In fact a mature person does not fall in love, he rises in love. The word ’fall’ is not right. Only immature people fall; they stumble and fall down in love. Somehow they were managing and standing. They cannot manage and they cannot stand – they find a woman and they are gone, they find a man and they are gone. They were always ready to fall on the ground and to creep. They don’t have the backbone, the spine; they don’t have that integrity to stand alone.

A mature person has the integrity to be alone. And when a mature person gives love, he gives without any strings attached to it: he simply gives. And when a mature person gives love, he feels grateful that you have accepted his love, not vice versa. He does not expect you to be thankful for it – no, not at all, he does not even need your thanks. He thanks you for accepting his love. And when two mature persons are in love, one of the greatest paradoxes of life happens, one of the most beautiful phenomena: they are together and yet tremendously alone; they are together so much so that they are almost one. But their oneness does not destroy their individuality, in fact, it enhances it: they become more individual.


Two mature persons in love help each other to become more free. There is no politics involved, no diplomacy, no effort to dominate. How can you dominate the person you love? Just think over it. Domination is a sort of hatred, anger, enmity. How can you think of dominating a person you love? You would love to see the person totally free, independent; you will give him more individuality. That’s why I call it the greatest paradox: they are together so much so that they are almost one, but still in that oneness they are individuals. Their individualities are not effaced – they have become more enhanced. The other has enriched them as far as their freedom is concerned.


Immature people falling in love destroy each other’s freedom, create a bondage, make a prison. Mature persons in love help each other to be free; they help each other to destroy all sorts of bondages. And when love flows with freedom there is beauty. When love flows with dependence there is ugliness.

Osho  (via thatkindofwoman)

brown-princess:

samanta-m:

rickysuavemami:

eyekhandy:

odditiesoflife:

The Tiny Rock Restaurant in the Sea

At beautiful Michanwi Pingwe Beach on Zanzibar’s coast in Africa is an incredibly unique restaurant. The restaurant is so small, it’s perched on a fossilized bed of coral located in the Indian ocean. Another surprise is that the interior is quite different than the interior. To reach the restaurant, it’s either a walk or boat ride because when the tide comes in, the restaurant is surrounded by water. The spot is so spectacular that it has been used by Vogue magazine for photo shoots.

The restaurant serves a wide variety of seafood as well as wine, beer and soft drinks. However, the Rock Restaurant is a little more pricey than one might expect. The least expensive items on the menu are the mango salad, octopus salad and fish carpaccio — each priced at $14.00 USD. The most expensive menu item is the Rock Special with grilled lobster, cigal, jumbo prawn, fish filet and calamari oil for $48.00 USD. But if you can make it to Zanzibar for a visit, a trip to the restaurant is a must.

sources 1, 2, 3, 4

i would like to visit

#goals

Dear, future husband plzzz bring me here!

Que lugar lindo!!!!!!!!!!

illuminatizeitgeist:

“He who is doing his true will is assisted by the momentum of the universe.”
—  Peter J. Caroll, Liber Null

illuminatizeitgeist:

“He who is doing his true will is assisted by the momentum of the universe.”

Peter J. Caroll, Liber Null

theyjustloveme:

Ig: Jorieanne
neurosciencestuff:

Genes discovered linking circadian clock with eating schedule
For most people, the urge to eat a meal or snack comes at a few, predictable times during the waking part of the day. But for those with a rare syndrome, hunger comes at unwanted hours, interrupts sleep and causes overeating.
Now, Salk scientists have discovered a pair of genes that normally keeps eating schedules in sync with daily sleep rhythms, and, when mutated, may play a role in so-called night eating syndrome. In mice with mutations in one of the genes, eating patterns are shifted, leading to unusual mealtimes and weight gain. The results were published in Cell Reports today.
"We really never expected that we would be able to decouple the sleep-wake cycle and the eating cycle, especially with a simple mutation," says senior study author Satchidananda Panda, an associate professor in Salk’s Regulatory Biology Laboratory. "It opens up a whole lot of future questions about how these cycles are regulated."
More than a decade ago, researchers discovered that individuals with an inherited sleep disorder often carry a particular mutation in a protein called PER2. The mutation is in an area of the protein that can be phosphorylated—the ability to bond with a phosphate chemical that changes the protein’s function. Humans have three PER, or period, genes, all thought to play a role in the daily circadian clock and all containing the same phosphorylation spot.
The Salk scientists joined forces with a Chinese team led by Ying Xu of Nanjing University to test whether mutations in the equivalent area of PER1 would have the same effect as those in PER2 that caused the sleep disorder. So they bred mice to lack the mouse period genes, and added in a human PER1 or PER2 with a mutation in the phosphorylation site. As expected, mice with a mutated PER2 had sleep defects, dozing off earlier than usual. The same wasn’t true for PER1 mutations though.
"In the mice without PER1, there was no obvious defect in their sleep-wake cycles," says Panda. "Instead, when we looked at their metabolism, we suddenly saw drastic changes."
Mice with the PER1 phosphorylation defects ate earlier than other mice—causing them to wake up and snack before their sleep cycle was over—and ate more food throughout their normal waking period. When the researchers looked at the molecular details of the PER1 protein, they found that the mutated PER1 led to lower protein levels during the sleeping period, higher levels during the waking period, and a faster degradation of protein whenever it was produced by cells.
Panda and his colleagues hypothesize that normally, PER1 and PER2 are kept synchronized since they have identical phosphorylation sites—they are turned on and off at the same times, keeping sleep and eating cycles aligned. But a mutation in one of the genes could break this link, and cause off-cycle eating or sleeping.
"For a long time, people discounted night eating syndrome as not real," says Panda. "These results in mice suggest that it could actually be a genetic basis for the syndrome." The researchers haven’t yet tested, however, whether any humans with night eating syndrome have mutations in PER1.
When Panda and Xu’s team restricted access to food, providing it only at the mice’s normal meal times, they found that even with a genetic mutation in PER1, mice could maintain a normal weight. Over a 10-week follow-up, these mice—with a PER1 mutation but timed access to food—showed no differences to control animals. This tells the researchers that the weight gain caused by PER1 is entirely caused by meal mistiming, not other metabolic defects.
Next, they hope to study exactly how PER1 controls appetite and eating behavior—whether its molecular actions work through the liver, fat cells, brain or other organs.

