Issue 3, 2007

There are a lot of articles in this issue because they included the papers from the first Edmonton aging symposium.

"Human Reproductive Costs and the Predicted Response to Dietary Restriction" by Robert Arking. Attempts to predict the effects of CR on human longevity with a model based on energy allocation (I think).

"Autophagy in the Heart and Liver During Normal Aging and Calorie Restriction" by Stephanie E. Wohlgemuth, David Julian, Debora E. Akin, Joanna Fried, Kristin Toscano, Christiaan Leeuwenburgh, and William A. Dunn, Jr. Autophagy rates in the heart and liver are not affected by age in rats that eat what they want. It is increased by CR in old rats only in the heart, not in the liver.

"Apolipoprotein E Genotypic Frequencies Among Down Syndrome Patients Imply Early Unsuccessful Aging for ApoE4 Carriers" by Giusi I. Forte, Maria Piccione, Letizia Scola, Antonino Crivello, Cristina Galfano, Massimiliano M. Corsi, Martina Chiappelli, Giuseppina Candore, Mario Giuffrè, Roberto Verna, Federico Licastro, Giovanni Corsello, Calogero Caruso, and Domenico Lio. ApoE4 carriers go down as a proportion of the population at older ages (16% of people under 40, 13% of those in their 70s, and 4% of people over 90 in a study of 360 people). Down syndrome patients at 9% (106 DS average age 9). They use frequency difference between 5-year old DS people to those older to claim that DS is a good model of early aging.

"Dietary Intake of Elderly Living in Toronto Long-Term Care Facilities: Comparison to the Dietary Reference Intake" by Elaheh Aghdassi, Margaret McArthur, Barbara Liu, Alison McGeer, Andrew Simor, and Johane P. Allard. Old people in long term care facilities don't get a perfect diet, but not too bad either.

"Cytochrome c Oxidase Rather than Cytochrome c is a Major Determinant of Mitochondrial Respiratory Capacity in Skeletal Muscle of Aged Rats: Role of Carnitine and Lipoic Acid" by Jayavelu Tamilselvan, Kumarasamy Sivarajan, Muthuswamy Anusuyadevi, and Chinnakkannu Panneerselvam. I don't really understand much more than the title. They did experiments on naked mitochondria that had lost their cytochrome c and where bathing them in cytochrome c didn't recover their natural activity.

"A Model of Metabolic Changes in Respiration-Deficient Human Cells" by F. Mathias Bollmann. A model of how cells with damaged mitochondria survive long term through the combination of glycolysis and a 'partly reversed TCA cycle'. Needs to export succinate.

Following papers from the Edmonton aging symposium

"Mitochondria in Aging and Alzheimer's Disease" by P.J. Crouch, K. Cimdins, J.A. Duce, A.I. Bush, and I.A. Trounce. They postulate that mtDNA mutations are an important factor in amyloid beta production. They say amyloid beta accumulates in mitochondria in Alzheimered brains.

"Engineering Away Lysosomal Junk: Medical Bioremediation" by Bruce E. Rittmann and John Schloendorn. Strains of Nocardia (a bacteria) can degrade 7-ketocholesterol, although it's tricky to tell from the grammar of the sentence to what, or if it can be degraded without modifications. They have some analysis of the intermediate molecules in the degradation pathway.

"Therapeutic Ultrasound Applications in Craniofacial Growth, Healing and Tissue Engineering" by Tarek El-Bialy. Ultrasound being trialled/used to trigger/speed up bone formation/healing and dental formation. This paper claims to explain the molecular basis for this.

"Time, Damage, and Aging: What Really Matters?" by Huber R. Warner. Not sure.

"Nutrition as a Determinant of Successful Aging: Description of the Quebec Longitudinal Study NuAge and Results from Cross-Sectional Pilot Studies" by Pierrette Gaudreau, José A Morais, Bryna Shatenstein, Katherine Gray-Donald, Abdel Khalil, Isabelle Dionne, Guylaine Ferland, Tamàs Fülöp, Danielle Jacques, Marie-Jeanne Kergoat, Daniel Tessier, Richard Wagner, and Hélène Payette. Longitudinal study of 1800 >68 year olds tracking lots of variables. Hasn't finished yet, this is just the description.

