However, once it was combined with the TAK-1 inhibitor, Dr Melisi and his colleagues saw a 78% reduction in tumour volumes. "The median average survival for the control, TAK-1 inhibitor, gemcitabine on its own, or TAK-1 inhibitor combined with gemcitabine was 68, 87, 82 and 122 days respectively," he said.
"This is the first time that TAK-1 has been indicated as a relevant target for the treatment of a solid tumour and that it is a valid approach to reverting the intrinsic drug resistance of pancreatic cancer. The TAK-1 inhibitor used in this study is an exciting drug that warrants further development for the treatment of pancreatic cancer. In the near future, we will study whether it is also able to make other chemotherapeutic agents, such as oxaliplatin, 5-FU or irinotecan, work against pancreatic cancer in mice.
"Our main goal is to translate this combination approach from the bench to the bedside, conducting a clinical trial that could demonstrate the safety of this TAK-1 inhibitor in combination with gemcitabine, and its efficacy, in pancreatic cancer patients."
Abstract no: 1002, Basic science/translational research session.
[1] ECCO 15 - ESMO 34 is the 15th congress of the European CanCer Organisation and the 34th congress of the European Society for Medical Oncology.
Source:
Emma Mason
ECCO-the European CanCer Organisation
Cancer Treatment Options
Diagnosed w/Pancreas Cancer? Learn About New Treatment Options at CTCA
www.CancerCenter.com
Pancreatitis Questions?
Capital Digestive Care has the answers you need. Learn more.
www.capitaldigestivecare.com
Ovarian cancer clinical trials
Pharmaceutical Research Trial Expertise for Phase I - IV Oncology
INCResearch.com
What memories that need released in me that cause others to have Pancreas Cancer?
Main Category: Pancreatic Cancer
Also Included In: Radiology / Nuclear Medicine
http://www.medicalnewstoday.com/articles/165293.php
For the first time researchers have shown that by inhibiting the action of an enzyme called TAK-1, it is possible to make pancreatic cancer cells sensitive to chemotherapy, opening the way for the development of a new drug to treat the disease.
Dr Davide Melisi told Europe's largest cancer congress, ECCO 15 - ESMO 34 [1], in Berlin, that resistance to chemotherapy was the greatest challenge to treating pancreatic cancer.
"Pancreatic cancer is an incurable malignancy, resistant to every anti-cancer treatment. Targeting TAK-1 could be a strategy to revert this resistance, increasing the efficacy of chemotherapy," said Dr Melisi, who until the start of September was a Fellow at the M.D. Anderson Center in Houston (Texas, USA); he has now moved to a staff position at the National Cancer Institute in Naples (Italy). "During the past few years we have been studying the role played by a cytokine or regulatory protein called Transforming Growth Factor beta (TGFbeta) in the development of pancreatic cancer. Recently we focused our attention on a unique enzyme activated by TGFbeta, TAK-1, as a mediator for this extreme drug resistance."
Dr Melisi and his colleagues investigated the expression of TAK-1 (TGFbeta-Activated Kinase-1) in pancreatic cell lines and developed a drug that was capable of inhibiting TAK-1. They tested the activity of the TAK-1 inhibitor on its own and in combination with the anti-cancer drugs gemcitabine, oxaliplatin and SN-38 (a metabolite of the anti-cancer drug irinotecan) in cell lines, and the activity of the TAK-1 inhibitor combined with gemcitabine against pancreatic cancer in mice.
"The use of this TAK-1 inhibitor increased the sensitivity of pancreatic cells to all three chemotherapeutic drugs. By combining it with classic anti-cancer drugs, we were able to use doses of drugs up to 70 times lower in comparison with the control to kill the same number of cancer cells. In mice, we were able to reduce significantly the tumour volume, to prolong the mice survival, and to reduce the toxicity by combining the TAK-1 inhibitor with very low doses of a classic chemotherapeutic drug, gemcitabine, that would have been ineffective otherwise," said Dr Melisi.
The use of gemcitabine on its own against the cancer in mice was ineffective because of the drug resistant nature of the disease. However, once it was combined with the TAK-1 inhibitor, Dr Melisi and his colleagues saw a 78% reduction in tumour volumes. "The median average survival for the control, TAK-1 inhibitor, gemcitabine on its own, or TAK-1 inhibitor combined with gemcitabine was 68, 87, 82 and 122 days respectively," he said.
"This is the first time that TAK-1 has been indicated as a relevant target for the treatment of a solid tumour and that it is a valid approach to reverting the intrinsic drug resistance of pancreatic cancer. The TAK-1 inhibitor used in this study is an exciting drug that warrants further development for the treatment of pancreatic cancer. In the near future, we will study whether it is also able to make other chemotherapeutic agents, such as oxaliplatin, 5-FU or irinotecan, work against pancreatic cancer in mice.
"Our main goal is to translate this combination approach from the bench to the bedside, conducting a clinical trial that could demonstrate the safety of this TAK-1 inhibitor in combination with gemcitabine, and its efficacy, in pancreatic cancer patients."
Abstract no: 1002, Basic science/translational research session.
[1] ECCO 15 - ESMO 34 is the 15th congress of the European CanCer Organisation and the 34th congress of the European Society for Medical Oncology.
Source:
Emma Mason
ECCO-the European CanCer Organisation
Cancer Treatment Options
Diagnosed w/Pancreas Cancer? Learn About New Treatment Options at CTCA
www.CancerCenter.com
Pancreatitis Questions?
