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Monday, December 3, 2018

IIT-Bombay team creates tiny bubbles for cancer drugs that can make chemo pain-free

SANDHYA RAMESH 6 November, 2018

Patients receiving chemotherapy (Representational image) | Daniel Bockwoldt/picture alliance via Getty Images
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IIT-Bombay team has devised a drug carrier that can be used in combination with chemo to deliver treatment to exact site of tumour, keeping healthy cells safe.
Bengaluru: IIT-Bombay scientists have developed a therapy whereby two microscopic “bubbles” can deliver drugs straight to tumours, thus reducing the amount of healthy cells that would be affected in chemotherapy.
The mice on which the study was carried out reportedly demonstrated a 100 per cent survival rate.
The research has been published in the journal Scientific Reports.
Cancer has affected humans for millennia, and, so far, chemotherapy has proved to be one of the most effective treatments.
However, cancer cells tend to multiply quickly and chemotherapy simply targets the cells that are dividing.
This means that even healthy cells that aren’t affected by cancer will be targeted by chemo drugs, which induce suicide in cells. Thus, whether the treatment is effective or not, the patient invariably tends to be in a lot of pain.

To improve the accuracy of drugs — so they target only an infected tumour and not healthy cells — as well as to reduce cancer cells developing immunity to drugs, lots of experimental work is underway around the world on ‘combination therapy’.
These include the administration of two or more drugs to treat the same disease. With cancer, this is increasingly becoming the norm.

Ball-shaped carriers
The IIT-Bombay team has devised a drug carrier that can be used in combination with chemotherapy to deliver treatment to the exact location of a solid cancerous tumour, keeping healthy cells safe.
The study has been performed on both lab-grown cells (in-vitro), as well as animals (in-vivo), with promising results.
The injectable consists of two microscopic ball-shaped carriers attached together: The smaller one is a capsule that will contain the potent drug to fight a cancer cell, and the bigger one a gas bubble that will act as a tracker that can be seen using ultrasound imaging.
The latter is 500 nanometres in diameter, and known as a “nanobubble”, while the drug carrier is about 200 nanometres and called a “nanocapsule”.
The tiny blobs will have two different effects in the body. First, they will be able to allow tracking through ultrasound as they travel through the bloodstream.
We can monitor their progress and wait for them to reach the precise point of the cancerous tumour. When they hit the region where the affected tumour is, ultrasound therapy can be administered to the exact target area. This process is known as guided cancer therapy.
The second occurs as tissues loosen when ultrasound is applied to the right spot. As the tumour area is administered ultrasound, the tumour tissues relax. The gas bubble undergoes multiple expansions and contractions, before eventually bursting.
The tiny nanocapsule has now been given an easy passageway to enter the tumour, thanks to tissue expansion. The capsule is made up of lipids that occur naturally in our bodies, and thus they are compatible to deliver the drug within the tumour at a precise location.

‘Improved targeting’
“This research presents an image-guided, ultrasound trigger-responsive platform for improved tumour cell targeting, along with real-time monitoring of the disease,” said Rinti Banerjee from the department of biosciences and bioengineering at IIT-Bombay, who led the study.
The two individual bubbles aren’t a new invention. Both technologies exist independently. But they have not been used in conjunction before for treating cancer.
“To the best of our knowledge this is the first time a smart combination therapy with a pro-apoptotic biomolecule, a drug, and nanobubbles have been used together,” said Banerjee.
The study showed that ultrasound with the combination of the two bubbles is much more effective than any other combination of treatments and components.
Ultrasound image-guided therapy and ultrasound application therapy are growing fields in cancer research, and this study could help expedite more efficient treatments based on this technology.

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Saturday, March 3, 2018

Scientists say diabetes is five separate diseases, and treatment could be tailored to each form.

Could there be five types of diabetes rather than just two?

Scientists say diabetes is five separate diseases, and treatment could be tailored to each form.
Diabetes - or uncontrolled blood sugar levels - is normally split into type 1 and type 2.

But researchers in Sweden and Finland think the more complicated picture they have uncovered will usher in an era of personalised medicine for diabetes. 

Experts said the study was a herald of the future of diabetes care but changes to treatment would not be immediate. 
Diabetes affects about one in 11 adults worldwide and increases the risk of heart attack, stroke, blindness, kidney failure and limb amputation.
Type 1 diabetes is a disease of the immune system, which affects around 10% of people with the condition in the UK. It errantly attacks the body's insulin factories (beta-cells) so there is not enough of the hormone to control blood sugar levels. 
Type 2 diabetes is largely seen as a disease of poor lifestyle as body fat can affect the way the insulin works. 
The study, by Lund University Diabetes Centre in Sweden and the Institute for Molecular Medicine Finland, looked at 14,775 patients including a detailed analysis of their blood.
The results, published in The Lancet Diabetes and Endocrinology, showed the patients could be separated into five distinct clusters. 
  • Cluster 1 - severe autoimmune diabetes is broadly the same as the classical type 1 - it hit people when they were young, seemingly healthy and an immune disease left them unable to produce insulin
  • Cluster 2 - severe insulin-deficient diabetes patients initially looked very similar to those in cluster 1 - they were young, had a healthy weight and struggled to make insulin, but the immune system was not at fault
  • Cluster 3 - severe insulin-resistant diabetes patients were generally overweight and making insulin but their body was no longer responding to it
  • Cluster 4 - mild obesity-related diabetes was mainly seen in people who were very overweight but metabolically much closer to normal than those in cluster 3
  • Cluster 5 - mild age-related diabetes patients developed symptoms when they were significantly older than in other groups and their disease tended to be milder

