Humans could achieve ‘super-intelligence’ in as little as FIVE YEARS by implanting tiny computer chips into our brains, expert claims

• Researchers working to develop smart brain implants for non-medical reasons 
• These chips could serve as brain-computer interface to boost our intelligence
• Neuroscientist developing a chip of his own predicts they'll be here in 5 years

High-tech chips implanted in the brain could soon give humans an intelligence boost.

Researchers have been working to develop minimally invasive methods to hack the human brain and squeeze out more of its potential.

Recent technological advancements could make this possible within the next five years, Northwestern University neuroscientist Dr. Moran Cerf told CBS – but, he warns the move could also create new forms of social inequality.

High-tech chips implanted in the brain could soon give humans an intelligence boost. Researchers have been working to develop minimally invasive methods to hack the human brain and squeeze out more of its potential. Stock image

‘Make it so that it has an internet connection, and goes to Wikipedia, and when I think this particular thought, it gives me the answer,’ Cerf told CBS.

The neuroscientist and business professor is currently working to develop one such chip, with the goal of improving human intelligence by melding it with technology.

This idea has taken off in recent years, with initiatives such as Elon Musk-backed Neuralink working to develop brain-computer interfaces.

DARPA has also expressed continued interest in the field as it works to enhance soldiers’ cognitive abilities and grasp on technology.

‘Everyone is spending a lot of time right now trying to find ways to get things into the brain without drilling a hole in your skull,’ Cerf told CBS.Can you eat something that will actually get to your brain? Can you eat things in parts that will assemble inside your head.’

According to Cerf, we may be just a few years away from the solution. But, its use in everyday society could make for extreme intelligence gaps within a given population. 

Just this past summer, the Pentagon’s research arm made moves in a project that intends to bridge the gap between humans and machines.

Recent technological advancements could make smart brain chips possible within the next five years, Dr Moran Cerf (pictured) says

DARPA selected a number of teams in July to develop a neural interface as part of its new N3 program, with a goal of developing systems that would allow troops to send and receive information using their brainwaves, according to Nextgov.

This means troops could one day control drones, cyber defense systems, and other technology with their mind.

It might sound like science fiction, but the agency is looking to see this done in one of two ways: a non-invasive device outside of the body, or a non-surgical system that could be swallowed, injected, or delivered up the nose.

And in spring of 2017, the agency funded eight separate research efforts to determine if electrical stimulation can safely be used to 'enhance learning and accelerate training skills.'

The program, called the Targeted Neuroplasticity Training (TNT) program, aimed to use the body's peripheral nervous system to accelerate the learning process.

This would be done by activating a process known as 'synaptic plasticity' – a key process in the brain involved in learning – with electrical stimulation.

Ultimately, doing this could allow a person to quickly master complex skills that would normally take thousands of hours of practice.

HOW IS THE US MILITARY HOPING TO 'HACK' SOLDIERS BRAINS?

Darpa's four-year Targeted Neuroplasticity Training (TNT) program aims to use the body's peripheral nervous system to accelerate the learning process.

This would be done by activating a process known as 'synaptic plasticity' – a key process in the brain involved in learning – with electrical stimulation.

Some teams will be working with intelligence analysts and foreign language specialists to shape the platform around currently training practices.

Researchers will look into using the technique across a wide range of applications, including decision-making and spatial navigation, speech perception and threat recognition.

'Imagine you're struggling to learn something new, like multiplication tables or how to hit a golf ball,' said Dr Robert Rennaker, of the University of Texas at Dallas’ Texas Biomedical Device Center.

'When you get it right, when that light bulb comes on, this system is being activated.

'By stimulating the vagus nerve during the learning process, we're artificially releasing these chemicals to enhance those connections active during learning.' 

Medications Older Adults Should Avoid

































You might be on one of the drugs listed below. It may be fine for you to be taking that drug. If you are taking a medication listed here it would be prudent to discuss that medication with the healthcare provider who prescribed it for you. It is always in your best interest to have your medications reviewed as some may no longer be necessary or may not be doing what they were intended to do for your health. Keep a list of your medications in your wallet, along with dosage and how many times a day, so you can refer to that list if you need to remind someone what you are taking. Also, if you are being seen by more than one healthcare provider be sure that ALL know your medication list as well as herbals and vitamins that you are taking. Some medications and herbals do not work together….

