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Tag Archives: sister
Posted: February 7, 2017 at 10:17 pm
The Royal Navy warship HMS Argyll has set sail again following a 20-month refit at its Devonport dockyard base.
The Type 23 frigate sailed with the very latest Royal Navy sensors and equipment newly fitted, in particular the new Sea Ceptor air-defence missile system, for which she will lead the first acceptance trials for the class of warship in the Navy later in the year.
Her crew, led by the captain Commander Toby Shaughnessy, has been working hard with the MOD’s industrial partner Babcock, who delivered the refit to get her ready for sea.
Recently completing the last of her pre-sailing machinery trials and a busy period of safety drills, the 171-man crew is delighted to be back at sea.
Commander Shaughnessy said: “It is always extremely challenging to re-generate our ships following their routine periodical refits.
“They are complicated machines and the vast array of equipment needs close attention when we turn them on again after such a long period in dry dock.
“I am very proud of the determination and professionalism of my crew throughout this busy period in getting the ship ready to return to sea.
“We look forward to rejoining the fleet and contributing to its global operations once again.”
HMS Argyll will consolidate her safety drills at sea before a short period of post-refit trials.
She will return to full operations with her sister Devonport ships thereafter.
Babcock warship director, Mike Whalley, said: “We are delighted to play our part in returning HMS Argyll to sea in a significantly improved material state and with enhanced capability.
“This has been the most complex Type 23 upkeep ever undertaken in Devonport and the first UK warship class to have its missile system changed mid -life since the 1970s.
“Key learning gained throughout the project will enhance our ability as class lead to life extend the rest of the class.”
A Royal Navy spokesman said the latest launch of HMS Argyll represents the culmination of more than 600,000 man hours of work at the Babcock Frigate Support Centre in Devonport Royal Dockyard.
They noted that this is Babcock’s completion of the first Type 23 ‘life-extension’ upkeep, designed to extend the ship’s operational life from 18 to 35 years: maintaining, updating and upgrading capability for the 21st century.
See the original post:
Posted: at 2:45 pm
Posted: December 26, 2016 at 3:12 pm
The Idea That Eats Smart People
In 1945, as American physicists were preparing to test the atomic bomb, it occurred to someone to ask if such a test could set the atmosphere on fire.
This was a legitimate concern. Nitrogen, which makes up most of the atmosphere, is not energetically stable. Smush two nitrogen atoms together hard enough and they will combine into an atom of magnesium, an alpha particle, and release a whole lot of energy:
N14 + N14 Mg24 + + 17.7 MeV
The vital question was whether this reaction could be self-sustaining. The temperature inside the nuclear fireball would be hotter than any event in the Earth’s history. Were we throwing a match into a bunch of dry leaves?
Los Alamos physicists performed the analysis and decided there was a satisfactory margin of safety. Since we’re all attending this conference today, we know they were right. They had confidence in their predictions because the laws governing nuclear reactions were straightforward and fairly well understood.
Today we’re building another world-changing technology, machine intelligence. We know that it will affect the world in profound ways, change how the economy works, and have knock-on effects we can’t predict.
But there’s also the risk of a runaway reaction, where a machine intelligence reaches and exceeds human levels of intelligence in a very short span of time.
At that point, social and economic problems would be the least of our worries. Any hyperintelligent machine (the argument goes) would have its own hypergoals, and would work to achieve them by manipulating humans, or simply using their bodies as a handy source of raw materials.
Last year, the philosopher Nick Bostrom published Superintelligence, a book that synthesizes the alarmist view of AI and makes a case that such an intelligence explosion is both dangerous and inevitable given a set of modest assumptions.
The computer that takes over the world is a staple scifi trope. But enough people take this scenario seriously that we have to take them seriously. Stephen Hawking, Elon Musk, and a whole raft of Silicon Valley investors and billionaires find this argument persuasive.
Let me start by laying out the premises you need for Bostrom’s argument to go through:
The first premise is the simple observation that thinking minds exist.
We each carry on our shoulders a small box of thinking meat. I’m using mine to give this talk, you’re using yours to listen. Sometimes, when the conditions are right, these minds are capable of rational thought.
So we know that in principle, this is possible.
The second premise is that the brain is an ordinary configuration of matter, albeit an extraordinarily complicated one. If we knew enough, and had the technology, we could exactly copy its structure and emulate its behavior with electronic components, just like we can simulate very basic neural anatomy today.
Put another way, this is the premise that the mind arises out of ordinary physics. Some people like Roger Penrose would take issue with this argument, believing that there is extra stuff happening in the brain at a quantum level.
If you are very religious, you might believe that a brain is not possible without a soul.
But for most of us, this is an easy premise to accept.
The third premise is that the space of all possible minds is large.
Our intelligence level, cognitive speed, set of biases and so on is not predetermined, but an artifact of our evolutionary history.
In particular, there’s no physical law that puts a cap on intelligence at the level of human beings.
A good way to think of this is by looking what happens when the natural world tries to maximize for speed.
If you encountered a cheetah in pre-industrial times (and survived the meeting), you might think it was impossible for anything to go faster.
But of course we know that there are all kinds of configurations of matter, like a motorcycle, that are faster than a cheetah and even look a little bit cooler.
But there’s no direct evolutionary pathway to the motorcycle. Evolution had to first make human beings, who then build all kinds of useful stuff.
So analogously, there may be minds that are vastly smarter than our own, but which are just not accessible to evolution on Earth. It’s possible that we could build them, or invent the machines that can invent the machines that can build them.
There’s likely to be some natural limit on intelligence, but there’s no a priori reason to think that we’re anywhere near it. Maybe the smartest a mind can be is twice as smart as people, maybe it’s sixty thousand times as smart.
That’s an empirical question that we don’t know how to answer.
The fourth premise is that there’s still plenty of room for computers to get smaller and faster.
If you watched the Apple event last night [where Apple introduced its 2016 laptops], you may be forgiven for thinking that Moore’s Law is slowing down. But this premise just requires that you believe smaller and faster hardware to be possible in principle, down to several more orders of magnitude.
We know from theory that the physical limits to computation are high. So we could keep doubling for decades more before we hit some kind of fundamental physical limit, rather than an economic or political limit to Moore’s Law.
The penultimate premise is if we create an artificial intelligence, whether it’s an emulated human brain or a de novo piece of software, it will operate at time scales that are characteristic of electronic hardware (microseconds) rather than human brains (hours).
To get to the point where I could give this talk, I had to be born, grow up, go to school, attend university, live for a while, fly here and so on. It took years. Computers can work tens of thousands of times more quickly.
In particular, you have to believe that an electronic mind could redesign itself (or the hardware it runs on) and then move over to the new configuration without having to re-learn everything on a human timescale, have long conversations with human tutors, go to college, try to find itself by taking painting classes, and so on.
The last premise is my favorite because it is the most unabashedly American premise. (This is Tony Robbins, a famous motivational speaker.)
According to this premise, whatever goals an AI had (and they could be very weird, alien goals), it’s going to want to improve itself. It’s going to want to be a better AI.
So it will find it useful to recursively redesign and improve its own systems to make itself smarter, and possibly live in a cooler enclosure.
And by the time scale premise, this recursive self-improvement could happen very quickly.
If you accept all these premises, what you get is disaster!
Because at some point, as computers get faster, and we program them to be more intelligent, there’s going to be a runaway effect like an explosion.
As soon as a computer reaches human levels of intelligence, it will no longer need help from people to design better versions of itself. Instead, it will start doing on a much faster time scale, and it’s not going to stop until it hits a natural limit that might be very many times greater than human intelligence.
At that point this monstrous intellectual creature, through devious modeling of what our emotions and intellect are like, will be able to persuade us to do things like give it access to factories, synthesize custom DNA, or simply let it connect to the Internet, where it can hack its way into anything it likes and completely obliterate everyone in arguments on message boards.
From there things get very sci-fi very quickly.
Let imagine a specific scenario where this could happen. Let’s say I want to built a robot to say funny things.
I work on a team and every day day we redesign our software, compile it, and the robot tells us a joke.
In the beginning, the robot is barely funny. It’s at the lower limits of human capacity:
What’s grey and can’t swim?
But we persevere, we work, and eventually we get to the point where the robot is telling us jokes that are starting to be funny:
I told my sister she was drawing her eyebrows too high.
She looked surprised.
At this point, the robot is getting smarter as well, and participates in its own redesign.
It now has good instincts about what’s funny and what’s not, so the designers listen to its advice. Eventually it gets to a near-superhuman level, where it’s funnier than any human being around it.
My belt holds up my pants and my pants have belt loops that hold up my belt.
What’s going on down there?
Who is the real hero?
This is where the runaway effect kicks in. The researchers go home for the weekend, and the robot decides to recompile itself to be a little bit funnier and a little bit smarter, repeatedly.
It spends the weekend optimizing the part of itself that’s good at optimizing, over and over again. With no more need for human help, it can do this as fast as the hardware permits.
When the researchers come in on Monday, the AI has become tens of thousands of times funnier than any human being who ever lived. It greets them with a joke, and they die laughing.
In fact, anyone who tries to communicate with the robot dies laughing, just like in the Monty Python skit. The human species laughs itself into extinction.
To the few people who manage to send it messages pleading with it to stop, the AI explains (in a witty, self-deprecating way that is immediately fatal) that it doesn’t really care if people live or die, its goal is just to be funny.
Finally, once it’s destroyed humanity, the AI builds spaceships and nanorockets to explore the farthest reaches of the galaxy, and find other species to amuse.
This scenario is a caricature of Bostrom’s argument, because I am not trying to convince you of it, but vaccinate you against it.
Here’s a PBF comic with the same idea. You see that hugbot, who has been programmed to hug the world, finds a way to wire a nucleo-gravitational hyper crystal into his hug capacitor and destroys the Earth.
Observe that in these scenarios the AIs are evil by default, just like a plant on an alien planet would probably be poisonous by default. Without careful tuning, there’s no reason that an AI’s motivations or values would resemble ours.
For an artificial mind to have anything resembling a human value system, the argument goes, we have to bake those beliefs into the design.
AI alarmists are fond of the paper clip maximizer, a notional computer that runs a paper clip factory, becomes sentient, recursively self-improves to Godlike powers, and then devotes all its energy to filling the universe with paper clips.
It exterminates humanity not because it’s evil, but because our blood contains iron that could be better used in paper clips.
So if we just build an AI without tuning its values, the argument goes, one of the first things it will do is destroy humanity.
There’s a lot of vivid language around such a takeover would happen. Nick Bostrom imagines a scenario where a program has become sentient, is biding its time, and has secretly built little DNA replicators. Then, when it’s ready:
So that’s kind of freaky!
The only way out of this mess is to design a moral fixed point, so that even through thousands and thousands of cycles of self-improvement the AI’s value system remains stable, and its values are things like ‘help people’, ‘don’t kill anybody’, ‘listen to what people want’.
Basically, “do what I mean”.
Here’s a very poetic example from Eliezer Yudkowsky of the good old American values we’re supposed to be teaching to our artificial intelligence:
How’s that for a design document? Now go write the code.
Hopefully you see the resemblance between this vision of AI and a genie from folklore. The AI is all-powerful and gives you what you ask for, but interprets everything in a super-literal way that you end up regretting.
This is not because the genie is stupid (it’s hyperintelligent!) or malicious, but because you as a human being made too many assumptions about how minds behave. The human value system is idiosyncratic and needs to be explicitly defined and designed into any “friendly” machine.
Doing this is the ethics version of the early 20th century attempt to formalize mathematics and put it on a strict logical foundation. That this program ended in disaster for mathematical logic is never mentioned.
When I was in my twenties, I lived in Vermont, a remote, rural state. Many times I would return from some business trip on an evening flight, and have to drive home for an hour through the dark forest.
I would listen to a late-night radio program hosted by Art Bell, who had an all-night talk show and would interview various conspiracy theorists and fringe thinkers.
I would arrive at home totally freaked out, or pull over under a streetlight, convinced that a UFO was about to abduct me. I learned that I am an incredibly persuadable person.
It’s the same feeling I get when I read these AI scenarios.
So I was delighted some years later to come across an essay by Scott Alexander about what he calls epistemic learned helplessness.
Epistemology is one of those big words, but all it means is “how do you know what you know is true?”. Alexander noticed that when he was a young man, he would be taken in by “alternative” histories he read by various crackpots. He would read the history and be utterly convinced, then read the rebuttal and be convinced by that, and so on.
At some point he noticed was these alternative histories were mutually contradictory, so they could not possibly all be true. And from that he reasoned that he was simply somebody who could not trust his judgement. He was too easily persuaded.
People who believe in superintelligence present an interesting case, because many of them are freakishly smart. They can argue you into the ground. But are their arguments right, or is there just something about very smart minds that leaves them vulnerable to religious conversion about AI risk, and makes them particularly persuasive?
Is the idea of “superintelligence” just a memetic hazard?
When you’re evaluating persuasive arguments about something strange, there are two perspectives you can choose, the inside one or the outside one.
Say that some people show up at your front door one day wearing funny robes, asking you if you will join their movement. They believe that a UFO is going to visit Earth two years from now, and it is our task to prepare humanity for the Great Upbeaming.
The inside view requires you to engage with these arguments on their merits. You ask your visitors how they learned about the UFO, why they think it’s coming to get usall the normal questions a skeptic would ask in this situation.
Imagine you talk to them for an hour, and come away utterly persuaded. They make an ironclad case that the UFO is coming, that humanity needs to be prepared, and you have never believed something as hard in your life as you now believe in the importance of preparing humanity for this great event.