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Prof Leif Groop, one of the researchers, told the BBC: "This is extremely important, we're taking a real step towards precision medicine.
"In the ideal scenario, this is applied at diagnosis and we target treatment better."
The three severe forms could be treated more aggressively than the two milder ones, he said.
Cluster 2 patients would currently be classified as type 2 as they do not have an autoimmune disease. 
However, the study suggests their disease is probably caused by a defect in their beta-cells rather than being too fat.
And perhaps their treatment should more closely mirror patients who are currently classed as type 1.
Cluster 2 had a higher risk of blindness while cluster 3 had the greatest risk of kidney disease, so some clusters may benefit from enhanced screening. 
Better classification
Dr Victoria Salem, a consultant and clinical scientist at Imperial College London, said most specialists knew that type 1 and type 2 was "not a terribly accurate classification system".
She told the BBC: "This is definitely the future of how we think about diabetes as a disease."
But she cautioned the study would not change practice today.
The study was only on Scandinavians and the risk of diabetes varies considerably around the world, such as the increased risk in South Asians.
Dr Salem said: "There is still a massively unknown quantity - it may well be that worldwide there are 500 subgroups depending on genetic and local environment effects.
"Their analysis has five clusters, but that may grow."
Sudhesh Kumar, a professor of medicine at Warwick Medical School, said: "Clearly this is only the first step. 
"We also need to know if treating these groups differently would produce better outcomes."
Dr Emily Burns, from Diabetes UK, said understanding the diseases could help "personalise treatments and potentially reduce the risk of diabetes-related complications in the future".
She added: "This research takes a promising step toward breaking down type 2 diabetes in more detail, but we still need to know more about these subtypes before we can understand what this means for people living with the condition."

