Machine learning systems, fair or biased, reflect our moral standards

  • While machine learning systems and algorithms are theoretically more objective than humans, this does not necessarily result in different or fairer results
  • There needs to be a concerted effort by regulators, governments and practitioners to ensure the technology stems inequities rather than perpetuates them
Mohan Jayaraman

Mohan Jayaraman

Published: 6:45am, 30 Jun, 2020Why you can trust SCMP

While machine learning systems and algorithms are theoretically more objective than humans, this does not necessarily result in different or fairer results. Image: Dreamstime/TNS
While machine learning systems and algorithms are theoretically more objective than humans, this does not necessarily result in different or fairer results. Image: Dreamstime/TNS

While machine learning systems and algorithms are theoretically more objective than humans, this does not necessarily result in different or fairer results. Image: Dreamstime/TNS

Discrimination in the real world is an ugly reality we have yet to change despite many years of effort. And recent events have made it clear that we have a long, long way to go.

Some companies and governments have turned to automation and algorithms in a bid to remove the human bias that leads to discrimination. However, while machine learning (ML) systems and algorithms are theoretically more objective than humans, the ability to apply the same decision structure unwaveringly does not necessarily result in different or fairer results.

Why is that? Given humans are their progenitors, bias is often built into these ML systems, leading to the same discrimination they were created to avoid. Recently, concerns have emerged that stem from the growing use of these ML systems, when unfiltered for bias, in such areas that could impact human rights and financial inclusion.

Today, ML algorithms are used in hiring, which could be biased by historical pay divides by gender; in parole profiling systems, impacted by historical trends of racial or geography-linked crime rates; and credit decisions, influenced by the economic status of a consumer segment that may have a racial tilt.

These biases stem from flaws in current processes which in turn, colour the training or modelling data set. This can then result in discrimination, and with the growing use of these systems at scale, existing social biases can be further amplified.

Computer, your biases are showing23 Jun 2020

How then can we filter out built-in biases and discrimination within these ML systems and make them “fairer” across every segment of society?

Let’s start by understanding what we mean by discrimination. Today, various forms of discrimination in making decisions about consumers have been identified and are subject to regulatory scrutiny. These include:

  • Direct discrimination: when specific sensitive attributes like race, national origin, religion, sex, family status, disability, marital status or age are used to differentiate treatment.
  • Indirect discrimination: when sensitive attributes are indirectly identified and used in the decision model. A typical example would be an attribute like postcode, which, while not categorised as a protected attribute, may still have a racial, religious and/or socio-economic concentration.
  • Statistical discrimination: when decision-makers use average group statistics to judge an individual of the group, with racial profiling as a typical example.
  • Systemic discrimination: policies or customs that are a part of the culture or structure of an organisation that may perpetuate discrimination against certain population subgroups, gender or racial stereotypes.

Too white, too male: scientist stakes out inclusive future for AI12 Feb 2019

ML systems learn from past decisions or from other feedback loops that are set up based on current decision agents, typically human. Consequently, they inherit human biases.

An ML algorithm typically optimises based on a finite data set. It is, therefore, subject to bias because an algorithm works on assumptions or classifiers. These assumptions and classifiers are necessary as without them, the algorithm would produce no better than random results. Unfortunately, this also means that the decision and outcomes from these algorithms can consequently be unfair and discriminatory.

Discrimination in the real world is an ugly reality we have yet to change despite many years of effort. And recent events have made it clear that we have a long, long way to go.

When evaluating fairness within ML systems, the metrics fall into two distinct categories – group and individual fairness. Group fairness is founded on the fair treatment of groups to ensure that members of all segments receive a fair share of the beneficial outcome(s). Individual fairness focuses on similar outcomes for similar individuals.

The commonly used group fairness metrics are:

  • Demographic parity: acceptance rates are tracked across demographic profiles seen as disadvantaged to get them on par with the relatively advantaged segment. The fairness metric is achieved when the model’s classification is independent of the sensitive attribute(s).
  • Equalised odds: no matter whether an applicant is part of an advantaged or disadvantaged segment, so long as they qualify, they are equally likely to get approved. If they do not qualify, they are equally likely to get rejected.
  • Predictive (rate) parity: the fairness metric is met when the acceptance rate of a given classifier, e.g. race, is equivalent for each subgroup. This is also referred to as predictive parity.

