Science is Cool....

[Fish]

This is a repository for all cool scientific discussion and fascination. Scientific facts, theories, and overall cool scientific stuff that you'd like to share with others. Stuff that makes you smile and wonder at the amazing shit going on around us, that most people don't notice.

Post pictures, vidoes, stories, or links. Ask questions. Share science.

Why should I care?:

[Dave Lane]

Originally Posted by Buehler445

I happened to be watching the 10:00 news on NBC out of Wichita. I normally try not to watch that crap, but there was a news report that said 1 in 5 teachers don't even record grades for Science.

WHAT. THE. ****.

That is crap!

Of and if you didn't see this in the lounge try this... Amazing

http://workshop.chromeexperiments.com/stars/

[ZepSinger]

Originally Posted by Dave Lane

That is crap!

Of and if you didn't see this in the lounge try this... Amazing

http://workshop.chromeexperiments.com/stars/

incredible. Almost incomprehensible how small our little world is in relation to everything else...

[cyborgtable]

The US Navy has unveiled plans to make jet fuel out of seawater, with the help of electrochemistry and gas-to-liquid fuels technology.


Researchers at the Naval Research Laboratory (NRL) in Washington, DC, have demonstrated that it is possible to obtain CO2 and hydrogen from seawater, then convert these to hydrocarbons suitable for fuelling aircraft.

Keeping ships and aircraft fuelled is a major operation for any navy. The US Navy has 15 refuelling ships — known as oilers — and last year these delivered 600 million gallons of fuel to ships under way. Generating their own fuel would free up the ships from these logistics and make the navy less dependent on imported oil, said Nancy Willauer, a research chemist who worked on the project.




Refuelling at sea is an expensive process that often relies on imported oil

The technology uses electrochemistry to recover CO2 from seawater, where it is present at a concentration 140 times greater than in air, mostly as bicarbonate with traces of carbonate and dissolved CO2 gas (carbonic acid). The navy team developed a device called an electrochemical acidification cell, which uses ion-permeable polymer membranes and an electric current to lower the pH of the seawater. The three forms of carbon in the water exist in a state of equilibrium, and making the water more acidic alters the balance between them, making gaseous CO2 the most stable form. The cell produces hydrogen gas at its cathode as a by-product.

After demonstrating this at a small scale, the NRL team scaled it up to a skid process — a freestanding unit on a scale similar to that which might be used in the field — which can reportedly recover up to 92 per cent of the CO2 from seawater taken from the Gulf of Mexico.


The skid unit at NRL, which can recover up to 92 per cent of the CO2 from seawater

Converting these two gases into hydrocarbons uses a technology similar to the Fischer-Tropsch process, which has been used for many years to make fuel from ‘synthesis gas’, a mixture of hydrogen and carbon monoxide. ‘By modifying the surface compositions of iron catalysts in fixed-bed reactors, NRL has successfully improved CO2 conversion efficiencies by up to 60 per cent,’ Willauer said.

The iron-catalysed process produces short-chain unsaturated hydrocarbons, which can then be combined to make compounds containing nine to 16 carbon atoms; treating these with a catalyst supported on porous nickel converts them into a liquid suitable as jet fuel, the researchers said.

NRL is now looking into improving the efficiency of the process and scaling it up and believes that the final process should be able to produce fuel at a price of between $3 and $6 per gallon (between fifty pence and £1 per litre). The process could be powered using nuclear electricity or by a method known as solar OTEC, which uses the natural temperature gradient between different levels of the ocean to power electricity generation, the team suggested. The research can be read in this paper.


Read more: http://www.theengineer.co.uk/sectors...#ixzz2CRICukih

[cyborgtable]

(CBS News) Two men who've had HIV for years may now be free of the disease following bone marrow transplants, researchers at Brigham and Women's Hospital in Boston announced Thursday.


The new research has some attendees at the XIX International AIDS Conference in Washington, D.C. hopeful for a cure.

Timothy Ray Brown, man thought to be first "cured" of AIDS, says he's still cured
Man "cured" of AIDS: Timothy Ray Brown

Both patients were being treated for cases of cancer. One of the patients underwent a bone marrow transplant two years ago at the Dana-Farber/Brigham and Women's Cancer Center in Boston, the other had the procedure done four years ago at the same hospital. NBCNews.com reports that one of the patients is in his 50s and has been infected since the early 1980s towards the beginning of the AIDS epidemic and the other man, in his 20s, was infected at birth.

Both stayed on their antiretroviral medication regimens, the standard treatment of HIV, following the transplants.