neurosciencestuff:

Genes discovered linking circadian clock with eating schedule

For most people, the urge to eat a meal or snack comes at a few, predictable times during the waking part of the day. But for those with a rare syndrome, hunger comes at unwanted hours, interrupts sleep and causes overeating.

Now, Salk scientists have discovered a pair of genes that normally keeps eating schedules in sync with daily sleep rhythms, and, when mutated, may play a role in so-called night eating syndrome. In mice with mutations in one of the genes, eating patterns are shifted, leading to unusual mealtimes and weight gain. The results were published in Cell Reports today.

"We really never expected that we would be able to decouple the sleep-wake cycle and the eating cycle, especially with a simple mutation," says senior study author Satchidananda Panda, an associate professor in Salk’s Regulatory Biology Laboratory. "It opens up a whole lot of future questions about how these cycles are regulated."

More than a decade ago, researchers discovered that individuals with an inherited sleep disorder often carry a particular mutation in a protein called PER2. The mutation is in an area of the protein that can be phosphorylated—the ability to bond with a phosphate chemical that changes the protein’s function. Humans have three PER, or period, genes, all thought to play a role in the daily circadian clock and all containing the same phosphorylation spot.

The Salk scientists joined forces with a Chinese team led by Ying Xu of Nanjing University to test whether mutations in the equivalent area of PER1 would have the same effect as those in PER2 that caused the sleep disorder. So they bred mice to lack the mouse period genes, and added in a human PER1 or PER2 with a mutation in the phosphorylation site. As expected, mice with a mutated PER2 had sleep defects, dozing off earlier than usual. The same wasn’t true for PER1 mutations though.

"In the mice without PER1, there was no obvious defect in their sleep-wake cycles," says Panda. "Instead, when we looked at their metabolism, we suddenly saw drastic changes."

Mice with the PER1 phosphorylation defects ate earlier than other mice—causing them to wake up and snack before their sleep cycle was over—and ate more food throughout their normal waking period. When the researchers looked at the molecular details of the PER1 protein, they found that the mutated PER1 led to lower protein levels during the sleeping period, higher levels during the waking period, and a faster degradation of protein whenever it was produced by cells.

Panda and his colleagues hypothesize that normally, PER1 and PER2 are kept synchronized since they have identical phosphorylation sites—they are turned on and off at the same times, keeping sleep and eating cycles aligned. But a mutation in one of the genes could break this link, and cause off-cycle eating or sleeping.

"For a long time, people discounted night eating syndrome as not real," says Panda. "These results in mice suggest that it could actually be a genetic basis for the syndrome." The researchers haven’t yet tested, however, whether any humans with night eating syndrome have mutations in PER1.

When Panda and Xu’s team restricted access to food, providing it only at the mice’s normal meal times, they found that even with a genetic mutation in PER1, mice could maintain a normal weight. Over a 10-week follow-up, these mice—with a PER1 mutation but timed access to food—showed no differences to control animals. This tells the researchers that the weight gain caused by PER1 is entirely caused by meal mistiming, not other metabolic defects.

Next, they hope to study exactly how PER1 controls appetite and eating behavior—whether its molecular actions work through the liver, fat cells, brain or other organs.

ladytatyana:

Dreads 2k14

Sex

I’m still convinced that control of our sexual passions is a basic step we take on the path to self knowledge. It’s the source of our creativity. Sex creates. All those wasted nuts. Smh.

ladytatyana:

ladytatyana:

Good afternoon 🌞

On my dash 😁

ladytatyana:

ladytatyana:

Good afternoon 🌞

On my dash 😁