"The Cancer–Aging Interface and the Significance of Telomere Dynamics in Cancer Therapy" by Gesche Tallen, Mohamed A. Soliman, and Karl Riabowol. Chemotherapy triggers faster cell regeneration in healthy tissue to compensate for lost cells. This leads to shorter telomeres, which could have some impact down the line.

"Loss of Muscle Strength During Aging Studied at the Gene Level" by Geoffrey Goldspink. Mechano-growth factor, an alternative splicing of IGF-1, increases muscle contractile strength by activating muscle satellite stem cells that do local muscle repair.

Issue 2, 2007

By the abstracts.

"Allotopic mRNA Localization to the Mitochondrial Surface Rescues Respiratory Chain Defects in Fibroblasts Harboring Mitochondrial DNA Mutations Affecting Complex I or V Subunits" by Crystel Bonnet, Valérie Kaltimbacher, Sami Ellouze, Sébastien Augustin, Paule Bénit, Valérie Forster, Pierre Rustin, José-Alain Sahel, and Marisol Corral-Debrinski. Another mitoSENS contribution like the one in issue 4 of 2006 by Bokori-Brown, this one claiming success in both getting the proteins to migrate to the mitochondria and them functioning as expected and rescuing cells with mtDNA mutations in their ATP6 and ND4 genes. They seem to be stressing the result for ATP6 so maybe the result for ND4 isn't as clear-cut. How many left out of the 13 then?

"Microsatellite Instability and Compromized Mismatch Repair Gene Expression During In Vitro Passaging of Monoclonal Human T Lymphocytes" by Simona Neri, Graham Pawelec, Andrea Facchini, and Erminia Mariani. I don't know enough about T-cells, mismatch repair or microsatellite instability to even understand what this study was about.

"The Olive Constituent Oleuropein Exhibits Proteasome Stimulatory Properties In Vitro and Confers Life Span Extension of Human Embryonic Fibroblasts" by Magda Katsiki, Niki Chondrogianni, Ioanna Chinou, A. Jennifer Rivett, and Efstathios S. Gonos. 15% is the claimed lifespan extension on fibroblasts.

"Oxidative Stress of Neural, Hematopoietic, and Stem Cells: Protection by Natural Compounds" by R. Douglas Shytle, Jared Ehrhart, Jun Tan, Jennifer Vila, Michael Cole, Cyndy D. Sanberg, Paul R. Sanberg, and Paula C. Bickford. Lower oxidative stress-induced apoptosis in some human cells in vitro when given some code-named natural compound.

"Examination of Cognitive Function During Six Months of Calorie Restriction: Results of a Randomized Controlled Trial" by Corby K. Martin, Stephen D. Anton, Hongmei Han, Emily York-Crowe, Leanne M. Redman, Eric Ravussin, Donald A. Williamson, and for the Pennington CALERIE Team. Randomised controlled CR study on humans. These are rare. Checked to see if there was any cognitive impairment but found none. 12 people per group, so it would have had to have been a big effect to have been found, but still something.

"Oxidative DNA Damage Repair and parp 1 and parp 2 Expression in Epstein-Barr Virus-Immortalized B Lymphocyte Cells from Young Subjects, Old Subjects, and Centenarians" by Marta Chevanne, Corinne Calia, Michele Zampieri, Barbara Cecchinelli, Riccardo Caldini, Daniela Monti, Laura Bucci, Claudio Franceschi, and Paola Caiafa. They find some properties of B-cells in centenarians that resemble the properties found in young people and differ from old non-centenarians (sub-centenarians?). I never buy these ones.

"Mathematical Models for the Proliferation of Neural Stem/Progenitor Cells in Clonogenic Culture" by Bao Feng Ma, Xiao Mei Liu, Ai Xia Zhang, Peng Wang, Xiu Ming Zhang, Shu Nong Li, Bruce T. Lahn, and Andy Peng Xiang. What it says on the title. Without access to the paper, can't tell anything about the model.

