The fingerprints of a mighty creator in Proteomics, impact factor >5

Creationism/intelligent design is not really an issue for me as I am a biologist working with mitochondria and stem cells, also a life extension supporter, whose angle on things and projections are based on the recent advancements in science and technology. As far as I know, creationism/ID neither suggests any new experiments or heuristic solutions in my research field, nor does it help to plan&build new technologies to extend healthy lifespan. From my point of view, thinking about creationism is a waste of valuable scientific/technological processor time.

But I am not used to encounter with explicit creationism and the fingerprints of a mighty creator as an explanatory force behind a natural phenomenon in scientific peer-review journals. That’s exactly what happened to me in a recent review published online by the Wiley journal, Proteomics (ISI Impact Factor 2006: 5.735) by Mohamad Warda and Jin Han, entitled Mitochondria, the missing link between body and soul: Proteomic prospective evidence.

Last week when I wrote the post Can you tell a good article from a bad based on the abstract and the title alone? on the review I had only 10 minutes for figuring out the post between 2 experiments in the lab during lunchtime. The only thing that came into my mind reading the abstract - popped out of PubMed feeds - was that something stinks here. Now it’s Mardi Gras day and I have a couple of minutes more to address this issue and hopefully no more.

Myrmecologist and blogger Alex Wild picked one sentence from the paper in a comment, and here is the complete paragraph:

Alternatively, instead of sinking in a swamp of endless debates about the evolution of mitochondria, it is better to come up with a unified assumption that all living cells undergo a certain degree of convergence or divergence to or from each other to meet their survival in specific habitats. Proteomics data greatly assist this realistic assumption that connects all kinds of life. More logically, the points that show proteomics overlapping between different forms of life are more likely to be interpreted as a reflection of a single common fingerprint initiated by a mighty creator than relying on a single cell that is, in a doubtful way, surprisingly originating all other kinds of life.

This is the closing paragraph of the section Mitochondrial integrated function disproves endosymbiotic hypothesis of mitochondrial evolution. The mitochondrial part of the well established evolutionary endosymbiotic theory claims that ATP-producing mitochondria were ancient prokariotic invaders of host prokariotic cells eventually turned out to be the common ancestors of eukaryotic cells. I always found this hypothesis one of the most fruitful scientific concepts as it constantly suggest new ideas and warns that current eukaryotic cells are the products of an evolutionary, accidental and instable alliance between the mitos and their hosts. As the endosymbiotic theory is the mainstream academic theory of mitochondrial evolution it is a challenge for scientists to attack it with counterarguments and that’s what Warda and Han are aiming for in that section. What they are doing seems like a legitimate discussion of a scientific theory but ends with the logically unacceptable jump to the fingerprints of a mighty creator as an alternative explanation.

Before I cite the section in question in full length and recommend to my readers to analyze it, I also like to suggest the detailed comment of D. Spencer saying amongst others:

If Wiley and the journal Proteomics allow this into print (it is currently only “published” online) they can kiss goodbye to any hope that Proteomics will ever again be regarded as a serious scientific publication.

Here is the complete section by Warda and Han without references that could be found in the full text:

Michael Rose, evolutionary SENS and aging as a loss of adaptation (slides)

Embedded on the slideshow below 9 slides of Michael Rose’s presentation called Slowing and then stopping aging on the SENS3 conference on the 9th of September. (Photos made by me with the iPhone.) Rose’s argument was: Aubrey de Grey’s original SENS proposal is based on the non-evolutionary assumption that aging is a process of accumulating damage, while according to the evolutionary SENS version of Rose aging should be interpreted as a loss of adaption. The script is: breed mice with delayed reproduction over multiple generations (let evolution by natural selection give us the answer of how to build a long-lived animal), and then reverse engineer this answer to develop anti-aging therapies for genetically unaltered humans. The experimental basis of this proposal: Rose’s own ancient experiments with fruit flies (sorry, no reference yet, that’s what I’ve heard) showed that there is a plateau in mortality rates after many generations of breeded Drosophilas with delayed reproduction time which leads to the cessation of the aging process.

Does this method sound as one that gives us a complete engineering toolkit to achieve robust healthy life extension for early generations of humans under the reverse engineered treatment?