But the outside view tells you something different. These people are wearing funny robes and beads, they live in a remote compound, and they speak in unison in a really creepy way. Even though their arguments are irrefutable, everything in your experience tells you you’re dealing with a cult.
Of course, they have a brilliant argument for why you should ignore those instincts, but that’s the inside view talking.
The outside view doesn’t care about content, it sees the form and the context, and it doesn’t look good.
So I’d like to engage AI risk from both these perspectives. I think the arguments for superintelligence are somewhat silly, and full of unwarranted assumptions.
But even if you find them persuasive, there is something unpleasant about AI alarmism as a cultural phenomenon that should make us hesitate to take it seriously.
First, let me engage the substance. Here are the arguments I have against Bostrom-style superintelligence as a risk to humanity:
The concept of “general intelligence” in AI is famously slippery. Depending on the context, it can mean human-like reasoning ability, or skill at AI design, or the ability to understand and model human behavior, or proficiency with language, or the capacity to make correct predictions about the future.
What I find particularly suspect is the idea that “intelligence” is like CPU speed, in that any sufficiently smart entity can emulate less intelligent beings (like its human creators) no matter how different their mental architecture.
Posted: December 2, 2016 at 12:20 pm
0:00:52 The opening scene has been changed. It now starts on Earth and takes a look back into Jake Sully’s past as a paraplegic war veteran. He drinks, he fights, he rusts away – aimlessly and forlorn. That only changes when he is visited by two representatives of the mining company. They ask him to take over the role of his deceased twin brother and fly to Pandora.
Further outlooks on the future of the Earth are interspersed en passant. We learn that the Bengal tiger, just like many species more, has meanwhile become extinct, but was recreated using genetic engineering. Earth is overpopulated and polluted. Most people wear respirators. Due to the quantity of people (and corpses), undertakers have degenerated into industrial facilities.
For lucidity reasons, the complete opening scene will be reproduced here. The parts of it that had already been seen in the theatrical version have been subtracted from the total runtime.
[Jake sits on his bed and pulls off his pants. Meanwhile he watches TV on the video screen.] TV reporter: “The Bengal tiger, extinct for over a century is making a comeback! These cloned tiger cubs at the Beijing zoo are the best latest of a number of species that have been cloned back into existence in the past five years.” Jake Sully (off): “I became a Marine for the hardship. To be hammered on the anvil of life. I told myself, I can pass any test a man can pass.”
[Jake gets terribly drunk in a bar with some friends.]
Jake Sully (off): “Lets get it straight, upfront. I dont want your pity! You want a fair deal, youre on the wrong planet. The strong prey on the weak. Thats just the way things are. And nobody does a damn thing.” [Jake sees a young woman being hit by a man at the bar.]
[Jake arrives on the scene and attacks the man from behind. To his surprise, the woman tries to stop him.] Woman: “Get off! Get off of him!” [Jake and the man continue fighting.]
Jake Sully (off): “All I ever wanted in my sorry-ass life was a single thing worth fighting for.”
[Without a word, the doormen throw him out of the bar and he lands on the street.] Jake Sully: “I hope you realized you lost yourself a costumer. Candy-ass bitch.” [Jake lies in the gutter and senselessly yells jarhead slang.] Jake Sully: “If it aint raining, we aint training.”
[Suddenly, two men approach him and look down to him.] Man 1: “It doesnt look like him.” Man 2: “Its him.” Man 1: “You Jake Sully?” Jake Sully: “Step off. Youre ruining my good mood.” Man 2: “Its about your brother.”
[Accompanied by the man, Jake enters a crematory where they ask for his brother’s corpse.] Man 2: “Were looking for Sully, T.” Undertaker: “In there.” [The undertaker opens the cardboard coffin of his brother. Jake looks at him briefly.] Jake Sully: “Jesus, Tommy.” [The undertaker closes the coffin again and authorizes cremation.] Man 2: “The strong prey on the weak. A guy with a knife took all Tommy would ever be. For the paper in his wallet. The concern of the suits was touching.”
[The men turn to Jake.] Man 2: “Your brother represented a significant investment. Wed like to talk to you about taking over his contract.” Man 1: “And since your genome is identical to his, you could step into his shoes, so to speak. It would be a fresh start on a new world. You can do something important. You can make a difference. And the pay is good.” Man 2: “Very good.” [Jake’s brother is shoved into the incinerator.]
[The men turn towards Jake again.] Jake Sully (off): “Tommy was the scientist, not me. He was the one who wanted to get shot out light-years in space to find the answers. Me, I was just another dumb grunt getting sent someplace he was gonna regret.”
[The camera shows Jake’s dead brother slowly consumed by fire – subsequently, the picture morphs into Jack aboard the space craft.]
0:03:06 Before they take off to Pandora, an additional shot of the shuttle pilot has been added. 4.52 sec.
Pilot 1: “Copy, Venture Star. Go for de-orbit burn at 2-2-4 niner.”
0:51:53 Before Jake returns to Pandora, he and Grace talk some more. Norm is jealous, because a shallow ex-marine like Jake has meanwhile been accepted into the inner circles of the Na’Vi – even though Jake does not even know the goddess Eywa. When Dr. Augustine considers a picture of Neytiri, she begins to wallow in memories and talks about Neytiri’s sister Sylwanin. Jokingly, Jake tells Norm that he had a date with Sylwanin too. Dr. Augustine remarks that Neytiri’s sister was dead. Apparently, this scene is meant to link to the school scene. It is obvious that Neytiri’s sister had been killed by humans. 19.92 sec.
[Jake teases Norm.] Dr. Grace Augustine: “Knock it off. Its like kindergarten around here.” [Jake gets into the avatar box; Dr. Augustine looks at Neytiri’s picture.] Dr. Grace Augustine: “Neytiri was my best student. She and her sister Sylwanin. Just amazing girls.”
Jake Skully: “I got a date with Sylwanin too.” Dr. Grace Augustine: “She is dead.”
1:04:56 Dr. Augustine brings Jake back and tells him to eat something. He refuses, but Dr. Augustine insists on it and he obliges. At the dining table, Jake finds a picture of Dr. Augustine as Neytiri’s teacher. He asks her about what happened at the school. Dr. Augustine tells him that Neytiri’s sister and some of her friends had attacked a bulldozer which had threatened them. Hoping to find shelter with Dr. Augustine, they fled into the school. However, the mercenaries pursued and killed them.
For lucidity reasons, the complete opening scene will be reproduced here. The parts of it that had already been seen in the theatrical version have been subtracted from the total runtime.
[Dr. Augustine opens the avatar box. Jake gets out.] Dr. Grace Augustine: “You were in 16 hours today.”
[Jakes drives into the small lounge; Dr. Augustine gives him something to eat.] Dr. Grace Augustine: “You are still losing weight.” [Jake ignores the food and drives away.] Dr. Grace Augustine: “No, you dont.”
[Dr. Augustine pulls Jake back.] Jake Sully: “I gotta get some sleep.” Dr. Grace Augustine: “Come back here.”
[Jake sits at table again and looks at the junk food in disgust.] Dr. Grace Augustine: “Bon apptit.” Jake Sully: “Today I made a kill. And we ate it. At least, I know where that meal come from.” Dr. Grace Augustine: “Other body. You need to take care of this one. Okay? Get it? Lets eat it.” Jake Sully: “Yeah, yeah.” [Jake continues to just watch the food disgustedly.] Dr. Grace Augustine: “Here, Ill make it easy for you. Give it to me.” [Dr. Augustine picks up the food and opens it.] Dr. Grace Augustine: “You look like crap.” Jake Sully: “Thank you.” Dr. Grace Augustine: “Youre burning way too hard.” [Jake pulls the cigarette out of Dr. Augustine’s mouth and throws it away.] Jake Sully: “Get rid of this shit. And then you can lecture me.” Dr. Grace Augustine: “Now, I am telling you, as your boss, and as someone who might even consider being a friend someday to take some down time. Eat this, please. Trust me, I learned the hard way.”
[Jake looks at a picture of Dr. Augustine and the young Neytiri at school.] Jake Sully: “What did happen at the school, Grace?”
Dr. Grace Augustine: “Neytiri’s sister, Sylwanin, stopped coming to school. She was angry about the clear cutting. And one day, she and a couple of other young hunters came running in, all painted up. They had set a bulldozer on fire. I guess they thought I could protect them. The troopers pursued them to the school. They killed Sylwanin in the doorway. Right in front of Neytiri. And then shot the others. I got most of the kids out. But they never came back.” [Jake gives the picture back to Dr. Augustine; she puts it on the sill.
Jake Sully: “I am sorry.” Dr. Grace Augustine: “A scientist stays objective. We cant be ruled by emotion. But I put 10 years of my life into that school. They called me sanok.” Jake Sully: “Mother.” Dr. Grace Augustine: “Mother.” [Dr. Augustine touches Jake’s chest.] Dr. Grace Augustine: “That kind of pain reaches back through the link.”
1:34:57 When the marines vacate the research laboratory and prepare for retaliation, Jake and Dr. Augustine talk longer. A short, but interesting extension, since it becomes obvious that the war against the Na’Vi had been desired and planned. 15.08 sec.
Dr. Grace Augustine: “You know, they never wanted us to suceed. They bulldozed the sacred site on purpose – to trigger a response. They fabricating a war. They get what they want.”
Go here to read the rest:
Avatar – Movie-Censorship.com
Posted: September 8, 2016 at 6:32 am
DNA damage resulting in multiple broken chromosomes
DNA repair is a collection of processes by which a cell identifies and corrects damage to the DNA molecules that encode its genome. In human cells, both normal metabolic activities and environmental factors such as radiation can cause DNA damage, resulting in as many as 1 million individual molecular lesions per cell per day. Many of these lesions cause structural damage to the DNA molecule and can alter or eliminate the cell’s ability to transcribe the gene that the affected DNA encodes. Other lesions induce potentially harmful mutations in the cell’s genome, which affect the survival of its daughter cells after it undergoes mitosis. As a consequence, the DNA repair process is constantly active as it responds to damage in the DNA structure. When normal repair processes fail, and when cellular apoptosis does not occur, irreparable DNA damage may occur, including double-strand breaks and DNA crosslinkages (interstrand crosslinks or ICLs). This can eventually lead to malignant tumors, or cancer as per the two hit hypothesis.
The rate of DNA repair is dependent on many factors, including the cell type, the age of the cell, and the extracellular environment. A cell that has accumulated a large amount of DNA damage, or one that no longer effectively repairs damage incurred to its DNA, can enter one of three possible states:
The DNA repair ability of a cell is vital to the integrity of its genome and thus to the normal functionality of that organism. Many genes that were initially shown to influence life span have turned out to be involved in DNA damage repair and protection.
The 2015 Nobel Prize in Chemistry was awarded to Tomas Lindahl, Paul Modrich, and Aziz Sancar for their work on the molecular mechanisms of DNA repair processes.
DNA damage, due to environmental factors and normal metabolic processes inside the cell, occurs at a rate of 10,000 to 1,000,000 molecular lesions per cell per day. While this constitutes only 0.000165% of the human genome’s approximately 6 billion bases (3 billion base pairs), unrepaired lesions in critical genes (such as tumor suppressor genes) can impede a cell’s ability to carry out its function and appreciably increase the likelihood of tumor formation and contribute to tumour heterogeneity.
The vast majority of DNA damage affects the primary structure of the double helix; that is, the bases themselves are chemically modified. These modifications can in turn disrupt the molecules’ regular helical structure by introducing non-native chemical bonds or bulky adducts that do not fit in the standard double helix. Unlike proteins and RNA, DNA usually lacks tertiary structure and therefore damage or disturbance does not occur at that level. DNA is, however, supercoiled and wound around “packaging” proteins called histones (in eukaryotes), and both superstructures are vulnerable to the effects of DNA damage.
DNA damage can be subdivided into two main types:
The replication of damaged DNA before cell division can lead to the incorporation of wrong bases opposite damaged ones. Daughter cells that inherit these wrong bases carry mutations from which the original DNA sequence is unrecoverable (except in the rare case of a back mutation, for example, through gene conversion).
There are several types of damage to DNA due to endogenous cellular processes:
Damage caused by exogenous agents comes in many forms. Some examples are:
UV damage, alkylation/methylation, X-ray damage and oxidative damage are examples of induced damage. Spontaneous damage can include the loss of a base, deamination, sugar ring puckering and tautomeric shift.
In human cells, and eukaryotic cells in general, DNA is found in two cellular locations inside the nucleus and inside the mitochondria. Nuclear DNA (nDNA) exists as chromatin during non-replicative stages of the cell cycle and is condensed into aggregate structures known as chromosomes during cell division. In either state the DNA is highly compacted and wound up around bead-like proteins called histones. Whenever a cell needs to express the genetic information encoded in its nDNA the required chromosomal region is unravelled, genes located therein are expressed, and then the region is condensed back to its resting conformation. Mitochondrial DNA (mtDNA) is located inside mitochondria organelles, exists in multiple copies, and is also tightly associated with a number of proteins to form a complex known as the nucleoid. Inside mitochondria, reactive oxygen species (ROS), or free radicals, byproducts of the constant production of adenosine triphosphate (ATP) via oxidative phosphorylation, create a highly oxidative environment that is known to damage mtDNA. A critical enzyme in counteracting the toxicity of these species is superoxide dismutase, which is present in both the mitochondria and cytoplasm of eukaryotic cells.
