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Replicative senescence…
Is always detrimental to the organism
Causes uncontrolled cell proliferation
Is achieved when cell divisions hit Hayflick limit
Is only encountered in the process of aging
increases individual's fitness
Is achieved when cell divisions hit Hayflick limit
Cellular senescence is involved in the following EXCEPT
inflammation
Tumor promotion
increasing force of selection
Tumor suppression
Aging
increasing force of selection
Normal human cells will divide ______ times before reaching senescence or apoptosis.
More than 200
100-115
40-60
infinite number of times
Less than 15
40-60
Caloric restriction mediates its effect on a lifespan via the following mechanism
metformin
TOR pathway
increased amino acids concentration
ncrease in Hayflick limit
DAF-16
TOR Pathway
TAME trial used metformin, which is the widely prescribed medication for
weight loss
Type I diabetes
Gram-positive infections
Cancer
Type II diabetes
Type II diabetes
Senescent cells
Spontaneously revert to a “young” phenotype
Are “invisible” to the immune system
harbor bacteria promoting infectious disease
Are biochemically inert
Secrete proinflammatory mediators
Secrete proinflammatory mediators
Which statement about Senolytics is incorrect?
can be natural or synthetic
can be found in regular foods
Are experimental
Are widely used in clinical practice
are found in natural products
Are widely used in clinical practice
The ____________ theory proposes: Genes that are beneficial early in life may not be later in life.
expendable soma
Evolutionary theory
Rate of living theory
Mutation theory
Antagonistic Pleiotropy theory
Antagonistic Pleiotropy theory
Insulin resistance is characterized by
Decreased sensitivity of peripheral tissues to insulin
Decreased insulin production
Generalized weight loss
Elevated HDL (high density lipoprotein)
Increased risk of type I diabetes
Decreased sensitivity of peripheral tissues to insulin
aging
progressive decline
age specific
senescence
occurs throughout lifespan
senescent cells
number inc with age
aid in wound healing
relase pro inflamm factors
Mccay theory of caloric restriction in rats
reduction in energy rather than nutrients was responsible for increased longevity
hoped to disprove vitamins
rats with decreased energy/nutrients = didn’t live long
restriction worked better in M
what did barton observed about yeast cells
they can die
replicative aging
number of times a cell can divide to produce a daughter
Medawar theories
father of transplantation
discovered acquired immunity
endocrine theory
new uses of “old” hormones
why has evolution allowed senesce
senescent cells are “old”
when an org is done reproducing what happens to it “doesn’t matter”
selection shadow… deleterious mutation show up late in life. these mutations are not “seen” by natural selection
antagonistic pleiotropy
trade off
higher reproducitivty but shorter life span
Hayflick theory
normal human cells can divide a limited amount of times
GRIM reaper genes
AGE 1
DAF 2
Sir 2
TOR pathway
TOR= sensor for how many amino acids are available
high amino acids = grow
what cells are “good citizens but bad neighbors”
senescent cells
Francesci theory
chronic inflammation → early death
TAME trial
metformin (T2D treatment) and placebo
M/F ages 65-90 with age released diseases
does metformin aid in age releated diseases?
Metformin in mice
makes mice life longer and look healthier
senolytics
destroy senescent cells
ex: fisetin, curcumin
Senolytics in cancer
curcumin = induce senescence (cancer→ senescent cells)9
fisetin= destroy senescent cells
lifespan vs healthspan
lifespan= how long you live
healthspan= how long you stay healthy