Friday, October 6, 2017



Why did it take us so long to realise sugar, not fat, was the enemy? In a move that would make most big pharma companies proud, new research published in JAMA Internal Medicine found sugar companies paid to downplay the white stuff's role in heart disease during the 1960s. Scary stuff, even more so because it's had lasting effects on public perceptions. It's time everyone woke up to the truth about fat and sugar. MH investigates...
This morning, as I do most days, I breakfasted on a three egg omelette cooked in coconut oil, with a whole milk coffee. I enjoyed a wedge of full fat cheese with my lunch, poured a liberal dose of olive oil on my evening salad and snacked on nuts throughout the day. In short, I ingested a fair amount of fat and, as a cardiologist who has treated thousands of people with heart disease, this may seem a particularly peculiar way to behave. Fat, after all, furs up our arteries and piles on the pounds – or at least that’s what prevailing medical and dietary advice has had us believe. As a result, most of us have spent years eschewing full fat foods for their ‘low fat’ equivalents, in the hope it will leave us fitter and healthier.
Yet I’m now convinced we have instead been doing untold damage: far from being the best thing for health or weight loss, a low fat diet is the opposite. In fact, I would go so far as to say the change in dietary advice in 1977 to restrict the amount of fat we were eating helped to fuel the obesity epidemic unfolding today. It’s a bold statement, but one I believe is upheld by an array of recent research.
These days I make a point of telling my patients – many of whom are coping with debilitating heart problems – to avoid anything bearing the label ‘low fat’. Better instead, I tell them, to embrace full fat dairy and other saturated fats within the context of a healthy eating plan. It’s an instruction that is sometimes greeted with open-mouthed astonishment, along with my request to steer clear of anything that promises to reduce cholesterol – another of those edicts we are told can promote optimum heart and artery health.
As we will see, the reality is far more nuanced: in some cases lowering cholesterol levels can actually increase cardiovascular death and mortality, while in healthy people over sixty a higher cholesterol is associated with a lower risk of mortality. Why, exactly, we will come to later.
First though, let me make it clear that until very recently, I too assumed that keeping fat to a minimum was the key to keeping healthy and trim. In fact, to say my diet revolved around carbohydrates is probably an understatement: sugared cereal, toast and orange juice for breakfast, a panini for lunch and pasta for dinner was not an uncommon daily menu. Good solid fuel, or so I thought, especially as I am a keen sportsman and runner. Still, I had a wedge of fat round my stomach which no amount of football and running seemed to shift.
That, though, wasn’t the reason I started to explore changing what I ate. That process started in 2012, when I read a paper called ‘The toxic truth about Sugar’ by Robert Lustig in the science journal Nature.  In it, Lustig, a Professor of Paediatrics who also works at the University of California’s Centre for Obesity Assessment, said that the dangers to human health caused by added sugar were such that products packed with it should carry the same warnings as alcohol. It was an eye-opener: as a doctor I already knew too much of anything is bad for you, but here was someone telling us that something most of us ate unthinkingly every day was, slowly, killing us.
The more I looked into it, the more it became abundantly clear to me that it was sugar, not fat, which was causing so many of our problems – which is why, along with a group of fellow medical specialists I launched the lobbying group Action on Sugar last year with the aim of persuading the food industry to reduce added sugar in processed foods
Then earlier this year I had another light-bulb moment. In February Karen Thomson, the granddaughter of pioneering heart transplant surgeon Christian Barnard, and Timothy Noakes, a highly-respected Professor of Exercise and Sports Medicine at the University of Cape Town, invited me to speak at the world’s first ‘low carb’ summit in South Africa. I was intrigued, particularly as the conference hosts are both fascinating characters. A former model, Thomson has courageously battled a number of addictions including alcohol and cocaine, but lately it is another powder – one she labels ‘pure, white and deadly’ – that has resulted in her opening the world’s first carbohydrate and sugar addiction rehab clinic in Cape Town
Noakes, meanwhile, has recently performed a remarkable U-turn on the very dietary advice he himself expounded for most of his illustrious career: that is, that athletes need to load up on carbohydrates to enhance performance. A marathon runner, he was considered the poster boy for high carbohydrate diets for athletes – then he developed Type 2 diabetes. Effectively tearing pages out of his own textbook, Noakes has now said athletes – and this goes for those of us who like to jog around the park too – can get their energy from ketones, not glucose. That is, from fat not sugar.
Alongside them were fifteen international speakers ranging from doctors, academics and health campaigners who between them produced an eloquent and evidence-based demolition of “low fat” thinking – as well as suggesting that it is carbohydrate consumption, not fatty foods, which is fuelling our obesity epidemic.
Opening the conference was Gary Taubes, a former Harvard physicist who wrote The Diet Delusion, in which he argued that it is refined carbohydrates that are responsible for heart disease, diabetes, obesity, cancer, and many other of our Western maladies. The book caused controversy when it was released seven years ago, but his message is finally gaining traction. And that message is this: obesity is not about how many calories we eat, but what we eat. Refined carbohydrates fuel the over production of insulin, which in turn promotes fat storage. In other words: it’s not calories from fat themselves that are the problem.
It’s a robust message that was reinforced time and again at the conference. Take Swedish family physician Dr Andreas Eenfeldt, who runs the country’s most popular health blog Diet Doctor. In his home country, studies show that up to twenty three percent of the population are embracing a high fat, low carbohydrate diet. A ticking time bomb you might think – but contrary to expectations, while obesity rates are soaring everywhere else, they are now starting to show a decline there
More research on this correlation is yet to be done – but in the meantime The Swedish Council on Health Technology has made its position clear. After a two year review involving sixteen scientists, it concluded that a high fat, low carb diet may not only be best for weight loss, but also for reducing several markers of cardiovascular risk in the obese. In short, as Dr Eenfeldt told the conference, ‘You don’t get fat from eating fatty foods just as you don’t turn green from eating green vegetables.’
This, of course, is a difficult message for many to swallow; particularly for heart patients, most of whom have spent years pursuing a low fat, low cholesterol diet as the best way to preserve heart health.
It’s a public health message that was first promoted in the sixties, after the globally respected Framingham Heart study sanctified high cholesterol as a major risk factor for heart disease. It’s a cornerstone of government and public health messages – yet what people didn’t know was that the study also threw up some more complex statistics. Like this one: for every 1mg/dl per year drop in cholesterol levels in those who took part in the study there was a 14% increase in cardiovascular death and an 11% increase in mortality in the following 18 years for those aged over 50.
It’s not the only statistic that doesn’t sit with the prevailing anti-cholesterol message: in 2013, a group of academics studied previously unpublished data from a seminal study done in the early seventies, known as the Sydney Diet Heart study. They discovered that cardiac patients who replaced butter with margarine had an increased mortality, despite a 13% reduction in total cholesterol. And the Honolulu heart study published in the Lancet in 2001 concluded that in the over-sixties a high total cholesterol is inversely associated with risk of death. Startling, isn’t it? A lower cholesterol is not in itself the mark of success, it only works in parallel with other important markers, like a shrinking waist size and diminishing blood markers for diabetes.
Conversely, a mounting slew of evidence suggests that far from contributing to heart problems, having full fat dairy in your diet may actually protect you from heart disease and type 2 diabetes. What most people fail to understand is that, when it comes to diet, it’s the polyphenols and omega 3 fatty acids abundant in extra virgin olive oil, nuts, fatty fish and vegetables that help to rapidly reduce thrombosis and inflammation independent of changes in cholesterol. Yet full fat dairy has remained demonized – until now.
In 2014, two Cambridge Medical Research Council studies concluded that the saturated fats in the blood stream that came from dairy products were inversely associated with Type 2 diabetes and heart disease. Meaning that in moderate amounts – no-one is talking about devouring a cheese board in one sitting here – cheese is actually a proponent of good health and longevity. The same study, incidentally, found that the consumption of starch, sugar and alcohol encourages the production of fatty acids made by the liver that correlate with an increased risk of these killer diseases.
It is around type 2 Diabetes, in fact, that the anti-fat pro-carb message of recent decades has done some of the greatest damage. A lot of patients suffering from Type 2 Diabetes – the most common kind – are laboring under the dangerous misapprehension that a low fat, starchy carbohydrate fuelled diet will help their medication work most effectively. They couldn’t be more wrong. Earlier this year, a critical review in the respected journal Nutrition concluded that dietary carbohydrate restriction is one of the most effective interventions for reducing features of metabolic syndrome. 
It would be better to rename type 2 diabetes “carbohydrate intolerance disease”. Try telling this to the public though. Like the man who called into a national radio show in Cape Town on which I was taking part to discuss the relationship between diet and heart disease. Diagnosed with Type 2 diabetes, he was under the impression he had to consume sugar so his diabetes medications could ‘work’ – when in fact it was going to worsen his symptoms. And how many doctors and patients know that although some of these medications to control blood sugar may marginally reduce the risk of developing kidney disease, eye disease and neuropathy, they don’t actually have any impact on heart attack, stroke risk or reduce death rates? On the contrary dangerously low blood sugar from overmedicating on diabetes drugs has been responsible for approximately 100,000 emergency room visits per year in the United States
But who can blame the public for such misguided perceptions? In my opinion a perfect storm of biased research funding, biased reporting in the media and commercial conflicts of interest have contributed to an epidemic of misinformed doctors and misinformed patients. The result is a nation of over-medicated sugar addicts who are eating and pill-popping their way to years of misery with chronic debilitating diseases and an early grave.
It’s why, these days, I very seldom touch bread, have got rid of all added sugars and have embraced full fat as part of my varied Mediterranean-inspired diet. I feel better, have more energy and – even though I didn’t set out to do so – I’ve lost that fatty tyre around my waist, despite reducing the time I spend exercising.
Perhaps you can’t face making all those changes in one go. In which case, if you do one thing, make it this: next time you are in the supermarket and are tempted to pick up a pack of low-fat spread, buy a pack of butter instead or, better still, a bottle of extra virgin olive oil. Your heart will thank you for it. The father of modern medicine Hippocrates once said, “let food be thy medicine and medicine be thy food”. It’s now time we let “fat” be that medicine.
Dr Aseem Malhotra is a cardiologist, founding member of the Public Health Collaboration and advisor to the National Obesity Forum. 