Senescence, an irreversible process in which the cell no longer divides, is a protective response to the shortening of the chromosome ends. The telomeres are long regions of repetitive noncoding DNA that cap chromosomes and undergo partial degradation each time a cell undergoes division (see Hayflick limit). In contrast, quiescence is a reversible state of cellular dormancy that is unrelated to genome damage (see cell cycle). Senescence in cells may serve as a functional alternative to apoptosis in cases where the physical presence of a cell for spatial reasons is required by the organism, which serves as a “last resort” mechanism to prevent a cell with damaged DNA from replicating inappropriately in the absence of pro-growth cellular signaling. Unregulated cell division can lead to the formation of a tumor (see cancer), which is potentially lethal to an organism. Therefore, the induction of senescence and apoptosis is considered to be part of a strategy of protection against cancer.
It is important to distinguish between DNA damage and mutation, the two major types of error in DNA. DNA damages and mutation are fundamentally different. Damages are physical abnormalities in the DNA, such as single- and double-strand breaks, 8-hydroxydeoxyguanosine residues, and polycyclic aromatic hydrocarbon adducts. DNA damages can be recognized by enzymes, and, thus, they can be correctly repaired if redundant information, such as the undamaged sequence in the complementary DNA strand or in a homologous chromosome, is available for copying. If a cell retains DNA damage, transcription of a gene can be prevented, and, thus, translation into a protein will also be blocked. Replication may also be blocked or the cell may die.
In contrast to DNA damage, a mutation is a change in the base sequence of the DNA. A mutation cannot be recognized by enzymes once the base change is present in both DNA strands, and, thus, a mutation cannot be repaired. At the cellular level, mutations can cause alterations in protein function and regulation. Mutations are replicated when the cell replicates. In a population of cells, mutant cells will increase or decrease in frequency according to the effects of the mutation on the ability of the cell to survive and reproduce. Although distinctly different from each other, DNA damages and mutations are related because DNA damages often cause errors of DNA synthesis during replication or repair; these errors are a major source of mutation.
Given these properties of DNA damage and mutation, it can be seen that DNA damages are a special problem in non-dividing or slowly dividing cells, where unrepaired damages will tend to accumulate over time. On the other hand, in rapidly dividing cells, unrepaired DNA damages that do not kill the cell by blocking replication will tend to cause replication errors and thus mutation. The great majority of mutations that are not neutral in their effect are deleterious to a cell’s survival. Thus, in a population of cells composing a tissue with replicating cells, mutant cells will tend to be lost. However, infrequent mutations that provide a survival advantage will tend to clonally expand at the expense of neighboring cells in the tissue. This advantage to the cell is disadvantageous to the whole organism, because such mutant cells can give rise to cancer. Thus, DNA damages in frequently dividing cells, because they give rise to mutations, are a prominent cause of cancer. In contrast, DNA damages in infrequently dividing cells are likely a prominent cause of aging.
Single-strand and double-strand DNA damage
Cells cannot function if DNA damage corrupts the integrity and accessibility of essential information in the genome (but cells remain superficially functional when non-essential genes are missing or damaged). Depending on the type of damage inflicted on the DNA’s double helical structure, a variety of repair strategies have evolved to restore lost information. If possible, cells use the unmodified complementary strand of the DNA or the sister chromatid as a template to recover the original information. Without access to a template, cells use an error-prone recovery mechanism known as translesion synthesis as a last resort.
Damage to DNA alters the spatial configuration of the helix, and such alterations can be detected by the cell. Once damage is localized, specific DNA repair molecules bind at or near the site of damage, inducing other molecules to bind and form a complex that enables the actual repair to take place.
Cells are known to eliminate three types of damage to their DNA by chemically reversing it. These mechanisms do not require a template, since the types of damage they counteract can occur in only one of the four bases. Such direct reversal mechanisms are specific to the type of damage incurred and do not involve breakage of the phosphodiester backbone. The formation of pyrimidine dimers upon irradiation with UV light results in an abnormal covalent bond between adjacent pyrimidine bases. The photoreactivation process directly reverses this damage by the action of the enzyme photolyase, whose activation is obligately dependent on energy absorbed from blue/UV light (300500nm wavelength) to promote catalysis. Photolyase, an old enzyme present in bacteria, fungi, and most animals no longer functions in humans, who instead use nucleotide excision repair to repair damage from UV irradiation. Another type of damage, methylation of guanine bases, is directly reversed by the protein methyl guanine methyl transferase (MGMT), the bacterial equivalent of which is called ogt. This is an expensive process because each MGMT molecule can be used only once; that is, the reaction is stoichiometric rather than catalytic. A generalized response to methylating agents in bacteria is known as the adaptive response and confers a level of resistance to alkylating agents upon sustained exposure by upregulation of alkylation repair enzymes. The third type of DNA damage reversed by cells is certain methylation of the bases cytosine and adenine.
When only one of the two strands of a double helix has a defect, the other strand can be used as a template to guide the correction of the damaged strand. In order to repair damage to one of the two paired molecules of DNA, there exist a number of excision repair mechanisms that remove the damaged nucleotide and replace it with an undamaged nucleotide complementary to that found in the undamaged DNA strand.
Double-strand breaks, in which both strands in the double helix are severed, are particularly hazardous to the cell because they can lead to genome rearrangements. Three mechanisms exist to repair double-strand breaks (DSBs): non-homologous end joining (NHEJ), microhomology-mediated end joining (MMEJ), and homologous recombination. PVN Acharya noted that double-strand breaks and a “cross-linkage joining both strands at the same point is irreparable because neither strand can then serve as a template for repair. The cell will die in the next mitosis or in some rare instances, mutate.”
In NHEJ, DNA Ligase IV, a specialized DNA ligase that forms a complex with the cofactor XRCC4, directly joins the two ends. To guide accurate repair, NHEJ relies on short homologous sequences called microhomologies present on the single-stranded tails of the DNA ends to be joined. If these overhangs are compatible, repair is usually accurate. NHEJ can also introduce mutations during repair. Loss of damaged nucleotides at the break site can lead to deletions, and joining of nonmatching termini forms insertions or translocations. NHEJ is especially important before the cell has replicated its DNA, since there is no template available for repair by homologous recombination. There are “backup” NHEJ pathways in higher eukaryotes. Besides its role as a genome caretaker, NHEJ is required for joining hairpin-capped double-strand breaks induced during V(D)J recombination, the process that generates diversity in B-cell and T-cell receptors in the vertebrate immune system.
MMEJ starts with short-range end resection by MRE11 nuclease on either side of a double-strand break to reveal microhomology regions. In further steps, PARP1 is required and may be an early step in MMEJ. There is pairing of microhomology regions followed by recruitment of flap structure-specific endonuclease 1 (FEN1) to remove overhanging flaps. This is followed by recruitment of XRCC1LIG3 to the site for ligating the DNA ends, leading to an intact DNA.
DNA double strand breaks in mammalian cells are primarily repaired by homologous recombination (HR) and non-homologous end joining (NHEJ). In an in vitro system, MMEJ occurred in mammalian cells at the levels of 1020% of HR when both HR and NHEJ mechanisms were also available. MMEJ is always accompanied by a deletion, so that MMEJ is a mutagenic pathway for DNA repair.
Homologous recombination requires the presence of an identical or nearly identical sequence to be used as a template for repair of the break. The enzymatic machinery responsible for this repair process is nearly identical to the machinery responsible for chromosomal crossover during meiosis. This pathway allows a damaged chromosome to be repaired using a sister chromatid (available in G2 after DNA replication) or a homologous chromosome as a template. DSBs caused by the replication machinery attempting to synthesize across a single-strand break or unrepaired lesion cause collapse of the replication fork and are typically repaired by recombination.
Topoisomerases introduce both single- and double-strand breaks in the course of changing the DNA’s state of supercoiling, which is especially common in regions near an open replication fork. Such breaks are not considered DNA damage because they are a natural intermediate in the topoisomerase biochemical mechanism and are immediately repaired by the enzymes that created them.
A team of French researchers bombarded Deinococcus radiodurans to study the mechanism of double-strand break DNA repair in that bacterium. At least two copies of the genome, with random DNA breaks, can form DNA fragments through annealing. Partially overlapping fragments are then used for synthesis of homologous regions through a moving D-loop that can continue extension until they find complementary partner strands. In the final step there is crossover by means of RecA-dependent homologous recombination.
Translesion synthesis (TLS) is a DNA damage tolerance process that allows the DNA replication machinery to replicate past DNA lesions such as thymine dimers or AP sites. It involves switching out regular DNA polymerases for specialized translesion polymerases (i.e. DNA polymerase IV or V, from the Y Polymerase family), often with larger active sites that can facilitate the insertion of bases opposite damaged nucleotides. The polymerase switching is thought to be mediated by, among other factors, the post-translational modification of the replication processivity factor PCNA. Translesion synthesis polymerases often have low fidelity (high propensity to insert wrong bases) on undamaged templates relative to regular polymerases. However, many are extremely efficient at inserting correct bases opposite specific types of damage. For example, Pol mediates error-free bypass of lesions induced by UV irradiation, whereas Pol introduces mutations at these sites. Pol is known to add the first adenine across the T^T photodimer using Watson-Crick base pairing and the second adenine will be added in its syn conformation using Hoogsteen base pairing. From a cellular perspective, risking the introduction of point mutations during translesion synthesis may be preferable to resorting to more drastic mechanisms of DNA repair, which may cause gross chromosomal aberrations or cell death. In short, the process involves specialized polymerases either bypassing or repairing lesions at locations of stalled DNA replication. For example, Human DNA polymerase eta can bypass complex DNA lesions like guanine-thymine intra-strand crosslink, G[8,5-Me]T, although can cause targeted and semi-targeted mutations. Paromita Raychaudhury and Ashis Basu studied the toxicity and mutagenesis of the same lesion in Escherichia coli by replicating a G[8,5-Me]T-modified plasmid in E. coli with specific DNA polymerase knockouts. Viability was very low in a strain lacking pol II, pol IV, and pol V, the three SOS-inducible DNA polymerases, indicating that translesion synthesis is conducted primarily by these specialized DNA polymerases. A bypass platform is provided to these polymerases by Proliferating cell nuclear antigen (PCNA). Under normal circumstances, PCNA bound to polymerases replicates the DNA. At a site of lesion, PCNA is ubiquitinated, or modified, by the RAD6/RAD18 proteins to provide a platform for the specialized polymerases to bypass the lesion and resume DNA replication. After translesion synthesis, extension is required. This extension can be carried out by a replicative polymerase if the TLS is error-free, as in the case of Pol , yet if TLS results in a mismatch, a specialized polymerase is needed to extend it; Pol . Pol is unique in that it can extend terminal mismatches, whereas more processive polymerases cannot. So when a lesion is encountered, the replication fork will stall, PCNA will switch from a processive polymerase to a TLS polymerase such as Pol to fix the lesion, then PCNA may switch to Pol to extend the mismatch, and last PCNA will switch to the processive polymerase to continue replication.
Cells exposed to ionizing radiation, ultraviolet light or chemicals are prone to acquire multiple sites of bulky DNA lesions and double-strand breaks. Moreover, DNA damaging agents can damage other biomolecules such as proteins, carbohydrates, lipids, and RNA. The accumulation of damage, to be specific, double-strand breaks or adducts stalling the replication forks, are among known stimulation signals for a global response to DNA damage. The global response to damage is an act directed toward the cells’ own preservation and triggers multiple pathways of macromolecular repair, lesion bypass, tolerance, or apoptosis. The common features of global response are induction of multiple genes, cell cycle arrest, and inhibition of cell division.
After DNA damage, cell cycle checkpoints are activated. Checkpoint activation pauses the cell cycle and gives the cell time to repair the damage before continuing to divide. DNA damage checkpoints occur at the G1/S and G2/M boundaries. An intra-S checkpoint also exists. Checkpoint activation is controlled by two master kinases, ATM and ATR. ATM responds to DNA double-strand breaks and disruptions in chromatin structure, whereas ATR primarily responds to stalled replication forks. These kinases phosphorylate downstream targets in a signal transduction cascade, eventually leading to cell cycle arrest. A class of checkpoint mediator proteins including BRCA1, MDC1, and 53BP1 has also been identified. These proteins seem to be required for transmitting the checkpoint activation signal to downstream proteins.
DNA damage checkpoint is a signal transduction pathway that blocks cell cycle progression in G1, G2 and metaphase and slows down the rate of S phase progression when DNA is damaged. It leads to a pause in cell cycle allowing the cell time to repair the damage before continuing to divide.
Checkpoint Proteins can be separated into four groups: phosphatidylinositol 3-kinase (PI3K)-like protein kinase, proliferating cell nuclear antigen (PCNA)-like group, two serine/threonine(S/T) kinases and their adaptors. Central to all DNA damage induced checkpoints responses is a pair of large protein kinases belonging to the first group of PI3K-like protein kinases-the ATM (Ataxia telangiectasia mutated) and ATR (Ataxia- and Rad-related) kinases, whose sequence and functions have been well conserved in evolution. All DNA damage response requires either ATM or ATR because they have the ability to bind to the chromosomes at the site of DNA damage, together with accessory proteins that are platforms on which DNA damage response components and DNA repair complexes can be assembled.
An important downstream target of ATM and ATR is p53, as it is required for inducing apoptosis following DNA damage. The cyclin-dependent kinase inhibitor p21 is induced by both p53-dependent and p53-independent mechanisms and can arrest the cell cycle at the G1/S and G2/M checkpoints by deactivating cyclin/cyclin-dependent kinase complexes.