"Mitochondrial Oxygen Consumption and Reactive Oxygen Species Production are Independently Modulated: Implications for Aging Studies" by Gustavo Barja. Claims that sometimes higher oxygen consumption means lower ROS production. eg aerobic exercise, chronic exercise, hyperthyroidism and dietary restriction. Also, that it is lower in long-lived birds than in mammals of the same size.

"Long-Term Low-Calorie Low-Protein Vegan Diet and Endurance Exercise are Associated with Low Cardiometabolic Risk" by Luigi Fontana, Timothy E. Meyer, Samuel Klein, and John O. Holloszy. Raw vegans and runners were healthier than normal people, all groups around 53 (11) years. Lower weight, plasma lipids, lipoproteins, glucose, C-reactive protein, blood pressure and carotid artery intima-mdedia thickness. Also, raw vegans had lower BP than runners.

In the first page of the now-seemingly-regular column surveying theses, there is a thesis looking at parental imprinting comparison in cattle between cloned and natural animals, and finding big variability among cloned animals, and differences from natural animals, especially mentioning IGF2.

Issue 1, 2007

Back to not having access to the full text on this issue.

"Old Rhesus Macaques Treated with Interleukin-7 Show Increased TREC Levels And Respond Well to Influenza Vaccination" by Richard Aspinall, Jeffrey Pido-Lopez, Nesrina Imami, Sian M. Henson, Pa Tamba Ngom, Michel Morre, Henk Niphuis, Ed Remarque, Brigitte Rosenwirth, and Jonathan L. Heeney. What it says on the title. TREC are T-cell receptor excision circles, wikipedia tells me, which are small circles of DNA created during the time the T-cell spends in the thymus while creating the huge variety of receptors, and are a marker for mature T-cells. Old here is 18.5 to 23.9 years.

"A Novel Possible Approach to The Creation of Genetically Personalized Human Embryonic Stem-Like Cell Lines" by Wenqing Fu. Proposal for a technique to create tailored hESCs by repeatedly merging a generic line of hESCs with the target human's line, growing it to a blastocyst, pulling hESCs from that and repeating the process. I'd think the invention of iPSCs obviated the need for doing this.

"Correction of Proliferation And Drug Sensitivity Defects in The Progeroid Werner's Syndrome by Holliday Junction Resolution" by Ana M. Rodriguez-Lopez, Matthew C. Whitby, Christine M. Borer, Marcus A. Bachler, and Lynne S. Cox. They insert a bacterial enzyme that removes Holliday junctions from Werner's syndrome cells. The cells do better afterwards.

"Impaired Mononuclear Cell Immune Function in Extreme Obesity Is Corrected by Weight Loss" by Luigi Fontana, J. Christopher Eagon, Marco Colonna, and Samuel Klein. Very small study on six extremely fat people. They had very low production of two immune-system stimulating factors. Losing 30% of their weight fixed that. The whys for the low immune system stimulation and recovery seem not to be known.

"Reactive Oxygen Species, Isotope Effect, Essential Nutrients, and Enhanced Longevity" by Mikhail S. Shchepinov. Change the carbons and hydrogens to heavier isotopes than normal to slow down ROS reaction and therefore live longer.

"Evidence That Aging And Amyloid Promote Microglial Cell Senescence" by Barry E. Flanary, Nicole W. Sammons, Cuong Nguyen, Douglas Walker, and Wolfgang J. Streit. Shorter telomeres in human microglia when demented. Shorter telomeres and lower telomerase activation in rat microglia with aging. Microglia dystrophy in demented and amyloidal humans compared to non-demented non-amyloidal.

"Cumulative Index of Elderly Disorders And Its Dynamic Contribution to Mortality And Longevity" by Anatoli I. Yashin, Konstantin G. Arbeev, Alexander Kulminski, Igor Akushevich, Lucy Akushevich, and Svetlana V. Ukraintseva. An absolute and relative risk function of age that I think I need to see to understand.

"Cellular Therapy Using Microglial Cells" by John Schloendorn, Sebastian Sethe, and Alexandra Stolzing. Sounds like a theoretical paper on what we could do to keep microglia functioning properly and also improve their function by inserting proteases from other species into precursors that can then cross the blood-brain barrier. Might have to look for it.

