Really Want To Get Tough? Then ....

Why do people say "Grow some balls"? Balls are weak and fucking sensitive!
If you really want to get tough, like seriously,u want to get tough? Then grow a vagina! Yes! Vejayjay! I mean those things really take some pounding!

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Health:Young or Old,Stomach Infection Can Cause Arthritis, Joint Pains(See How To Prevent It)

Bacteria in Your belle(Stomach),Gut feelings, may train the immune system to attack joints 

 

The bacteria that live in your intestines are a mixed blessing. Scientists have known for decades that this so-called microbiota helps us digest our food and crowds out infectious germs. The bugs have also been implicated in allergies and obesity. Now, a new study adds one more potential malady to the list: rheumatoid arthritis.

"It's been suspected for years and years, both in humans and in the animal model, that the development of autoimmune diseases like arthritis is dependent on the gut microbiota," says immunologist Diane Mathis of Harvard Medical School in Boston. Now, she says, those suspicions are beginning to be confirmed in humans. "It's a very striking finding.”

Rheumatoid arthritis is a mysterious disease. It can strike at any age, typically beginning in young and middle-aged adults and causing painfully stiff, swollen joints in the hands and feet. It can also destroy bone and cartilage and damage organs like the lungs and kidneys. Scientists aren’t sure what causes rheumatoid arthritis, but they do know that it’s an autoimmune disorder, meaning that the body's immune system is attacking its own tissues. And that's where gut bacteria come in.

Gut bacteria have an intricate relationship with our immune system. We need to be able to tolerate helpful microbes while still recognizing and fighting invaders. Immunologist Dan Littman of New York University knew that gut microbes are important to the development of a particular type of immune cell his team studies, known as a Th17 cell. Mice that are reared in sterile conditions produce very few of these cells, and his group had previously found that mice bought from one supplier had far more Th17 cells than those that came from a different supplier. The difference turned out to be due to the rodents' gut microbes.

When Littman presented that result at a conference several years ago, Mathis, who was in the audience, told him that she had seen a change in her lab animals when they were moved to a lab in a different town. Instead of spontaneously developing a mouse version of arthritis, they remained healthy. Littman and Mathis collaborated to find out why and tracked down the difference to a particular type of bacterium that, when present in the intestines, trains the immune system to produce 

Th17 cells, which in turn release molecules that cause inflammation and bone damage in arthritis.

Littman wondered if rheumatoid arthritis in humans might also be due to specific gut microbes. His team tested fecal samples (which reflect the population of gut bacteria) from 114 residents of the New York City area. Some subjects were healthy; others had been living with rheumatoid arthritis for years; still others had psoriatic arthritis, a different autoimmune disease whose causes are also unknown; and some had been recently diagnosed with rheumatoid arthritis. Members of this latter group were especially important because, although they had rheumatoid arthritis, they hadn't yet been treated for it. In this group, a bacterium named Prevotella copri was present in 75% of patients' intestines, the researchers will report online tomorrow in eLife. P. copri only appeared in 37% of patients living with either rheumatoid or psoriatic arthritis and 21% of healthy controls. This last number is similar to the prevalence of P. copri that previous studies found in the general population in industrialized countries.

"That they were able to associate one bacterium with one pathology is remarkable," says Yasmine Belkaid, an immunologist at the National Institute of Allergy and Infectious Diseases in Bethesda, Maryland, who was not involved in the work.

But the results aren't enough to convict P. copri as the mastermind behind rheumatoid arthritis, she notes. The authors can't ethically give the bacterium to healthy subjects, so they couldn't prove that P. copri caused arthritis in patients, just that the bacterium and the disease tend to occur together. Genetics and other environmental factors, like smoking, have been associated with rheumatoid arthritis, so even if P. copri is the culprit, it doesn't necessarily act alone. "The next step is to be able to understand how causative these microbes are," Belkaid says. That would require surveying people's microbes and waiting to see who develops the disease.

To build its case against the bacterium, Littman's team gave a lab-grown strain of P. copri to mice and watched what happened in the rodents' guts. P. copri easily took up residence, and the researchers found that the mice developed increased inflammation, especially in the gut. They didn't get arthritis, possibly because the strain of P. copri was different from the human ones, but Littman says the gut inflammation corroborates the idea that gut microbes are prodding immune cells to develop and that those cells then go forth and lead an attack on other parts of the body.

That is the most exciting possibility, Mathis says. But, she explains, other hypotheses can't be ruled out. It's possible that arthritis patients' immune systems allow P. copri to grow out of control, or perhaps a third factor affects both the microbes and the immune system independently. Rheumatoid arthritis, Littman says, seems to have several environmental triggers, but how and whether they combine is not well understood.

