Beetroot juice supplements may help enhance exercise capacity in patients with heart failure, according to a new study published in the Journal of Cardiac Failure.
The researchers looked at the impact of dietary nitrate in the form of beetroot juice supplements on the exercise capacity of eight heart failure patients with reduced ejection fraction, a condition in which the heart muscle doesn’t contract effectively and can’t pump enough blood to the rest of the body.
Tens of millions of people suffer from heart failure. In about half of all such people, the ejection fraction of the heart is reduced.
Because of their condition, these patients find it harder to breathe, have diminished peak oxygen uptake and use more energy while exercising than would otherwise be the case.
Researchers found that the beetroot supplement resulted in significant increases in exercise duration, peak power and peak oxygen uptake while exercising.
Those improvements were not accompanied by any changes in the breathing responses of the patients, and there was no change in their exercise efficiency, a measure of how much external work a person gets for a certain input of energy.
Andrew Coggan, one of the researchers who conducted the study, said: Abnormalities in aerobic exercise responses play a major role in the disability, loss of independence and reduced quality of life that accompany heart failure. Perhaps more importantly, elevations in ventilatory demand and decreases in peak oxygen uptake are highly predictive of mortality in patients with heart failure.’
The data suggests that dietary supplementation may be a valuable addition to treatment for exercise intolerance among heart failure patients with reduced ejection fraction.
People with major depressive disorder (MDD) have reduced arginine levels, according to a new study by the University of Eastern Finland.
Arginine is an amino acid which the body uses to produce nitric oxide, a nervous system and immune defence mediator that also plays a role in vascular regulation.
The study, which has been published in the Journal of Affective Disorders, shows that people suffering from MDD have reduced arginine bioavailability.
Toni Ali-Sisto, the study’s lead author, said: ‘It is possible that depression-induced inflammatory responses lead to reduced arginine levels. This may result in insufficient production of nitric oxide for the needs of the nervous system and circulation. However, we don’t know yet what exactly causes reduced arginine bioavailability in people with depression.’
The study involved 99 adults with diagnosed major depressive disorder and 253 non-depressed controls. The concentrations of three amino acids, namely arginine, citrulline and ornithine, were analysed from fasting glucose samples. The findings were then compared between the depressed and the non-depressed controls.
People with depression had weaker arginine bioavailability than their non-depressed controls. The use of anti-depressants or anti-psychotics did not affect the concentrations, either. There were also no clear differences in the concentrations measured from people who had recovered from depression and people who remained depressed.
‘Although our study shows that people with depression have reduced arginine bioavailability, this doesn’t mean that taking an arginine supplement would protect against depression. That’s an area for further research,’ Ali-Sisto says.
Exercising for just a few minutes a day is linked to a lower risk of death in older men, according to new research published in the British Journal of Sports Medicine.
The study suggests that the total volume of exercise matters. Current exercise guidelines recommend accumulating at least 150 minutes a week of moderate to vigorous physical activity in bouts lasting longer than ten minutes. But such a pattern is not always easy for older adults to achieve, say the researchers.
This lower level of intensity is also likely to be a better fit for older men, say the researchers.
To find out if other patterns of activity might still contribute to lowering the risk of death, the researchers drew on data from the British Regional Heart Study.
This involved 7735 participants from 24 British towns, who were between the ages of 40 and 59 when the study began in 1978-80.
In 2010-12, the 3137 survivors were invited for a check-up, which included a physical examination, and questions about their lifestyle, sleeping patterns, and whether they had ever been diagnosed with heart disease.
They were also asked to wear an accelerometer during waking hours for 7 days. Their health was then tracked until death or June 2016, whichever came first.
In all, 1566 (50 per cent) men agreed to wear the device, but after excluding those with pre-existing heart disease and those who hadn’t worn their accelerometer enough during the 7 days, the final analysis was based on 1181 men, with an average age of 78.
The accelerometer findings indicated that total volume of physical activity, from light intensity upwards, was associated with a lower risk of death from any cause.
Each additional 30 minutes a day of light intensity activity, such as gentle gardening or taking the dog for a walk, for example, was associated with a 17 per cent reduction in the risk of death. This association persisted even after taking account of potentially influential lifestyle factors, such as sedentary time.