Sunday, August 13, 2017

Exclusive: Woman Can Move Again After a Breakthrough Stroke Treatment - Time Health

The first person to receive deep brain stimulation (DBS) for stroke recovery is performing far better than her doctors anticipated.

Two years ago, J udy Slater, a 59 year old in Pulaski, Pennsylvania, was getting out of bed when she had a severe stroke. She fell down and couldn’t get back up; the stroke had left her entire left side paralyzed.

With time, Slater was able to regain her ability to walk, but her left arm remained almost entirely immobile, hanging against her side with her elbow stuck tightly at 90 degrees. Her hands and fingers had curled up, and she couldn’t extend them on her own. “I depended so much on my family,” says Slater, who lives with her husband and daughter.

Slater’s experience is not unique. In the United States, stroke is the leading cause of serious long-term disability among Americans, and about half of the 800,000 Americans who have a stroke every year end up disabled. With physical therapy, people can regain some motor function, but more than half of all people with stroke will continue to have severe movement impairments.

After the stroke, Slater couldn’t bathe or cook on her own, and she longed for her former independence. That’s why she agreed to become the first person in the world to receive deep brain stimulation (DBS) for stroke recovery: a procedure in which electrodes are implanted in the brain to provide small electric pulses. She is part of a new clinical trial at the Cleveland Clinic aimed at helping people disabled by stroke regain control of their movements.

A medical first

“Despite advances in physical therapy and acute treatment of stroke, there are still too many people who live with longterm disabilities, and new technologies are needed,” says trial leader Dr. Andre Machado, chairman of the Cleveland Clinic Neurological Institute.


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Slater is the first person to receive the treatment. Machado and his team spent more than a decade testing DBS for stroke recovery in animals, and DBS has been used to treat tremors associated with Parkinson’s disease, but in that scenario, doctors are trying to get rid of tremors. In the case of stroke, Machado and his team are trying to make movement come back—a goal that's considered harder to pull off.

In December 2016, Slater's skull was opened and doctor's surgically implanted electrodes in the area of her brain called the cerebellum. The electrodes provide small pulses that target damaged areas of the brain to help recover movement. The electrodes are attached to a wire that connects them to a small battery pack doctors surgically embedded under the skin in her chest. After she recovered from the initial surgery, Slater started physical therapy, and soon after that, her doctors turned on the device.

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Four months after the electrodes were turned on, Slater is doing better than investigators expected. “Judy is performing exceptionally well,” says Machado. “Since we’ve turned on the device, we’ve seen an acceleration in her recovery, and we have not yet seen the limit of her gains.”

People with severe impairments from stroke can improve with physical therapy alone, but typically the gains are small and then plateau. Machado had originally hoped that Slater would experience improved movement beyond what was expected from physical therapy (DBS is not intended to replace physical therapy, but to make it work better). Machado expected the effects of DBS to eventually reach a similar plateau within about four months, at which point his team would measure how much the procedure contributed to her overall improvement.

But Slater has yet to stop improving.

“Week by week and month by month, we see improvements,” says Machado. “There is no flattening or tipping point. No one can predict where that point will be.”

Not only can Slater open up her left hand, but she can also move her wrist and elbow. She can open her purse, reach into her bag and grab what she needs. She can get dressed and do the dishes. “I am so excited I can move my fingers and my hand, and reach in front of me and to the side,” says Slater. "I can cook, cut vegetables and get dinner ready. It’s still a little bit hard, but I can do it.”

“What excites me is that we have reduced her dependence on other people," says Machado. "She has exceeded my expectations, and this gives us courage to continue.”
An ethical dilemma

Slater’s case has been inspiring and an encouraging proof of concept study. But her results have put Machado in an ethical quandary. The study protocol states that Slater’s stimulation should be turned off now that she has used it for four months. That’s largely because no one—not Machado or the other doctors who advised his research team—thought she would improve beyond that time frame.

From a scientific standpoint, researchers including Machado want to turn off the device so they can learn whether a person keeps or loses the improvements they made with the brain stimulation. Scientists need to discover whether DBS for stroke is something a person uses for a few months, or if it’s a lifelong implant.

But Machado says he can’t bring himself to turn off Slater’s device—not yet, at least. "Judy took a risk by becoming the first person ever to have this surgery done," he says. "Imagine you are in my shoes. Would you have the courage to turn it off? I’m an investigator and a physician, and the physician side of me wins—I will continue to treat her. No one has the heart to stop it.”

For now, Slater will continue her physical therapy with the device turned on, and Machado will work with the U.S. Food and Drug Administration—the agency that would eventually review the device for possible market approval—to change the study protocol. Cleveland Clinic has already enrolled the second patient into the clinical trial and implanted them with the electrodes; researchers will turn the device on after the patient recovers. They don't plan to stop there: Researchers are currently screening more people to potentially enter the trial.

Slater says she is pleased to keep working with the device. “I’ve been thinking about what happens if they turn it off,” she says. “I don’t want to go back and start over where I was."

"I am happy I did it," she adds. "I still have a way to go, but I am going to get there.”