There's a summary of PhD dissertations there that would be interesting to see too.

Issue 4, 2006

For some reason, this issue is free so I can read any articles I feel interested in, but since I don't really have any time to read papers, I will stick mostly to the abstracts.

There is a series of comment articles that are followups to the Special Interest Group on Societal Implications of Anti-Aging Research at the the 2005 Gerontology Society of America's conference discussing the usual SENS vs nonSENS.

"Site-Specific Integration into the Human Genome: Ready for Clinical Application?". A commentary piece on the possibilities of practical use of adeno-associated virus (AAV) for clinical gene insertion. AAV can insert its genome into a specific part of chromosome 19 (AAVS1), but it can only carry a very small payload. To enlarge the payload it's usually used without the site-specific integration gene (Rep) which ruins the reason for using AAV in the first place. What was new work at the time was a development of a hybrid between the herpes simplex virus and AAD to keep the site-specific integration while enlarging the payload and not overdoing the Rep expression which otherwise causes problems. Article says it isn't good enough for the clinic yet because the site-specificity isn't good enough (70%) and because of low efficiency of gene transfer which they claim to be 20% for stable cell lines (my problem here is that I don't know what the efficiency means. That 20% of the cells get the gene inserted into them sounds like the most likely meaning).

"Mitochondrial Transfer Between Eukaryotic Animal Cells and Its Physiologic Role". Another commentary piece on a paper that appeared in PNAS reporting the rescue of cells grown without mtDNA when grown among normal human skin fibroblasts and mesenchymal stem cells in vitro. By rescue, they mean that after a while, the sans-mtDNA cells appear to acquire functional mitochondrial and they multiply as normal. The commentary is on the mechanism of mitochondrial transfer and on whether the usual function of mitotransfer is that good mitochondria flow from good cells to bad cells or the reverse, the first one as an analogy to entropy, the second seeing mitochondria as selfish agents. The author prefers the first option.

"Expression of Algal Nuclear ATP Synthase Subunit 6 in Human Cells Results in Protein Targeting to Mitochondria but No Assembly into ATP Synthase" by M Bokori-Brown and IJ Holt. Very interesting and thorough attempt at introducing a version of the human subunit a (A6) of ATP synthase gene into a human cell's nuclear DNA. They tried many versions and the one that targeted to the mitochondria best was a version from an algae (Chlamydomonas reinhardtii) that is naturally in the nDNA, with various hybrids working less well. The problem is that the better the protein was targetted, the worse the cell did. Some more imagery shows that the protein doesn't colocalise with the ATP synthase on the mitochondria, so it's just gunking up the mitochondria, not doing anything useful.

"Erythrocyte Plasma Membrane Redox System in Human Aging" by SI Rizvi, R Jha and PK Maurya. Correlation of 0.78 between the level of export of electrons by red blood cells through the plasma membrane redox system, and age in 80 people. Similar inverse correlation between plasma antioxidant capacity and age.

"Selegiline Induces Neuronal Phenotype and Neurotrophins Expression in Embryonic Stem Cells" by F Esmaeili, T Tiraihi, M Movahedin and SJ Mowla. What the title says.

"VEGF Gene and Phenotype Relation with Alzheimer's Disease and Mild Cognitive Impairment" by M Chiappelli, B Borroni, S Archetti, E Calabrese, MM Corsi, M Franceschi, A Padovani and F Licastro. Link between a variant in the vascular enthelial growth factor (VEGF) gene promoter and Alzheimer's and mild cognitive impairment in a study of about 1000 people total. AA variant were 1.6 times more common than expected among AD. Also deteriorated fast 6 times more often if they had an ApoE4 allele. AA variant had more VEGF in circulation.

Issue 3, 2006

By the abstracts:

"Targeting Telomerase". Review of techniques and issues regarding hammering telomerase as an anti-cancer treatment, and whether that would select for ALT-cancers (ALT constitute 10-15% of cancers atm). Of note, the existence of a TERT vaccine.

"Telomere and TRF2/MTBP Localization in Respect to Satellite DNA During the Cell Cycle of Mouse Cell Line L929" About what happens to telomeres as the cells goes through its cycle in mice. Mostly goes over my head.