Whilst the equivalent reduction in the risk of death was around 33 per cent for each additional 30 minutes of moderate to vigorous intensity physical activity a day, the benefits of light intensity activity were large enough to mean that this too might prolong life.
And there was no evidence to suggest that clocking up moderate to vigorous activity in bouts of 10 minutes or more was better than accumulating it in shorter bouts. Sporadic bouts of activity were associated with a 41 per cent lower risk of death; bouts lasting 10 or more minutes were associated with a 42 per cent lower risk.
‘The results suggest that all activities, however modest, are beneficial. The finding that low intensity physical activity is associated with lower risk of mortality is especially important among older men, as most of their daily physical activity is of light intensity,’ the researchers say.
‘Furthermore, the pattern of accumulation of physical activity did not appear to alter the associations with mortality, suggesting that it would be beneficial to encourage older men to be active irrespective of bouts.’
Excessive levels of calcium in brain cells may lead to the formation of toxic clusters that are the hallmark of Parkinson’s disease, according to new research by the University of Cambridge.
The researchers found that calcium can mediate the interaction between small membranous structures inside nerve endings, which are important for neuronal signalling in the brain, and alpha-synuclein, the protein associated with Parkinson’s disease.
Excess levels of either calcium or alpha-synuclein may be what starts the chain reaction that leads to the death of brain cells.
The findings, which have been published in the journal Nature Communications, take us a step closer towards understanding how and why people develop Parkinson’s, which is currently incurable.
Parkinson’s disease is one of a number of neurodegenerative diseases caused when naturally occurring proteins fold into the wrong shape and stick together with other proteins, eventually forming thin filament-like structures called amyloid fibrils. These deposits of alpha-synuclein, also known as Lewy bodies, are indicative of Parkinson’s disease.
It hasn’t been clear until now what alpha-synuclein actually does in the cell. It is implicated in various processes, such as the smooth flow of chemical signals in the brain and the movement of molecules in and out of nerve endings, but exactly how it behaves is unclear.
Dr. Gabriele Kaminski Schierle, the study’s senior author, said: ‘Alpha-synuclein is a very small protein with very little structure, and it needs to interact with other proteins or structures in order to become functional, which has made it difficult to study.’
Thanks to super-resolution microscopy techniques, it is now possible to look inside cells to observe the behaviour of alpha-synuclein. The researchers observed that when calcium levels in the nerve cell increase, such as upon neuronal signalling, the alpha-synuclein binds to synaptic vesicles at multiple points causing the vesicles to come together.
Understanding the role of alpha-synuclein in physiological or pathological processes may aid in the development of new treatments for Parkinson’s disease. One possibility is that drug candidates developed to block calcium, for use in heart disease for instance, might also have potential against Parkinson’s disease.
There is a heartwarming video on Youtube of Jamie Oliver showing a group of children how chicken nuggets are made in an attempt to deter them from eating them. He blends up a gruesome mix of bones, skin and offal, slaps some flour on it and sticks it in the pan. ‘Now,’ he says triumphantly, ‘who would still eat this?’
The look of disappointment on Oliver’s face when every hand goes up is one of the most delightful images ever shown on television. It never fails to cheer me up.
After watching it for the umpteenth time, I noticed something. None of the children appear to be obese. In fact, it is difficult to spot many obese kids in any of Oliver’s series involving children. Jamie’s School Dinners was filmed at the height of the childhood obesity ‘epidemic’ and yet there was little sign of it in the cafeteria. Fat kids were also surprisingly rare in Jamie’s Return to School Dinners and Jamie’s Dream School. There were one or two, of course – as there always has been – but at a glance there were far fewer pudgy hands, chubby faces and double chins than one would expect in a country where a third of secondary school children are said to be overweight or obese.
You may have noticed the same thing if you drop your children off at the school gates or flick through the school news in your local paper. You may even be one of the bemused parents up and down the country who receives a letter from school informing you that your seemingly healthy child is borderline obese.
And yet, one in ten kids are classified as obese when they start primary school and one in five are obese by the time they start secondary school. According to the latest figures, 23 per cent of 11-15 year olds are obese. And that’s before we add those who are merely overweight.
These are shocking statistics and we are reminded about them at every opportunity. Organisations like Public Health England repeat the claim that ‘more than a third of children [are] leaving primary school overweight or obese’ like a mantra whenever they have a new anti-obesity wheeze to push. So where are they all?