The researchers discovered that overtime as the patients' cells were replaced by cells from the donor, evidence of HIV in the patients' blood tests disappeared. The researchers also said both patients have no signs of HIV in their DNA or RNA and levels of their disease-fighting antibodies have also decreased. The researchers think the medications helped allow these cells to be replaced.

"This gives us some important information," one of the researchers Dr. Daniel Kuritzkes, an infectious disease specialist at the hospital and Harvard Medical school said in a press release. "It suggests that under the cover of antiretroviral therapy, the cells that repopulated the patient's immune system appear to be protected from becoming re-infected with HIV."

The researchers themselves won't call it a cure yet, saying they still need to check more tissues for traces of the disease. But they were surprised to see no signs of HIV beyond what's seen in a blood test.

"We expected HIV to vanish from the patients' plasma, but it is surprising that we can't find any traces of HIV in their cells," said co-resarcher Dr. Timothy Henrich, also of BWH and Harvard. "The next step is to determine if there are any traces of HIV in their tissue."

The researchers' announcement comes days after Timothy Ray Brown, the man known as the "Berlin Patient," held a press conference in Washington, D.C., to say he's still cured of AIDS five years after undergoing a bone marrow blood transplant.

However, the researchers noted differences in their two patients' treatment compared to that of Brown.

In Brown's case, his donor was specifically chosen because he possessed a genetic mutation that's found in one person of Caucasian people that makes them resistant to developing HIV. But the donors for the two Boston patient were selected at random. Additionally, Brown had stopped taking his antiretroviral medications following his transplant, while the Boston patients have stayed on the drugs.

Traces of HIV have been found in Brown's tissues, causing some to say the virus had returned, but he denied that at his press conference, saying those are merely dead remnants of the virus still in his body.

"We can't say we've replicated the Berlin patient's cure at this point because our patients remain on antiretroviral therapy," Kuritzkes told NPR. He did add to the station that it's "entirely possible" the two patients will remain disease-free.

Dr. Steven Deeks, an HIV researcher at the University of California, San Francisco, told The Washington Post, "Today might be considered a day when the research agenda moves from basic science and the lab into the clinic," adding that "it is an absolutely critical advancement."

Not all experts were impressed. Dr. Jay Levy, another HIV researcher at UC San Francisco, told The Boston Globe, "The real news would be if they could stop the drugs and not have the virus come back."

[cyborgtable]

Potential magic bullet vs caner?

PHILADELPHIA — A year ago, when chemotherapy stopped working against his leukemia, William Ludwig signed up to be the first patient treated in a bold experiment at the University of Pennsylvania. Mr. Ludwig, then 65, a retired corrections officer from Bridgeton, N.J., felt his life draining away and thought he had nothing to lose.
Multimedia
Graphic
Gene Therapy

Attacking a Tumor

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University of Pennsylvania

Tiny magnetic beads force the larger T-cells to divide before they are infused into the patient.
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Jessica Kourkounis for The New York Times

FULL OF LIFE William Ludwig, 66, in his RV parked at his home in New Jersey.
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Jessica Kourkounis for The New York Times

MAJOR ADVANCE Dr. Bruce Levine lifted cells from a freezer in his lab in Philadelphia last week. Special cell-culturing techniques may have contributed to the lab’s success.
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Doctors removed a billion of his T-cells — a type of white blood cell that fights viruses and tumors — and gave them new genes that would program the cells to attack his cancer. Then the altered cells were dripped back into Mr. Ludwig’s veins.

At first, nothing happened. But after 10 days, hell broke loose in his hospital room. He began shaking with chills. His temperature shot up. His blood pressure shot down. He became so ill that doctors moved him into intensive care and warned that he might die. His family gathered at the hospital, fearing the worst.

A few weeks later, the fevers were gone. And so was the leukemia.

There was no trace of it anywhere — no leukemic cells in his blood or bone marrow, no more bulging lymph nodes on his CT scan. His doctors calculated that the treatment had killed off two pounds of cancer cells.

A year later, Mr. Ludwig is still in complete remission. Before, there were days when he could barely get out of bed; now, he plays golf and does yard work.

“I have my life back,” he said.

Mr. Ludwig’s doctors have not claimed that he is cured — it is too soon to tell — nor have they declared victory over leukemia on the basis of this experiment, which involved only three patients. The research, they say, has far to go; the treatment is still experimental, not available outside of studies.