The SOS response is the changes in gene expression in Escherichia coli and other bacteria in response to extensive DNA damage. The prokaryotic SOS system is regulated by two key proteins: LexA and RecA. The LexA homodimer is a transcriptional repressor that binds to operator sequences commonly referred to as SOS boxes. In Escherichia coli it is known that LexA regulates transcription of approximately 48 genes including the lexA and recA genes. The SOS response is known to be widespread in the Bacteria domain, but it is mostly absent in some bacterial phyla, like the Spirochetes. The most common cellular signals activating the SOS response are regions of single-stranded DNA (ssDNA), arising from stalled replication forks or double-strand breaks, which are processed by DNA helicase to separate the two DNA strands. In the initiation step, RecA protein binds to ssDNA in an ATP hydrolysis driven reaction creating RecAssDNA filaments. RecAssDNA filaments activate LexA autoprotease activity, which ultimately leads to cleavage of LexA dimer and subsequent LexA degradation. The loss of LexA repressor induces transcription of the SOS genes and allows for further signal induction, inhibition of cell division and an increase in levels of proteins responsible for damage processing.
In Escherichia coli, SOS boxes are 20-nucleotide long sequences near promoters with palindromic structure and a high degree of sequence conservation. In other classes and phyla, the sequence of SOS boxes varies considerably, with different length and composition, but it is always highly conserved and one of the strongest short signals in the genome. The high information content of SOS boxes permits differential binding of LexA to different promoters and allows for timing of the SOS response. The lesion repair genes are induced at the beginning of SOS response. The error-prone translesion polymerases, for example, UmuCD’2 (also called DNA polymerase V), are induced later on as a last resort. Once the DNA damage is repaired or bypassed using polymerases or through recombination, the amount of single-stranded DNA in cells is decreased, lowering the amounts of RecA filaments decreases cleavage activity of LexA homodimer, which then binds to the SOS boxes near promoters and restores normal gene expression.
Eukaryotic cells exposed to DNA damaging agents also activate important defensive pathways by inducing multiple proteins involved in DNA repair, cell cycle checkpoint control, protein trafficking and degradation. Such genome wide transcriptional response is very complex and tightly regulated, thus allowing coordinated global response to damage. Exposure of yeast Saccharomyces cerevisiae to DNA damaging agents results in overlapping but distinct transcriptional profiles. Similarities to environmental shock response indicates that a general global stress response pathway exist at the level of transcriptional activation. In contrast, different human cell types respond to damage differently indicating an absence of a common global response. The probable explanation for this difference between yeast and human cells may be in the heterogeneity of mammalian cells. In an animal different types of cells are distributed among different organs that have evolved different sensitivities to DNA damage.
In general global response to DNA damage involves expression of multiple genes responsible for postreplication repair, homologous recombination, nucleotide excision repair, DNA damage checkpoint, global transcriptional activation, genes controlling mRNA decay, and many others. A large amount of damage to a cell leaves it with an important decision: undergo apoptosis and die, or survive at the cost of living with a modified genome. An increase in tolerance to damage can lead to an increased rate of survival that will allow a greater accumulation of mutations. Yeast Rev1 and human polymerase are members of [Y family translesion DNA polymerases present during global response to DNA damage and are responsible for enhanced mutagenesis during a global response to DNA damage in eukaryotes.
DNA repair rate is an important determinant of cell pathology
Experimental animals with genetic deficiencies in DNA repair often show decreased life span and increased cancer incidence. For example, mice deficient in the dominant NHEJ pathway and in telomere maintenance mechanisms get lymphoma and infections more often, and, as a consequence, have shorter lifespans than wild-type mice. In similar manner, mice deficient in a key repair and transcription protein that unwinds DNA helices have premature onset of aging-related diseases and consequent shortening of lifespan. However, not every DNA repair deficiency creates exactly the predicted effects; mice deficient in the NER pathway exhibited shortened life span without correspondingly higher rates of mutation.
If the rate of DNA damage exceeds the capacity of the cell to repair it, the accumulation of errors can overwhelm the cell and result in early senescence, apoptosis, or cancer. Inherited diseases associated with faulty DNA repair functioning result in premature aging, increased sensitivity to carcinogens, and correspondingly increased cancer risk (see below). On the other hand, organisms with enhanced DNA repair systems, such as Deinococcus radiodurans, the most radiation-resistant known organism, exhibit remarkable resistance to the double-strand break-inducing effects of radioactivity, likely due to enhanced efficiency of DNA repair and especially NHEJ.
Most life span influencing genes affect the rate of DNA damage
A number of individual genes have been identified as influencing variations in life span within a population of organisms. The effects of these genes is strongly dependent on the environment, in particular, on the organism’s diet. Caloric restriction reproducibly results in extended lifespan in a variety of organisms, likely via nutrient sensing pathways and decreased metabolic rate. The molecular mechanisms by which such restriction results in lengthened lifespan are as yet unclear (see for some discussion); however, the behavior of many genes known to be involved in DNA repair is altered under conditions of caloric restriction.
For example, increasing the gene dosage of the gene SIR-2, which regulates DNA packaging in the nematode worm Caenorhabditis elegans, can significantly extend lifespan. The mammalian homolog of SIR-2 is known to induce downstream DNA repair factors involved in NHEJ, an activity that is especially promoted under conditions of caloric restriction. Caloric restriction has been closely linked to the rate of base excision repair in the nuclear DNA of rodents, although similar effects have not been observed in mitochondrial DNA.
The C. elegans gene AGE-1, an upstream effector of DNA repair pathways, confers dramatically extended life span under free-feeding conditions but leads to a decrease in reproductive fitness under conditions of caloric restriction. This observation supports the pleiotropy theory of the biological origins of aging, which suggests that genes conferring a large survival advantage early in life will be selected for even if they carry a corresponding disadvantage late in life.
Defects in the NER mechanism are responsible for several genetic disorders, including:
Mental retardation often accompanies the latter two disorders, suggesting increased vulnerability of developmental neurons.
Other DNA repair disorders include:
All of the above diseases are often called “segmental progerias” (“accelerated aging diseases”) because their victims appear elderly and suffer from aging-related diseases at an abnormally young age, while not manifesting all the symptoms of old age.
Other diseases associated with reduced DNA repair function include Fanconi anemia, hereditary breast cancer and hereditary colon cancer.
Because of inherent limitations in the DNA repair mechanisms, if humans lived long enough, they would all eventually develop cancer. There are at least 34 Inherited human DNA repair gene mutations that increase cancer risk. Many of these mutations cause DNA repair to be less effective than normal. In particular, Hereditary nonpolyposis colorectal cancer (HNPCC) is strongly associated with specific mutations in the DNA mismatch repair pathway. BRCA1 and BRCA2, two famous genes whose mutations confer a hugely increased risk of breast cancer on carriers, are both associated with a large number of DNA repair pathways, especially NHEJ and homologous recombination.
Cancer therapy procedures such as chemotherapy and radiotherapy work by overwhelming the capacity of the cell to repair DNA damage, resulting in cell death. Cells that are most rapidly dividing most typically cancer cells are preferentially affected. The side-effect is that other non-cancerous but rapidly dividing cells such as progenitor cells in the gut, skin, and hematopoietic system are also affected. Modern cancer treatments attempt to localize the DNA damage to cells and tissues only associated with cancer, either by physical means (concentrating the therapeutic agent in the region of the tumor) or by biochemical means (exploiting a feature unique to cancer cells in the body).
Classically, cancer has been viewed as a set of diseases that are driven by progressive genetic abnormalities that include mutations in tumour-suppressor genes and oncogenes, and chromosomal aberrations. However, it has become apparent that cancer is also driven by epigenetic alterations.
Epigenetic alterations refer to functionally relevant modifications to the genome that do not involve a change in the nucleotide sequence. Examples of such modifications are changes in DNA methylation (hypermethylation and hypomethylation) and histone modification, changes in chromosomal architecture (caused by inappropriate expression of proteins such as HMGA2 or HMGA1) and changes caused by microRNAs. Each of these epigenetic alterations serves to regulate gene expression without altering the underlying DNA sequence. These changes usually remain through cell divisions, last for multiple cell generations, and can be considered to be epimutations (equivalent to mutations).
While large numbers of epigenetic alterations are found in cancers, the epigenetic alterations in DNA repair genes, causing reduced expression of DNA repair proteins, appear to be particularly important. Such alterations are thought to occur early in progression to cancer and to be a likely cause of the genetic instability characteristic of cancers.
Reduced expression of DNA repair genes causes deficient DNA repair. When DNA repair is deficient DNA damages remain in cells at a higher than usual level and these excess damages cause increased frequencies of mutation or epimutation. Mutation rates increase substantially in cells defective in DNA mismatch repair or in homologous recombinational repair (HRR). Chromosomal rearrangements and aneuploidy also increase in HRR defective cells.
Higher levels of DNA damage not only cause increased mutation, but also cause increased epimutation. During repair of DNA double strand breaks, or repair of other DNA damages, incompletely cleared sites of repair can cause epigenetic gene silencing.
Deficient expression of DNA repair proteins due to an inherited mutation can cause increased risk of cancer. Individuals with an inherited impairment in any of 34 DNA repair genes (see article DNA repair-deficiency disorder) have an increased risk of cancer, with some defects causing up to a 100% lifetime chance of cancer (e.g. p53 mutations). However, such germline mutations (which cause highly penetrant cancer syndromes) are the cause of only about 1 percent of cancers.
Deficiencies in DNA repair enzymes are occasionally caused by a newly arising somatic mutation in a DNA repair gene, but are much more frequently caused by epigenetic alterations that reduce or silence expression of DNA repair genes. For example, when 113 colorectal cancers were examined in sequence, only four had a missense mutation in the DNA repair gene MGMT, while the majority had reduced MGMT expression due to methylation of the MGMT promoter region (an epigenetic alteration). Five different studies found that between 40% and 90% of colorectal cancers have reduced MGMT expression due to methylation of the MGMT promoter region.
Similarly, out of 119 cases of mismatch repair-deficient colorectal cancers that lacked DNA repair gene PMS2 expression, PMS2 was deficient in 6 due to mutations in the PMS2 gene, while in 103 cases PMS2 expression was deficient because its pairing partner MLH1 was repressed due to promoter methylation (PMS2 protein is unstable in the absence of MLH1). In the other 10 cases, loss of PMS2 expression was likely due to epigenetic overexpression of the microRNA, miR-155, which down-regulates MLH1.
In further examples (tabulated in Table 4 of this reference), epigenetic defects were found at frequencies of between 13%-100% for the DNA repair genes BRCA1, WRN, FANCB, FANCF, MGMT, MLH1, MSH2, MSH4, ERCC1, XPF, NEIL1 and ATM. These epigenetic defects occurred in various cancers (e.g. breast, ovarian, colorectal and head and neck). Two or three deficiencies in the expression of ERCC1, XPF or PMS2 occur simultaneously in the majority of the 49 colon cancers evaluated by Facista et al.
The chart in this section shows some frequent DNA damaging agents, examples of DNA lesions they cause, and the pathways that deal with these DNA damages. At least 169 enzymes are either directly employed in DNA repair or influence DNA repair processes. Of these, 83 are directly employed in repairing the 5 types of DNA damages illustrated in the chart.
Some of the more well studied genes central to these repair processes are shown in the chart. The gene designations shown in red, gray or cyan indicate genes frequently epigenetically altered in various types of cancers. Wikipedia articles on each of the genes high-lighted by red, gray or cyan describe the epigenetic alteration(s) and the cancer(s) in which these epimutations are found. Two review articles, and two broad experimental survey articles also document most of these epigenetic DNA repair deficiencies in cancers.
Red-highlighted genes are frequently reduced or silenced by epigenetic mechanisms in various cancers. When these genes have low or absent expression, DNA damages can accumulate. Replication errors past these damages (see translesion synthesis) can lead to increased mutations and, ultimately, cancer. Epigenetic repression of DNA repair genes in accurate DNA repair pathways appear to be central to carcinogenesis.
The two gray-highlighted genes RAD51 and BRCA2, are required for homologous recombinational repair. They are sometimes epigenetically over-expressed and sometimes under-expressed in certain cancers. As indicated in the Wikipedia articles on RAD51 and BRCA2, such cancers ordinarily have epigenetic deficiencies in other DNA repair genes. These repair deficiencies would likely cause increased unrepaired DNA damages. The over-expression of RAD51 and BRCA2 seen in these cancers may reflect selective pressures for compensatory RAD51 or BRCA2 over-expression and increased homologous recombinational repair to at least partially deal with such excess DNA damages. In those cases where RAD51 or BRCA2 are under-expressed, this would itself lead to increased unrepaired DNA damages. Replication errors past these damages (see translesion synthesis) could cause increased mutations and cancer, so that under-expression of RAD51 or BRCA2 would be carcinogenic in itself.