You can’t see them because most of them do not exist. They are a statistical invention. The childhood obesity figures in Britain are simply not worth the paper they are printed on and the childhood obesity rate is much lower than 23 per cent. Let me explain.
Obesity in adults is easy enough to measure. Body Mass Index (BMI) is weight in kilograms divided by the square of height in centimetres. A BMI of 30 or more is classified as obese. In theory, the cut-off of 30 is used because this is the point at which being fat increases the risk of premature death, but it also happens to be a round number. A BMI of 25 or more makes you overweight, but this isn’t really based on anything. It is purely a round number.
There are well known problems with BMI, not least the fact that it does not distinguish between muscle weight and fat weight. It is excess body fat that we are interested in and this is best diagnosed by clinical examination, but when that is not possible (as when estimating figures for an entire nation), the BMI system correctly identifies obesity around 80 per cent of time.
But it doesn’t work with children. Kids are not shaped like adults, do not have the same fat/muscle ratio and are growing. They rarely have a BMI over 30. An obese child can easily have a BMI of less than 25. Moreover, obese girls have different BMIs than obese boys.
To make up for this, clinicians use a chart like the one below which gives bespoke, age-specific and gender-specific BMI cut-offs for children. For example, at the age of six and a half, boys are considered obese if their BMI exceeds 20.2. By the time the boy is eleven, the cut-off has risen to 25.1.
To see how these cut-offs are derived, we need to look at the work of Professor Tim Cole and his colleagues. In 1995, they published a much-cited study upon which the chart above is based. They studied the BMIs of children at different ages and divided them into percentiles. This allowed clinicians to compare the BMI of their patient to that of their peers. For example, if a girl’s BMI was at the 90th percentile, only ten per cent of her peers had a higher BMI while 90 per cent of her peers had a lower BMI.
The data used by Cole et al. were taken from between 1978 and 1990, before the rise in childhood obesity got underway and gave us a reference point from which future changes in obesity could be measured. For example, if obese 11 year old boys in 1990 had a BMI of 26 and were in the 99th (top) percentile, the obesity rate was one per cent in 1990. To update the statistics, we only need to measure today’s 11 year old boys and see how many of them would have been in the 99th percentile in 1990. If four per cent of them have a BMI over 26, they would have been in the 99th percentile and the obesity rate is four per cent.
This system made it possible to estimate child obesity rates nationwide without clinicians having to examine anybody. Detailed figures have been collected by the UK government since 1995 and all the child obesity estimates published by the NHS and Office for National Statistics are based on Cole’s reference curves from 1990.
It seems relatively straightforward. The problem is that we don’t really know how many children were obese in 1990. Cole’s solution was to infer the rate of child obesity from the rate of obesity among young adults. Common sense dictates that the child obesity and adult obesity figures should ‘link up’. Both systems should produce similar estimates for young adults. It would be strange if 17 year olds had an obesity rate of, say, eight per cent while 18 year olds had a rate of one per cent, especially since BMI tends to rise with age
Cole et al. noticed that the 20 years olds in 1990 who had a BMI of 29 (and were therefore nearly obese) appeared at the 98th percentile, which is to say that the rate of obesity was a little under two per cent. They also noticed that the 20 year olds in the 99.6th percentile (the top 0.4 per cent) had BMIs of at least 32.8. They therefore concluded that:
‘These centiles seem to be reasonable definitions of child obesity and superobesity respectively.’
They came to a similar conclusion when they published further research in 2000. Looking at BMIs in Britain between 1978 and 1993 (‘predating the recent increase in prevalence of obesity’), they found that obese 18 year olds were at the 99th percentile. In other words, only one per cent of people who had recently become adults were obese by the usual adult definition.
They found similarly low rates of obesity for 18 year olds in the Brazil and Singapore over the same time period. The Netherlands had an even lower rate of 0.3 per cent but the USA had a much higher rate of 3.3 per cent for men and 4 per cent for women.
Taken together, this suggested that the obesity rate among young British adults circa 1990 was less than two per cent and that a realistic cut-off point for childhood obesity was the 98th or 99th percentile. In a later study, Cole and Lobstein concluded that ‘the obesity cut-off is well above the 98th centile’.
So that means we use the 98th percentile as the cut-off when estimating child obesity figures today, right?
Wrong. We use the 95th percentile.