But scientists say the treatment that helped Mr. Ludwig, described recently in The New England Journal of Medicine and Science Translational Medicine, may signify a turning point in the long struggle to develop effective gene therapies against cancer. And not just for leukemia patients: other cancers may also be vulnerable to this novel approach — which employs a disabled form of H.I.V.-1, the virus that causes AIDS, to carry cancer-fighting genes into the patients’ T-cells. In essence, the team is using gene therapy to accomplish something that researchers have hoped to do for decades: train a person’s own immune system to kill cancer cells.

Two other patients have undergone the experimental treatment. One had a partial remission: his disease lessened but did not go away completely. Another had a complete remission. All three had had advanced chronic lymphocytic leukemia and had run out of chemotherapy options. Usually, the only hope for a remission in such cases is a bone-marrow transplant, but these patients were not candidates for it.

Dr. Carl June, who led the research and directs translational medicine in the Abramson Cancer Center at the University of Pennsylvania, said that the results stunned even him and his colleagues, Dr. David L. Porter, Bruce Levine and Michael Kalos. They had hoped to see some benefit but had not dared dream of complete, prolonged remissions. Indeed, when Mr. Ludwig began running fevers, the doctors did not realize at first that it was a sign that his T-cells were engaged in a furious battle with his cancer.

Other experts in the field said the results were a major advance.

“It’s great work,” said Dr. Walter J. Urba of the Providence Cancer Center and Earle A. Chiles Research Institute in Portland, Ore. He called the patients’ recoveries remarkable, exciting and significant. “I feel very positive about this new technology. Conceptually, it’s very, very big.”

Dr. Urba said he thought the approach would ultimately be used against other types of cancer as well as leukemia and lymphoma. But he cautioned, “For patients today, we’re not there yet.” And he added the usual scientific caveat: To be considered valid, the results must be repeated in more patients, and by other research teams.

Dr. June called the techniques “a harvest of the information from the molecular biology revolution over the past two decades.”

Hitting a Genetic Jackpot

To make T-cells search out and destroy cancer, researchers must equip them to do several tasks: recognize the cancer, attack it, multiply, and live on inside the patient. A number of research groups have been trying to do this, but the T-cells they engineered could not accomplish all the tasks. As a result, the cells’ ability to fight tumors has generally been temporary.

The University of Pennsylvania team seems to have hit all the targets at once. Inside the patients, the T-cells modified by the researchers multiplied to 1,000 to 10,000 times the number infused, wiped out the cancer and then gradually diminished, leaving a population of “memory” cells that can quickly proliferate again if needed.

The researchers said they were not sure which parts of their strategy made it work — special cell-culturing techniques, the use of H.I.V.-1 to carry new genes into the T-cells, or the particular pieces of DNA that they selected to reprogram the T-cells.

The concept of doctoring T-cells genetically was first developed in the 1980s by Dr. Zelig Eshhar at the Weizmann Institute of Science in Rehovot, Israel. It involves adding gene sequences from different sources to enable the T-cells to produce what researchers call chimeric antigen receptors, or CARs — protein complexes that transform the cells into, in Dr. June’s words, “serial killers.”

Mr. Ludwig’s disease, chronic lymphocytic leukemia is a cancer of B-cells, the part of the immune system that normally produces antibodies to fight infection. All B-cells, whether healthy or leukemic, have on their surfaces a protein called CD19. To treat patients with the disease, the researchers hoped to reprogram their T-cells to find CD19 and attack B-cells carrying it.

But which gene sequences should be used to reprogram the T-cells, from which sources? And how do you insert them?

Various research groups have used different methods. Viruses are often used as carriers (or vectors) to insert DNA into other cells because that kind of genetic sabotage is exactly what viruses normally specialize in doing. To modify their patients’ T-cells, Dr. June and his colleagues tried a daring approach: they used a disabled form of H.I.V.-1. They are the first ever to use H.I.V.-1 as the vector in gene therapy for cancer patients (the virus has been used in other diseases).

The AIDS virus is a natural for this kind of treatment, Dr. June said, because it evolved to invade T-cells. The idea of putting any form of the AIDS virus into people sounds a bit frightening, he acknowledged, but the virus used by his team was “gutted” and was no longer harmful. Other researchers had altered and disabled the virus by adding DNA from humans, mice and cows, and from a virus that infects woodchucks and another that infects cows. Each bit was chosen for a particular trait, all pieced together into a vector that Dr. June called a “Rube Goldberg-like solution” and “truly a zoo.”

“It incorporates the ability of H.I.V. to infect cells but not to reproduce itself,” he said.