29 Medications Older Adults Should Avoid




The risks of using certain prescription and OTC drugs change as you get older. Are you taking something you shouldn’t be?

Even if you’re as sharp and active as you were in your 20s, there’s no denying your body has changed over the years. And while some of those changes might be obvious, others are not as easily noticeable. One important example: how your body responds to medication.

As you age, your kidney function changes, so it takes longer for many drugs to leave your system. Meanwhile, your body is less able to hold on to water and your body fat percentage increases, says Donna Marie Fick, Ph.D., R.N., director of the Center of Geriatric Nursing Excellence at Penn State College of Nursing.

These shifts, among others, mean a drug that worked well for you when you were younger might no longer do the trick—or, worse, it could leave you vulnerable to serious side effects or adverse events.

Benzodiazepines, for example, are often prescribed for anxiety and related conditions, but can increase the risk for cognitive impairment, falls, and motor vehicle accidents—leading to fractures and other serious injuries. Despite these risks, six percent of men and more than 10 percent of women 65 to 80 years old use benzodiazepines, according to a study in JAMA Psychiatry.

In an effort to keep older adults and their doctors in the loop about these risks, the American Geriatric Society (AGS) maintains a list of drugs that might be dangerous in older patients. And you might very well be taking one or more of the drugs on this list.
Is Your Doctor Up to Speed?

If you’re thinking your doctor should already know which drugs are off-limits for seniors, don’t be so sure. Unless you’re seeing a geriatrician, your provider might not be an expert in treating older adults.

You should also know that the 2019 version of the AGS list—called the AGS Beers Criteria for Potentially Inappropriate Medication Use in Older Adults—just came out in late January 2019. The previous update was in 2015, so if your doctor is still relying on that version, their info could be outdated.

Another common issue: “You might have been put on a drug when you were 55 or 60, but now you’re 65 or 75 and still taking it,” says Fick, who was a panel co-chair for the 2019 update.

That could be problematic if a doctor hasn’t recently assessed all of the meds you’re taking. She recommends going over all your prescription and over-the-counter (OTC) drugs, as well as any dietary supplements you may be using, with a doctor at least every six months.

Fick adds that it’s a good idea to periodically ask your doctor if you still need to be taking everything that’s part of your current drug regimen, or if any of them can be stopped.



“There’s a big push now to do what’s called ‘deprescribing,’ because the sheer number of drugs you’re taking is the biggest risk factor for adverse events,” she says.

Whether you’re taking one pill or 10 (or more!), you and your doctor should consult the new AGS guide to help make sure it’s safe for you. The guide puts drugs into five categories:
Medications that are potentially inappropriate for most older adults
Medications that should typically be avoided in older adults with certain conditions
Medications to use with caution
Medications that can react negatively with other medications (drug-drug interactions)
Medications that may need a dosage adjustment based on your kidney function

You can get most of the highlights of the report by visiting HealthinAging.org. If your doctor hasn’t already seen the full version, point them to the AGS professional site or the January edition of the Journal of the American Geriatric Society.

In the meantime, here is a list of relatively common medications that older adults are now advised to avoid or use with caution.
Drugs Older Adults Should Avoid
Diabetes drugs: glyburide (DiaBeta or Micronase) and chlorpropamide (Diabinese)
Muscle relaxants: cyclobenzaprine (Flexeril), methocarbamol (Robaxin), carisoprodol (Soma), and similar medications
Anxiety drugs: benzodiazepines, such alprazolam (Xanax), lorazepam (Ativan), diazepam (Valium), and chlordiazepoxide (Librium)
Insomnia drugs: zaleplon (Sonata), zolpidem (Ambien), and eszopiclone (Lunesta)
Antidepressants: amitriptyline (Elavil) and imipramine (Tofranil)
Parkinson’s drug: trihexyphenidyl (Artane)
Irritable bowel syndrome drug: dicyclomine (Bentyl)
Prescription pain reliever: meperidine (Demerol)
Drugs for menopause symptoms: estrogen pills and patches
OTC antihistamines: diphenhydramine (Benadryl), except for the treatment of severe allergic reaction, and chlorpheniramine (Aller-Chlor and Chlor-Trimeton)
OTC sleep aids that contain antihistamines: Tylenol PM (contains diphenhydramine) and similar medications
Drugs Older Adults Should Use with Caution
Pain relievers in the NSAID class: celecoxib, aspirin, ibuprofen, and naproxen. Avoid them if you have heart failure with symptoms, and use them with caution if you have heart failure without symptoms. Also, consider avoiding aspirin, ibuprofen, and naproxen entirely if you’re older than 75, taking an oral steroid, or taking a prescription blood thinner.
Heart failure or irregular heartbeat medication: digoxin (Lanoxin). Ask about safer alternatives.
Antipsychotic medications, unless you are being treated for schizophrenia, bipolar disorder, or chemotherapy side effects: haloperidol (Haldol), risperidone (Risperdal), or quetiapine (Seroquel)
How to Use This List