Why? There is little justification for it in the scientific literature other than that it is the convention. Cole himself says that the methodology is ‘all built on sand.‘ The most likely explanation for dropping the cut-off to the 95th percentile – if we exclude the possibility that it was deliberately intended to exaggerate the size of the problem – is that the USA did it first and we copied them.
By the end of the 1990s, the USA had started using the 95th percentile as the cut-off for ‘overweight’, with the 85th percentile used to define ‘at risk of overweight’ – terms that would later be changed to ‘obese’ and ‘overweight’. This was not wholly unreasonable. The rise of obesity in America began earlier than it did in Britain and rates of obesity have always been higher. It is likely that around five per cent of American children were at least overweight, if not obese, by the end of the 1980s and would therefore have been above the 95th percentile.
But Britain is not America. Cole’s figures showed that the obesity rate among 18 year olds in Britain was much lower than it was in the USA – at one per cent – and while he recognised the need for a cut-off, he asked the obvious question:
‘… why base it on data from the United States, and why use the 85th or 95th centile? Other countries are unlikely to base a cut off point solely on American data, and the 85th or 95th centile is intrinsically no more valid than the 90th, 91st, 97th, or 98th centile.’
Whatever the reason for using the 95th percentile, it has had the effect of greatly inflating childhood obesity figures in Britain for as long as they have been recorded. It implicitly assumes that five per cent of 18 year olds were obese in 1990 when we know that the real figure was less than two per cent. Starting from this false premise, everything that follows from it is wrong. Forced to pretend that the child obesity rate in 1990 was more than twice as high as it was, we are given child obesity statistics for the present day that are likely to be off by a similar margin.
We are classifying huge numbers of children as obese who would not have been diagnosed as such by a doctor in 1990 and would not be diagnosed as such today. If you look at the chart above, you will see that the 95th percentile is not even shown on it. It is of no clinical relevance.
The result is that we get figures which defy credibility. Take a look at the latest obesity statistics for adults from the Health Survey for England. The pattern is typical of a developed country, with rates rising steadily as people get older and then dipping in old age.
Now let’s add the childhood obesity figures which are measured in a totally different way. As you can see, they do not link up at all. Both groups of children have a higher rate of obesity than the young adults, with the rate among 11-15 year olds being more than twice as high as that of 16-24 year olds.
To take these statistics seriously, we have to believe that obesity rises rapidly in secondary school, affecting nearly a quarter of children, before suddenly plummeting to barely a tenth of children once they become adults.
These figures are for 2016, but the same picture emerges if you go further back in time. Since 2001, every year (except one) shows rates of obesity for 11 to 15 year olds at between 18 and 25 per cent while the rates for 16-24 year olds are between 10 and 13 per cent. The current batch of 16-24 year olds have an obesity rate of 11 per cent, but when they were in school a few years ago they had an obesity rate of around 20 per cent. This is a remarkable feat of weight loss, especially when you consider that we have recently been told that ‘four out of five obese schoolchildren will remain dangerously overweight for the rest of their lives’.
When parents are asked about their supposedly obese children, only 52 per cent of them say that they are ‘too heavy’. When it comes to children who are ‘overweight’ – a truly meaningless category based on the 85th percentile – only 11 per cent think they are ‘too heavy’. The children themselves agree. Only 51 per cent of ‘obese’ children and 17 per cent of ‘overweight’ children think that they are too heavy.
Never mind Goldilocks. The Emperor’s New Clothes is the more appropriate fairy tale analogy here. We are told that obese children roam the streets in vast numbers: one in five 11 year olds, rising to one in three if you include the ‘overweight’. No one can see this many obese kids with their own eyes and yet we go along with the illusion, perhaps assuming that they live elsewhere. If you met these ‘overweight’ kids, you would probably agree with their parents and say that most of them are not fat. A doctor who examined the ‘obese’ kids would reject the diagnosis of obesity in hundreds of thousands of cases.
This is not to deny that child obesity, like adult obesity, has risen over the years. Comparing today’s figures with those of 1990 shows a rise in children’s BMI, albeit one that peaked in 2004 before going into reverse. But we have no idea how many children are obese because the official statistics do not really measure obesity. Claims about a quarter, or a third, of children being dangerously overweight are for the birds. The true figures – if they ever emerge – are bound to be much lower than the numbers bandied around in the newspapers.