To administer the treatment, the researchers collected as many of the patients’ T-cells as they could by passing their blood through a machine that removed the cells and returned the other blood components back into the patients’ veins. The T-cells were exposed to the vector, which transformed them genetically, and then were frozen. Meanwhile, the patients were given chemotherapy to deplete any remaining T-cells, because the native T-cells might impede the growth of the altered ones. Finally, the T-cells were infused back into the patients.

Then, Dr. June said, “The patient becomes a bioreactor” as the T-cells proliferate, pouring out chemicals called cytokines that cause fever, chills, fatigue and other flulike symptoms.

The treatment wiped out all of the patients’ B-cells, both healthy ones and leukemic ones, and will continue to do for as long as the new T-cells persist in the body, which could be forever (and ideally should be, to keep the leukemia at bay). The lack of B-cells means that the patients may be left vulnerable to infection, and they will need periodic infusions of a substance called intravenous immune globulin to protect them.

So far, the lack of B-cells has not caused problems for Mr. Ludwig. He receives the infusions every few months. He had been receiving them even before the experimental treatment because the leukemia had already knocked out his healthy B-cells.

One thing that is not clear is why Patient 1 and Patient 3 had complete remissions, and Patient 2 did not. The researchers said that when Patient 2 developed chills and fever, he was treated with steroids at another hospital, and the drugs may have halted the T-cells’ activity. But they cannot be sure. It may also be that his disease was too severe.

The researchers wrote an entire scientific article about Patient 3, which was published in The New England Journal of Medicine. Like the other patients, he also ran fevers and felt ill, but the reaction took longer to set in, and he also developed kidney and liver trouble — a sign of tumor lysis syndrome, a condition that occurs when large numbers of cancer cells die off and dump their contents, which can clog the kidneys. He was given drugs to prevent kidney damage. He had a complete remission.

What the journal article did not mention was that Patient 3 was almost not treated.

Because of his illness and some production problems, the researchers said, they could not produce anywhere near as many altered T-cells for him as they had for the other two patients — only 14 million (“a mouse dose,” Dr. Porter said), versus 1 billion for Mr. Ludwig and 580 million for Patient 2. After debate, they decided to treat him anyway.

Patient 3 declined to be interviewed, but he wrote anonymously about his experience for the University of Pennsylvania Web site. When he developed chills and a fever, he said, “I was sure the war was on — I was sure C.L.L. cells were dying.”

He wrote that he was a scientist, and that when he was young had dreamed of someday making a discovery that would benefit mankind. But, he concluded, “I never imagined I would be part of the experiment.”

When he told Patient 3 that he was remission, Dr. Porter said, they both had tears in their eyes.

Not Without Danger to Patients

While promising, the new techniques developed by the University of Pennsylvania researchers are not without danger to patients. Engineered T-cells have attacked healthy tissue in patients at other centers. Such a reaction killed a 39-year-old woman with advanced colon cancer in a study at the National Cancer Institute, researchers there reported last year in the journal Molecular Therapy.

She developed severe breathing trouble 15 minutes after receiving the T-cells, had to be put on a ventilator and died a few days later. Apparently, a protein target on the cancer cells was also present in her lungs, and the T-cells homed in on it.

Researchers at Memorial Sloan Kettering Cancer in New York also reported a death last year in a T-cell trial for leukemia (also published in Molecular Therapy). An autopsy found that the patient had apparently died from sepsis, not from the T-cells, but because he died just four days after the infusion, the researchers said they considered the treatment a possible factor.

Dr. June said his team hopes to use T-cells against solid tumors, including some that are very hard to treat, like mesothelioma and ovarian and pancreatic cancer. But possible adverse reactions are a real concern, he said, noting that one of the protein targets on the tumor cells is also found on membranes that line the chest and abdomen. T-cell attacks could cause serious inflammation in those membranes and mimic lupus, a serious autoimmune disease.

Even if the T-cells do not hit innocent targets, there are still risks. Proteins they release could cause a “cytokine storm”— high fevers, swelling, inflammation and dangerously low blood pressure — which can be fatal. Or, if the treatment rapidly kills billions of cancer cells, the debris can damage the kidney and cause other problems.

Even if the new T-cell treatment proves to work, the drug industry will be needed to mass produce it. But Dr. June said the research is being done only at universities, not at drug companies. For the drug industry to take interest, he said, there will have to be overwhelming proof that the treatment is far better than existing ones.

“Then I think they’ll jump into it,” he said. “My challenge now is to do this in a larger set of patients with randomization, and to show that we have the same effects.”