Of course, there are exceptions to everything, and there are some cases in which one or more of the drugs listed above truly is best for an older adult.

“All drugs have risks,” Fink says. “Our panel—which included clinicians, research scientists, private practice providers, pharmacists, and nurses—really tried to weigh the risk and benefits to figure out which ones belong on this list.”

Your own doctor can take it a step further by factoring in your medical history, health conditions, current medications, and any personal risk factors. If you’re concerned about a medication you are taking, continue taking it as directed, but call your doctoras soon as possible. After reviewing your information, your doctor will decide if it’s best for you to continue, change, or stop your medication.

A college degree may NOT protect against dementia as previously thought, study finds

• Higher education has been associated with lower dementia risk and slower decline
• But a new Rush University study found no link to support that

Having a higher level of education may not protect the brain against dementia as previously thought, a new study finds.

Plenty of research has found an active brain is a healthy brain - being bilingual, having a college degree, reading and even playing chess have all been associated with lower risk.

But a new paper by US scientists found that, after extending the time frame of these studies, there was no correlation at all.

They say it could be that people with higher education may have life experiences or biological factors that influence their risk.But based solely on letters after their name, there was little evidence of a link.

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People with a higher education did not necessarily have a slower cognitive decline than their peers, nor did it delay the age at which they were diagnosed - as previously suggested

'The strengths of this analysis include that it was based on more participants who were observed for a longer period of time than previous analyses,' said study author Robert S Wilson, PhD, of Rush University Medical Center in Chicago. 

'It's possible that the contribution of education to cognitive reserve depends on other factors, such as life experiences or biological factors, but these results did not show a relationship between a higher level of education and a slower rate of decline of thinking and memory skills or a later onset of the accelerated decline that happens as dementia starts.'

For the study, published today in Neurology, the medical journal of the American Academy of Neurology, used national and local data of 2,899 older adults. 

The local data came from the Rush Memory and Aging project, including older people in Chicago. 

The national data came from the Religious Orders Study, of older Catholic clergy members from across the United States. 

All of the people involved - who had an average age of 78 when they entered - agree to annual evaluations and a brain autopsy after death.

Over the eight years they were studied, 696 participants developed dementia. By the end, 752 died and had the brain autopsy, of whom 405 were diagnosed with dementia.

Analyzing the data, the researchers divided people into three education level groups - 12 years or fewer (up to a high school diploma), 13 to 16 years (from high school to bachelor's), and 17 or more years (higher than a bachelor's).

At the start of the study, those with higher education levels were sharper, with better memory skills and faster responses to questions. 

After that, the gap narrowed. 

People with a higher education did not necessarily have a slower cognitive decline than their peers, nor did it delay the age at which they were diagnosed - as previously suggested. 

The study also managed to dispel concerns that higher education could speed up decline once it started. There was no evidence of that. 

And the researchers found no evidence that highly educated people with high levels of Alzheimer's biomarkers declined slower than others.  

'This finding that education apparently contributes little to cognitive reserve is surprising given that education affects cognitive growth and changes in brain structure,' Dr Wilson said. 

'But formal education typically ends decades before old age begins, so late-life activities involving thinking and memory skills such as learning another language or other experiences such as social activities, cognitively demanding work and having a purpose in life may also play a role in cognitive reserve than may be more important than remote experiences such as schooling.'

There is one clear limitation of the study: many of the people involved had a fairly high level of education. 

The researchers concede that more work is needed on a broader spectrum of education levels to consolidate their findings.

But Dr Wilson said the study's finding that people with higher education levels were sharper at the start should not be dismissed lightly.  