"Werner Syndrome as an Example of Inflamm-aging: Possible Therapeutic Opportunities for a Progeroid Syndrome?" Title is a good summary of the abstract.

"Stimulation of Macroautophagy Can Rescue Older Cells from 8-OHdG mtDNA Accumulation: A Safe and Easy Way to Meet Goals in the SENS Agenda" They stimulate macroautophagy by injecting agents that stop the breakdown of triglycerides in rat liver cells. This gets rid of 8-OHdG accumulation in the mtDNA in six hours.

Also, a report on SENS 2 by Aubrey de Grey that I'd like to read.

Overall, I don't mind as much not having access to the articles in this issue.

Cryopreservation of Complex Systems: The Missing Link in the Regenerative Medicine Supply Chain

Interestingness: 6

By Gregory M. Fahy, Brian Wowk, and Jun Wu. Rejuvenation Research. Summer 2006, 9(2): 279-291. doi:10.1089/rej.2006.9.279.

They pump the idea of using cryogenics to store pre-produced organs for use in transplants. They start with some interesting numbers regarding yearly US deaths that could be prevented if there were available organs:

• Heart  710,760
• Lung 122,009
• Kidney 37,251
• Liver 16,214

in total forming 36.2% of all yearly US deaths. They seem to be assigning all heart disease deaths as solvable by a heart transplant, etc. They also have a corresponding graph showing survival curves (ie age vs percentage alive) for status quo vs with those transplants, assuming no deaths during the transplants, with the transplant curve really diverging after 70 years of age with the transplant survival to status quo survival ratio of two at 80 and of 18 at 90. I don't know why they chose to show numbers that are so clearly not conservative.

They see cryopreservation as a necessary tool to manage the supply chain of organs manufactured through regenerative medicine to make mass organ availability viable. This is seen by them as the interim solution until in-situ recreation of the organ becomes a possibility.

They then describe a brief history of the cryopreservation of organs by straight freezing:

• 1950s - Freezing of guinea pig uteri to dry ice temperature (< -79C) and back. Contractile responses in vitro.
• 1973 - Freezing of dog intestines to liquid nitrogen temperature (< -196C). Long term survival of small parts of it.
• 2002 - Freezing of rat ovaries. Survival of some and offspring in one after transplantation back into rats. They say this is not a good test since the ovaries can regenerate even if completely screwed up.
• 2003 - Freezing of sheep ovaries. Vascular patency (unobstructed) retained in 3 of 11 grafts and follicle-stimulating hromone levels kept to normal limits. Second report claiming higher patency rates using directional freezing.

They claim straight-freezing of vital organs won't work because the vascular system is too easily damaged by freezing. This leads to methods that try to avoid freezing damage by avoiding ice formation.

In 1965, red blood cells and guinea pig uteri were lowered to -79C by lowering the freezing point of water and keeping it liquid all the way to the target temperature. Then in the 1980s, vitrification experiments started where the material is cooled into a glass without forming ice, starting with the vitrification of mouse embryos in 1985.

Experiments with vitrifications suggest that toxicity of cryoprotectant is due to reduced water availability for biomolecules. "Winner" of the cryoprotectants is M22 which seems to be used only below -22C with some other cryoprotectant (VMP) used to go from room temperature to -22C. Not much idea of what M22 consists of but it has a carrier solution that is meant to lower the toxicity combined with many anti-nucleating substances.

When ten rabbit kidneys were cooled to -22C, M22ised, deM22ised and rewarmed, then transplanted into rabbits, all rabbits survived (the non-cooled kidney is extracted in the experiments to make sure that the rabbits depend on the transplanted kidney), but there is more injury to the M22-ised kidneys than what is seen when just cooling them to -3C with VMP. Eight rabbit kidneys taken to -50C using M22 seem fine once rewarmed/deM22ised. Extra injury in M22-ised kidneys might be due to extra handling or extra time at cold temperature.

Newest experiment (2005) does the same rabbit kidney vitrification and transplantation on one rabbit with the rabbit surviving for 48 days after transplantation before it is killed. The cryoprotected kidney is cooled to below the glass transition temperature for M22 (-123C). Lots of damage to the kidney on this one, with hints that more even perfusion is needed.