Most medical disorders have well-defined physical characteristics seen in tissues, organs and bodily fluids. Psychiatric disorders, in contrast, are define by behaviour.
A new study by the University of California, Los Angeles has found that autism, schizophrenia and bipolar disorder share some physical characteristics at the molecular level, specifically, patterns of gene expression in the brain. Researchers also pinpointed important differences in these disorders’ gene expression.
The study’s senior author, Daniel Geschwind, said: ‘These findings provide a molecular, pathological signature of these disorders, which is a large step forward. The major challenge now is to understand how these changes arose.’
Researchers know that certain variations in genetic material put people at risk for psychiatric disorders, but DNA alone doesn’t tell the whole story. Every cell in the body contains the same DNA; RNA molecules, on the other hand, play a role in gene expression in different parts of the body, by ‘reading’ the instructions contained within DNA.
Geschwind and the study’s lead author, Michael Gandal, reasoned that taking a close look at the RNA in human brain tissue would provide a molecular profile of these psychiatric disorders.
Researchers analyzed the RNA in 700 tissue samples from the brains of deceased subjects who had autism, schizophrenia, bipolar disorder, major depressive disorder or alcohol abuse disorder, comparing them to samples from brains without psychiatric disorders.
The molecular pathology showed significant overlap between distinct disorders, such as autism and schizophrenia, but also specificity, with major depression showing molecular changes not seen in the other disorders.
Geschwind said: ’We show that these molecular changes in the brain are connected to underlying genetic causes, but we don’t yet understand the mechanisms by which these genetic factors would lead to these changes.’
‘So, although now we have some understanding of causes, and this new work shows the consequences, we now have to understand the mechanisms by which this comes about, so as to develop the ability to change these outcomes.’
Engineers, doctors and scientists at UCLA and Rutgers University have developed a tool that measures the physical strength of individual cells 100 times faster than current technologies.
The new device could make it easier and faster to test and evaluate new drugs for diseases associated with abnormal levels of cell strength, including hypertension, asthma and muscular dystrophy.
It is the first tool that can measure the strength of thousands of individual cells at a time. The study’s co-author, Dr. Reynold A. Panettieri Jr, said: ‘We took a fresh approach to identify molecules that could serve as drugs to meet an unmet need for new treatments to treat or cure chronic disease.’
‘Our new experimental platforms are capable of screening millions of molecules to identify the best drug candidates for the right patients.’
‘The system leverages the state of the art bioengineering techniques and use of human cells derived from patients with chronic diseases that offers greater likelihood of predicting therapeutic responses.’
Cells use physical force for essential biological functions – both as individual cells, for example in cell division or immune function, and as large groups of cells in tissue, for example, when muscles contract.
Disruptions in a cell’s ability to control the levels of force they exert can lead to diseases or loss of important bodily functions. For example, asthma is caused by the smooth muscle cells that line the airways squeezing more than normal. And abnormally weak cell forces are associated with heart failure, muscular dystrophy and migraine headaches.
The device is called fluorescently labeled elastomeric contractible surfaces, or FLECS. Its key component is a flexible rectangular plate with more than 100,000 uniformly spaced X-shaped micropatterns of proteins that are sticky so cells settle on and attach to them.
‘Our platform can markedly improve the speed and fidelity of screening of millions of potential molecules in order to find new candidates that can rapidly progress through the approval process to become new drugs in asthma, cancer and heart disease,’ Panettieri said.
To test the tool, the researchers analyzed drugs that make cells either contract or relax, using human smooth muscle cells that line airways in the body. The researchers compared the results of those tests to what was already known about how lung tissue reacts to the drugs and found that FLECS captured the same types of reactions, only more precisely because it could analyse the reactions in cell-by-cell detail.
They also tested the force of macrophages, cells in the immune system that rid the body of potentially harmful particles, bacteria and dead cells. They found that when a typical macrophage receives a signal that an infection is present, it can exert force approximately 200,000 times its own weight in water. But some macrophages were more than three times stronger than that.
The researchers also used FLECS to analyze cell force and then compared the results of that test to a current standard test, which judges cell force by analysing the amount of calcium in the cells. They were surprised that the results of the calcium test did not correlate well with how much cells contracted. The finding suggests that the calcium test may be limited, because, unlike that tes, FLECS looks at a level of detail down to an individual cell.
