"Weight Loss in Obese Men Is Associated with Increased Telomere Length and Decreased Abasic Sites in Rectal Mucosa" by Nathan J. O'Callaghan, Peter M. Clifton, Manny Noakes, and Michael Fenech. One year study putting obese men on CR and making them drop 10kg. Dunno how many men. Telomere length from cells taken from colon biopsies were 10 times longer at the end of the study, and abasic sites in the DNA dropped by two thirds. Initial telomere length was only weakly negatively correlated with BMI so not sure how much this is a "change" effect. The effects sound too big.
"Characteristics of 400-Meter Walk Test Performance and Subsequent Mortality in Older Adults" by Sonja Vestergaard, Kushang V. Patel, Stefania Bandinelli, Luigi Ferrucci, and Jack M. Guralnik. Time to walk 400 metres and its variance were predictors of 6-year mortality in 1000 Italians >65 years old after adjusting for age, sex, MMSE, depression, education, smoking, BMI, sedentarity, disease burden and lower extremity performance (that last one is surprising).
"The Expression of CYP2D22, An Ortholog of Human CYP2D6, in Mouse Striatum and Its Modulation in 1-Methyl 4-Phenyl-1,2,3,6-Tetrahydropyridine-Induced Parkinson's Disease Phenotype and Nicotine-Mediated Neuroprotection" by Seema Singh, Kavita Singh, Devendra Kumar Patel, Chetna Singh, Chandishwar Nath, Vinod Kumar Singh, Raj Kumar Singh, and Mahendra Pratap Singh. Brain stuff.
"Nuclear DNA Damage as a Direct Cause of Aging" by Benjamin P. Best. Trying to build a case for nDNA damage as a cause of aging. Might need to find it and read it...ok. The paper is a collection of correlations between aging and nDNA damage. No claim of causality is made but a call to maybe-look-into-it since SENS dismisses nDNA as non-important outside of cancer and senescence. The paper is hard to summarise since it is almost in point form to begin with.
"Age-Dependent Down-Regulation of Mitochondrial 8-Oxoguanine DNA Glycosylase in SAM-P/8 Mouse Brain and Its Effect on Brain Aging" by Feng Tian, Tan-Jun Tong, Zong-Yu Zhang, Michael A McNutt, and Xin-Wen Liu. They compare mitochondrial 8-Oxoguanine DNA glycosylase (OGG1) expression and COX III expression in the brains of SAM-P/8, an accelerated-aging mouse, and SAM-R/1, its normally-aging counterpart, and find higher downregulation in SAM-P/8. They say this causes imbalances in mtDNA damage repair systems.
"How Is Mutant Mitochondrial DNA Clonally Amplified? Much New Evidence, Still No Answers" by Aubrey D.N.J. de Grey. Some commentary on how recent results affect two theories of clonal expansion of mitochondria with mtDNA mutations: his theory of clonal mitochondrial expansion (mt survive due to low superoxide creation) and another theory that says that mt with mtDNA deletions replicate fastest. Three pieces of new information:
- Clonal expansion in fast-dividing gut stem cells and slow dividing stem cells. Point mutations mostly. Doesn't go with either theory.
- mt with larger deletions replicate faster in mice. Goes nicely with deletion-related theory, but against superoxide-dependent since the size of deletion shouldn't matter
- Protein parkin binds to dysfunctional mt promoting their destruction. Goes against superoxide theory since it predicts the opposite (that mutants will survive). Reasonable attempt at salvaging theory by type of dysfunction in experiment (uncoupled, not respiratory chain malfunction)
The first thesis in the thesis discussion section is about grafts into rat hearts. They try genetically adding a growth factor receptor into the cells-to-be-grafted, and also building 3D grafts consisting of either pure cardiomyocytes and of cardiomyocytes, endothelial cells and fibroblasts.
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