Issue 2, 2006

This issue is the second part of the papers presented in SENS 2005. By the abstracts:

Section 5: Mitochondria and Oxidative Damage

"Extracellular Redox State: Refining the Definition of Oxidative Stress in Aging" suggests that blood glutathione/glutathione disulfide ratio does not equilibrate with blood cysteine/cystine ratio, that the latter is not just a diagnostic but that it affects cell proliferation and oxidant-induced apoptosis, and that both ratios are good controlling indicators of oxidative stress. Or something like that, I haven't done this for a while and seem to have lost the knack. Lots of citations for this one.

"Factors That Might Affect the Allotopic Replacement of a Damaged Mitochondrial DNA-Encoded Protein". Review of successful allotopic expression of mitochondrial genes ported to the nuclear DNA and possible issues with getting those proteins into the inner membrane of the mitochondria. Sounds interesting.

"Can a Single Subunit Yeast NADH Dehydrogenase (Ndi1) Remedy Diseases Caused by Respiratory Complex I Defects?" They introduced NDi1, which transfers electrons from NADH to ubiquinone in yeast, into mammalian cells, some missing Complex 1. NDi1 inserted itself into the inner membrane of mitochondria and rescued the cells that were lacking Complex 1. They got it working on mice muscles and brains. Interesting.

"Protective Efficacy of α-Lipoic Acid on Acetylcholinesterase Activity in Aged Rat Brain Regions". Pumped alpha-lipoic acid into old rats, saw acetylcholinesterase levels restored in some parts of their brain.

"Cytochemical Estimation of Cytochrome Oxidase Activity as a Morphofunctional Mitochondrial Check-Up". They propose that measuring the ratio of cytochemical precipitate to mitochondrial area would give a good indication of mitochondrial function since the ratio decreased by 25% with aging.

"From Disease-Oriented to Aging/Longevity-Oriented Studies". Not sure what this is. Abstract sounds like the general aging IS a disease drive, with a focus on epigenetics, but hard to tell. Quite a few citations.

"Tissue-Specific Effect of Age and Caloric Restriction Diet on Mitochondrial DNA Content". CR reversed the drop in mtDNA in old rat livers and leg muscles, and increased the mtDNA of the brain, even though there is no drop there in ad-libitum rats.

"Testing Mitochondrial Metabolic Competence by Cytochrome Oxidase Preferential Cytochemistry Versus Immunoreactivity of Subunits I and IV". COX activity dropped with age in rats but not levels of two of its subunits.

"Caloric Restriction Protects Mitochondrial Function with Aging in Skeletal and Cardiac Muscles" 25 to 46% drop in oxidative capacity markers for ad-libitum-fed 'animals' (who knows what animals). None for CR. A lot of citations.

"Mitochondrial Genome Anatomy and Species-Specific Lifespan"  Maximum lifespan is correlated with amount of cytosine in the DNA of mammal species, especially for primates. Vaguely interesting.

"Relationship Between Aging and Susceptibility of Erythrocytes to Oxidative Damage: In View of Nutraceutical Interventions". Placebo-controlled study feeding fermented papaya preparation to old people. Rescued abnormal higher concentration of nitric oxide synthase and malondialdehyde (a marker for oxidative stress) in red blood cells of old people compared to young people.

"Aging-Related Cell Surface ECTO-NOX Protein, arNOX, a Preventive Target to Reduce Atherogenic Risk in the Elderly". Cell-surface electron-transport protein associated with aging that can produce superoxide and thus oxidise circulating lipoproteins.


Section 6: Molecular Crosslinking and Aggregation

"Emerging Strategies for the Treatment of Hereditary Metabolic Storage Disorders" looks at solutions other than enzyme replacement for Gaucher and Fabry disease, which are diseases caused by mutations to enzymes that break down the stuff left over when senescent cells die.

"Advanced Atherosclerotic Foam Cell Formation Has Features of an Acquired Lysosomal Storage Disorder". Reviews the evidence for the foam cells in atherosclerosis to be due to an acquired lysosomal storage disorder. That is, the lysosomes are failing to break down what is sent to them so the material acumulates in the cell. Quite a few citations for this one.

