Aha! Interesting

(May 22, 2015 at 6:52 pm)francismjenkins Wrote: ...

haha ... well, couldn't figure out how to delete a post (although it's easy to edit a post). Maybe I missed something (I am a newbe after all)

Exactly how did something come from nothing across the inorganic/organic divide?

What's your thoughts on teleomerose (spelling?) Production into late life stages in lobsters? Can this be an applicable avenue of research?

(May 23, 2015 at 4:36 pm)whateverist Wrote: Exactly how did something come from nothing across the inorganic/organic divide?

Come from nothing across organic/inorganic divide?

You mean chemical compound containing carbon came from absolutly nothing?

Hey, I was going for dramatic effect. Jeez.

But let me be more specific. What's the best thinking say about how organic molecules become a critter? Are there any critters nowadays whose status fluctuates between being a critter and a compound? Maybe something like a prion?

(May 23, 2015 at 4:51 pm)Lemonvariable72 Wrote: What's your thoughts on teleomerose (spelling?) Production into late life stages in lobsters? Can this be an applicable avenue of research?

In human cells, proteins involved in DNA damage repair are localized at the telomere region of the chromosome (e.g. specific binding of the six sub-unit protein complex shelterin to the telomeric repeat sequence TTAGGG). Our telomere are shorted with each cell division, and eventually, depletion reaches a critical point where it triggers the DNA damage response and replicative senescence (the cell is no longer able to divide). It also influences other cell signaling pathways. So for example, senescent cells are thought to drive human aging through the secretion of inflammatory factors, and eventually mitochondrial DNA (mDNA) damage, induces apoptosis (cell death).
 
Lobsters do not age in the way humans age (age does not increase chances of death at all in lobsters), and yes, they do retain telomere length throughout their lives. However, this is because cells in lobsters express telomerase (an enzyme which can restore telomere length). The problem is, in humans, while telomerase could perform the same function, it's also implicated in virtually all forms of cancer.

However, there's much better research on telomeres these days e.g. a recent study conducted at Stamford was able to deliver modified mRNA, which encodes a telomere extending protein to human cells, and cell proliferation capacity increased dramatically, essentially turning back the aging clock in transfected cells. This research shows a pathway to overcome the traditional problem with telomere lengthening strategies (which usually rely on introduction of telomerase). 
 
https://med.stanford.edu/news/all-news/2015/01/telomere-extension-turns-back-aging-clock-in-cultured-cells.html
 
The above link is to an article discussing the study (the study itself was published in the FASEB Journal, but you have to pay for access). The potential here is remarkable, because this research demonstrates the possibility of dissociating concerns related to inducing oncogenesis from life extension strategies involving telomere extension. 
 

(May 23, 2015 at 6:30 pm)francismjenkins Wrote:

(May 23, 2015 at 4:51 pm)Lemonvariable72 Wrote: What's your thoughts on teleomerose (spelling?) Production into late life stages in lobsters? Can this be an applicable avenue of research?

In human cells, proteins involved in DNA damage repair are localized at the telomere region of the chromosome (e.g. specific binding of the six sub-unit protein complex shelterin to the telomeric repeat sequence TTAGGG). Our telomere are shorted with each cell division, and eventually, depletion reaches a critical point where it triggers the DNA damage response and replicative senescence (the cell is no longer able to divide). It also influences other cell signaling pathways. 

So for example, senescent cells are thought to drive human aging through the secretion of inflammatory factors, and eventually mitochondrial DNA (mDNA) damage, induces apoptosis (cell death).

Lobsters do not age in the way humans age. In fact, age (in lobsters) does not increase chances of death at all, and yes, they retain telomere length throughout their lives. However, this is because cells in lobsters express telomerase (an enzyme which can restore telomere length). In humans, while telomerase could perform the same function, it's also implicated in virtually all forms of cancer. In other words, inducing telomerase expression in humans would trigger aggressive cancers.  

However, there's much better research on telomeres these days e.g. a recent study conducted at Stamford was able to deliver modified mRNA, which encodes a telomere extending protein to human cells, and cell proliferation capacity increased dramatically, essentially turning back the aging clock in transfected cells. This research shows a pathway to overcome the traditional problem with telomere lengthening strategies (which usually rely on introduction of telomerase). 

https://med.stanford.edu/news/all-news/2...cells.html

The above link is to an article discussing the study (the study itself was published in the FASEB Journal, but you have to pay for access). The potential here is remarkable, because this research demonstrates the possibility of dissociating concerns related to inducing oncogenesis from life extension strategies involving telomere extension. 

Omg that is cool!

I should elaborate a bit more. The TERT gene encodes for one of the proteins in the telomerase enzyme complex (telomerase has several subunits, an RNA subunit, TERC, a protein subunit, TERT, and dyskerin or DKC1). In the above mentioned research, a modified mRNA** that encodes for TERT was used to extend telomere. But the important difference is rather than completely restoring telomere, it only adds about 1,000 nucleotides (which increases replicative capacity by up to ~40 additional cell divisions), and then TERT meets the fate of most other proteins, proteolysis (degradation). So while this treatment can (in theory) be readministered, it doesn't create the sort of permanent change in cells that can lead to cancer formation (at least hypothetically). 

**mRNA are "messenger" RNA (ribonucleic acid) involved in the translation of proteins, which work in cooperation with ribosomes.

(May 23, 2015 at 7:15 pm)francismjenkins Wrote: I should elaborate a bit more. The TERT gene encodes for one of the proteins in the telomerase enzyme complex (telomerase has several subunits, an RNA subunit, TERC, a protein subunit, TERT, and dyskerin or DKC1). In the above mentioned research, a modified mRNA** that encodes for TERT was used to extend telomere. But the important difference is rather than completely restoring telomere, it only adds about 1,000 nucleotides (which increases replicative capacity by up to ~40 additional cell divisions), and then TERT meets the fate of most other proteins, proteolysis (degradation). So while this treatment can (in theory) be readministered, it doesn't create the sort of permanent change in cells that can lead to cancer formation (at least hypothetically). 

**mRNA are "messenger" RNA (ribonucleic acid) involved in the translation of proteins, which work in cooperation with ribosomes.

I can still think of plenty of uses for it treatment wise. Such as staving off dementia in the elderly or as they mention in the article muscular dystrophy