The most commonly used individual fairness metrics are:

  • Fairness through unawareness: this approach excludes sensitive attributes that lead to direct discrimination from the modelling data. While relatively easy to use, a key flaw is the availability of a multitude of correlated features that could indicate sensitive attributes in a typical ML model.
  • Individual fairness or fairness through awareness: the fairness metric is reached when two applicants with a similar profile have the same probability of being approved.
  • Counterfactual fairness: when a classifier produces the same result for one individual as it does for another identical individual, except for one or more sensitive attributes.

This gives us a starting point to measure fairness but there simply is no one-size-fits-all solution. It is impossible to satisfy all of the fairness constraints at once except in certain special cases. The fairness metric, therefore, needs to take into account the use case and the population distribution.

There needs to be a concerted effort by regulators, governments and practitioners to make sure that these algorithms and systems reflect the best in us, which helps to stem inequities, instead of the worst in us, which perpetuates them.

Recently, a lot of progress has been made to remove bias from ML through a variety of techniques. These include pre-processing, which focuses on the primary source of bias data; and post-processing, or altering the decision of the models to get to fair outcomes. Interestingly, a lot of academic research is currently centred around a third approach, which focuses on introducing a fairness definition into the model training process.

The decisions made through ML reflect our moral standards. There needs to be a concerted effort by regulators, governments and practitioners to make sure that these algorithms and systems reflect the best in us, which helps to stem inequities, instead of the worst in us, which perpetuates them. Only then can we hope to move towards a fairer world.Sign up now for a 50% early bird discount on the 100+ page China Internet Report 2020 Pro Edition, which includes deep-dive analysis, trends, and case studies on the 10 most important internet sectors. Now in its 3rd year, this go-to source for understanding China tech also comes with exclusive access to 6 webinars with C-level executives. Offer valid until 30 June 2020.

Boosting Cellular Energy at Sites of Myelin Loss May Stop MS Progression



Boosting Cellular Energy at Sites of Myelin Loss May Stop MS Progression

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Loss of myelin in nerve cell fibers — the hallmark of multiple sclerosis (MS) — leads to a shortage of mitochondria, a cell’s powerhouse, denying these damaged fibers the energy they need to work as intended, a new study shows.

Boosting the migration of mitochondria to affected nerve fibers, supplying them with needed energy, may help to protect nerves from degeneration and halt disease progression. Indeed, it may offer a new way of treating progressive MS.

The study “Enhanced axonal response of mitochondria to demyelination offers neuroprotection: implications for multiple sclerosis” was published in the journal Acta Neuropathologica.

MS is caused by the destruction of myelin, the fat-rich substance that wraps around and insulates nerve cell fibers (axons). Axons are projections of nerve cells that conduct the electric impulses that allow these cells to communicate.

To work as intended, damaged axons require large amounts of energy, which is provided by mitochondria. To compensate for the resulting energy imbalance, neurons respond by increasing their mitochondrial content. Mitochondria are small cellular organelles that work as the cell’s power plant: they produce energy molecules such as ATP, the most common cellular energy source.

However, in nerve cells of MS patients, mitochondria function is often affected. Evidence suggests people with progressive MS have genetic alterations that impair energy production.

A team led by researchers at the University of Edinburgh investigated whether targeting mitochondria in neurons could help mitigate the loss of myelin (demyelination). The study was supported by the National MS Society.

Researchers hypothesized that neurons would respond to demyelination by moving mitochondria from the neuron’s body to the damaged axon.

Real-time imaging of fluorescent mitochondria showed that in healthy neurons in mice — namely, in Purkinje neurons (found in the cerebellum, the center for motor coordination) and sensory dorsal root ganglia (DGR) neurons — mitochondria migrated into the region of the axon where demyelination was present. They named this process “axonal response of mitochondria to demyelination” or ARMD.