Capital Digestive Care has the answers you need. Learn more.
www.capitaldigestivecare.com
Ovarian cancer clinical trials
Pharmaceutical Research Trial Expertise for Phase I - IV Oncology
INCResearch.com
What memories that need released in me that cause others to have Pancreas Cancer?
Pancreatic Cancer Treatment
New Hope for Treatment of
Pancreatic Cancer Slideshow
FRIDAY, Sept. 25 (HealthDay News) -- Inhibiting the action of an enzyme called TAK-1 reverses pancreatic cancer resistance to chemotherapy, a finding that could lead to the development of a new way to treat the disease, researchers say.
Pancreatic cancer is resistant to every currently available anti-cancer treatment.
"During the past few years we have been studying the role played by a cytokine or regulatory protein called transforming growth factor-beta [TGFbeta] in the development of pancreatic cancer. Recently we focused our attention on a unique enzyme activated by TGFbeta, TAK-1, as a mediator for this extreme drug resistance" in pancreatic cancer, study author Dr. Davide Melisi said in a news release from the European Cancer Organization.
He and his colleagues developed a TAK-1 inhibitor and tested it on its own and in combination with the anti-cancer drugs gemcitabine, oxaliplatin and SN-38 (a metabolite of the anti-cancer drug irinotecan) in pancreatic cancer cell lines. They also tested the TAK-1 inhibitor combined with gemcitabine against pancreatic cancer in mice.
"The use of this TAK-1 inhibitor increased the sensitivity of pancreatic cells to all three chemotherapeutic drugs," Melisi said.
"By combining it with classic anti-cancer drugs, we were able to use doses of drugs up to 70 times lower in comparison with the control to kill the same number of cancer cells. In mice, we were able to reduce significantly the tumor volume, to prolong the mice survival, and to reduce the toxicity by combining the TAK-1 inhibitor with very low doses of a classic chemotherapeutic drug, gemcitabine, that would have been ineffective otherwise," Melisi added.
The study was scheduled for presentation Sept. 24 at the joint meeting of the European Cancer Organization and the European Society for Medical Oncology in Berlin.
"This is the first time that TAK-1 has been indicated as a relevant target for the treatment of a solid tumor and that it is a valid approach to reverting the intrinsic drug resistance of pancreatic cancer," Melisi stated. "The TAK-1 inhibitor used in this study is an exciting drug that warrants further development for the treatment of pancreatic cancer."
-- Robert Preidt
Copyright © 2009 ScoutNews, LLC. All rights reserved.
SOURCE: European Cancer Organization, news release, Sept. 24, 2009
http://www.medicinenet.com/script/main/art.asp?articlekey=105937
Cancer Treatment Options One option is to clean my memories that make cause pancreas cancer in others? Diagnosed w/Pancreas Cancer? Learn About New Treatment Options at CTCA www.CancerCenter.com
Pancreatic Cancer Slideshow
FRIDAY, Sept. 25 (HealthDay News) -- Inhibiting the action of an enzyme called TAK-1 reverses pancreatic cancer resistance to chemotherapy, a finding that could lead to the development of a new way to treat the disease, researchers say.
Pancreatic cancer is resistant to every currently available anti-cancer treatment.
"During the past few years we have been studying the role played by a cytokine or regulatory protein called transforming growth factor-beta [TGFbeta] in the development of pancreatic cancer. Recently we focused our attention on a unique enzyme activated by TGFbeta, TAK-1, as a mediator for this extreme drug resistance" in pancreatic cancer, study author Dr. Davide Melisi said in a news release from the European Cancer Organization.
He and his colleagues developed a TAK-1 inhibitor and tested it on its own and in combination with the anti-cancer drugs gemcitabine, oxaliplatin and SN-38 (a metabolite of the anti-cancer drug irinotecan) in pancreatic cancer cell lines. They also tested the TAK-1 inhibitor combined with gemcitabine against pancreatic cancer in mice.
"The use of this TAK-1 inhibitor increased the sensitivity of pancreatic cells to all three chemotherapeutic drugs," Melisi said.
"By combining it with classic anti-cancer drugs, we were able to use doses of drugs up to 70 times lower in comparison with the control to kill the same number of cancer cells. In mice, we were able to reduce significantly the tumor volume, to prolong the mice survival, and to reduce the toxicity by combining the TAK-1 inhibitor with very low doses of a classic chemotherapeutic drug, gemcitabine, that would have been ineffective otherwise," Melisi added.
The study was scheduled for presentation Sept. 24 at the joint meeting of the European Cancer Organization and the European Society for Medical Oncology in Berlin.
"This is the first time that TAK-1 has been indicated as a relevant target for the treatment of a solid tumor and that it is a valid approach to reverting the intrinsic drug resistance of pancreatic cancer," Melisi stated. "The TAK-1 inhibitor used in this study is an exciting drug that warrants further development for the treatment of pancreatic cancer."
-- Robert Preidt
Copyright © 2009 ScoutNews, LLC. All rights reserved.
SOURCE: European Cancer Organization, news release, Sept. 24, 2009
http://www.medicinenet.com/script/main/art.asp?articlekey=105937
Cancer Treatment Options One option is to clean my memories that make cause pancreas cancer in others? Diagnosed w/Pancreas Cancer? Learn About New Treatment Options at CTCA www.CancerCenter.com
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Insurance Jacksonville
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Online Cricket Games
Online Cricket Games
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Online Cricket Games
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Insurance Fort Lauderdale
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Insurance Fort Lauderdale
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