Mr. Ludwig said that when entered the trial, he had no options left. Indeed, Dr. June said that Mr. Ludwig was “almost dead” from the leukemia, and the effort to treat him was a “Hail Mary.”

Mr. Ludwig said: “I don’t recall anybody saying there was going to be a remission. I don’t think they were dreaming to that extent.”

The trial was a Phase 1 study, meaning that its main goal was to find out whether the treatment was safe, and at what dose. Of course, doctors and patients always hope that there will be some benefit, but that was not an official endpoint.

Mr. Ludwig thought that if the trial could buy him six months or a year, it would be worth the gamble. But even if the study did not help him, he felt it would still be worthwhile if he could help the study.

When the fevers hit, he had no idea that might be a good sign. Instead, he assumed the treatment was not working. But a few weeks later, he said that his oncologist, Dr. Alison Loren, told him, “We can’t find any cancer in your bone marrow.”

Remembering the moment, Mr. Ludwig paused and said, “I got goose bumps just telling you those words.”

“I feel wonderful,” Mr. Ludwig said during a recent interview. “I walked 18 holes on the golf course this morning.”

Before the study, he was weak, suffered repeated bouts of pneumonia and was wasting away. Now, he is full of energy. He has gained 40 pounds. He and his wife bought an R.V., in which they travel with their grandson and nephew. “I feel normal, like I did 10 years before I was diagnosed,” Mr. Ludwig said. “This clinical trial saved my life.”

Dr. Loren said in an interview, “I hate to say it in that dramatic way, but I do think it saved his life.”

Mr. Ludwig said that Dr. Loren told him and his wife something he considered profound. “She said, ‘We don’t know how long it’s going to last. Enjoy every day,’ ” Mr. Ludwig recalled.

“That’s what we’ve done ever since.”

[Fish]

Ammonites. Giant prehistoric squid/snail predators that could grow as large as a Smartcar....




http://animals.nationalgeographic.co...ric/ammonites/

Ammonites are named after the Egyptian god Ammon, who is often depicted with rams' horns behind each ear.

Female ammonites grew up to 400 percent larger than males, presumably to make room to lay eggs.

Ammonites were predatory, squidlike creatures that lived inside coil-shaped shells. Like other cephalopods, ammonites had sharp, beaklike jaws inside a ring of tentacles that extended from their shells to snare prey such as small fish and crustaceans. Some ammonites grew more than three feet (one meter) across—possible snack food for the giant mosasaur Tylosaurus.

Ammonites constantly built new shell as they grew, but only lived in the outer chamber. They scooted through the warm, shallow seas by squirting jets of water from their bodies. A thin, tubelike structure called a siphuncle reached into the interior chambers to pump and siphon air and helped them move through the water.

Ammonites first appeared about 240 million years ago, though they descended from straight-shelled cephalopods called bacrites that date back to the Devonian, about 415 million years ago. Ammonites were prolific breeders, lived in schools, and are among the most abundant fossils found today. They went extinct with the dinosaurs 65 million years ago. Scientists use the various shapes and sizes of ammonite shells that appeared and disappeared through the ages to date other fossils.

Fibonacci Sequence

[EDIT: And what's really interesting to me about this 240 million year old snail/squid monster, is that it's another awesome natural occurrence of the Fibonacci sequence. To me, another glimpse of the fascinating math at the root of all life. Another amazing repeatable mathematical pattern evident throughout the chaos of random evolving life. Natural beauty, definable by math and science.]

The shape of the ammonite shell (and the shell of all nautiloids) are aesthetically pleasing because they are one of the natural expressions of the Fibonacci spiral, or golden spiral (also observed in galaxies, the unfurling of fern fiddleheads, the arrangement of leaves around a stem, the fruitlets of a pineapple, the flowering of artichoke, and the arrangement of a pinecone, just to name a few...). A "golden spiral" is easy to construct: 1**2 + 1**2 + . . . + F(n)**2 = F(n) x F(n+1)

The golden spiral is a symbol of beauty and proportional perfection/fit with unlimited room for expansion. The logarithmic proportions of the spiral are consistent throughout, no matter how large the spiral becomes, and the unique spiral can be found throughout the human body and in nature.

The spiral follows a specific mathematical formula: Fn = Fn-1 + Fn-2. Each number in the sequence is the sum of the previous two. If you construct a series of squares with lengths equal to the Fibonacci numbers (1,1,2,3,5, etc) and trace a line through the diagonals of each square, it forms a Fibonacci spiral.