ARMD peaked at five days post-demyelination in the cerebellum neurons, and by day seven in the DGR neurons, showing that axons are vulnerable for a few days after myelin is destroyed, and the therapeutic window to target this response process is short.

Next, researchers evaluated several ways of enhancing mitochondrial numbers and migration. One was by boosting the levels of the peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1-alpha), a key protein involved in mitochondria production. This boost led to an increase in the content and transport of mitochondria to axons, mimicking the ARMD process.

Based on this result, researchers tested pioglitazone, a type 2 diabetes medicine (sold as Actos, among other brand names) known to boost the PGC1-alpha pathway. The treatment was seen to recreate previous findings, with the therapy enhancing mitochondria transport to the axons.

“Taken together, these findings indicate the potential of targeting mitochondrial dynamics and biogenesis in neurons to enhance ARMD,” researchers wrote.

Since mitochondria function is deficient in progressive MS, namely in the complex IV (a key component for the production of energy), researchers evaluated whether ARMD could still be neuroprotective for neurons lacking sufficient complex IV.

They observed that in six out of 18 progressive MS cases analyzed, a positive correlation existed between complex IV deficient neurons and mitochondria content, area, and number. This supported the idea that, despite complex IV deficiency, neurons affected by MS still respond to demyelination by mobilizing mitochondria to their axons.

Researchers then developed a mouse model deficient for the complex IV (called COX10Adv mutant mice), and tested pioglitazone.

The treatment was given in the animal’s diet for six weeks. Results showed that mitochondrial content in axons increased significantly, and protected neurons from demyelinating lesions.

Researchers also observed that pioglitazone not only provided protection to myelin loss, but also helped to maintain synaptic function, meaning the neurons remained capable of transmitting signals.

“Our findings clearly illustrate a key compensatory role for mitochondria as part of the neuronal response to demyelination,” the researchers wrote. “Increased mobilisation of mitochondria from the neuronal cell body to the axon is a novel neuroprotective strategy for the vulnerable, acutely demyelinated axon.”

Overall, these findings support the potential neuroprotective benefits of therapies that enhance ARMD for diseases like MS.

“We propose that promoting ARMD is likely to be a crucial preceding step for implementing potential regenerative strategies for demyelinating disorders,” the team added.

In addition to the National MS Society, this research project was funded by the MS Society of the United Kingdom, the National Institutes of Health (NIH), and a Challenge Award from the International Progressive MS Alliance.

Aphantasia Challenges Some of our Most Basic Assumptions About the Human Mind

NEWS   Jun 29, 2020 | Original story by UNSWAphantasia Challenges Some of our Most Basic Assumptions About the Human Mind

Credit: Pixabay Read Time: 4 min

Aphantasia – being blind in the mind’s eye – may be linked to more cognitive functions than previously thought, new research from UNSW Sydney shows.

Picture the sun setting over the ocean.

It’s large above the horizon, spreading an orange-pink glow across the sky. Seagulls are flying overhead and your toes are in the sand.

Many people will have been able to picture the sunset clearly and vividly – almost like seeing the real thing. For others, the image would have been vague and fleeting, but still there.

If your mind was completely blank and you couldn’t visualise anything at all, then you might be one of the 2-5 per cent of people who have aphantasia, a condition that involves a lack of all mental visual imagery.

“Aphantasia challenges some of our most basic assumptions about the human mind,” says Mr Alexei Dawes, PhD Candidate in the UNSW School of Psychology.

“Most of us assume visual imagery is something everyone has, something fundamental to the way we see and move through the world. But what does having a ‘blind mind’ mean for the mental journeys we take every day when we imagine, remember, feel and dream?”

Mr Dawes was the lead author on a new aphantasia study, published in Scientific Reports. It surveyed over 250 people who self-identified as having aphantasia, making it one of the largest studies on aphantasia yet.

“We found that aphantasia isn’t just associated with absent visual imagery, but also with a widespread pattern of changes to other important cognitive processes,” he says.

