List of aging-relevant bionumbers/basic units

  • The amount of lysosomal lipofuscin was significantly higher (6-fold) in cell bodies of aged neurons (28
  • Moreover, we observed a drastic reduction in doublecortin expression, a neuronal precursor marker, from 14 to 28 DIV, as described previously
  • John Wentworth and CANanonymity@fightaging also have good lists

I really mitoSENS solves ATP loss with aging due to oxidized redox cell environment.

From 0 tp 40 years old, the plasma redox is roughly -140 mV, then +7 mv/decade rise, until at 70-85 years old, it is -110 mV.
At that high mV current the cell is a continuous oxidative stress state. It is why humans end up dying at 122 years old MLSP.

Lipofuscin granules, which range between 1 and 3 μm in diameter, appear as brownish particles in neuronal cytoplasm and are probably indigestible residues of lysosomes materials

33% of human proteins have four consecutive positive charged amino acids.


for GENERAL bionumbers, see Rob Phillip, Sara Walker, ppl tha Gaurav follow

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The protein concentration in our cells is ~ 200 mg / ml.

bionumbers claims 9%-22% of cellular protein is ribosomal, so multiplying through that would be ~5-10% of energy

That is to say, despite the thousands of noncovalent interactions existing in the structures of folded proteins [27], they are merely 5 to 15 kcal/mol more stable than the unfolded chain [28–30]. For comparison, the dissociation of a single covalent bond requires ~65 to 175 kcal/mol [3]. The low stability of proteins can be explained in two ways. First, even in the lower stability limit (−5 kcal/mol) the folded state is over 99.9% occupied

timescales of motions in proteins

The pK a values of cysteine residues are of critical importance in redox-regulated processes. At physiological pH, the pK a values of protein cysteine thiols vary from 8.2 to 9.9 for solvent-accessible cysteines and therefore have low deprotonation ability [47]. Cysteine thiols within a basic three-dimensional environment (low pK a) are more susceptible to deprotonation and oxidation to sulfenic acid in the presence of ROS

Cytoplasmic and nuclear NAD+/NADH ratios are typically maintained between 60 and 700 in eukaryotes depending on cell type, while the mitochondrial ratio is much lower, around 7–8 (Veech et al., 1972, Williamson et al., 1967, Zhang et al., 2002). Additionally, mitochondria contain a large proportion of cellular NAD+, with estimates ranging from 40%–70% of the total cellular NAD+ pool (Alano et al., 2007, Di Lisa et al., 2001, Tischler et al., 1977).

Due to its low redox potential, guanine is the most vulnerable nucleobase to oxidation. The dominant product of guanine oxidation is 8-hydroydeoxy-guanosine (8-OH-dG) and is, therefore, used as a cellular biomarker of oxidative stress

micronucleus frequency

urinary 1-hydroxypyrene (1-OHP)

Crypts from individuals with POLE L424V showed an average SBS mutation rate of 331 per year (linear mixed-effects model 95% confidence interval (CI) 259–403, P = 10−12) (Fig. 1a,b and Supplementary Note). The POLD1 S478N germline mutations were associated with an SBS rate of 152 per year (linear mixed-effects model 95% CI 128–176*, P* = 10−17), and POLD1 D316N and L474P were associated with an SBS rate of 58 per year (linear mixed-effects model 95% CI 51–65*, P* = 10−22). By comparison, intestinal crypts from healthy individuals acquire 49 SBS per year28 (linear mixed-effects model 95% CI 46–52, P = 10−36). Therefore increased somatic SBS rates are present in all normal intestinal cells of individuals with POLE or POLD1 germline mutations (Fig. 1), although there are differences in mutation rates between POLE (~sevenfold higher than normal individuals) and POLD1 (up to threefold higher) germline mutations, and between different POLD1 mutations

Scientists already knew that occasionally the cell’s protein-building machinery fails to stop where it should. When the machinery doesn’t stop — a phenomenon called readthrough — it creates extended forms of proteins that sometimes function differently than the regular forms.

Cells are highly crowded, with macromolecular concentrations estimated to be between 80 and 400 mg/mL (Cayley et al., 1991; Zimmerman and Trach, 1991). Macromolecular crowding retards diffusion, influences protein volume and association equilibria (Dix and Verkman, 2008; Ellis, 2001; Zhou et al., 2008), including, for example condensate formation in vitro and in vivo (Delarue et al., 2018; Woodruff et al., 2017). These effects are caused by steric exclusion, next to weak chemical interactions (Gnutt and Ebbinghaus, 2016; Rivas and Minton, 2016; Sarkar et al., 2013), and depend on the concentration, size, and shape of the molecules involved and are larger when crowders are smaller sized than the reacting molecule (Marenduzzo et al., 2006; Rivas and Minton, 2016). For example, an increased number of ribosomes slows down diffusion of 20 nm and 40 nm particles, but not average-sized proteins

Charles Brenner, PhD


something like 1 in a million fibroblasts treated w yamanaka factors become iPSCs lots die, others become weird stuff or stay fibroblasts some become tumors & teratomas skilled ppl clone out the iPSCs in vitro in vivo reprogramming is unlikely to be ever tested in ppl