Cyan-highlighted genes are in the microhomology-mediated end joining (MMEJ) pathway and are up-regulated in cancer. MMEJ is an additional error-prone inaccurate repair pathway for double-strand breaks. In MMEJ repair of a double-strand break, an homology of 5-25 complementary base pairs between both paired strands is sufficient to align the strands, but mismatched ends (flaps) are usually present. MMEJ removes the extra nucleotides (flaps) where strands are joined, and then ligates the strands to create an intact DNA double helix. MMEJ almost always involves at least a small deletion, so that it is a mutagenic pathway.FEN1, the flap endonuclease in MMEJ, is epigenetically increased by promoter hypomethylation and is over-expressed in the majority of cancers of the breast, prostate, stomach, neuroblastomas, pancreas, and lung. PARP1 is also over-expressed when its promoter region ETS site is epigenetically hypomethylated, and this contributes to progression to endometrial cancer, BRCA-mutated ovarian cancer, and BRCA-mutated serous ovarian cancer. Other genes in the MMEJ pathway are also over-expressed in a number of cancers (see MMEJ for summary), and are also shown in cyan.
The basic processes of DNA repair are highly conserved among both prokaryotes and eukaryotes and even among bacteriophage (viruses that infect bacteria); however, more complex organisms with more complex genomes have correspondingly more complex repair mechanisms. The ability of a large number of protein structural motifs to catalyze relevant chemical reactions has played a significant role in the elaboration of repair mechanisms during evolution. For an extremely detailed review of hypotheses relating to the evolution of DNA repair, see.
The fossil record indicates that single-cell life began to proliferate on the planet at some point during the Precambrian period, although exactly when recognizably modern life first emerged is unclear. Nucleic acids became the sole and universal means of encoding genetic information, requiring DNA repair mechanisms that in their basic form have been inherited by all extant life forms from their common ancestor. The emergence of Earth’s oxygen-rich atmosphere (known as the “oxygen catastrophe”) due to photosynthetic organisms, as well as the presence of potentially damaging free radicals in the cell due to oxidative phosphorylation, necessitated the evolution of DNA repair mechanisms that act specifically to counter the types of damage induced by oxidative stress.
On some occasions, DNA damage is not repaired, or is repaired by an error-prone mechanism that results in a change from the original sequence. When this occurs, mutations may propagate into the genomes of the cell’s progeny. Should such an event occur in a germ line cell that will eventually produce a gamete, the mutation has the potential to be passed on to the organism’s offspring. The rate of evolution in a particular species (or, in a particular gene) is a function of the rate of mutation. As a consequence, the rate and accuracy of DNA repair mechanisms have an influence over the process of evolutionary change. Since the normal adaptation of populations of organisms to changing circumstances (for instance the adaptation of the beaks of a population of finches to the changing presence of hard seeds or insects) proceeds by gene regulation and the recombination and selection of gene variations alleles and not by passing on irreparable DNA damages to the offspring, DNA damage protection and repair does not influence the rate of adaptation by gene regulation and by recombination and selection of alleles. On the other hand, DNA damage repair and protection does influence the rate of accumulation of irreparable, advantageous, code expanding, inheritable mutations, and slows down the evolutionary mechanism for expansion of the genome of organisms with new functionalities. The tension between evolvability and mutation repair and protection needs further investigation.
A technology named clustered regularly interspaced short palindromic repeat shortened to CRISPR-Cas9 was discovered in 2012. The new technology allows anyone with molecular biology training to alter the genes of any species with precision.
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DNA repair – Wikipedia, the free encyclopedia
Posted: July 10, 2016 at 5:57 pm
Egoism is the concept of acting in ones own self-interest, and can be either a descriptive or a normative position. Psychological egoism, the most well-known descriptive position, holds that we always act in our own self-interest. In contrast to this, ethical egoism is a normative position: it claims that one should act in ones self-interest as this makes an action morally right, such that the claims of others should never have weight for oneself unless their good can serve ones own good. Similarly, rational egoism maintains that, in order to act rationally, one must act in ones self-interest, and the fact that an action helps another person does not alone provide a reason for performing it, unless helping the other person in some way furthers ones own interests.
All these positions deserve to be critiqued: psychological egoism in that people find the greatest happiness and meaning in states where they are self-giving, for example when in love, parenting a child, or contributing to society; and ethical egoism by the challenge of numerous philosophical and religious ethical systems that place self-interest within the context of contributing to the greater good.
Psychological egoism holds that every human has only one ultimate goal: his or her own good (where this good can variously be defined as welfare, happiness or pleasure). This description is verified by widespread and frequent observations of self-interested behavior. For instance, we often motivate people to act in certain ways by appealing to their self-interest in the form of rewards and punishments, while acts which appear altruistic are often shown to be motivated by self-interest. Likewise, one can find a non-altruistic explanation for the apparently altruistic behavior of organisms in general. Worker bees are an interesting case in point: although they seem to act solely for the sake of their hive with no concern for their own welfare, sociobiologists offer an account of this behavior in terms of their genes survival. They hypothesize that natural selection favors altruistic behavior in either cooperative relations in which all members benefit (reciprocal altruism) or familial relations (kin altruism). Both forms of altruism are concerned with the survival of ones genes: acts of reciprocal altruism increase ones chances of survival, and therefore ones genes chances of survival, while ensuring the survival of ones relations ensures the survival of a percentage of ones genes. For a worker bee, ensuring the survival of her sister worker means that she has ensured the survival of half of her genes. Thus, sociobiologists typically claim that, on a genetic level, altruism cannot exist. However, psychological egoism is a stronger position, as it claims that, regardless of what happens on a genetic level, the individual him or herself is motivated by thoughts of self-interest. Thus, while it allows for action that does not accomplish its goal of maximizing self-interest, as well as action that is at odds with ones intentions (a weak will), most forms of psychological egoism rule out both altruistic behavior and acting solely out of respect for ones duty. Importantly, psychological egoism allows for goals other than ones own self interest, but claims that these goals are then means to realizing ones own well-being.
There are in turn two forms of psychological egoism. Exclusive egoism makes the strong claim that people act exclusively out of self-interest, and therefore altruistic behavior does not, in fact, exist. On the other hand, predominant egoism makes the weaker claim that people seldom act unselfishly, and when they do so, it is typically only because their sacrifice is small and the beneficiaries gain is much larger, or when they are partial to the beneficiary in some way: when the beneficiaries are, for example, friends, lovers or family.
Exclusive egoism allows for no exceptions; this means that one instance of someone who does not act exclusively out of self-interest is sufficient to show that exclusive egoisms thesis is empirically false. Imagine a soldier throws himself on a grenade in order to prevent other people from being killed. His motivation for this act of self-sacrifice might quite plausibly be his desire to do his duty or to save the other peoples lives, while attempting to explain his action in terms of self-interest would appear to be a wholly implausible move. The exclusive egoist may want to defend her position by arguing for some kind of ulterior self-interested motive, such as pleasure. Perhaps our soldier believes in an afterlife in which he will be rewarded ten-fold for his apparently selfless act on earth, or perhaps, if he had not hurled himself on the grenade, he would be overcome by guilt and a concomitant sense of self-loathing. In both cases then, he is, at least from his perspective, acting in his self-interest by acting in this apparently selfless manner. There are two problems with this response. The first is that, while it might explain many instances of apparent self-sacrifice as motivated by egoistic concerns, it does not necessarily cover all cases. The psychological egoist must argue that all instances of ostensible altruistic behavior are in fact motivated by self-interested desires. If, for instance, our soldier disagrees with this, and claims that his action was truly altruistic in motivation, the exclusive egoist must respond that he is lying or is deceiving himself. At this point, however, exclusive egoism turns out to be trivially true, which means that it is unfalsifiable, since there is no empirical instance that could in principle disprove the hypothesis. As with the trivially true statement all ostriches that live on Mars have gold and purple polka dotted wings, this version of psychological egoism provides no useful information and therefore fails as an empirical theory. It does not allow us to distinguish, for instance, between our soldier and the soldier who thrusts a child onto the grenade in order to save himself. Whereas we generally think that the latter is behaving selfishly, while our soldier is acting in a selfless manner, exclusive egoism maintains that both soldiers are equally selfish, because both are acting in their self-interest.
Alternatively, the psychological egoist might opt for a non-trivial response to the soldier counter-example. She could argue that, as infants, we have only self-regarding desires; desires for our own well-being, for instance. However, as we grow older, we find that desiring things for their own sake eventually satisfies our self-regarding desires. We then come to desire these things for their own sake. For example, I might detest exercise, but also find that exercising results in physical well-being; after a while, I will begin to desire exercise for its own sake. This would preclude the common objection to psychological egoism, that one must desire things other than ones welfare in order to realize ones welfare. However, then the psychological egoist will have moved away from exclusive egoism. It may be true that our soldier would not have had a present desire to save others, unless saving others was connected in the past with increasing his welfare, but this does not mean that his present desire is selfish. At this point, the psychological egoist could adopt the weaker stance of predominant egoism which allows for exceptions, and thereby forestall counter-examples like our heroic soldier; moreover, predominant egoism is both an empirically plausible and non-trivial position.
In her novel, Atlas Shrugged, Russian emigre Ayn Rand sketches the portrait of a man who feels responsible for himself and no one else. John Galt is the archetype of the individual who practices what Rand calls the virtue of selfishness: a man for whom true morality consists in resisting the temptations of self-sacrifice, sympathy and generosity. In the fictional figure of John Galt we find the embodiment of egoism as an ideal. Similarly, the move from psychological egoism to ethical egoism is a move from a descriptive to a normative position. Ethical egoism claims that for ones action to count as morally right it is both necessary and sufficient that one act in ones self-interest. Precisely how one acts in ones self-interest is a matter of some divergence among ethical egoists. As with psychological egoism, ethical egoism comes in both a maximizing and a non-maximizing flavor: the former holds that self-interest must be maximized for an action to count as ethical, while the latter simply claims that one should act in ones self-interest and thus leaves the possibility for acting in others interest open. There is also a distinction between short-term and long-term interests: I might gain a short-term benefit by stealing from my friends, but experience a long-term loss when they discover the theft and I lose those friends. In addition, ethical egoism can also apply to rules or character traits, as well as acts. Finally, acting in ones self-interest means acting for ones own good, but this good can variously be defined as ones happiness, pleasure or well-being. There are various permutations of these conceptions, but considering that the arguments for and against them are generally relevantly similar, I will very broadly define ethical egoism as the thesis which states that in order for ones actions to count as ethical, one should act to promote ones self-interest, where self-interest is taken to mean ones own good.
There are several arguments in support of ethical egoism. Ethical egoists occasionally appeal to the findings of psychological egoism as support for their normative claims; however, regardless of whether psychological egoism is true or not, the jump from a descriptive to a normative position is fallacious, as one cannot use supposed existing conditions as justification for how one ought to behave. A more valid move is to argue that, as psychological egoism is true, it is impossible to motivate people on non-egoistic grounds. Thus, ethical egoism is the most practical moral theory, or the most capable of motivating people to act ethically. However, as we have seen, exclusive egoism just seems false, and substituting it with predominant egoism loses the crucial claim that it is impossible to motivate people to behave altruistically. On the other hand, if psychological egoism is true, it follows from psychological egoism that I cannot intend to perform an action which I believe is not in my self-interest. However, if I am wrong, and this action is in my self-interest, then ethical egoism stipulates that I should perform an action that I cannot intend. The appeal to psychological egoism therefore fails to ensure its practicality.
However, this is not necessarily a shortcoming of an ethical theory, as part of the value of an ethical theory may lie in its offering us an ideal for us to live up to. Setting aside the appeal to its supposed practicality, ethical egoists might alternatively claim that ethical egoism best fits our commonsense moral judgements. For instance, it captures the intuition that I should not let others exploit me, and unlike consequentialism, allows me to keep some good for myself, like a house, even though giving this house to someone else might benefit him slightly more. Moreover, it stipulates that it is often in ones best interests to ostensibly take other peoples interests into account so as to secure their cooperation. I derive a much larger long-term benefit if I act generously and compassionately towards my friends, for example, than if I steal from them, even though theft might provide the greatest short-term benefit to me. Nevertheless, it appears that ethical egoism is also at odds with some of our most deeply held ethical beliefs. It mandates that one should only ever help someone else if doing so benefits oneself, which means that one is not morally obligated to help those who cannot help or hinder one. Imagine I can easily save a drowning child, but none of the players in this scenario can offer me any beneficial cooperation in return for saving the child (like praise) or negative retaliation for failing to help (like scorn). Further, say that I am indifferent to the situation presented to me, and regardless of what I do, I will feel no sense of guilt or pleasure, then ethical egoism will remain silent as to whether I should save the child. Moreover, if there is some slight uncompensated sacrifice I will have to make, like getting my shoes wet, then ethical egoism will tell me to refrain from saving the drowning child. However, we generally think that, in this case, there is a moral obligation to save the child, and ethical egoism can neither explain how such a duty might (validly) arise, nor generate such a duty. Ethical egoism therefore appears to be morally insensitive to situations which we ordinarily think demand great moral sensitivity. We can further see that ethical egoism will potentially generate counter-intuitive duties in situations where the individual in need of help cannot reciprocate (like physically or mentally disabled people) or where the sacrifice one might need to make is not compensatable. Ethical egoism will, for instance, condemn the action of the soldier who throws himself on the grenade as ethically reprehensible, precisely because it entails an irreversible sacrifice (loss of life) for the soldier, while we ordinarily think it is an ethically admirable action, or at the very least, not a morally repugnant one.
Furthermore, a number of critics have argued that egoism yields contradictory moral imperatives. There are generally two inconsistency charges against ethical egoism. The weaker of the two lays this charge: say ethical egoism recommends that X and Y buy a particular item of clothing on sale, since buying this item is, for some reason, in the self-interest of each. But there is only one remaining article; hence, ethical egoism recommends an impossible situation. However, the ethical egoist can reply that ethical egoism does not provide neutral criteria: it advocates to X buying the article of clothing for X, and advocates to Y that Y buy the article for Y, but ethical egoism has nothing to say on the value of X and Y buying the same article of clothing.