Monday, August 7, 2017

Crying has often been touted as a good way to relieve stress. Does science back this belief up?

Crying has often been touted as a good way to relieve stress. Does science back this belief up? 

  • By Jason G Goldman
13 March 2017

Until recently, scientists and authors were at stark disagreement over the point of crying. In King Henry VI, Shakespeare wrote, "to weep is to make less the depth of grief", and the American writer Lemony Snicket said "unless you have been very, very lucky, you know that a good, long session of weeping can often make you feel better, even if your circumstances have not changed one bit".
Charles Darwin, on the other hand, thought that the production of tears (the act of crying notwithstanding) was merely a useless side effect of the way that the muscles around the eye worked. For him, those muscles had to contract from time to time so that they didn’t overflow with blood; the expulsion of tears was simply an unintended consequence of that evolved physiological process. (He did acknowledge that crying could help young infants attract the attention of their parents, though.)
Perhaps weeping is a literal cry for attention, a means of soliciting support and help from our friends when we need it the most 
We now know that crying – at least, the sort that adults do – is a complex physiological response to some kind of emotional stimulus. The most prominent feature is of course the shedding of tears, but it also includes changes in facial expressions and breathing patterns. "Sobbing," for example, refers to the rapid inhalation and exhalation that so often accompanies crying.

The reasons why we cry are still largely a mystery (Credit: iStock)

From a scientific perspective, that means crying is different from the production of tears in response to a chemical irritant, like when you accidentally rub your eyes after eating spicy foods. Even the tears themselves are different. In 1981, Minnesota psychiatrist William H Frey II discovered that tears brought on by sad movies had more protein in them than those that flowed in response to some freshly chopped onions.
As anyone who has attended a side-splitting comedy act or listened to a groom read wedding vows to his bride, emotional tears aren't limited to feelings of melancholy. But while all of us are familiar with the feelings that are associated with crying, whether for joy or sorrow, there's not much that's known about why we do it as adults – but there are plenty of ideas.
One idea is that adult crying isn't actually all that different from the sort that babies do, at least when it comes to its social nature. In other words, perhaps weeping is a literal cry for attention, a means of soliciting support and help from our friends when we need it the most. It's a way of communicating our inner emotional state at a time when we may not be able to fully articulate it.
While this may explain some forms of crying, many researchers have found that adults often cry when they're completely alone. Another possibility that is that crying might serve as a means of "secondary appraisal," helping people to realise just how upset they are, a way of helping them understand their own feelings – it's a provocative idea, with at  least some evidence to support it, in some cases.

Private crying may be a way for people to appraise how they are feeling (Credit: iStock)

And then there's the notion of catharsis: crying provides for relief from emotionally stressful situations. The idea is consistent not only with the words of Shakespeare, but with the Roman poet Ovid, who wrote: "It is a relief to weep; grief is satisfied and carried off by tears." The Greek philosopher Aristotle also wrote that crying "cleanses the mind". In a 1986 study of popular US magazines and newspapers, one psychologist found that 94% of articles about crying suggested that it helped to relieve psychological tension.
Indeed, a 2008 study of nearly 4,300 young adults from 30 countries found that most reported improvements in both their mental and physical wellbeing after a bout of crying, but not all. Some reported no change after a crying session, and some even said that they felt worse afterwards.
The notion of having "a good cry" is not without merit, but it seems to necessitate the right kind of social support to be effective   
The difference seems to lie in the social context: if a person felt embarrassed about crying in public, for example, they might feel less resolved than if they cried alone or with a single close friend. The study also found that when people tried to suppress or hide their crying, they also wound up feeling less relief afterwards.
So the notion of having "a good cry" is not without merit, but it seems to necessitate the right kind of social support to be effective. Which means, in the end, that adults might just cry for much the same reason as human infants: to seek help from their friends and family.

Is Too Much Sitting Killing You?

Is Too Much Sitting Killing You? 

Is too much sitting killing Indian Americans? Are you having problems sleeping at night, controlling your weight, or managing your blood sugar, pressure, or cholesterol? If you are a white collar worker, you are probably sitting too much and for too long.  And this may be the greatest health hazard you face.
The human body is a product of millions of years of evolution. It was never meant to be sedentary. New science is revealing that being immobile and sitting at the same place for hours has dire consequences.

If you are an average Indian American, your usual day begins with sitting at the table eating your breakfast, then sitting in your car, bus or train going to work. At work, you will sit at your desk for eight hours and then return home while sitting in a motorized vehicle. You will have dinner while sitting, and then watch television while relaxing on a couch. Some may go for a run or lift weights for an hour at the gym. In total, the average Indian American is sitting more than nine hours in a day. This is an all-time high in recorded history.

Now, there is a vast amount of data linking a physically active lifestyle to lower rates of morbidity and mortality. Decades earlier, this connection was not studied or understood. In 1949, it was  Professor Jerry Morris who made a significant discovery linking exercise to heart health. He studied the heart attack rates among drivers and conductors on London’s transit system. Even though drivers and condutors were drawn from similar backgrounds and social status, drivers had a statistically significant difference in heart attack rates that adversely affected them.  After his study was published in the Lancet in 1953, recommendations for exercise have become mainstream and widely followed all over the world.

Health organizations recommend  around one hour of exercise a day. The American Heart Association and American College of Sports Medicine call for a minimum of 30 minutes of moderate to intense physical activity five days a week or 20 minutes of vigorous intense physical activity three days a week. But new research reveals that one hour of activity is not enough to mitigate the harms of 23 hours of inactivity. This new finding is revolutionizing how we think about exercise.