“People with aphantasia reported a reduced ability to remember the past, imagine the future, and even dream.”~

Study participants completed a series of questionnaires on topics like imagery strength and memory. The results were compared with responses from 400 people spread across two independent control groups.

For example, participants were asked to remember a scene from their life and rate the vividness using a five-point scale, with one indicating “No image at all, I only ‘know’ that I am recalling the memory”, and five indicating “Perfectly clear and as vivid as normal vision”.

“Our data revealed an extended cognitive ‘fingerprint’ of aphantasia characterised by changes to imagery, memory, and dreaming,” says Mr Dawes.

“We’re only just starting to learn how radically different the internal worlds of those without imagery are.”

Subsets of aphantasia

While people with aphantasia wouldn’t have been able to picture the image of the sunset mentioned above, many could have imagined the feeling of sand between their toes, or the sound of the seagulls and the waves crashing in.

However, 26 per cent of aphantasic study participants reported a broader lack of multi-sensory imagery – including imagining sound, touch, motion, taste, smell and emotion.

“This is the first scientific data we have showing that potential subtypes of aphantasia exist,” says Professor Joel Pearson, senior author on the paper and Director of UNSW Science’s Future Minds Lab.

Interestingly, spatial imagery – the ability to imagine distance or locational relationship between things – was the only form of sensory imagery that had no significant changes across aphantasics and people who could visualise.

“The reported spatial abilities of aphantasics were on par with the control groups across many types of cognitive processes,” says Mr Dawes. “This included when imagining new scenes, during spatial memory or navigation, and even when dreaming.”

In action, spatial cognition could be playing Tetris and imagining how a certain shape would fit into the existing layout, or remembering how to navigate from A to B when driving.

In dreams and memories

While visualising a sunset is a voluntary action, involuntary forms of cognition – like dreaming – were also found to occur less in people with aphantasia.

“Aphantasics reported dreaming less often, and the dreams they do report seem to be less vivid and lower in sensory detail,” says Prof Pearson.

“This suggests that any cognitive function involving a sensory visual component – be it voluntary or involuntary – is likely to be reduced in aphantasia.”

Aphantasic individuals also experienced less vivid memories of their past and reported a significantly lower ability to remember past life events in general.

“Our work is the first to show that aphantasic individuals also show a reduced ability to remember the past and prospect into the future,” says Mr Dawes. “This suggests that visual imagery might play a key role in memory processes.”

Looking ahead

While up to one million Australians could have aphantasia, relatively little is known about it – to date, there have been less than 10 scientific studies on the condition.

More research is needed to deepen our understanding of aphantasia and how it impacts the daily lives of those who experience it.

“If you are one of the million Australians with aphantasia, what do you do when your yoga teacher asks you are asked to ‘visualise a white light’ during a meditation practice?” asks Mr Dawes.

“How do you reminisce on your last birthday, or imagine yourself relaxing on a tropical beach while you’re riding the train home? What’s it like to dream at night without mental images, and how do you ‘count’ sheep before you fall asleep?”

The researchers note that while this study is exciting for its scope and comparatively large sample size, it is based on participants’ self-reports, which are subjective by nature.

Next, they plan to build on the study by using measurements that can be tested objectively, like analysing and quantifying people’s memories.


Alexei J. Dawes et al. A cognitive profile of multi-sensory imagery, memory and dreaming in aphantasia. Scientific Reports doi:10.1038/s41598-020-65705-7

This article has been republished from the following materials. Note: material may have been edited for length and content. For further information, please contact the cited source.

Can’t Sleep? Behavioral Therapy May Ease Insomnia

By Katherine Kamwoman with insomnia

June 29, 2020 — Sleep expert Rachel Manber, PhD, has seen the pervasive miseries of insomnia. Patients who are frustrated and fatigued tell her they toss in bed all night, seeking that elusive comfortable spot. Others give up evening outings or vacations to avoid messing up their sleep schedules. Still others get anxious at bedtime, pondering whether to take sleep medications or wind down with a nightcap.