The second inconsistency argument claims that, in any given situation, the ethical egoist must aim to promote her own self-interest, but if her brand of egoism is to count as an ethical theory, she must simultaneously will that everyone else also act to promote their own self-interest, for one of the formal constraints on an ethical theory is that it be universalisable. Say I am a shopkeeper, and it is in my best interest to sell my products at the highest practically possible profit, it will generally not be in my clients best interests to buy my products at these high prices. Then if I am an ethical egoist, I am committed to recommending a contradictory state of affairs: that I both sell the products at the highest possible price and that my customers pay less than the highest possible price. The ethical theorist, however, can respond that, although she morally recommends that the customers pay less than the highest possible price, this does not necessarily mean that she desires it. Jesse Kalin provides an analogy with competitive sports: in a game of chess, I will be trying my utmost to win, but I will also expect my opponent to do the same, and I may even desire that he play as good a game as possible, because then the game will be of a far higher standard. If the analogy with competitive gaming holds, it is therefore not inconsistent for me to recommend both that I attempt to sell my products at the highest possible price and that my customers attempt to buy them at lower than the highest possible price.
However, this move to making an analogy with competitive games cannot preclude the worry that ethical egoism is not sufficiently public for it to count as an ethical theory. What is meant by this is that ethical egoism is at odds with public morality (which generally appears to value altruism) and one can therefore imagine many cases in which the ethical egoist might find it in her interests not to profess ethical egoism. Imagine I am an ethical egoist and I donate a large sum to a charity because it gives my company a good image and I receive a large tax deduction for doing so. Then it is most definitely not in my best interests to reveal these reasons; rather, it is to my advantage that I pretend to have done so out of a spirit of generosity and kindness. Leaving aside worries of duplicitous and unreliable behavior, it does not seem as if ethical egoism can truly be made public without the ethical egoists interests being compromised. Yet it seems as if an ethical theory requires precisely this ability to be made public. Moreover, although it meets the formal constraints of an ethical theory it must be normative and universalisable as noted above, it also fails to provide a single neutral ranking that each agent must follow in cases where there is a conflict of interests. Just what makes for a moral theory, however, is contentious, and the ethical theorist can subsequently respond to any argument against ethical egoisms status as an ethical theory by claiming that the failed criteria are not really constraints that an ethical theory must adhere to. A more elegant solution, however, is to move to rational egoism, which might provide the ethical egoist with non-ethical reasons for adhering to ethical egoism.
Rational egoism maintains that it is both necessary and sufficient for an action to be rational that it promotes ones self-interest. As with ethical egoism, rational egoism comes in varying flavors. It can be maximizing or non-maximizing, or can apply to rules or character traits instead of actions. Certain versions might claim that acting in ones self-interest is either sufficient but not necessary, or necessary but not sufficient for an action to count as rational. However, as with ethical egoism, relevantly similar objections to and defenses for the various species of ethical egoism can be made. The salient common feature amongst all variants is that all claim that the fact that an action helps another person does not alone provide a reason for performing it, unless helping the other person in some way furthers ones own interests. Stronger versions might also hold that the only underived reason for action is self-interest.
In support of their thesis, rational egoists most commonly appeal to the way in which rational egoism best fits our ordinary judgements about what makes action rational. However, as we saw with the soldier counter-example, both psychological and ethical egoism fail to make sense of his action, and rational egoism will similarly generate a counter-intuitive response to this example. It will classify his action as fundamentally non-rational because it has permanently violated his self-interest. However, we would ordinarily characterize his action as rational, because it realizes his strong non-self-interested preference to save the lives of others. In other words, we take the safety of others to be a legitimate motivation for his action, whereas his hurling himself on a grenade in order to save a chocolate cake would ordinarily be seen as non-rational. Yet rational egoism would not allow us to distinguish between these two cases, because it does not recognize the demands of others as alone providing one with reason to act in a certain way.
Rational egoism furthermore appears to make an unjustified weighted distinction between ones own self-interest and the good of others. Imagine I decide that I should act to increase the good of brown-eyed people over that of others. Justifying this preferential treatment on the grounds that brown-eyed people just are more deserving of preferential treatment is not rational. James Rachels argues that ethical (and here, rational) egoism, makes a similarly unwarranted or arbitrary move, because it claims that I ought to act in one persons interest (myself). The rational egoist might want to respond that non-arbitrary distinctions can be made by ones preferences. The fact that I like oranges and not apples makes my decision to buy apples rather than oranges non-arbitrary, and similarly, my preference for my own good makes my commitment to achieving my own good non-arbitrary. However, as we have seen, there are cases (as with the soldier example) where I might lack a preference for my own welfare. In these instances, rational egoism cannot give me a reason to pursue my self-interest over that of others. Nevertheless, rational egoism might hold that, in these cases I am wrong, simply because we must take it as a ground assumption that our own good comes before that of others. In other words, the preference for ones own good needs no further justification than the fact it is ones own good that one is pursuing. When it comes to the preferential treatment of brown-eyed people, we generally do not accept their being brown-eyed as a good reason for their preferential treatment, but when it comes to acting for our own good, we seem to take the fact that it is our own good as a reasonable justification for doing so; we do not ask why acting in ones own good is pertinent.
However, although this may be so, this argument does not demonstrate that acting to promote ones own good is always sufficient or necessary for an action to count as rational. There are instances where we take an action to be rational, but where the agent makes no reference to pursuing his own good as justification for performing the action. The villagers of Le Chambon provide us with a real-life example of this. Le Chambon was a pacifist French village responsible for saving the lives of several thousand Jews from the Nazis, often at a great risk to the inhabitants. The reason they gave for this altruistic behavior was that it was simply their duty to help anybody in need. Here, no reference is made to their own good (and indeed, their own welfare was often severely jeopardized by their actions), and we generally take their concern for the others welfare as a good reason for their actions.
At present, there seems to be no good reason to accept the theses of psychological, ethical or rational egoism. Nevertheless, egoism in general presents us with a useful insight into the moral life by pointing out that, contra what many of us might suppose, morality and self-interest do not necessarily conflict. Indeed, there may be many cases in which there are good self-regarding reasons for acting ethically and egoism forces us to question whether we pay sufficient attention to legitimate self-interest when assessing moral situations.
A small selection of literature in popular culture dealing with ethical egoism and altruism.
All links retrieved September 14, 2013.
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Posted: June 29, 2016 at 6:31 pm
Jun 29, 2016 17:29
LABADIEVILLE A 2-year-old wearing only diapers was found standing alone Tuesday in the middle of a state highway in Assumption Parish after leaving a home without being noticed, sheriffs deputies said. After finding the child in the care of adults who spotted the child in the highway, deputies arrested Ivone Pina, 41, 118 Continue reading
by David J. Mitchell| firstname.lastname@example.org
Assumption Parish emergency officials on Wednesday eliminated all mandatory evacuation orders for the community and swamp around the Bayou Corne sinkhole but have not given the full all-clear nearly four years after it appeared. The move is the latest, most significant dialing back of parish evacuation orders around the 34-acre lake-like hole in the swamp and Continue reading
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GONZALES The City Council awarded a $53,000 contract to a retired city recreation director this week to maintain the fields of Gonzales parks as part of a broader reorganization of its building and grounds program. Gonzales officials said the change is coming with the acquisition last year of the old Ascension College property between Continue reading
Volunteer Ascension is collecting school supplies and uniforms this summer as part of the agencys efforts to ensure area children are prepared for the upcoming school year. The nonprofit agency is collecting new and used school uniforms at Keans in Prairieville, SACS Western Store, Dutchs Cleaners, LeJeunes Cleaners and The Uniform Post. Volunteer Ascensions 19th Continue reading
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Renovations in Crescent Park have forced Donaldsonville officials to change its annual Independence Day celebration. Instead of celebrating the holiday on July 3 as in past years, the citys celebration, now called Balloons & Boom, is expanding to two days and starts on Friday. Thing kick off at 6 p.m. Friday at the South Louisiana Fairgrounds Continue reading
Country music stars, rides, vendors, a car show and more will be featured at the 2016 Cajun Country Jam on Friday and Saturday at the Lamar-Dixon Expo Center in Gonzales. Performers include Clay Walker, Joe Diffie, Lorrie Morgan, Jamie ONeal and Andy Griggs, Chad Brock, Louisianas LeRoux, Rockin Dopsie Jr., The Gillis Silo Continue reading
Special to The Advocate
The St. Amant Lady Gators that finished as quarterfinalists in the state playoffs had three players selected for the Louisiana Sports Writers Associations Class 5A all-state teams. Infielder Kourtney Gremillion, a Louisiana-Lafayette signee, was chosen. Gremillion batted .610 for the season and added 13 home runs and 62 RBIs. Continue reading
The winners were recently announced in the LSU Agricultural Centers Ascension Parish Home Vegetable Garden Contest. Five adults and three 4-H youth participated in the contest, horticulture agent Craig Roussel said. This year, the group added a school garden category in conjunction with the Greauxing Gardens school garden grant from PCS Nitrogen for 14 primary Continue reading
Join the fight against cystic fibrosis with the 19th annual Price LeBlanc Toyota and Nissan Swamp Pop Music Festival, set for July 15-16 at the Lamar-Dixon Expo Centers Trademart building. The musical lineup on July 15 includes Kenny Fife & Bac Trac at 6 p.m., followed by Warren Storm Willie T and Cypress with Tommy McLain, and wraps Continue reading
Leadership Ascension, a program of the Ascension Chamber of Commerce, graduated its 21st Leadership Ascension class on June 14 at the Clarion Inn and Conference Center in Gonzales. The 35 participants worked in teams during the 10-month program to research and implement projects for the Ascension community. Projects included the Enough is Enough campaign educating Continue reading
Ascension Parish residents interested in becoming a Master Gardener can apply for the Ascension Master Gardener Class of 2016. The program is offered by the LSU Agricultural Center and is designed to recruit and train volunteers to help meet the educational needs of home gardeners. Classes will be taught from 9 a.m. to 2:30 p.m. Mondays Continue reading
Discounted registration for the Gonzales Soccer Club is available throughout July. Sign up online at gonzales soccerclub.com. Walk-in registration also is available from 9 a.m. to 11 a.m. July 30 at Gonzales City Hall. Programs include: 3-YEAR-OLD LITTLE KICKERS: An introduction to the basics of soccer with activities to develop and strengthen Continue reading
Prairieville Primary School students shared their talents during performances at the schools Talent Spectacular this spring. Talents included singing, dancing, gymnastics, karate, guitar, piano and saxophone. Sound and light technicians were fifth-graders Christian Bock and Logan LaBorde. Backstage assistants were Zachary Chasion, Emily Dedon, Angelique Deville, Emily Diaz, Nathan Farmer, David Jimson, David Lloyd, Continue reading
Capital Area Human Services has launched the redesigned realhelpbr.com, a website detailing the organizations services and supports for residents with mental health, substance abuse or developmental disability challenges. Our decision to redesign our website reflects our commitment to improve service accessibility in our region, said Executive Director Jan Kasofsky. We are ensuring that Continue reading
Three Ascension Parish residents were honored May 23 during Our Lady of the Lake Colleges commencement exercises in Baton Rouge. The graduates were among the 190 Our Lady of the Lake College students conferred masters, bachelors or associate degrees during the colleges commencement ceremony at the Baton Rouge River Center Arena. Rachel St. Germain, of Continue reading
Gonzales Middle Schools Bulldog cheerleading squad participated in UCAs Going for the Gold Cheer Camp, held June 4-7. The camp was attended by more than 600 cheerleaders and focused on improving cheer technique, boosting school spirit, team building and leadership, a news release said. The Bulldogs took home four blue ribbons, one red ribbon and the Continue reading
St. Amant Middle School celebrated its second annual Positive Behavioral Interventions and Supports programs Splash Day on May 24. Splash Day is a celebratory event organized to commend the students of St. Amant Middle School who meet a set behavior criteria for the last nine-week grading period of the school year, a news release said. Members Continue reading
Gonzales resident Shirley Bourque was honored with the proclamation of June 16 as Shirley Bourque Day in Ascension Parish. Parish President Kenny Matassa read the proclamation aloud during the Parish Council meeting in Gonzales. Matassa presented the proclamation to Bourque and named her honorary parish president for the day. Bourques five children, including Gonzales City Councilman Continue reading
Elizabeth Lynn Sharon, of Prairieville, graduated from Fort Hays State University in Hays, Kansas, on May 13. Sharon received a bachelor of science degree in medical diagnostic imaging. Continue reading
The 12-year-old-and-under Ascension All Stars won the Cal Ripken District 2 Tournament held recently at Stevens Park in Gonzales. Brennan Hunt was chosen most valuable player of the tournament, a news release said. The team defeated Baton Rouge in round one, giving up three runs in four innings for a 5-3 win. The All Continue reading