The association between sitting and mortality is dose dependent; the more you sit, the less you live. This is independent of leisure activity or baseline BMI (body mass index) so that no matter how much exercise we get or how healthy our food choices are, the dangers of prolonged sitting will still cause harm.

Studies have shown that even four hours of sitting changes your metabolism and sitting is especially harmful for women. Women who sit for more than six hours per day have a 40 percent increased all-cause death rate compared to those sitting less than three hours per day. This association is not affected by the amount of physical activity women receive.

If we look back in history, until very recently, humans have always been moving. In the beginning, we were all hunter-gatherers, and we used to forage for food. Then the economy switched to pastoral, agricultural and after the industrial revolution, things began to change rapidly as fossil fuels and electricity replaced physical labor. In this digital age, almost everything can be done seated. Although tools and technology changed our environment, our body has not had time to evolve. Scientists and anthropologists conclude that the human body has not changed much over the last 40,000 years.

Most Indian-Americans are white collar workers. They may argue that the kind of work that they do demands that they sit to focus and concentrate. They may say, “Deep thinking and contemplation requires the meditative stillness of sitting.” This may seem like a valid argument, but even this argument does not stand up in the light of scientific research. The brain has enormous plasticity. It can produce new neurons and make new synaptic connections throughout life. Scientists have found that a protein called Brain Derived Neurotropic Factor (BDNF) plays an important role in brain function. It improves memory, attention, mood and concentration. We produce more of this protein when we exercise and move. Therefore, moving more may not only make us healthier, it may also make us smarter.
Now, the challenge becomes how to create circumstances where we can coax our bodies to move. We see that the market has responded to our need to increase movement with many creative fitness gadgets that make it easier for us to exercise.
One such innovation is the Standing desk, which makes you stand and work, and the Treadmill desk, which makes you walk and work. As companies are becoming aware of the cost of sitting and the sedentary life, some are offering standing and treadmill desks for their employees.

As a practicing Indian American psy chiatrist I had to spend a lot of time sitting and listening to people’s stories, and then documenting them. As my practice got busier, I began to develop back and neck pain from prolonged sitting. And then there was the weight gain, despite my eating healthy and exercising regularly. It made me rethink the way in which I structured my day.

I made changes to my schedule. I placed a small table on top of my desk and converted it into a standing desk. I try to do all my reading, typing and writing while standing. When I get tired I sit down and take rest, then I will stand again and continue. Some of my coworkers saw me make this change, and now they have also put a small platform over their desk in order to use the computer keyboard while standing. Many of us suffered from back, neck and wrist pain in the past and we have seen this disappear after we changed our posture from sitting to standing.

I strongly encourage everyone to have a standing desk or make one. There are inexpensive DIY options as well. You can make a workable standing desk using a box or stool over the regular desk. A spare treadmill or standing cycle can be placed under the desk. Pedometer smart phone apps are available that will record all steps and movements of the day.

Seek all opportunities to move. While you are working, get up and move every 15 minutes. Use a pedometer or a fitness tracker. A mundane activity like walking and moving can become fun and competitive once you measure and compare with family and friends. I wear a Fit-bit Charge and try to do the recommended 10,000 steps per day. Stand while you talk on the phone. Some offices are holding standing and walking meetings. I got rid of the copier and printer in my office. This forces me to walk down the hallway to get papers. I stopped bringing bottled water and now use a recyclable mug. Every time I get thirsty, I walk to the common area to refill my water.
Prolonged sitting increases the risk of death from all causes, including cardiovascular diseases, irrespective of a person’s BMI, leisure activities, and exercise.

The solution is simple—move. Make use of fitness gadgets and tools available to make you less sedentary. Make a personal commitment to stand more, move more, and sit less. Keep a daily activity log noting your position at each hour. Try to find more opportunities to move rather than sit. It has been established that we  become healthier, happier, and smarter as we move more. As you finish reading now, you may stand up, and ponder what Nietzsche meant when he said “Only thoughts reached by walking have value.”

Dr. Panchajanya Paul, MD, ABIHM, ABPN, is an American Board certified  Child, Adolescent, and Adult Psychiatrist. He is a diplomate of the American Board of Integrative and Holistic Medicine. He holds adjunct faculty position at Emory University School of Medicine; University of Georgia & Georgia Regents University, and University of Central Florida School of Medicine. He is a fellow of the American Psychiatric Association. He is a freelance writer who lives in Atlanta.

Have a look at this review on Standing desks in the Market

Scientists Have Uncovered The Atomic Structure of a Key Alzheimer's Protein For The First Time

Scientists Have Uncovered The Atomic Structure of a Key Alzheimer's Protein For The First Time

This is huge.

6 JUL 2017

For the first time, scientists have revealed the chemical structure of one of the key markers of Alzheimer's disease, capturing high-resolution images of the abnormaltau protein deposits suspected to be behind Alzheimer's and other neurodegenerative conditions.

The results will now give scientists an unprecedented glimpse at how these harmful deposits function at a molecular level, and could lead to a number of new treatments to prevent them from forming – and in doing so, help to combat Alzheimer's and dementia.

"This is a tremendous step forward," says one of the team, Bernardino Ghetti from Indiana University.

"It's clear that tau is extremely important to the progression of Alzheimer's disease and certain forms of dementia. In terms of designing therapeutic agents, the possibilities are now enormous."

In the new study, researchers led by the MRC Laboratory of Molecular Biology (LMB) in the UK extracted tau protein filaments from the brain of a deceased patient with a confirmed diagnosis of Alzheimer's disease, and imaged them using a technique called called cryo-electron microscopy (cryo-EM).

Tau protein filaments. Credit: Scheres Group MRC-LMB

Alzheimer's disease is linked to the build-up of two kinds of abnormal protein deposits – tau filaments, which form inside nerve cells, and amyloid beta proteins, which builds up outside cells.