But trying so hard to fall asleep works against you, says Manber, a professor of insomnia and behavioral sciences at Stanford University Medical Center and a behavioral sleep medicine specialist.SLIDESHOW

Slideshow: Insomnia Myths and Facts

Man enjoying a glass of wine at sunset
1/11A Drink Will Help You SleepMyth. Insomnia — chronic trouble getting to sleep or staying asleep — can leave you desperate for a good night’s rest. Think a cocktail before bed will offer relief? Think again. This myth probably persists because alcohol can help you fall asleep. But as it moves through your body it may lead to disturbed, restless sleep, or it may make you wake earlier.
Young female insomniac awakened with worry
2/11Insomnia Is Strictly MentalMyth. It’s true that psychological issues can cause insomnia. As a matter of fact, stress is the No. 1 reason people report a lack of sleep. But it’s not the only insomnia trigger. Many things can cause insomnia, including poor sleep hygiene, illness, drug side effects, chronic pain, restless legs syndrome, or sleep apnea.
Woman jogger stretching against a tree at sunrise
3/11Exercise Helps You SleepFact. Regular exercise can be a great way to help stimulate better sleep. If you have trouble sleeping, avoid working out too late. Strenuous exercise can make you more alert. It also increases your body temperature, which may stay elevated for as many as six hours. Steer clear of workouts too close to bedtime. Aim to complete a workout two or three hours before you plan on going to sleep.
Hispanic woman kept awake by glowing television
4/11Screen Time Helps You Wind DownMyth. It’s tempting to try to wind down by reading on the computer or watching TV before bed, but both can actually stimulate you. The light and noise of TVs and computers can be engaging and can reduce brain melatonin levels. You want your melatonin levels to increase around bedtime to help you fall asleep. Need just a little noise to help you drift off? Try listening to relaxing music or download a relaxing, sleep app.
Woman asleep with sleeping pills nearby
5/11Sleep Aids Are Risk-FreeMyth. It’s true that today’s sleeping pills are safer and more effective than many older drugs. But all medications have potential risks, including the risks of dependency. Always talk to your doctor before using sleeping pills. Some sleep aids can help relieve insomnia symptoms temporarily. They can’t cure insomnia. Resolving underlying health issues and addressing your sleep environment is often the best approach to insomnia.
Woman silencing alarm clock late in the day
6/11You Can Make Up For Lost SleepMyth. It’s unlikely that you can fully catch up on sleep you’ve lost. Sleeping in one or two days a week or over the weekend may actually upset your natural body clock. The disruption may make it harder to get to sleep the next time. The only way to catch up on lost sleep is to get back into a regular sleep schedule.
Woman napping in hammock
7/11Napping Helps Offset InsomniaMyth. Naps affect everyone differently. For some people, a brief 10- to 20-minute nap taken midday can be refreshing. For many people with insomnia, however, a late afternoon nap can decrease the brain’s sleep drive. That can make it even harder to fall asleep at night.
Man nodding off in a business meeting
8/11You’ll Learn to Need Less SleepMyth. Believing this myth can lead to serious consequences. Everyone is born with a set sleep need. Most adults need 7-8 hours. You can learn to get by on less sleep, but you can’t train your body to need less sleep. If you’re sleep deprived, it’s harder to pay attention or remember things. Being chronically tired can have serious consequences, including poor work performance, an increased risk of accidents, and even poor health.
Man in pajamas watering plants late at night
9/11Get Out of Bed If You Can’t SleepFact. Tossing and turning for a half hour or more in bed? It’s OK to get up to read or listen to relaxing music. A quiet activity can help you relax and feel sleepy. Staying in bed may lead to frustration and clock-watching. Over time, you may associate your bed with wakefulness, not rest. Serious health conditions have been associated with severe, chronic lack of sleep, including obesity, high blood pressure, diabetes, heart attack, and stroke.
Woman meditating on bed before going to sleep
10/11You Can Train Yourself to SleepFact. You can train your body to associate certain restful behaviors with sleep. The key, of course, is consistency. Read for an hour or take a warm bath before bed. Maybe meditating or daydreaming will help you drop off to sleep. Find what works for you, and then make those rituals a regular part of preparing for bed every night.
Fatigued woman leaning against car at night
11/11Sleep Problems Go Away on Their OwnMyth. Until you know what’s causing your insomnia — whether it’s stress, medication, illness, or another issue — don’t expect it to disappear on its own. If you’ve had problems getting to sleep or staying asleep, or if you’re consistently tired after a night’s sleep, you may have a sleep disorder, and it’s time to talk to your doctor about treatment.