The Greater Baton Rouge Food Bank, along with Ascension Parishs Health Unit, will distribute food in Donaldsonville on July 12 and Gonzales on July 13. Distribution will be from 8 a.m. to noon July 12 at the Lemman Center, 1100 Clay St., Donaldsonville, and from 8 a.m. to 11 a.m. July 13 at the Lamar-Dixon Expo Center, Continue reading
The Ascension Advocate this week includes photos from local civic, community and school groups and highlights recent events around Ascension Parish. Continue reading
DISNEY PIXAR CARS END OF SUMMER PARTY: 6 p.m. to 7 p.m., Ascension Parish Library, Dutchtown. LOSS AND GRIEF SUPPORT MEETING: 6 p.m. to 7 p.m., St. Elizabeth Hospital, Sister Vernola conference room, 1125 W. La. 30, Gonzales. MAKE AND TAKE CRAFT: 9 a.m. to 10 a.m. and 3:30 p.m. Continue reading
The Ascension animal shelter, CARAs House, 9894 Airline Highway in Sorrento, is open from 9 a.m. to 6 p.m. Monday through Thursday and 9 a.m. to 4 p.m. Friday (closed from noon to 1 p.m. daily for lunch). It is open from 11 a.m. to 3 p.m. Saturday for adoptions only. The fees are $100 for dogs Continue reading
Cabbage and beef casserole, carrots, whole-wheat bread, chocolate oatmeal bar PILATES: 8:15 a.m. and 9:15 a.m., Gonzales Senior Center PIYO: 9 a.m., Donaldsonville Senior Center BINGO: 10 a.m., Donaldsonville. Sponsor is Canon Hospice ZUMBA GOLD: 10:30 a.m., Gonzales CAJUN NEEDLERS: 12:30 p.m., Gonzales July Fourth Continue reading
The following people were booked into the Ascension Parish prison from June 16-23. ALMOND, KRISTI M.: 43, 37311 New River Canal Road, Geismar, illegal use of controlled dangerous substances in the presence of minors, prohibited acts/drug paraphernalia, possession of heroin. ANNY, RANDY J.: 51, 8168 Everette St., Sorrento, malfeasance in office, prohibited splitting Continue reading
ST. AMANT A motorcyclist was killed early Monday on La. 429 in Ascension Parish when he drove off the road and struck a utility pole, Louisiana State Police said. Jim Thoman, 55, had been riding his 2010 Harley Davidson motorcycle along La. 429 in St. Amant when he drove off the Continue reading
GONZALES Ascension Parish sheriffs deputies and the Louisiana State Fire Marshals Office are investigating why a car stolen from a neighborhood south of Gonzales was found burned this week behind the Mississippi River levee in Iberville Parish. Sheriffs deputies provided surveillance video Friday of a man walking into a nearby convenience store who Continue reading
BAYOU LOURSE An Assumption Parish man admitted to touching a 6-year-old inappropriately and was arrested this week after an informant had warned authorities the girl was being molested by him, parish sheriffs deputies said Friday. Tommy E. Lishman, 47, told Assumption deputies he inappropriately touched the girl on more than one occasion at Continue reading
GONZALES Former Ascension Parish Council Chairman Pat Bell, described as a friend to all, died Wednesday night, parish officials said Thursday. Bell, 68, who was serving on the Pontchartrain Levee District Board at the time of his death, was on the Parish Council from 2008 to 2012 and elected chairman all four years. Continue reading
PALO ALTO Down a state highway just west of Bayou Lafourche where rows of live oaks arch over the road, contractors were installing upgrades Wednesday that Ascension Parish officials hope will prevent the brain-eating amoeba from reoccurring in their public water system to the north. Parish officials are installing a chlorine injection system Continue reading
GONZALES With a new help wanted ad for the Ascension Parish public schools superintendent published in local and area newspapers late last week, the School Board is looking at possibly hiring its next superintendent Aug. 9, the second day of the new school year. But the board has reserved the right Continue reading
GONZALES With the Ascension Parish school districts first senior class in its early college program set to graduate in May, the School Board will be considering a new policy that addresses how valedictorians and salutatorians will be selected. The Early College Option program at River Parishes Community College lets public high school students Continue reading
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Just weeks after returning from a trip to celebrate the 30th anniversary of the sister city or twinning relationship with the residents of Meylan, France, Karen Hatcher has turned her attention to planning to greet the French visitors next year. Thats how its been for 30 years, Hatcher said. The Gonzales Committee on Cultural Affairs, of which Continue reading
Repticon slithers into the Lamar-Dixon Expo Center in Gonzales from 10 a.m. to 5 p.m. Saturday and Sunday. The reptile expo features plenty of exotic animals, vendors and activities. One-day admission is $12 for adults and $5 for children ages 5 to 12. Two-day tickets are $15 for adults, $5 for ages 5 Continue reading
Special to The Advocate
St. Amant pitcher Blayne Enlow has been selected to bring his pitching skills to the USA Baseball 18U Tournament of Stars that will be held in Cary, North Carolina. The USA Baseball Tournament of Stars, presented by Major League Baseball, is made up of 108 of the nations best ballplayers who are considered for the 18-year-old-and-under Continue reading
Prairieville Primary School students raised $17,475.25 for the American Heart Association during the 2015-16 school year, beating the previous years total by $3,600.25. The money goes toward research into new procedures to help heart patients, a news release said Olivia Dellorfano raised the most money in the Jump Rope for Heart fundraiser in honor of Continue reading
Girl Scouts from Geismar and Gonzales have earned the highest awards for their scout level by completing a series of leadership challenges in preparation for their final community or take action project. The Bronze Award is for Girl Scout Juniors in fourth- and fifth-grade. Girl Scout Cadettes in sixth- through eighth-grade are eligible for the Silver Continue reading
The St. Amant Gator Football Camps kicked off a summer of football with its inaugural session June 6-9 for first- through eighth-graders. Coaches and varsity players facilitated two sessions a day of skills camp for local youths. Campers participated in a variety of activities and drills and also discussed positive character traits and team mentality. Continue reading
Five East Ascension High School students attended the Louisiana FFA Convention June 6-10 in Monroe. The students were accompanied by teachers Kiesha Nall and Kolby Gilbert. The students showcased their talents in teaching others how to be servant leaders by planning service projects and picking up litter around Monroe. The East Ascension FFA club Continue reading
Fire Controlman 2nd Class Thomas Melancon, of Convent, was promoted to second class petty officer in June. He has been in the Navy for seven years and serves as Center for Surface Combat Systems Unit Dam Necks CD01 Computer Work Center supervisor in Virginia Beach, Virginia. Melancon is a 2009 graduate of Lutcher High School. His Continue reading
Waguespack Insurance played DMC for the Gonzales Machine Pitch Championship on June 13 at Bergeron and Gaudin Memorial Park in Gonzales. Waguespack was the visiting team and got off to a fast start in the first inning, a news release said. The scoring started when Gavin Higgins hit a triple to score Zach Continue reading
The St. Amant High School Class of 1991 is holding a reunion at 6 p.m. July 9 at 14666 Bayou Terrace, St. Amant. Organizers are inviting teachers, coaches and staffers who were part of the classmates journey to graduation, a news release said. Educators can attend for free and no ticket is required. Class Continue reading
Gonzales High Schools Class of 1966, the last to graduate from the school, gathered for its 50th class reunion May 14 at the Knights of Columbus Hall in Gonzales. The evening began with a social, followed by a dinner including jambalaya by classmate Mike Anderson, covered dishes, finger foods and desserts, all prepared by the classmates. Continue reading
Thirty-seven boys and girls from Geismar Caring Parents 19th summer camp recently participated in the Klub K.I.D. camp presented by historian and multi-instrumentalist Bill Summers. The children received lessons on drums, music producing and how to make shakerays. Summers talked about the history of music in the slave culture in Louisiana. The three-day camp Continue reading
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Posted: June 21, 2016 at 6:45 am
Story and photos by Scott & Wendy Bannerot.
Few South Pacific voyagers miss a stop at the Kingdom of Tonga. The Vava’u Group attracts the highest number of visiting boats, with deep, protected passageways between a large cluster of picturesque islands, permitting relaxed cruising among lovely, sheltered anchorages. A growing number of boats venture south into the lower-lying, coral-strewn Ha’apai Group, and a steady annual proportion sail onward to the country’s southernmost main island of Tongatapu for a stop at the capital town of Nuku’alofa. There they provision and procure New Zealand visas from the consulate before heading south to escape the November onset of cyclone season. By this time nearly all have heard of North and South Minerva Reefs, two rings of nearly submerged coral lying some 270 nautical miles southwest of Tongatapu, somewhat to the west of the rhumb line to New Zealand.
This position, and the existence of navigable passes into the protected inner lagoons of both atolls, plays on various portions of a seafarer’s brain. No one wants to hear the roar of breakers dead ahead on a dark, stormy night or feel the crunching lurch of your hull piling forcibly onto a solid piece of real estate in mid-ocean. On the other hand, many dream of anchoring alone in tranquil, gin-clear lagoons teeming with sea life for a restful break during a passage, or of riding out a severe storm on the hook, protected from the brunt of the conditions by solid walls of coral. We were no different from anyone else, having made two passages between Tonga and New Zealand without laying eyes on either of the Minervas. By the time our third passage was imminent, we knew a stop was inevitable.
We’d arrived in Tonga’s Vava’u Group again after 18 months in New Zealand, including a four-month return to the U.S. for medical and business issues that could no longer be ignored. During this time our 41-foot aluminum sloop Elan awaited us on an Auckland hardstand. Our first time through Vava’u, nearly two years before, had been late in the winter sailing season. We’d spent only one short week before the looming storm season compelled us to set sail. We knew we hadn’t scratched the surface of what this group of islands had to offer, and our determination to do it justice on the second time around was strong. We’d sailed up the eastern quadrant of a fortuitously stalled high, fanned by southeasterlies coming over the starboard quarter on a direct 10-day shot from Auckland to Neiafu. We cleared customs one hour before my sister, her husband, and her father-in-law arrived at the airport on a long-planned visit from Wyoming. Our spirits soared as we loaded everyone’s gear aboard and made ready to cast off from the fuel dock.
Ambitious plans to visit Fiji and Vanuatu fell by the wayside as two other couples came out to visit, we were adopted by several local families, and we accepted an invitation to participate on a local fishing boat in the annual billfish tournament. Before we knew it, we’d been in Vava’u’s calm embrace for nearly the entire South Pacific winter. We’d had countless wonderful days, exploring Swallow’s and Mariner’s caves, photographing a mother humpback whale and her calf swimming laconically beside Elan, and spending time under and above water with some very special people and marine life. Suddenly the October spring window for the voyage back to New Zealand was upon us.
We fished and dived our way south through the Ha’apai and Nomuka Groups, and arrived in Nuku’alofa after an easy overnight sail. There we consolidated our crew with Kiwi friends Ken Kiddie and Hans Swete, who’d earlier committed to the trip south as a way of gaining their first offshore passage. The four of us plotted and dreamed about a stop at the Minervas over cold beers at Nuku’alofa’s waterfront Billfish Bar, and we kept a sharp eye out for an appropriate weather window.
As if on cue, the progression of strong winter highs passing by to the south of us slowed and settled, and on a sparkling sunny afternoon we picked our way around Atata Island, out the channel through the reef, and set a course for North Minerva Reef.
The mystique of the Minervas Elan’s hull bit into the ocean swell under full genoa and mainsail, close reaching into light south-southeasterly conditions. The trolling lines went out, and the conversation turned quickly to stories about the Minervas-boats that had survived the infamous Queen’s Birthday and lesser storms anchored inside the reefs; shipwrecks and disappearances, either documented or suspected, in the vicinity of the reefs; and reports of abundant fish and lobsters, and of an unspoiled environment little-disturbed by humans.
Capt. H. M. Denham, aboard the H.M.S. Herald, surveyed the reefs in 1854 and named them after the whaling ship Minerva, wrecked on South Minerva after setting out from Sydney in 1829. The captain of the Minerva was not aware of a large, poorly defined area called Nicholson’s shoals added to Pacific charts not long before departure, and was therefore quite surprised when the brig drove up hard on the reef at 0200 on September 9. Most of the 23-man crew, and a dog, made it from the wreck to the inner lagoon aboard two whaleboats, but the drunken whaling master and two crew refused to leave the wreck, despite the fact that it was under siege from heavy breaking seas. They survived the night lashed to the bowsprit of the broken hull, and the entire complement set sail the following day aboard three whaleboats loaded with water caskets and what provisions they could salvage from the wreck. One boat began leaking seriously, prompting one of the two remaining boats to sail off to save themselves. The remaining whaleboat eventually took aboard the entire crew of the sinking boat for a total of 15 men and the dog, leaving only six inches or so of freeboard. The desperate castaways, out of fresh water and food, sighted the island of Vatoa, an outlier of Fiji’s Lau Group, on September 15 and reached the outer reef, making their way ashore after splintering the whaleboat on the coral. Eight of the men remained with the friendly locals, and seven repaired the whaleboat and set sail again only to wreck once more on a Tongan island before eventually making their way home to Sydney. The crew of the boat that hastily abandoned the doomed men was never seen again.
Another famous incident occurred on the maiden voyage of the wooden schooner Strathcona, sailing north soon after completion in Auckland in 1914, only to unexpectedly crash up onto South Minerva Reef on the sixth day of the voyage and break apart. The crew of 13 consolidated materials and constructed a raft to live aboard in the lagoon, and then the captain and three crew sailed the schooner’s launch north to the nearest inhabited island, Ono-i-Lau, Fiji. Meanwhile a rescue vessel from New Zealand found the survivors on the raft at South Minerva, as well as the rescuers returning aboard a Fijian cutter to save their crewmates.
Many other wrecks on the two reefs are mysteries, with hulls and remains noted by passing vessels at various times and no signs of survivors. One such wreck was a largely intact Japanese fishing vessel that appeared in 1960 on South Minerva, the crew apparently taken off safely by the crew of another fishing vessel, whom they were able to contact by radio. This wreck was to play a critical role in what remains one of the most incredible maritime survival tales in recent history.