'Of course, even if one declines at the same rate it is still better to start at a higher level of cognition,' Dr Wilson added.

Scientists discover a new kind of blood vessel in our bones that could help treat arthritis

• Capillaries - trans-cortical vessels - penetrate the shell of long bones in mice
• Provide most of bones' blood supply and take immune cells out of their marrow
• Similar canals found in human bones but unclear if they transport immune cells 

A new kind of blood vessels in our bones has been discovered by scientists.

The newly-discovered capillaries - called trans-cortical vessels (TCVs) - penetrate the hard shell of bones in mice.

Researchers found they provide most of the blood supply to the bones.

They also act as a 'shortcut' by carrying immune cells from the bone marrow to the injured area of the body - rather than the cells having to be 'picked up' by blood as it enters one end of the bone, travel through bone marrow, and exit the other end.

When analysing humans, the scientists found we too have similar blood vessels in the larger bones of our bodies.

The researchers hope their finding will lead to the development of new therapies that use this blood flow and immune cell migration to help treat inflammatory conditions, such as osteoarthritis.      

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Scientists have unveiled a new kind of blood vessels in our bones (stock)

The research was carried out by the University Duisburg-Essen, Germany, and led by Dr Anika Grüneboom, from the institute for experimental immunology and imaging.

Human anatomy is rarely the subject of scientific breakthroughs, with most experts being confident the major organs and tissues have already been discovered.   

'It is really unexpected being able to find a new and central anatomical structure that has not been described in any textbook in the 21st Century,' Dr Matthias Gunzer, study co-author and head of the institute, said.

He told NewScientist: 'It’s totally crazy there are still things to find out about human anatomy – we have discovered blood vessels in a new place that we didn’t know about before.'In their discovery, the scientists injected a fluorescent marker into the long bones of mice.

Long bones are hard and dense - providing strength, structure and mobility. An example is the femur, or thigh bone.

WHAT IS OSTEOARTHRITIS?

Osteoarthritis - sometimes called 'wear and tear' - is a condition that occurs when the surfaces within joints become damaged.

Cartilage covering the ends of bones gradually thin over time, and the bone thickens, according to Arthritis Research UK.    

Around a third of people aged 45 years and over in the UK suffer from the condition. This equates to roughly 8.75 million people. At least 20 million are known to suffer in the US.

It is different to rheumatoid arthritis, a long-term illness in which the immune system causes the body to attack itself, causing painful, swollen and stiff joints.  

Replacement joints are often necessary for osteoarthritis patients, because the joint has been worn down and causes agonising pain.The bones were then examined under a fluorescence microscope and X-ray.

Results  - published in the journal Nature Metabolism - revealed long bones in mice are supplied with oxygen and nutrients by hundreds of newly-discovered capillaries along the entire bone shaft. 

When the researchers looked at small pieces of human thigh bone, they found the same - albeit thicker - blood vessels, however, it is unclear if these carry immune cells. 

Professor Gunzer himself even took part - lying in a scanner for six hours while it imaged his lower leg. 

The discovered capillaries connect the inner and outer membranes that surround bones.  

They are thought to play a critical role in helping to transport blood in and out of the bones' hard shell. 

This blood also found to be rich in immune cells, which the capillaries carry from the bone marrow to the circulation.

Up until now, blood was assumed to enter long bones via arteries at the bones' end or through the few vessels along the bones' shaft, before passing through bone marrow and exiting the other end. 

'This is too oversimplified and does not correctly reflect the true natural situation,' Professor Gunzer said.

The researchers believe TCV re-modelling could play a role in the healing of fractures. 

To better understand this, they are calling for studies that investigate what 'maintains' these capillaries. 

Keep Exercising Mind And Body

Posted on 

Activity Tied To Cognition, Despite Brain Pathologies

Physical activity, motor skills independently correlated with reduced dementia

Higher levels of physical activity and motor abilities were independently associated with better cognition in older adults, even when brain lesions or biomarkers linked to dementia were present, a post-mortem study showed.

The study also showed no evidence that a more active lifestyle or better motor abilities modified associations between dementia pathologies and cognitive function, suggesting the cognitive reserve associated with activity may be unrelated to them, Aron Buchman, MD, of the Rush University Medical Center in Chicago, and colleagues wrote in Neurology.

