Health Services Facility

Here is an interesting open access paper at PLoS ONE: "We generated microarray gene expression data from livers of male mice fed high calorie or [calorie restriction] CR diets, and we find that CR significantly changes the expression of over 3,000 genes, many between 10- and 50-fold. We compare our data to the GenAge database of known aging-related genes and to prior microarray expression data of genes expressed differently between male and female mice. CR generally feminizes gene expression and many of the most significantly changed individual genes are involved in aging, hormone signaling, and p53-associated regulation of the cell cycle and apoptosis. Among the genes showing the largest and most statistically significant CR-induced expression differences are Ddit4, a key regulator of the TOR pathway, and Nnmt, a regulator of lifespan linked to the sirtuin pathway. ... Our data show that CR induces widespread gene expression changes and acts through highly evolutionarily conserved pathways, from microorganisms to mammals, and that its life-extension effects might arise partly from a shift toward a gene expression profile more typical of females." So yet another theory to add to the many on the cause of longevity differences by gender.

View the Article Under Discussion: http://dx.doi.org/10.1371/journal.pone.0005242
Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

A good example of the sort of cellular hacking going on in the laboratory and early trials these days via EurekAlert!: researchers "have developed a nanoparticle - about one thousandth smaller than a printed period - that can travel through the blood stream. 'Decorated' with a tumor-targeting antibody, the nanoparticle is able to locate primary and hidden metastatic tumor cells and deliver its payload: a fully functioning copy of the P53 tumor suppressor gene. ... Normal cells have two copies of the functioning P53 gene. The protein produced by the P53 gene is activated to either coordinate the repair process in cells or induce cell suicide. ... In earlier work using animal models, [researchers] delivered functional p53 genes to tumor cells and tumor metastases in 16 different types of cancer, including prostate, pancreatic, melanoma, breast cancer and head and neck cancer. The presence of the replacement genes dramatically improved the efficacy of conventional cancer therapy. ... When the job of reinstating a normal P53 suppressor gene is done, the nanoparticle - essentially a little fat droplet wrapped around the gene - simply melts away, unlike non-biodegradable delivery systems. ... Clinical trials are now underway ... The trial already has enrolled six patients with various cancers and anticipates a total of 14."

View the Article Under Discussion: http://www.eurekalert.org/pub_releases/2009-04/foas-fdn040509.php
Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

As I've mentioned in the past, autophagy - the process by which cells destroy and replace damaged or old components - seems to be very important in the natural longevity you are granted by the operation of your metabolism. It's required for the longevity boost given by calorie restriction, for example. Some groups would go so far as to say that most or all longevity-inducing tweaks to metabolism operate through increased autophagy: "Autophagy is involved in cellular protein and organelle degradation, which is mediated by the lysosomal pathway. [Autophagy] has a key role in cellular housekeeping by removing damaged organelles. During aging, the efficiency of autophagic degradation declines and intracellular waste products accumulate. In Caenorhabditis elegans, there is clear evidence that lifespan is linked to the capacity to regulate autophagy. Recent studies have revealed that the same signaling factors regulate both aging and autophagocytosis, thus highlighting the role of autophagy in the regulation of aging and age-related degenerative diseases. Here, we examine in detail the interactions of the signaling network involving longevity factors SIRT1, mTOR, FoxO3, NF-kappaB and p53 in the regulation of autophagy. We discuss the possibility that these well-known stress resistance and longevity factors regulate the aging process via autophagy."

View the Article Under Discussion: http://pmid.us/19380253
Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

Times are changing, and some very interesting and transformative technologies are emerging from the life sciences. Expect biotech to look increasingly like open source software development in years ahead: "at least three major technologies are shovel-ready: the programming of tissues, the ability to engineer cells, and robots. ... these discoveries mean that one can write out a life code, manipulate a cell, and execute a specific desired function. It means we can convert cells into programmable manufacturing entities. But this software builds its own hardware, allowing companies to begin using bacteria to produce chemicals, fuels, medicines, textiles, data storage, or any series of organic products. ... A second major tsunami is our increasing ability to grow complex organic structures, such as limbs, bladders, hearts, and tracheas. All complex organisms start out as undifferentiated, pluripotent cells, meaning these cells contain an entire genome and are able to produce all body parts. Mexico's dinosaur-like axolotl salamanders naturally regrow body parts, including sections of their hearts and brains as well as whole limbs. ... And soon, it may be possible to do this without a full body, just some cells. ... As innovators begin to read, reproduce, and program life, they will change almost every industry across the globe."

View the Article Under Discussion: http://www.npr.org/templates/story/story.php?storyId=103397134
Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

A report here on the recent conference at the Stanford Center for Longevity, representative of the dominant "work to slow aging through metabolic manipulation" faction in the research community: "Recent, near-miraculous advances in our understanding of biological processes at the cellular and molecular level offer the possibility of extending individual lives by slowing the aging process itself. ... Not that environment doesn't play a key role in aging-associated disease. For instance, the gene cited by Brunet is involved in the insulin pathway. Brunet, whose laboratory is studying aspects of this pathway in mammals as well as in C. elegans, noted that restricting caloric intake by about one-quarter to one-third - which suppresses insulin levels - has a life-span-increasing effect on all other species in which it's been tried: worms, flies, mice, even monkeys. Experiments with humans are ongoing, but our life spans are so long that data are dribbling out slowly. However, an apparent diminution in aging-related conditions such as type-2 diabetes, stroke and cancer is being seen, she said."

View the Article Under Discussion: http://news.stanford.edu/news/2009/april22/med-longevity-042209.html
Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/