[Buehler445]

That Fibonacci stuff in nature is profoundly interesting. I've looked at it a little bit while studying markets.

[Fish]

Nocturnal Penile Tumescence.... The Science of Morning Wood....



Nocturnal penile tumescence (NPT) is the spontaneous occurrence of an erection of the penis during sleep or when waking up. All men without physiological erectile dysfunction experience this phenomenon, usually three to five times during the night. It typically happens during REM sleep.

The existence and predictability of nocturnal tumescence is used by sexual health practitioners to ascertain whether a given case of erectile dysfunction (E.D.) is psychological or physiological in origin. A patient presenting with E.D. is fitted with an elastic device to wear around his penis during sleep; the device detects changes in girth and relays the information to a computer for later analysis. If nocturnal tumescence is detected, then the E.D. is presumed to be due to a psychosomatic illness such as sexual anxiety; if not, then it is presumed to be due to a physiological cause.

The cause of NPT is not known with certainty. Bancroft (2005) hypothesizes that the noradrenergic neurons of the locus ceruleus are inhibitory to penile erection, and that the cessation of their discharge that occurs during REM sleep may allow testosterone-related excitatory actions to manifest as NPT.

Evidence supporting the possibility that a full bladder can stimulate an erection has existed for some time and is characterized as a 'reflex erection'. The nerves that control a man’s ability to have a reflex erection are located in the sacral nerves (S2-S4) of the spinal cord. A full bladder is known to mildly stimulate nerves in the same region. This mild stimulus which during the day is normally suppressed in adult males by competing stimuli and other distractions; during sleep with the absence of such factors could instigate a reflex erection.

The possibility of a full bladder causing an erection, especially during sleep, is perhaps further supported by the beneficial physiological effect of an erection inhibiting urination, thereby helping to avoid nocturnal enuresis.

[Fish]

[Fish]

Ever seen a spider crab migration?

Stingray is boss...

[Third Eye]

A Fibonacci spiral is not the same as a golden spiral. Close, but not the same. Not sure why the article equates the two.

[Fish]

Originally Posted by Third Eye

A Fibonacci spiral is not the same as a golden spiral. Close, but not the same. Not sure why the article equates the two.

True. Good point. That's not exactly correct.

A*Golden spiral is very similar to the Fibonacci spiral but is based on a series of identically proportioned golden rectangles, each having a golden ratio of 1.618 of the length of the long side to that of the short side of the rectangle:



The Fibonacci spiral gets closer and closer to a Golden Spiral as it increases in size because of the ratio of each number in the Fibonacci series to the one before it converges on Phi, 1.618, as the series progresses (e.g., 1, 1, 2, 3, 5, 8 and 13 produce ratios of 1, 2, 1.5, 1.67, 1.6 and 1.625, respectively)

Fibonacci spirals and Golden spirals appear in nature, but not every spiral in nature is related to Fibonacci numbers or Phi. *Most spirals in nature are equiangular spirals, and Fibonacci and Golden spirals are special cases of the broader class of Equiangular spirals. *An Equiangular spiral itself is a special type of spiral with unique mathematical properties in which the*size of the spiral increases but its shape remains the same with each successive rotation of its curve. *The curve of an equiangular spiral has a constant angle between a line from origin to any point on the curve and the tangent at that point, hence its name. *In nature, equiangular spirals occur simply because they result in the forces that create the spiral are in equilibrium, and are often seen in non-living examples such as spiral arms of galaxies and the spirals of hurricanes. *Fibonacci spirals,*Golden spirals and golden ratio-based spirals generally appear in living organisms.

More info: http://www.goldennumber.net/spirals/

[notorious]

Water clouds on Mars:

[Fish]

Did you know that bananas are radioactive? They're radioactive enough in fact, their radioactivity has spawned its own unit of measurement of radioactivity. The banana equivalent dose (BED). The source of radioactivity is the Potassium. Potassium is actually a radioactive element. An important and necessary radioactive element that humans need in their diet.

A banana equivalent dose (abbreviated BED) is a nonstandard unit of radiation exposure, ostensibly defined as the additional dose a person will absorb from eating one banana.

The concept is based on the fact that bananas, like most organic material, naturally contain a certain amount of radioactive isotopes—even in the absence of any contamination due to human nuclear endeavors. The banana equivalent dose was meant to express the severity of exposure to radiation, such as resulting from nuclear power, nuclear weapons or medical procedures, in terms that would make sense to most people.

[Fish]