The findings, Mathis says, open the possibility of new therapies to prevent or treat rheumatoid arthritis. Current treatments for the disease include drugs with scary side effects—Remicade, for instance, seems to increase the risk of developing certain cancers and serious infections. Perhaps P. copri could be attacked with antibiotics, Littman says, or crowded out with probiotic pills full of good bacteria. Either way, patients may someday be able to relieve their joint pain by focusing on their guts

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Health:Late Nights,Smart Phones, Reduces Ur Immune System,Makes You Sick(See What To Do)

Timing is everything. Infection-fighting T_H17 cells (green) in the intestine cause disease when the body clock is  disrupted

Jet lag, shift work, and even late nights staring at your tablet or smartphone may be making you sick. That's because the body's internal clock is set for two 12-hour periods of light and darkness, and when this rhythm is thrown off, so is the immune system. One reason may be that the genes that set the body clock are intimately connected to certain immune cells, according to a new study.

The finding “was a happy accident," says Lora Hooper, an immunologist at the University of Texas Southwestern Medical Center in Dallas. She and her colleagues were studying NFIL3, a protein that guides the development of certain immune cells and turns on the activity of others. The gene for this protein is mutated in some human patients with inflammatory bowel disease, and mice lacking the gene for NFIL3, the team found, had more so-called T_H17 cells in their intestines.

These cells are a type of immune cell known as a T cell. They get their name from a signal they produce, called interleukin 17, which tells other T cells to increase the immune response. In normal numbers, T_H17 cells, which live in the intestines, help the body fight bacterial and fungal infections. But when there are too many, the immune defense begins to cause illness rather than prevent it. Boosting NFIL3 levels in T cells growing in lab cultures resulted in fewer of them turning into T_H17 cells, the researchers found, suggesting that the protein's job is to prevent T cells from going into that area of specialization. The absence of the protein, the team concluded, leads to runaway T_H17 activity.

At this point, the researchers had no reason to suspect a connection to our body’s internal timekeeping system—also known as our circadian clock—which responds to daily cycles of light and dark. But as they continued to explore the connection between NFIL3 and T_H17 cells, they found that some of the proteins produced by the body’s "clock genes” attach to the NFIL3 genes. What's more, cultured cells and mice whose clock genes were experimentally tampered with produced fewer T_H17 cells. The researchers surmise that a key protein in the clock network binds to the NFIL3 gene to keep the production of T_H17 cells synchronized with periods of light and darkness. And the team found that normal mice produce less NFIL3, and thus more T_H17 cells, during the day than at night.
In a final experiment, the researchers gave the mice jet lag. "We didn't fly them anywhere," Hooper jokes. Instead, the team shifted the rodents' light/dark cycles by 6 hours every 4 days. "It would be like flying from the U.S. to Europe, India, and Japan and spending 4 days in each country," she explains. Mice with altered light cycles had nearly twice as many T_H17 cells in their spleens and intestines, compared with mice having a normal day, the team reports online today in Science. The jet-lagged mice also mounted a stronger inflammatory response to irritation by an experimental chemical—a test used to gauge immune-system sensitivity that hints the animals may be more prone to inflammatory disease.

   The finding adds to a growing body of research showing that a healthy pattern of light and dark, sleeping and waking, is essential to keep the immune system in balance, Hooper says. She notes that inflammation is the basis of many chronic disorders, such as heart disease, asthma, chronic pain, and many things ending in "-itis," like bursitis and dermatitis. Inflammatory conditions are more prevalent in developed countries, where people's circadian rhythms are chronically disrupted. Even people who don't work shifts or cross time zones still wake and sleep out of sync with light and darkness, Hooper says. "We all have screwed up light cycles. We stay up late, keep the lights on, look at our lit-up iPhones at 2 a.m."
Immunologist Dan Littman of New York University in New York City finds the results in cultured cells convincing. He cautions, though, that the neatly defined pathway from clock gene to T_H17 suppression might not be so tidy in a living animal. "Even if NFIL3 is involved in the way they show, circadian disruption affects many other things." Stress hormones, gut bacteria, and the actions of other types of T cells may also account for the effects of the experimental jet lag, he says.
Littman also notes that the increased inflammation in the jet-lagged animals was a response to an induced chemical irritation, and more research is needed to prove a link to inflammatory or autoimmune disease.

Hooper agrees that the present study is probably the tip of the iceberg, and more research will yield deepening insight into the relationship between immune cells circadian rhythms. She is hoping to collaborate with other researchers to determine if T_H17 cells are increased in humans with chronically altered light cycles. For now, she says, she tries to keep her own sleeping patterns more aligned with nature, starting by limiting exposure to artificial light at night. "I turn off the lights, I draw the curtains, and I keep my iPhone off."

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