Man vs. Bacterium
A human cell can be divided only 50 times or so.
When this limit is reached, a cell dies. If many of cells of the human body die, a man will get old. And, the mechanism of this limited cell division capability is governed by the characteristics of the Telomere, the end parts of a DNA sequence. Each time a cell is divided, the length of a Telomere gets shorter. After 50 times of division, a Telomere gets too short to protect the main body of DNA, and a cell holding the DNA and the Telomere is forced to avoid using broken DNA so as to die eventually. It is to secure soundness of DNA and genes to be handed down to new cells created through cell division. But, there is something that can recover a Telomere, which is called Telomerase.
How Telomerase makes a telomere longer.
http://www.mls.sci.hiroshima-u.ac.jp/smg/education/telomere.html
This is the reason why telomeres are so important in context of successful cell division: They "cap" the end-sequences and themselves get lost in the process of DNA replication. But the cell has an enzyme called telomerase, which carries out the task of adding repetitive nucleotide sequences to the ends of the DNA. Telomerase, thus, "replenishes" the telomere "cap" of the DNA. In most multicellular eukaryotic organisms, telomerase is active only in germ cells, stem cells, and certain white blood cells. There are theories that claim that the steady shortening of telomeres with each replication in somatic (body) cells may have a role in senescence and in the prevention of cancer. This is because the telomeres act as a sort of time-delay "fuse", eventually running out after a certain number of cell divisions and resulting in the eventual loss of vital genetic information from the cell's chromosome with future divisions....
Since shorter telomeres are thought to be a cause of poorer health and aging, this raises the question of why longer telomeres are not selected for to ameliorate these effects. A prominent explanation suggests that inheriting longer telomeres would cause increased cancer rates (e.g. Weinstein and Ciszek, 2002). However, a recent literature review and analysis [13] suggests this is unlikely, because shorter telomeres and telomerase inactivation is more often associated with increased cancer rates, and the mortality from cancer occurs late in life when the force of natural selection is very low. An alternative explanation to the hypothesis that long telomeres are selected against due to their cancer promoting effects is the "thrifty telomere" hypothesis that suggests that the cellular proliferation effects of longer telomeres causes increased energy expenditures.[13] In environments of energetic limitation, shorter telomeres might be an energy sparing mechanism.
http://en.wikipedia.org/wiki/Telomere
On the other hand, a bacterium has no telomeres as its DNA has a shape of a loop. This single-cell creature can live forever while splitting itself as many times as possible in theory. No matter how many times it is divided into two, no deterioration of DNA information occurs.
Some cells of a multicellular animal or plant have a mechanism to commit a suicide for survival as a whole body. They go on growing or living while discarding unnecessary cells by forcing them to kill themselves. But, single-cell bacteria do not have the same mechanism, since they have each only one cell. To kill itself is to kill a whole body. Yet, it can kill itself.
When a myriad of bacteria get together and live like a big living thing, there is a situation that it is advantageous for a great majority of bacteria that some bacteria die or disappear. In this case, a special signal is sent from some bacterium to other member of a group which kills itself on receiving the signal.
How does EDF work? It mimics a portion of the MazE sequence important for its binding to MazF, especially with regard to the central tryptophan that corresponds to a critical tryptophan in MazE. The parallel interaction of EDF-MazF and MazE MazF awaits structural analysis of the EDF-MazF complex. But matters are more intricate, as seen by the presence of two binding sites on MazF for mRNA. This paper explains much of it, plus it introduces another toxin, ChpBK, that has equally tantalizing properties.
Added to the magic of EDF is the fact that it acts as a quorum sensing signal, meaning that it comes into play at high bacterial densities where interactions between cells become especially relevant . But the MazF protein also has unusual properties: It regulates the synthesis of both “death proteins and “survival proteins,” thus playing the role of a master regulator. This leads not only to the death of some members of the population but to the survival of the others. Neat or what?http://schaechter.asmblog.org/schaechter/2011/04/coping-with-hard-times-death-as-an-option.html
Even in the world of bacteria survival of a whole group counts more than one of its members. Maybe in a rare case death of one bacterium saves the whole group.
In this context, the death of Christ Jesus might be thought of. To save the whole group of human beings he died. But, "save" is not a simple act with a single meaning. Anyway, in the world of living things, every live living thing owes deaths and a myriad of deaths that have been performed and accumulated since the beginning of history of creatures.
(To be continued...)
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A showdown has come around Wall Street, far before Christmas.
Bloomberg defends raid on Occupy camp
By Tina Susman | 4:50 a.m.
"Protesters have had two months to occupy the park .... Now they will have to occupy the space with the power of their arguments," the New York mayor says. Full coverage
- NYPD arrests 70 Occupy protesters
- New York police evict Occupy protesters
- Oakland site cleared, but protest lives
http://latimesblogs.latimes.com/nationnow/2011/11/new-york-mayor-bloomberg-occupy-wall-street-zuccotti-park.html
Almost all the Japanese TV stations broadcast this situation. However, nobody thinks that this loose movement would change America drastically. Yet, it is Occupy Wall Street that emerged as if taking over the symbolic position of the era of the late Steve Jobs.
Maybe it implies that no more IT heroes will appear in the US; but the era of popular and social movement has come. It might match Japan's lost decade which has led to long-time deflation. Japan has suffered deflation due to too much use of cheap labor force in China. But it is globalization driven by the IT development that forced Japanese makers to use low-paid Chinese workers and reduce costs. The same dynamics have fostered unemployment in the US. It is deeply rooted in the global economic structure involving China and India both of which have hundreds of millions of work force.
In either case, this Occupy Wall Street movement must have a deep, obscure but decisive influence on the 2012 Presidential Election, though.
Joh 11:12 Then said his disciples, Lord, if he sleep, he shall do well.
Joh 11:13 Howbeit Jesus spake of his death: but they thought that he had spoken of taking of rest in sleep.
Joh 11:14 Then said Jesus unto them plainly, Lazarus is dead.
Joh 11:15 And I am glad for your sakes that I was not there, to the intent ye may believe; nevertheless let us go unto him.
Joh 11:16 Then said Thomas, which is called Didymus, unto his fellowdisciples, Let us also go, that we may die with him.
Joh 11:17 Then when Jesus came, he found that he had lain in the grave four days already.
Joh 11:18 Now Bethany was nigh unto Jerusalem, about fifteen furlongs off:
Joh 11:19 And many of the Jews came to Martha and Mary, to comfort them concerning their brother.
Joh 11:20 Then Martha, as soon as she heard that Jesus was coming, went and met him: but Mary sat still in the house.
Joh 11:21 Then said Martha unto Jesus, Lord, if thou hadst been here, my brother had not died.
Joh 11:22 But I know, that even now, whatsoever thou wilt ask of God, God will give it thee.
Joh 11:23 Jesus saith unto her, Thy brother shall rise again.