The UCLA researchers found that individuals cells from people who had died from severe asthma contract with more force, both generally and during an asthma attack, than they do in healthy people.
It is estimated that there are 10 million cats and 11.5 million dogs kept as pets in the UK – and new research suggests they could be improving the mental health of their human companions.
A new study, published in BMC Psychiatry, conducted by researchers from the universities of Liverpool, Manchester and Southampton, is the first systematic review of the evidence related to the comprehensive role of companion animals and how pets might contribute to the management of long-term mental health conditions.
The researchers reviewed 17 international research papers to explore the extent, nature and quality of the evidence implicating the role and utility of pet ownership for people living with a mental health condition, and to identify the positive, negative and neutral impacts of pet ownership.
The research highlighted the ‘intensiveness’ of connectivity people with companion animals reported, and the many ways in which pets contributed to the work associated with managing a mental health condition, particularly in times of crisis.
The negative aspects of pet ownership were also highlighted, including the practical and emotional burden of pet ownership and the psychological impact that losing a pet has.
The study’s lead author, Dr. Helen Brooks, said: ‘Our review suggests that pets provide benefits to those with mental health conditions. Further research is required to test the nature and extent of this relationship, incorporating outcomes that cover the range of roles and types of support pets confer in relation to mental health and the means by which these can be incorporated into the mainstay of support for people experiencing a mental health problem.’
Researchers from the Queensland University of Technology have identified a drug that could potentially help our brains reverse the damage caused by heavy alcohol consumption.
Their studies in adult mice show that two weeks of daily treatment with the drug tandospirone reversed the effects of 15 weeks of binge-like alcohol consumption on neurogenesis (the ability of the brain to grow and replace brain cells). The study’s findings have been published in the journal Scientific Reports.
Tandospirone is a relatively new drug, only currently available in China and Japan, where it is used to treat general anxiety.
It acts selectively on the serotonin receptor 5-HT1A, and has also been shown to stop anxiety-like behaviours associated with alcohol withdrawal in a mouse mofel. This was accompanied by a significant decrease in binge-like alcohol intake.
The study’s leader, neuroscientist Professor Selena Bartlett, said: ‘This is a novel discovery that tandospirone can reverse the deficit in neurogenesis caused by alcohol. We know that with heavy drinking you are inhibiting your ability to grow new neurons, brain cells. Alcohol is specifically very damaging for neurons.’
‘Other studies in mice have shown that tandospirone improves brain neurogenesis, but this is the first time it has been shown that it can totally reverse the neurogenic deficits induced by alcohol.’
‘This opens the way to look at if neurogenesis is associated with other substance-abuse deficits, such as in memory and learning, and whether this compound can reverse these.’
‘This is not just another drug that shows promise in helping to reduce binge drinking. While it could possibly have that effect, it might be able to help reboot the brain and reverse the deficits the alcohol abuse causes – both the inhibition to the brain’s ability to regenerate, and the behavioural consequences that come from what alcohol is doing to the brain, like increases in anxiety and depression.’
A new blood test developed by researchers at the University of Sheffield could provide a clue as to why some patients are at higher risk of cardiovascular disease after suffering a heart attack.
The research may help scientists to identify new targets for reducing the risk and eventually lead to more effective treatments.
During the study the team of researchers analysed blood plasma samples from more than 4300 patients with acute coronary syndrome as they were discharged from hospital.
They measured the maximum density of a clot and the time it took for the clot to break down, known as clot lysis time.
After adjustment for known clinical characteristics and risk factors, the study found that the patients with the longest clot lysis time had a 40 per cent increased risk of recurrent myocardial infarction or death due to cardiovascular disease.
Professor Storey, the study’s lead author, said: ‘We have made huge strides over the last two decades in improving prognosis following heart attacks but there is still plenty of room for further improvement.’
‘Our findings provide exciting clues as to why some patients are at higher risk after heart attack and how we might address this with new treatments in the future.’
The results, which have been published in the European Heart Journal, showed novel therapies targeting fibrin clot lysis time may improve prognosis in patients with acute coronary syndrome.
Professor Storey said: ‘We now need to press ahead with exploring possibilities for tailoring treatment to an individual’s risk following a heart attack and testing whether drugs that improve clot lysis time can reduce this risk.’
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