Reviewed by Sabrina Felson on 5/26/2020

“When you talk to somebody who sleeps well and you ask them, ‘How do you sleep? How do you do that?’ they will likely look at you with blank eyes. They don’t do anything. Sleep is an automatic process,” she says.

“When you talk to somebody who has trouble sleeping, they will name a long list of things that they’re doing to try to sleep. And that very effort to sleep ends up creating arousal and interfering with sleep.”

Instead of trying to sleep, allow sleep to happen, Manber says.

For more than two decades, she has helped patients undo habits that don’t work, stop their sleep medications, and drift into slumber on their own. Her method: cognitive behavioral therapy for insomnia (CBTI), a nondrug treatment that can improve sleep by helping patients change beliefs and behaviors.

More doctors have become aware of CBTI since the American College of Physicians issued a guideline in 2016 calling it the first-line treatment for chronic insomnia in adults, preferred over sleep medications.

It’s not that sleep drugs don’t work. They often do, but they can have side effects and drug interactions, and they aren’t meant for long-term use. Further, once patients stop taking them, insomnia might return, requiring another course of drugs.

In contrast, CBTI resolves insomnia without drugs and gives patients “skills that nobody can take away from them so they can use them should insomnia come back,” Manber says. “As you know, life happens. And when we become stressed, we tend to lose sleep over it.” By applying CBTI skills, people can prevent new bouts of chronic insomnia or recover from them.

When patients get CBTI with a sleep specialist, the insomnia typically improves with four to six sessions, Manber saysDuring the COVID-19 pandemic, some sleep specialists have been offering CBTI entirely through telemedicine. But many people can find relief with these at-home measures.

Wake Up at the Same Time Every Day

Insomnia is when it’s hard to go to sleep or stay asleep, a problem that can lead people to feel distressed or impaired in daily life. Symptoms include:

  • Trouble falling asleep at night
  • Waking up during the night and having trouble going back to sleep
  • Waking up too early in the morning
  • Not feeling rested or refreshed after sleeping at night
  • Feeling tired or sleepy during the day
  • Worries about sleep that won’t go away
  • Crankiness, depression, or anxiety
  • A hard time with paying attention, focusing on tasks, or memory
  • Making more mistakes or having accidents

You can’t control when you fall asleep, or you wouldn’t have insomnia. But you can control what time you wake up every day. “If you always wake up at the same time,” Manber says, “you are toning your internal biological clock that controls sleep and wakefulness.”

She suggests picking a regular wake time that fits your own circadian rhythm. That steady wake time sends cues to your body, she says. “It creates a very robust biological clock. If you vary the wake time, the amplitude of the signal becomes flatter, the signal is weaker. It’s not supporting your sleep.”

“When your clock is robust, you naturally start feeling sleepy more or less at the same time every night. That’s why I’m saying you have to start from the morning.”

Many sleep problems are caused by an irregular schedule, Manber says, so avoid the temptation to sleep in, even on your days off.

Go to Bed When You’re Sleepy, Not When You’re Tired

People often confuse being physically tired or mentally fatigued with being sleepy, “but these are distinct experiences,” Manber says. “We define ‘sleepy’ as the likelihood that if you put your head on the pillow, you’ll fall asleep quickly.”

Another way to understand the distinction: “Tired is a function of energy; sleepy is a function of sleep need.”

Sleep need builds during our waking hours, but people can’t feel it if they’re still in a state of high arousal or stimulation. “In other words, people can be tired, but wired. The feeling of ‘wired’ prevents them from feeling sleepy, and therefore, they cannot fall asleep.”