In healthy brains, tau acts as a stabiliser, but when the proteins become defective, they can form into bundles of tangled filaments, which are thought to impede communication between brain cells, leading to the neurodegeneration and reduced cognitive ability seen in conditions like Alzheimer's disease.

Researchers have studied the tau protein's involvement in Alzheimer's for decades, but up until now, we've never been able to see tau filaments up so close – and the molecular insights afforded by the cryo-EM imaging performed here could mean the opportunities for drug discovery targeting tau is a whole new ball game.

"Drugs that could clear away clumps of protein in the brain are a key goal for researchers, but to directly affect these proteins, molecules that make up a drug need to latch on and bind to their surface," explains the head of research at Alzheimer's Research UK, Rosa Sancho.

"Knowing the precise shape of these complex protein structures is enormously valuable in guiding the development of targeted drugs."

While there's no shortage of research examining how abnormal tau and amyloid beta proteins function, it's been unclear just how much artificial samples assembled in the lab differ from the structures that form in the lab.

Thanks to the tau structures obtained from the deceased patient, researchers now have the ability to investigate how abnormal filaments function at an atomic level in the human brain – and studying these tangles won't only benefit Alzheimer's research, the team says.

"This is a big step forward as far as tau goes but it is bigger than that," neuroscientist Michel Goedert from LMB told James Gallagher at BBC News.

"This is the first time anybody has determined the high-resolution structure [from human brain samples] for any of these diseases. The next step is to use this information to study the mechanisms of neurodegeneration."

We won't know the full ramifications of this discovery until scientists have a chance to follow up on the new findings presented here, but it's clear that this could be a major turning point in studying how to counter these harmful protein clumps, with Ghetti describing the result as one of the major discoveries of the last quarter century of Alzheimer's research.

That said, it may take many more years (or even decades) for new treatments to ultimately come out of this – but at least we're now a big step closer to that long-hoped-for eventuality, which before now may have been impossible.

"It's like shooting in the dark – you can still hit something but you are much more likely to hit if you know what the structure is," explains one of the team, LMB's Sjors Scheres.

"We are excited – it opens up a whole new era in this field, it really does."

The findings are reported in Nature.

New Engineered Liver Tissue Could Improve Transplants

New Engineered Liver Tissue Could Improve Transplants
Fri, 07/21/2017 - 12:06pm

Researchers have developed a new way to engineer liver tissue by organizing tiny subunits that contain three types of cells embedded into a biodegradable tissue scaffold. This image shows vascularized engineered human liver tissue that has self-organized into a lobule-like microstructure. Image: Chelsea 
Fortin/Bhatia Lab/Koch Institute for Integrative Cancer Research

With a shortage in available livers, researchers have found a new way to engineer liver tissue.

A team from the Massachusetts Institute of Technology (MIT), Rockefeller University and Boston University organized tiny subunits that contain three types of cells into a biodegradable tissue scaffold.

After being implanted in the abdomen, the tiny structures expanded 50-fold and were able to perform normal liver tissue functions in a study of mice with damaged livers.
Currently, approximately 17,000 Americans are waiting for liver transplants.

 “There are just not enough organs to go around,” Sangeeta Bhatia, the John and Dorothy Wilson Professor of Health Sciences and Technology and Electrical Engineering and Computer Science and a member of MIT’s Koch Institute for Integrative Cancer Research and Institute for Medical Engineering and Science, said in a statement. “Our goal is that one day we could use this technology to increase the number of transplants that are done for patients, which right now is very limited.”

Bhatia developed an engineered tissue scaffold in 2011 that could be implanted into the abdomen of a mouse and integrate with the mouse’s circulatory system to allow it to receive a blood supply and begin performing normal liver functions.
The researchers built on that work by taking advantage of a key trait of liver cells where they can multiply to generate new liver tissue. They designed microfabricated structures that incorporate spherical organoids made of hepatocytes and fibroblasts, as well as cords of endothelial cells that are building blocks of blood vessels.

The mice receive regenerative signals—including growth factors, enzymes and molecules—from the surrounding environment after the constructs are implanted. 

The engineered livers could help facilitate liver transplants for those suffering from cirrhosis and hepatitis, as well as help those suffering from chronic liver disease that don’t qualify for a transplant.

“These patients never really are transplant candidates, but they suffer from liver disease, and they live with it their whole lives,” Bhatia said. “In that population you could imagine augmenting their liver function with a small engineered liver, which is an idea we’re pretty excited about.”

The best way to fix broken bones might be with glass

The best way to fix broken bones might be with glass

Glass may not seem an obvious material for a bone replacement. But UK surgeons are finding that bioglass not only is stronger than bone: it can bend, bounce and even fight infection.
  • By David Cox
4 August 2017

In 2002, Ian Thompson, a specialist in facial reconstruction at King’s College, London, received an urgent phone call. A patient in his late 20s had been struck by an out-of-control car mounting the pavement. The impact had sent him catapulting over the bonnet of the car, smashing his face and shattering the fragile orbital floor – the tiny bone, no more than 1mm thick, which holds the eyeball in place in the skull.

“Without the orbital floor, your eye moves backwards into the skull, almost as a defensive mechanism,” Thompson explains. “But this results in blurred vision and lack of focus. This patient had also lost the ability to perceive colour. His job involved rewiring aircraft and as he could no longer detect a red wire from a blue one, he’d barely been able to work in three years.”
The accident had happened three years earlier. Since then, surgeons had desperately tried to reconstruct the bony floor and push the eye back into position, first using material implants and then bone from the patient’s own rib. Both attempts had failed. Each time, infection set in after a few months, causing extreme pain. And now the doctors were out of ideas.

