Our brains control pain perception

Pain perception is essential for survival, but how much something hurts can sometimes be amplified or suppressed: for example, soldiers who sustain an injury in battle often recall not feeling anything at the time. A new study published honed in on the brain circuitry responsible for upgrading or downgrading these pain signals, likening the mechanism to how a home thermostat controls room temperature.

The paper's senior author and a scientist for the National Center for Complementary and Integrative Health (NCCIH), told AFP the region responsible was the central amygdala, which according to her work appeared to play a dual role.

Studying mice, researchers found that the activity in neurons that express protein kinase C-delta amplified pain, while neurons that express somatostatin inhibited the chain of activity in the nerves required to communicate pain. The central amygdala isn't completely responsible for pain itself: if it were removed entirely, then "the 'ouch' of things, or the protective pain, would remain intact," he said.

"It seems to be sitting there waiting for something to happen," for example responding to stress or anxiety that amplifies pain, or being forced to focus on a task that diverts your attention and reduces pain. Experiencing pain can be a vital warning to seek help, for example in a person experiencing appendicitis or a heart attack.

People who are born with insensitivity to pain, meanwhile, often do not realize the severity of injuries and are at greater risk of early death. But not all pain is useful. According to a 2012 survey, about 11 per cent of US adults have pain every day and more than 17 per cent have severe levels of pain.

Often this leads to dependence on potent painkillers like opioids, or attempting to self-medicate through counterfeit or illicit drugs which are increasingly laced with deadly fentanyl. By better understanding the brain mechanisms responsible for pain modulation, researchers hope to eventually find better cures: potentially ones that target only those forms of pain that are "bad" and not useful.

"The healthy response is you get pain, it tells you something is wrong, it heals, and the pain goes away," he said. "In chronic pain, that doesn't happen, the system gets stuck. If we can identify what makes the system gets stuck, then we can reverse it."

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New molecule identified as key factor in anxiety disorder

A recent study has revealed that boosting a molecule named neurotrophin-3 in the brain can change ‘dispositional anxiety’. Researchers found that neurotrophin-3 can trigger neurons to grow and make new connections.

The study provides hope for new strategies focused on intervening early in life to treat people at risk for anxiety disorders, depression, and related substance abuse.

 

“There are millions of people worldwide who suffer from debilitating anxiety and depressive disorders ” said an assistant professort of Psychology.

Anxiety disorders often emerge around adolescence and can continue to affect people for most of their lives. Currently, researchers can identify children who display an extremely anxious or inhibited temperament these young people are at risk to develop-stress-related psychopathologies as they transition to adulthood.

The roots of the study come from research done by the group about eight years ago in preadolescent rhesus macaques (species of monkeys) when researchers got their first glimpse of molecular alterations in the dorsal amygdala, a brain region important in emotional responses.

The researchers used an altered virus to boost levels of neurotrophin-3 in the dorsal amygdala of juvenile rhesus macaques. They found that the increase of neurotrophin 0-3 in the dorsal amygdala leads to a decrease in anxiety-related behaviours, particularly behaviours associated with inhibition, a core feature of the early-life risk for developing anxiety disorders in humans. Subsequent brain imaging studies of these animals found that neurotrophin-3 changed activity throughout the distributed brain regions that contribute to anxiety.

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Taking antibiotics before liver transplants leads to better outcomes

A recent study has found that administering antibiotics to mice for 10 days prior to a liver transplant leads to better liver function after surgery, and the same holds true for human beings too.

After concluding the experiment in mice, scientists studied data from liver transplants performed between October 2013 and August 2015 revealing that the same phenomenon appears to hold true in humans.

The statistics from human patients even demonstrated that the people who were in worse health prior to their surgeries but received pre-surgery antibiotics fared better after their transplants than the patients who were healthier prior to their surgeries but did not receive antibiotics.

The researchers concluded that the antibiotics inhibited bacteria that cause inflammation, which in turn can lead to organ rejection.

Specifically, they found that in mice and humans, the treatment prior to a transplant reduced the damage that could occur when blood flow is restored to the liver after a period of time without oxygen; and it reduced inflammation and cell damage while accelerating the removal of damaged cells.

“The livers in the mice that received antibiotics were protected against transplant damage, as well as rejection later on because the antibiotics modulated their host microbiomes, which in turn stimulated cell protection,” the researcher said.