Mitochondria, the not so hidden superstars of current life sciences

If one thing is for sure, it is mitochondrion’s ascending career in late biology. Mitochondria are the power centers of the eukariotic cell and eventually tell the nucleus what to do next: die or live. Mitos do not exist stably as distinct, individual, autonomous organelles according to new results, but form a highly dynamic semi-tubular network.

Mitochondria are bacterium size, membrane-bound organelles in the eukaryotic cell and were descended from prokaryotic endosymbionts about two billion years ago.

Mitos are the main energy supplier, the power centers of the eukariotic cell, in the form of ATP, the vast majority of cellular Reactive Oxigen Species (ROS, oxidants), approximately 90% can be traced back to the mitochondria. The main apoptotic signals of programmed cell death come from there, so eventually mitochondria tell the cell (i.e. the nucleus) what to do next: die or live.

In the past decade a new concept of mitochondrial presence and spatial distribution in the host cell was articulated based on microscopy observation, which suggested the fusion and fission of different mitochondria: the mitochondrial network concept. Mitochondria form a highly dynamic semi-tubular network in the cell, the morphology of which is regulated by movements along the cytoskeleton and the balance of mitochondrial fusion and fission events. Recent developments identified some essential protein players in fusion and fission machinery of mitochondria in eukaryotic cells, like GTPases, Mfn1, Mfn2 in fusion and Drp1 in fragmentation. According to the new network mitochondrion concept, mitochondria do not exist stably as distinct, individual, autonomous organelles. Rather, mitochondria form a network within cells; their continous fusion and fission is a highly dynamic process, adapting to the role the mitochondrion actually has in the cell. Increasing results confirm the role of mitochondrial fission and fragmentation in most forms of apoptosis, even as a cause. This suggests that fragmented mitochondria are in a „bad“ condition, under oxidative stress. Conversely, for example fragmentation of mitochondria in hippocampal neurons seems to have a role in the proper function of neuronal protrusions. On the other hand, mitochondrial fusion is thought to have a role in the maintenance of correct mitochondrial function.

So if you ask a cell, what she intends to do, you’d better ask and take a look at her mitochondria first.

In regenerative medicine mitochondria’s role will be much more important as we become more and more familiar with their tricks. In my opinion a whole new and powerful subfield will arise in biomedicine, organellar therapy, which is subcellular (not cell transplantation) and supramolecular (not classical pharmacology).

Picture: (Human stem cell stained with Mitotracker Red, which specifically bind to mitochondria, visualized in a black-and-white retro style. You can see the mitochondrial structure of the cell, mitochondria in an elongated form. Author’s shot.)

Why is partial immortalization theoretically and technologically possible?

There are two main arguments supporting our modal statement:
i., negative: there is not any particular natural law, neither biological, nor physical which excludes this possibility.

ii., positive: we could extrapolate the technological draft of a regeneration treatment of the whole human body from the present results and methods of regenerative medicine.

Concerning the first argument, the impossibility proof of something which is not based on an outright logical contradicition, is very hard. But the argument does not say nothing about the realisation of pimm, it just opens some place in the possibility space. What if opposition considers, that entropy, in the statistical "disorder" sense, could cause a problem, say: the second law of thermodynamics necessarily excludes the possibility of pimm, because the total entropy of the human body increases over time and approaching a maximum value? Now the second law of thermodynamics states that the entropy of an isolated system will tend to increase over time, approaching a maximum value. One point, where this metaphorical counterargument goes wrong is "isolated system". In thermodynamics, an isolated system is a physical system that does not interact with its surroundings. The human body is not an isolated, and not even a closed system, because it can exchange heat, work, i.e. energy and matter with its environment. I am pleased to announce that the human body is an open system.

Another source of objection could be based on evolution, but I discuss the connection between pimm, evolution and ageing later.

The second, positive argument is a macroargument, and the technological part of the pimm book tries to explicate this draft. An assertive quote:

”The promise of scientifically verified immortality has gained credibility with every successful organ transplant.” Frank Pasquale: Two concepts of immortality. Yale Journal of Law & the Humaities

Next: Maximum or radical life extension?

Originally posted at May 4th, 2006, http://attilachordash.wordpress.com/

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