Eva Vertes Attention

Today I received an email from Dr. Edo McGowan who saw my post on Eva Vertes and her research on cancer. Dr. McGowan wanted to share with her some research information and was unable to locate her, thus asking if I would post the information here in hopes someone might be able to find a way to get this information to Eva.

Thank you Dr. McGowan for sharing and I hope your connection will be made.

Note from Dr. McGowan

Kristie, I have no way to reach this young woman, but this may be of interest to her. I tried to post but was rejected. Your help posting this or reaching Eva would be appreciated.

Thanks Dr Edo McGowan

Eva some rambling thoughts. In working with wound healing and tissue repair using topically applied hyperbaric, there was often no scar tissue. Other that using embryonic tissue, I am unaware of this phenomenon. Thus the stem cells seem to be turned on by the oxygen. If one were to prick damaged tissue and then bring up tissue fluids, subject the area to topically applied hyperbaric the area would often remodel without scar tissue----i.e., new skin. The topically applied hyperbaric closed Pyoderma gangrenosum very quickly when not much else would work. Too much oxygen was damaging to new tissue. The right amount was angiogenic. The electron microscopy demonstrated this. Oxygen acted as an irritant, the TNF involvement and the MAP kinase and the phospholation of threonine kinase had something to do with driving this. See if you can talk with Madalene Heng who has this all worked out. You can Google her, Heng MC. Also ask her about her rat brain studies.

In your Monterey address a year or so ago, you mentioned muscle tissue as being exempt from active cancer growth. This tissue is also susceptible to enormous shifts in oxygen supply. In the microvascular supply the endothelial cell is capable of metabolic activity that can be 100 times greater than that of other cells. To support this elevated and impressive metabolic activity, endothelial cells are also major oxygen sinks. In ischemia, reperfusion injury, and acute inflammatory states, the endothelial cell shifts to a prothrombotic mode, the consequences of which are microthrombi [5]. The postcapillary venules are the most prone to attack during the inflammatory response as well as during ischemia or reperfusion injury. Granger et al noted that venular endothelial cells are 1 to 3 times more sensitive to inflammatory mediators and peptide angiogenic factors than endothelial cells found in the aorta [6]. The implication is that venular endothelial cells contain the highest density of inflammatory mediator receptors.

You might look at this. Also in furtherance of the discussion, the following is noted.

Effect of acute hypoxia on microcirculatory and tissue oxygen levels in rat cremaster muscle Paul C. Johnson,1 Kim Vandegriff,2 Amy G. Tsai,1 and Marcos Intaglietta1 1Department of Bioengineering, University of California, San Diego, La Jolla; and 2Sangart, San Diego, California Submitted 9 June 2004 ; accepted in final form 29 November 2004 Repeated exposure to brief periods of hypoxia leads to pathophysiological changes in experimental animals similar to those seen in sleep apnea. To determine the effects of such exposure on oxygen levels in vivo, we used an optical method to measure PO2 in microcirculatory vessels and tissue of the rat cremaster muscle during a 1-min step reduction of inspired oxygen fraction from 0.21 to 0.07. Under control conditions, PO2 was 98.1 ± 1.9 Torr in arterial blood, 52.2 ± 2.8 Torr in 29.0 ± 2.7-µm arterioles, 26.8 ± 1.7 Torr in the tissue interstitium near venous capillaries, and 35.1 ± 2.6 Torr in 29.7 ± 1.9-µm venules. The initial fall in PO2 during hypoxia was significantly greater in arterial blood, being 93% complete in the first 10 s, whereas it was 68% complete in arterioles, 47% at the tissue sites, and 38% in venules. In the 10- to 30-s period, the fall in normalized tissue and venular PO2 was significantly greater than in arterial PO2. At the end of hypoxic exposure, PO2 at all measurement sites had fallen very nearly in proportion to that in the inspired gas, but tissue oxygen levels did not reach critical PO2. Significant differences in oxyhemoglobin desaturation rate were also observed between arterial and microcirculatory vessels during hypoxia. In conclusion, the fall in microcirculatory and tissue oxygen levels in resting skeletal muscle is significantly slower than in arterial blood during a step reduction to an inspired oxygen fraction of 0.07, and tissue PO2 does not reach anaerobic levels.

Hope this reaches you.

Good luck with your work.

Edo