"Indirect Antioxidant Protection Against Photooxidative Processes Initiated in Retinal Pigment Epithelial Cells by a Lipofuscin Pigment". Claims lipofuscin A2E triggers oxidation damage in retinal epithelial cells and is protected from this by glutathione and sulforaphane.

"Prevention and Repair of Protein Damage by the Maillard Reaction In Vivo". Equivalence between Maillard recation and advanced glycation end products (AGEs). 20 AGEs in human skin. No evidence of AGE breakers of breaking crosslinks in vivo. Maybe interesting, at least to learn about AGEs.

"Extracellular Glycation Crosslinks: Prospects for Removal". Two proposed methods of getting rid of glucosepane and K2P crosslinks. One is upping extracellular matrix turnover. A second one is high-throughput screening for molecules that can break those two down.


Section 7: Miscellaneous

"Cryopreservation of Complex Systems: The Missing Link in the Regenerative Medicine Supply Chain". On the potential use of vitrification to store organs, created through regenerative medicine, for transplanting when necessary. Claims routine recovery of vitrified rabbit kidneys cooled to -45 degrees celsius functioning properly after rewarming and being transplanted back into rabbits. Found the article. Might write one for it.

"Cryptobiosis, Aging, and Cancer: Yin-Yang Balancing of Signaling Networks". Aging as unbalanced complex signaling pathways.

"The Neurosecretory System Is Hypertrophied in Senescence-Accelerated Mice". Analysis of the neurosecretory system of senescence-accelerated mice.

"Natural Background Radioactive Carbon and the Natural Death Rate of People". Correlation between levels of carbon-14 in the atmosphere and death rates over the last 150 years. Notable mainly because the author's organisation is given as 'independent researcher'. Didn't think that was possible in this century.

"Radiocarbon Mechanism of Aging". More on carbon-14 and death rates by independent researchers, offering a mechanism of aging by carbon-14.

"Variations of Humans' Natural Death Rate and the Radiocarbon Aging Mechanism". More carbon-14 and mortality.

"Statistical Issues of Regression Analysis on Development of an Age-Predictive Equation". Equations to predict age from physical fitness measurements training on 31 Japanese males.

"Soft Strategies for Postponing Aging and Prolonging Human Life". Postponing aging by looking at things that cause discomfort and stopping things from becoming major.

"Psychosocial Aspects and Zinc Status: Is There a Relationship with Successful Aging?". Low albumin, as indicator for zinc, correlated with higher levels of depression in old Italians.

"Liver Exposure to Xenobiotics: The Aging Factor and Potentials for Functional Foods". Study on liver cells from young and old rats cultured with and without alpha-linolenic acid and given YHK (a herbal supplement I'd never heard of) or sylibin. They then gave them copper and iron. YHK did better at some things.

"The Aging Gut Motility Decay: May Symbiotics Be Acting as "Implantable" Biologic Pace-Makers?" Symbiotic (I don't know what that is) SCM-III (also no idea) does something to old rats' colons and jejunum.

"How Evolutionary Thinking Affects People's Ideas About Aging Interventions". From a person that belong to the group that think that aging is an evolutionarily programmed response. Mentions apoptosis and senescence via telomere shortening as behaviours that seem to shorten lifespan. Also, NSAIDs slowing arthritis, cancer and atherosclerosis as evidence for inflammation as programmed autoimmune response.

"Zinc Homeostasis in Aging: Two Elusive Faces of the Same 'Metal'". Aging creates zinc dyshomeostasis, not zinc deficiency.

"Aging and Oral Health Related to Quality of Life in Geriatric Patients". Survey of 53 70-year old Bulgarians regarding reasons they go to the dentist. 32% for acute pain and the rest for caries.

"Is Thrombolytic Therapy Effective in Elderly Patients?". Clinical (single-arm?) study doing thrombolytic therapy on 103 heart attacked people over 75. They say it had a positive effect.

"Negligible Senescence: How Will We Know It When We See It?". Suggests the use of global index of aging rate as units of functional change per time.