“Physical activity may provide cognitive reserve to maintain function independent of accumulating brain pathologies,” Buchman told MedPage Today.

“Similar findings have been reported for late-life cognitive activities,” he added. “Together, these suggest that even in the absence of treatment for Alzheimer’s disease and related disorders, a more active lifestyle including physical and cognitive activities may help maintain cognition in older adults.”

Numerous observational studies have supported an association between physical exercise and reduced cognitive decline, but the mechanisms remain unknown, noted James Mortimer, PhD, of the University of South Florida in Tampa, and Yaakov Stern, PhD, of Columbia University in New York, in an accompanying editorial.

“The results of randomized trials of physical exercise suggest that exercise leads to increases in brain tissue, including in the hippocampus, where atrophy is an early and important finding in Alzheimer’s disease,” they wrote. One trial showed aerobic exercise led to increased levels of brain-derived neurotrophic factor (BDNF) and increased hippocampal volume; other studies suggested higher BDNF gene expression may help slow cognitive decline. “Alternatively, physical exercise itself might reduce brain pathology,” Mortimer and Stern added: mouse models have shown that higher physical activity levels reduce Alzheimer’s pathology accumulation.

The study drew on data from the Rush Memory and Aging Project, a community-based cohort of older adults who agreed to annual detailed clinical examination and brain donation at the time of death. The analysis included 454 participants with an average age at death of 91; 73% were female. A total of 191 participants had been diagnosed with dementia and 263 with no dementia.

The researchers incorporated 10 supervised motor performance tests to determine a global motor ability score and relied on continuous multi-day accelerometer recordings to monitor physical activity. Activity results were collected about 2 years before death and were measured in counts/day. The overall average was 156,000 counts/day, with participants without dementia averaging 180,000 counts/day, and people with dementia averaging 130,000 counts/day.

At autopsy, the researchers assessed brain tissue for:

• Alzheimer’s disease pathology (neuritic plaques, diffuse plaques, and neurofibrillary tangles)
• Nigral neuronal loss
• Lewy body disease pathology
• TAR DNA-binding protein 43
• Hippocampal sclerosis
• Macroscopic cerebral infarcts
• Cerebral atherosclerosis
• Microscopic cerebral infarcts
• Cerebral arteriolosclerosis
• Cerebral amyloid angiopathy

On average, participants had three different brain pathologies, with one or more pathologies observed in nearly all cases.

Buchman and colleagues performed regression analyses to “examine whether motor abilities or the quantity of daily physical activity attenuates the association of indices of AD pathology with the level of cognitive function proximate to death,” they wrote. Higher levels of total daily activity (estimate 0.148 ± 0.049, 95% CI 0.053–0.0.244, P=0.003) and better motor abilities (estimate 0.283 ± 0.055, 95% CI 0.175–0.390, P<0.001) both were independently associated with better global cognition proximate to death. These independent associations remained significant when interaction terms for Alzheimer’s disease and other pathologies were added.

Each standard deviation increase of total daily activity or motor capacity was associated with a reduction of dementia risk (total daily activity 31%; motor abilities 55%). These associations were additive, as the association of total daily physical activity with cognition did not vary with motor abilities.

“These data provide support for the idea that strategies or behaviors that lead to a more active lifestyle and better motor abilities may provide cognitive reserve, which may maintain cognitive function in older adults despite the accumulation of Alzheimer’s disease and other common brain pathologies,” the researchers wrote. “Further work is needed to clarify to what extent the risk factors and the types and duration of interventions to increase total daily physical activity and motor abilities are distinct and can be disentangled.”

The authors noted several limitations to their research: the data were cross-sectional and causal inferences cannot be drawn. It’s possible some of the association resulted from reverse causality (that lower cognitive function led to less activity). Accelerometers used in the study did not differentiate between various physical activities (such as steps vs arm movements) And the researchers assessed activity only at one point later in life; whether physical activity in early life may have played a role is unknown.

The study was supported by the National Institutes of Health, the Illinois Department of Public Health, and the Robert C. Borwell Endowment Fund.

Buchman reported no disclosures relevant to the manuscript. Other researchers reported relationships with Grifols, Lilly, Genentech, the Michael J. Fox Foundation, and the National Hockey League.

