All Posts Tagged With: "genes"

Linda’s comment:  This is a great read……

Dr. Gordon’s Comments:

Finally they hit pay dirt with turning on Telomerase. This is the real thing; read it carefully!!! Yes, we will soon be able to substantially reverse aging even when you are near death! This is the most exciting proof that anti-aging will one day work that I have ever seen. This makes it worthwhile to really take good care of your body now, as this major breakthrough will happen for humans in our lifetime I am sure.

This Harvard associated study is the most credible research I have seen that we may one day really take years off our age even when we are very old and sick. This involved tweaking the genes to turn on Telomerase and worked even when the mice were near death’s doorstep. Then the mice still were able to grow new brain and other cells and clearly the effects are systemic and rejuvenating.

“These mice were equivalent to 80-year-old humans and were about to pass away,” says Ronald DePinho, co-author of the paper and a scientist at Dana-Farber Cancer Institute in Boston. After the experiment, “they were the physiological equivalent of young adults.”

Telomerase, as cancer treatment or cancer cause, needs to be understood since anti-aging benefits might be offset by increased cancer. Since enhancing telomerase has recently been shown to dramatically reverse aging then doing the opposite might be worth looking into for treating cancer. Please note, however, that this makes it clear why those who will be researching the antiaging benefits from inducing telomerase will be very concerned about the possibility that they will also increase cancer in those using the treatment.

I sent this research to you so that you will understand that Cancer is is a realistic possibility to consider. But there can be balance to this using non-toxic small conditional RNA’s that identify and kill cancer cells. And, since I lecture a great deal about How to Stem the Tide of Cancer, I am confident that a healthy outcome will be possible with telomerase induction, as we can monitor with tumor marker testing early tendencies toward developing cancer in patients receiving anti-aging telomerase therapy. 
We will plan to use therapies that we are already familiar with.  We can expect then that, in most instances, as Dr. Kobayashi proved in is ten year study in Japan that a World without Cancer is available now. He proved that simple things will bring early cancer marker tests back under control and death from cancer can be avoided.

But in case that is not sufficient control for some cases, then the new research about RNA curing cancer should be the safety blanket that will promote the safe use of antiaging based telomerase induction using gene tweaking, as described in Nature this week.  Their only fear from this approach is moving toward cancer and of course they have no idea about how nutritional and herbal approaches can keep that tendency under control.

So start exercising and detoxing now, as it now seems it is never too late to plan to live much longer with a healthy younger body!

Garry F. Gordon MD,DO,MD(H)
President, Gordon Research Institute
www.gordonresearch.com

Link 1: http://online.wsj.com/article/SB10001424052748703785704575642964209242180.html?mod=djemHL_t

Link 2: http://www.nature.com/news/2010/101128/full/news.2010.635.html

Link: http://www.biomedcentral.com/content/pdf/1471-2180-10-316.pdf

Excerpt:

he effect of Lactobacillus plantarum MB452 on tight junction integrity was determined by measuring trans-epithelial electrical resistance (TEER) across Caco-2 cell layers. L. plantarum MB452 caused a dose-dependent TEER increase across Caco-2 cell monolayers compared to control medium. Gene expression was compared in Caco-2 cells untreated or treated with L. plantarum MB452 for 10 hours. Caco-2 cell RNA was hybridised to human oligonucleotide arrays. Data was analysed using linear models and differently expressed genes were examined using pathway analysis tools. Nineteen tight junction-related genes had altered expression levels in response to L. plantarum MB452 (modified-P<0.05, fold-change>1.2), including those encoding occludin and its associated plaque proteins that anchor it to the cytoskeleton. L. plantarum MB452 also caused changes in tubulin and proteasome gene expression levels which may be linked to intestinal barrier function. Caco-2 tight junctions were visualised by fluorescent microscopy of immuno-stained occludin, zona occludens (ZO)-1, ZO-2 and cingulin. Caco-2 cells treated with L. plantarum MB452 had higher intensity fluorescence of each of the four tight junction proteins compared to untreated controls.

Conclusions

This research indicates that enhancing the expression of genes involved in tight junction signalling is a possible mechanism by which L. plantarum MB452 improves intestinal barrier function.

Central Role of the Holliday Junction Helicase RuvAB in vlsE Recombination and Infectivity of Borrelia burgdorferi

Lyme disease is the most prevalent tick-borne infection in North America and Eurasia. It is caused by the bacterium Borrelia burgdorferi and is transmitted to humans via the bite of infected ticks. These spirochetes can cause both acute and chronic infection and inflammation of the skin, joints, heart, and central nervous system. The persistence of infection despite the presence of an active immune response is dependent upon antigenic variation of VlsE, a 35 kDa surface-exposed lipoprotein. A large number of different VlsE variants are present in the host simultaneously and are generated by recombination of the vlsE gene with adjacent vls silent cassettes. To try to identify factors important in vlsE recombination and immune evasion, we selected mutants in genes involved in DNA recombination and repair and screened them for infectivity and vlsE recombination. Mutants in genes encoding RuvA and RuvB (which act together to promote the exchange of strands between two different DNA molecules) had reduced infectivity and greatly diminished vlsE recombination. In immunodeficient mice, ruvA mutants retained full infectivity, and no vlsE recombination was detected. Our findings reinforce the importance of vlsE variation in immune evasion and persistent infection. Continued