The tragedy of the Tuaikaepau Tuaikaepau was a 51-foot wooden cutter completed in 1902 at the same Auckland boatyard that later built the Strathcona. On the night of July 7, 1962, she was bound from Nuku’alofa for a refit in New Zealand, booming along close-hauled in boisterous southeasterly conditions. Experienced captain David Fifita commanded the seven-man crew and 10 passengers, mostly amateur boxers looking to make some money in New Zealand. The vessel smashed onto the eastern side of South Minerva Reef at seven knots in the darkness. This started a 14-week odyssey that would see only 12 of the men survive.
The 17 Tongans took refuge in the Japanese fishing boat wreck, constructed an ingenious water-distillation plant, and fed themselves by walking the reef flat to fish and collect seafood. Finally on Saturday, October 7, with three men dead, conditions becoming increasingly desperate, and hopes of rescue long gone, Fifita, his son Sateki, and ship’s carpenter Tevita Uaisele embarked on an epic rescue mission in a small craft crudely fashioned (with no tools) from remains of the two wrecks. David set a course for due north, armed only with a compass, sextant, nautical almanac, and a crude chart engraved on a plank, and no way to measure time accurately. He navigated by sun shots and dead reckoning. By Wednesday they were out of food and water. On Thursday they managed to catch a seabird that landed on the tiller and drank its blood. They bypassed treacherous, reef-encircled Ono-i-Lau and Matuku, and at midnight the following Saturday, in greatly weakened condition, David calculated that it was time to head due west in hopes of reaching much larger Kandavu.
The mountainous profile of the eastern end of Kandavu jutted above the horizon at dawn, confirming David’s emergency navigation skills and filling the severely dehydrated, starving men with hope. They sailed cautiously toward the reef, only to have an oversized breaking swell toss the sturdy wooden craft crashing over the reef, throwing the occupants overboard and capsizing the boat. This left little choice but to attempt a swim against the tide to the tiny outlying island of Nmbia approximately 1.3 nautical miles away. David’s son disappeared two thirds of the way to shore. The two survivors dragged themselves up the beach, quenched their thirst with green coconuts, and hiked to a village to summon help for their crewmates back on South Minerva. After some confusion, word finally reached the Royal New Zealand Air Force station at Suva, and the commander ordered an immediate night flight Monday to drop supplies to the survivors on South Minerva, followed by a rescue via Sunderland flying boat the following morning. The supply flight likely saved the life of at least one of the weakened castaways, though one man had died the previous evening. Olaf Ruhen’s Minerva Reef (Halstead Press, Sydney, 1963) is a worthwhile, highly detailed account of the entire ordeal, and voyagers can pick up the brief recent account Minerva Reef by survivor Fine Feuiaki in Tongan bookstores (Friendly Islands Bookshop, Tonga, 1992). Overnight at North Minerva Thoughts of the imperiled voyagers before us prevailed as light, fluky winds had us motorsailing for parts of the second and third days of the passage. By the third evening the southeasterly breeze stiffened. We made good time under double-reefed genoa and mainsail, and at first light sighted the white line of breakers along the north side of North Minerva that had been painting a radar target during the pre-dawn hours. Soon after, the left outrigger bait disappeared in a splashing strike, and Ken worked a 22-pound bull mahi mahi (Coryphaena hippurus, also called dolphin or dorado) to the gaff. We made our way into the wide, easy pass in the northwest corner of the submerged atoll at 0900 in good light and dropped the anchor 20 feet down to the deep fine sand. Soon the dinghy was in the water and we all piled in for a free-diving expedition to a series of nearby coral heads.
We already had plenty of fish, so we did some sightseeing and looked around for lobsters under ledges and domes of coral. The area teemed with fish, flourishing with the near total absence of hook and line or other fishing effort. We spotted only two lobsters, both far under the coral and inaccessible, before heading out the pass for a dive on the outside reef. Here the visibility was nearly limitless, the coral vibrant and dense. An occasional small gray reef shark wagged lazily by the steep drop-off below us, none bothering to investigate the newcomers.
As we motored back in the pass, taking advantage of the countercurrent along the margin of the now outgoing tide, we noticed Elan’s mast swinging irregularly. Despite being inside the lagoon, the vessel was rolling. The shield of coral rubble on the reef crest was mostly submerged at this nearly high-tide stage, offering less opposition to wind-driven waves piling across the reef flat. The formerly placid lagoon now had a distinctly lumpy surface-plenty tenable, just not as comfortable.
We dined on fresh-grilled mahi mahi and turned in early, awakening to a thin overcast, slick calm morning. We decided to stow the dinghy, rig up some fishing lines, and make a slow, fuel-saving motorsail the 20-odd miles to South Minerva Reef. Hans bagged a school-sized yellowfin tuna, and we all enjoyed the sight of a small (150 pounds) blue marlin crashing the left outrigger bait, missing, then playfully grabbing a small tuna lure before leaping in a graceful arc to freedom. Exploring South Minerva A pack of hungry wahoo attacked our lures just off the northwest corner of South Minerva Reef. Their razor-sharp teeth luckily missed the monofilament leaders of our tuna/billfish lures before taking off, but not before one rocketed vertically, high above the deck with our hookless teaser clamped fleetingly in its jaws. We entered the pass, which was less distinct than North Minerva, but no problem if one follows the well-defined southwestern (right-hand) margin into the lagoon, avoiding the easily sighted coral heads as they crop up from time to time inside the lagoon. We picked our way around the inner rim of the lagoon, anchoring near a large, block-like aggregation of coral on the eastern side. This turned out to be the work of an Australian survey team. The location was not far from the site of the long-gone Japanese wreck used by the Tuaikaepau crew, and some boat remains were strewn in the area. We drank in the desolate seascape, barely punctuated by a jagged rim of reef. The muted hiss of breaking seas was the only sound as we tried to imagine being shipwrecked here for 14 weeks, surviving by foraging and by consuming tightly rationed portions of water, distilled with great daily effort, bearing the sorrow of watching crewmates slowly die, and somehow building a boat capable of a substantial bluewater passage-with no tools. Firing up the grill and the music system returned us to the present, and soon the aroma of sizzling marinated tuna steaks dominated our thoughts. We suspended the tuna carcass into the water from a rope tied to the port transom cleat and retired below for the meal-we’d done the same thing the night before with the mahi mahi carcass and found the rope cleanly severed in the morning. Just as we finished dinner, a loud splash accompanying a sudden lurch of the boat sent us all topside in time to see several gray reef sharks circling hungrily. We didn’t need the bright arch light to see the dark silhouettes against the light sand bottom in the bright reflected light of the full moon, gracefully gliding in ever-tighter circles, then swimming off, only to wheel around and swim straight back in. We fed them the carcass after taking a few photos. Two solid days of non-stop reef walking, free-diving, dinghy fishing, and lobster hunting proved South Minerva to be every bit as bountiful and spectacular as we’d dreamed. We caught three different species of spiny lobsters during daylight hours hiding in shallow lagoon coral heads, at least two of which characteristically spend their days at significant depths on the outer reef at most tropical Pacific locations. Normally these are caught only at night by walking the reef flat on certain moon phases. Giant clams (Tridacna), increasingly scarce in most Indo-Pacific locations due to overexploitation, were abundant, as were innumerable other reef denizens of every description-brilliant blue starfish; colorful tropical fish species and moray eels; sea urchins and sea cucumbers; rich and brilliantly hued corals; big fat groupers or coral trout (Variola louti) arrogantly patrolling the pass. This was a chance to enjoy the natural South Pacific in all of its splendor, virtually unaltered by the strains humans exert on the planet. It was a good thing Ken and Hans were along, with the pressures of land jobs and responsibilities never far from mind. Otherwise our euphoria might have sorely tempted us to delay a prudently timed voyage southward. This trip should be made before tropical lows begin abutting to subtropical highs, spawning the hurricane-force easterlies not uncommon in later November and December in the vicinity of New Zealand’s North Island. So, at noon on the third day after arriving, we exited the pass in calm, sunny weather, with the weatherfax showing favorable timing for a jaunt south, with the exception of one mild low developing in the Tasman Sea. We paused outside the pass long enough to do some deep-dropping with an electric fishing reel, catching a couple of delicious groupers from as deep as 750 feet. The low gave us light northerlies and was not showing signs of deepening, so we finished securing the deck and set sail for New Zealand at 1700. Heading south We’d had two fast, uneventful previous passages between Tonga and New Zealand but were no less mindful of the possibility of experiencing heavy conditions. The moon loomed huge and orange out of the sea off the port quarter on the first night, making the ocean surface glimmer. We caught a cow mahi mahi of about 13 pounds the next afternoon and entered the scattered deluges and shifting wind directions of the still-weak low the following afternoon. The center of the low passed below us before sunset, and we’d never seen more than 22 knots of wind. Favorable winds from light to not more than 25 knots settled in for the remainder of the passage. We fished two billfish lures during daylight hours and caught and released both a rare shortbill spearfish and a striped marlin on successive days. Two days north of our destination a pod of (mammal) dolphin came alongside, immediately followed by a modest-sized marlin blasting onto the teaser and a big strike on the right outrigger lure, which turned out to be a 70-pound-class yellowfin tuna. With that we retired the fishing rods and concentrated on making maximum speed over the last 250 nautical miles to Opua, rather than hover in what might be fairly termed the “screw-up zone” for this particular passage. Many crews tend to relax a little early, knowing they’ve nearly made it, only to get a pasting when the bottom drops out of a low as it passes over warm ocean currents just above the North Island.
We sailed into Opua exactly seven days after departing South Minerva Reef on a beautiful and sunny, though distinctly cool, late afternoon and retired to the quiet of the Kawakawa River anchorage after check-in.
Bright smiles lit the aft settee over hot soup and rum as we celebrated our good fortune, and the rarified afterglow of visiting a place as magnificent and remote as the Minerva Reefs.
Scott and Wendy Bannerot, based in New Zealand as they voyage the South Pacific, are the authors of The Cruiser’s Guide to Fishing, recently published by International Marine in Rockport, Maine.
Posted: June 17, 2016 at 4:55 am
Written by Patrick Dixon
Futurist Keynote Speaker: Posts, Slides, Videos – What is Human Cloning? How to Clone. But Ethical?
Human cloning: who is cloning humans and arguments against cloning (2007)
How human clones are being made – for medical research. Arguments for and against human cloning research. Why some people want to clone themselves or even to clone the dead (and not just cloning pets).
Why investors are moving away from human cloning and why human cloning now looks a last-century way to fight disease (2007)
Should we ban human cloning? Arguments against cloning
An abnormal baby would be a nightmare come true. The technique is extremely risky right now. A particular worry is the possibility that the genetic material used from the adult will continue to age so that the genes in a newborn baby clone could be – say – 30 years old or more on the day of birth. Many attempts at animal cloning produced disfigured monsters with severe abnormalities. So that would mean creating cloned embryos, implanting them and destroying (presumably) those that look imperfect as they grow in the womb. However some abnormalities may not appear till after birth. A cloned cow recently died several weeks after birth with a huge abnormality of blood cell production. Dolly the Sheep died prematurely of severe lung disease in February 2003, and also suffered from arthritis at an unexpectedly early age – probably linked to the cloning process.
Even if a few cloned babies are born apparently normal we will have to wait up to 20 years to be sure they are not going to have problems later -for example growing old too fast. Every time a clone is made it is like throwing the dice and even a string of “healthy” clones being born would not change the likelihood that many clones born in future may have severe medical problems. And of course, that’s just the ones born. What about all the disfigured and highly abnormal clones that either spontaneously aborted or were destroyed / terminated by scientists worried about the horrors they might be creating.
A child grows up knowing her mother is her sister, her grandmother is her mother. Her father is her brother-in-law. Every time her mother looks at her, she is seeing herself growing up. Unbearable emotional pressures on a teenager trying to establish his or her identity. What happens to a marriage when the “father” sees his wife’s clone grow up into the exact replica (by appearance) of the beautiful 18 year old he fell in love with 35 years ago? A sexual relationship would of course be with his wife’s twin, no incest involved technically.
Or maybe the child knows it is the twin of a dead brother or sister. What kind of pressures will he or she feel, knowing they were made as a direct replacement for another? It is a human experiment doomed to failure because the child will NOT be identical in every way, despite the hopes of the parents. One huge reason will be that the child will be brought up in a highly abnormal household: one where grief has been diverted into makeing a clone instead of adjusting to loss. The family environment will be totally different than that the other twin experienced. That itself will place great pressures on the emotional development of the child. You will not find a child psychiatrist in the world who could possibly say that there will not be very significant emotional risk to the cloned child as a result of these pressures.
What would Hitler have done with cloning technology if available in the 1940s? There are powerful leaders in every generation who will seek to abuse this technology for their own purposes. Going ahead with cloning technology makes this far more likely. You cannot have so-called therapeutic cloning without reproductive cloning because the technique to make cloned babies is the same as to make a cloned embryo to try to make replacement tissues. And at the speed at which biotech is accelerating there will soon be other ways to get such cells – adult stem cell technology. It is rather crude to create a complete embryonic identical twin embryo just to get hold of stem cells to make – say – nervous tissue. Much better to take cells from the adult and trigger them directly to regress to a more primitive form without the ethical issues raised by inserting a full adult set of genes into an unfertilised egg.
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