As Manber suggests, “You will fall asleep faster if you go to sleep at the time in which you are no longer wired and are starting to feel sleepy.”

When people with insomnia lie in bed unable to sleep, they typically worry about another bad night and how awful they’ll feel the next day. Doing so conditions their minds to view the bed as a place of wakefulness, stress, and anxiety.

In contrast, if people spend most of their time in bed snoozing, the mind will learn to associate it with restful sleep.

One caveat, though: People should spend no less than 5½ hours in bed each night, even if they sleep less than that.

But Don’t Spend Too Much Time in Bed

People with insomnia tend to spend a much longer time in bed than they’re able to sleep, emphasizing quantity over quality. They’ll stay in bed for 8 hours, but only sleep a total of 6 hours.

And they tend to have low-quality, short periods of sleep, Manber says. “When people spend too much time in bed, many actually end up dozing off here and there. So the brain gets some sleep. It’s not very refreshing sleep, it’s not good sleep. But if you add all the crumbs of sleep, it does add up.”

Tired and Sleepless

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Tired and Sleepless

Is the stress of children, jobs, and daily life giving you insomnia? See how you can fix your poor sleep habits and get some rest!ABOUT

To avoid crummy sleep, try limiting time in bed to combine your sleep into one block. If you’re only averaging 6 hours of sleep per night, you would spend 6 hours in bed each night to aim for deeper, high-quality sleep. “If you’re getting 6 hours of sleep, it would be much nicer to get them in one piece,” Manber says.

You might be tired at first, but once you build a solid period of sleep, for example, 5 or 6 hours, you can extend your amount of time in bed, perhaps with the goal of reaching 7 or 8 hours of solid sleep.

But in the beginning, while you’re trying to build that solid block, limit your time in bed cautiously to avoid an unsafe level of sleepiness. “If you develop a significant level of sleepiness, back off and consult a CBTI therapist,” Manber says. These specialists can also check for other causes of sleepiness, such as sleep apnea.

There’s another good reason to avoid spending too much time in bed: You also allow ample time for the sleep drive to build during your waking hours, according to Manber.

“The sleep drive is something that accumulates in our system. The longer we’re awake, the stronger is our sleep drive,” she says.

If you don’t build up enough sleep pressure, “when you go to sleep, you actually have a lower sleep drive, which is not going to support a long bout of sleep, Manber says. “That’s one of the primary reasons why we don’t want people to spend too much time in bed: to make sure that your sleep drive is strong.”

Stay in Bed Only When You’re Asleep

People with chronic insomnia don’t just have a hard time falling asleep, but staying asleep. For example, if they wake up at 3 a.m., they might not fall back asleep for a couple of hours.

Under the standard CBTI recommendations, if people can’t fall asleep within 20 minutes at the beginning of the night, they should get out of bed and do something quiet, like read a book, and come back to bed when they’re sleepy.

Manber agrees. “You should stop trying.”

But it’s important to avoid any activity that creates a lot of physical or mental arousal; for example, cleaning the house or reading a political book that riles up your emotions.

Still, she says, not everyone can get out of bed in the middle of the night if they can’t go back to sleep; for example, those who are bedridden or staying in a hotel room with others. “In that situation, you go to the core of what is most important here, and the core is that you stop trying to sleep.”

Some research shows that for middle-of-the-night wakings, “if you just stay in bed and stop trying and do something calming, then that helps as well,” Manber says.

Some patients prefer to remain in bed and cozy up with an audiobook. “People choose to listen to books that they’ve heard before,” she says. If you use any electronic device, be sure to block the blue light, which can interfere with your biological clock. Once again, the trick is to find material that isn’t too stimulating. Instead, people should listen to things “that are pleasant but that grab their attention and are not boring,” she says.