Exercise DOES beat depression: Study finds evidence for long-held theory that running 15 minutes a day boosts mood

• For years, studies found a connection between working out and lower depression risk
• But there was no evidence to show a causal relationship
• Now researchers at Massachusetts General Hospital have found evidence for it

Scientists have found some concrete evidence that exercising a little bit every day does reduce depression symptoms and boost overall mood.

For years, studies have found a connection between working out and lower depression risk - we all know exercise releases endorphins and endorphins make you happy.

But until now, there was no evidence to show a causal relationship when it came to depression - whether physical activity really did affect the condition, or simply that people with depression exercised less.

Now, a study by researchers at Massachusetts General Hospital (MGH) has presented evidence based on genetic data showing that working out is beneficial - and found no evidence that depression affects your ability to work out.

The team says the findings could help doctors and officials to develop prevention strategies for the growing number of people battling symptoms of depression.  

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For years, studies found a connection between working out and lower depression risk. But there was no evidence to show a causal relationship. Now researchers at MGH have found evidence for it

'On average, doing more physical activity appears to protect against developing depression,' says Karmel Choi, PhD, of the Psychiatric and Neurodevelopmental Genetics Unit in the MGH Center for Genomic Medicine, lead author of the report.

'Any activity appears to be better than none; our rough calculations suggest that replacing sitting with 15 minutes of a heart-pumping activity like running, or with an hour of moderately vigorous activity, is enough to produce the average increase in accelerometer data that was linked to a lower depression risk.' 

WHY RESEARCHERS HAVE STRUGGLED TO CONNECT THE DOTS - BUT GENES COULD OFFER AN ANSWER

Epidemiology is the study of what causes health outcomes and disease, and how to control them. 

But very often the things we're trying to understand - why some people love to drink  alcohol, what causes anxiety, who is at higher risk for certain cancers - are hard to measure clearly. 

Most studies end up being observational. In other words, scientists track their variables - in this case, physical activity levels and depression diagnoses - to see if the theory matches up. 

However, that is very rarely enough to determine a causal relationship. Even if you try to account for all the variables again and again, there will still be a gap in your data.

In a bid to dig deeper, and to eliminate one of the biggest question marks, the MGH team employed a popular technique: using genes as a framework.     

Both depression and physical activity can be affected by our genes. Some people are more naturally athletic, some are more prone to depression. 

Using genomic data, we can stabilize that factor. We can determine whether people with depression are simply just less active, or not. 

The technique (known as Mendelian randomization) is not a silver bullet; you are still left with room for other explanations. But it gets us as close as possible to confirming a cause. 

They pooled data from the UK Biobank and a global research group.   

For physical activity, they had two pools of results: one in which 377,000 people reported their own physical activity, and another in which 91,000 people wore fitness trackers to monitor their movement. This was compared to genetic tests. 

For depression, they analyzed the genetic makeup of 143,000 who were diagnosed with depression.  

The results of the Mendelian randomization study found no connection between self-reported activity and lower rates of depression. 

But when they looked at data from the fitness trackers, they did see improvement: those who worked out regularly had fewer symptoms of depression. 

The researchers said there is a myriad of easy explanations for that gap. Firstly, our memories are not always perfectly accurate, and sometimes we are driven to slightly curate our own version of what happened. Secondly, and crucially, many may not count everyday movement, such as climbing the stairs or walking to the subway, as exercise, whereas a fitness tracker would. 

They found nothing to suggest depression could hamper physical activity, nor that people with depression were less physically capable.   

Senior author Jordan Smoller, MD, ScD, director of the Psychiatric and Neurodevelopmental Genetics Unit and a professor of Psychiatry at Harvard Medical School, says that gene variants do not determine a person's behaviors or outcomes.

However, he says: '[T]heir average associations with certain traits in these very large studies can help us look at a question such as whether physical activity - or the tendency to engage in more physical activity - has a likely causal effect on depression. 

'And the answers to those questions could help researchers design large-scale clinical trials.'

Choi adds: 'And of course it's one thing to know that physical activity could be beneficial for preventing depression; it's another to actually get people to be physically active. 

'More work needs to be done to figure out how best to tailor recommendations to different kinds of people with different risk profiles. 

'We currently are looking at whether and how much physical activity can benefit different at-risk groups, such as people who are genetically vulnerable to depression or those going through stressful situations and hope to develop a better understanding of physical activity to promote resilience to depression.'