Thompson’s answer was to build the world’s first glass implant, moulded as a plate which slotted in under the patient’s eye into the collapsed orbital floor. The idea of using glass – a naturally brittle material – to repair something so delicate may seem counterintuitive.

But this was no ordinary glass.
“If you placed a piece of window glass in the human body, it would be sealed off by scar tissue, basically wobble around in the body for a while and then get pushed out,” says Julian Jones, an expert in bioglass at Imperial College London. “When you put bioglass in the body, it starts to dissolve and releases ions which kind of talk to the immune system and tell the cells what to do. This means the body doesn’t recognise it as foreign, and so it bonds to bone and soft tissue, creating a good feel and stimulating the production of new bone.”

Bioglass actually works even better than the patient’s own bone – Ian Thompson 

For Thompson, the results were immediate. Almost instantaneously, the patient regained full vision, colour and depth perception. Fifteen years on, he remains in full health.
Thompson has gone on to use bioglass plates to successfully treat more than 100 patients involved in car or motorcycle accidents. “Bioglass actually works even better than the patient’s own bone,” Thompson says. “This is because we’ve found that it slowly leaches sodium ions as it dissolves, killing off bacteria in the local environment. So, quite by chance, you have this mild antibiotic effect which eliminates infections.”

Cutting edge
Bioglass was invented by US scientist Larry Hench in 1969. Hench was inspired by a chance conversation on a bus with an army colonel who recently had returned from the Vietnam War. The colonel told Hench that while modern medical technology could save lives on the battlefield, it could not save limbs. Hench decided to shelve his research into intercontinental ballistic missiles– and instead work on designing a bionic material which would not be rejected by the human body.
Hench ultimately took his research to London, and it has been in Britain where some of the most revolutionary bioglass innovations are being made in fields from orthopaedic surgery to dentistry.

Bioglass already is being used in many households in the form of toothpaste (Credit: Alamy)

Over the last 10 years, surgeons have used bioglass in a powdered form, which looks and feels like a gritty putty, to repair bone defects arising from small fractures. Since 2010, this same bioglass putty has hit the high street as the key component in Sensodyne’s Repair and Protect toothpaste, the biggest global use of any bioactive material. During the brushing process, the bioglass dissolves and releases calcium phosphate ions which bond to tooth mineral. Over time, they slowly stimulate regrowth.
But many scientists feel that the current applications of bioglass are barely scratching the surface of what could be possible. New clinical products are being developed which could revolutionise bone and joint surgery like never before.
Sitting in his office in Imperial College’s Department of Materials, Jones is holding a small, cube-shaped object he’s dubbed ‘bouncy bioglass’. It’s similar to the current bioglass but with a slight twist: subtle alterations in the chemical composition mean it’s no longer brittle. Instead it bounces,“like a kid’s power ball” as Jones describes it, and it’s incredibly flexible.

Bouncy bioglass, shown here, is the opposite of the brittle material most of us imagine when we think of glass (Credit: Julian Jones)

The point of this is that it can be inserted into a badly broken leg and can support both the patient’s weight and allow them to walk on it without crutches, without requiring any additional metal pins or implants for support. At the same time, the ‘bouncy bioglass’ also will stimulate and guide bone regrowth while slowly, naturally assimilating into the body.
“To regenerate large pieces of bone, for example in a really big fracture, it’s very important to be able to put weight on your leg,” Jones says. “And it’s really important that the bio-implant in your leg is able to transmit the force from your weight to the bone cells, like a signal. Our body makes its own bone in the architecture that it’s in, because the cells feel the mechanical environment. So to grow back a big piece of bone you need to be able to transmit the right signals to them. The reason why astronauts in space lose bone mass is because without gravity, the cells aren’t receiving the same information as they do on Earth.”
Further alterations to the chemical makeup of bioglass produce a different form which is much softer and has an almost rubbery feel. It feels almost like a piece of squid at a seafood restaurant. This bioglass is designed for possibly the holy grail of orthopaedic surgery: cartilage repair.
Right now, surgeons attempt to repair damaged cartilage in arthritic hips or damaged knee joints with a fiddly procedure called microfracture. This involves smoothing over the damaged area to expose the bone underneath, then pricking it to release stem cells from the bone marrow which stimulate repair. But this results in scar cartilage and within a few years, as many athletes have found, the original problem returns.
As a solution, Jones is looking to produce bioglass which can be 3D-printed and then slotted into any hole in the cartilage. For the cells to accept it, the material must retain all the natural properties of cartilage. To test its effectiveness, Jones uses a simulator that has human knee joints from cadavers donated for medical research.

Bioglass could be a solution to repairing cartilage in damaged knee joints (Credit: Alamy)

“We simulate the walking action, bending, all the things a knee would do, and make sure that the bioglass actually preserves the rest of the joint and behaves as it should do,” he says. “If that works then we’ll proceed to animal and then clinical trials.”
This same bioglass could find an additional use in aiding people with chronic back pain due to herniated discs. At the moment surgeons treat this by replacing the dysfunctional disc with a bone graft which fuses the vertebrae in the back together. But while this takes away the pain, it results in a considerable loss in mobility. Instead, a bioglass implant could be printed and simply inserted to replace the faulty disc.
“It seems the obvious thing to do,” Jones says. “So far nobody has been able to replicate the mechanical properties of cartilage synthetically. But with bioglass, we think we can do it.
“We’ve just got to prove that we can. If all goes well and we pass all the necessary safety tests, it could reach the clinic in 10 years.”

Using man-made materials which can fuse to the body may seem far-fetched – but it is appearing to be a more and more likely component of future medicine. Already, millions of people brush their teeth with it. And that may just be the start.