To substantiate the effect of the antibiotics, the researchers then transplanted faecal matter from the untreated mice into those that had been given the medication.

The mice that received the faecal transplants suffered inflammatory damage to their livers, despite the fact that they had been given antibiotics earlier in the experiment.

“That showed that antibiotic-mediated benefits clearly relate to the microbiota,” the researcher said.

The data on the patients covered 264 people who had received liver transplants — 156 who, because they were sicker before their surgeries received antibiotics for 10 or more days prior to the transplant, and 108 who were given antibiotics for less than 10 days, or not at all prior to surgery.

The researchers then narrowed their focus to human patients who had been given one specific antibiotic, rifaximin, prior to the transplants.

They found that in patients that received rifaximin, which stays in the bowel and has a low risk for inducing bacterial resistance, early liver failure was significantly delayed or stopped.

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Chili Consumption Slows Lung Cancer Progression

Besides spicing up your food, chili, it seems, also has some medicinal value. New research suggests the compound responsible for chili’s heat could help slow the spread of lung cancer, the leading cause of cancer death for both men and women.

Most cancer-related deaths occur when cancer spreads to distant sites, a process called metastasis.

“Lung cancer and other cancers commonly metastasise to secondary locations like the brain, liver or bone, making them difficult to treat,” said one of the study authors.

“Our study suggests the natural compound capsaicin from chili peppers could represent a novel therapy to combat metastasis in lung cancer patients,” said one of the researchers.

In experiments involving three lines of cultured human non-small cell lung cancer cells, researchers observed capsaicin inhibited invasion, the first step of the metastatic process.

They also found mice with metastatic cancer that consumed capsaicin showed smaller areas of metastatic cancer cells in the lung compared with mice not receiving the treatment.

Additional experiments revealed capsaicin suppresses lung cancer metastasis by inhibiting activation of the protein Src. This protein plays a role in the signalling that controls cellular processes like proliferation, differentiation, motility and adhesion.

“We hope one day capsaicin can be used in combination with other chemotherapeutics to treat a variety of lung cancers,” he said.

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Researchers hijack the common flu to make it a pancreatic cancer killer

As part of a new effort to halt one of the deadliest cancers in its tracks, researchers are recruiting a common flu virus as a powerful new weapon.

While the flu virus might be the last thing we want to hear about in the midst of what has been a particularly virulent flu season, it could prove to be a powerful new weapon in the fight against pancreatic cancer with a survival rate of just 5%.

The reason for its poor survival rate is due to both its late diagnosis and the cancer’s rapid development of resistance to current therapies leading to researchers searching for new strategies that won’t allow the cells to develop an immunity.

In a paper published , a team of researchers has revealed how the common flu can be modified to attack different parts of the body, in this case the pancreatic cancer cells.

“The new virus specifically infects and kills pancreatic cancer cells, causing few side effects in nearby healthy tissue,” said the study’s lead researcher.

“Not only is our targeting strategy both selective and effective, but we have now further engineered the virus so that it can be delivered in the blood stream to reach cancer cells that have spread throughout the body.”

The key to the breakthrough was down to a unique feature of pancreatic cancer cells: a specific molecule called alpha v beta 6 (αvβ6), which is found on the surface of many pancreatic cancer cells but, crucially, not on normal cells.

Could be used with existing treatments

With this knowledge, the team set about modifying the flu virus so that it displays an additional small protein on its outer coat that recognises and binds to αvβ6-molecules.

When the virus enters the cancer cells, the virus spreads producing thousands of copies of itself prior to bursting out of the cell and thereby destroying it in the process.

These new copies can then bind onto neighbouring cancer cells and repeat the same cycle, eventually removing the tumour mass altogether.

This seemingly astounding solution was tested on human pancreatic cancer cells grafted onto mice with the results showing they inhibited cancer growth.

“If we manage to confirm these results in human clinical trials, then this may become a promising new treatment for pancreatic cancer patients, and could be combined with existing chemotherapy drugs to kill persevering cancer cells,” the Dr. said.

She added that the team’s new virus is much more specific in its targeting compared with previous versions.

If the team secures funding for clinical trials within the next two years, early phase trials could be just a few years away.
 

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