In doing so, “their attention is away from sleep. They’re no longer trying to sleep, and sleep comes to the surface and takes them.”WebMD Health News Reviewed by Michael W. Smith, MD on June 29, 2020

Alphabet has Reportedly Acquired Canadian AR Smartglasses Company called ‘North’ which gives us a Peek at their Future

1 cover - Smartglasses from North  Google my have acquired them

(Click on image to enlarge)

Google’s parent company Alphabet has reportedly acquired a Canadian Company out of Kitchner Ontario called North. A company that makes AR Smartglasses branded “Focals.” They have sales outlets in Toronto and Brooklyn NY. While the glasses are smart technologically, they’re also smart looking, unlike Google Glass that failed miserably partly due to its bizarre look and its possibly intrusive spy camera. North’s introductory video below shows us just how natural they actually look on a user.  

More specifically, Focals are a pair of custom-built smart glasses with a transparent, holographic display that only the wearer can see. This display floats an arm’s length in front of you and connects you to the people you care about, the information you need and the places you want to go in an augmented way.

Focals let you see and respond to texts, get turn-by-turn directions, check the weather, request an Uber, talk to Amazon Alexa and more — seamlessly and immediately. Obviously Alexa will be ripped out and replaced with Google Assistant. 

The glanceable and minimalist interface gives users control over what’s happening in their digital world without pulling them away from what’s in front of them. Focals come in three colors (Black, Tortoise, and Grey Fade) and offer either prescription or non-prescription lenses.

Focals were originally sold for $999 USD ($1299 CAD) and then dropped to just US$599 last February (for non-prescription). They were custom-built using a unique sizing process to ensure a comfortable and attractive fit. The packaging includes Focals Classic frames, Loop, Charging Case and Sun Clips. Orders including prescription lenses are now on hold unless Alphabet decides to allow the company to continue.

The Glasses were to be sold to iPhone users as well as androiders as presented in the image below. One would expect Google didn’t want Apple to have the opportunity of selling them at Apple Stores. This is a common practice of late, with Apple pulling support for the whether App Dark Sky for Android.

2 X Focals for iPhone

(Click on image to Enlarge) 

Focals work with a ring-type of input device as presented in the image below. Apple invented a ring input device in 2015 which has already gained their second granted patent for in April 2020. Apple’s ring is far more advanced than the one used with focals but Apple could easily add navigation to future smartglasses as well if they thought it would be of benefit.

3 x Focals ring input

(Click on image to Enlarge) 

Focals use a brilliant, full-color holographic Project system as presented below. Apple was granted a killer interactive holographic display patent way back in 2014.  Another patent revealing work on this technology was published in 2019. 4

4 x holographic display

(Click on image to Enlarge) 

In fact, this past April Patently Apple posted another report pointing to further advancements being made regarding a holographic optical element that works with a projector that sends imagery to the glasses lens. One of the images from that patent filing is presented below.  

5 holographic apple

North’s focals works with prescription lenses. In a patent application report last week, we revealed  Apple’s possible modular smartglasses approach that a) pointed out vastly superior frame design with multiple components  and well beyond a mere holographic projector, and b) Apple presented one way that prescription lenses would be able to simply slide into the side frame (FIG. 14) or snap in (as in FIG. 13) as confirmed by their patent figures below.   

6 apple smartglasses patent filing

Last Thursday Canada’s Globe and Mail publishing house broke the news that Google was buying Waterloo Canada’s company called North.

The Kitchner publication ‘The Record‘ reported on on Saturday that analyst Carmi Levy,  a director at London’s Info-Tech Research Group had stated that “We know the company has been a technology success story, but less so a marketing success story. It often means you’re ahead of your time.”

North was Founded in 2012 as Thalmic Labs by a trio of University of Waterloo graduates.

Levy added that “If the acquisition by Alphabet is completed, it should be seen as validation of the innovation behind North’s technology, rather than the result of its failure from a business perspective. It’s a confirmation that North was very much on to something. Market conditions notwithstanding, it doesn’t take away from the achievements of the company to date.”

Levy Further added that “Ideally, Alphabet will take some of North’s talent ‘along for the ride,’ and benefit from its patents and intellectual property.”

You could check out TechCrunch’s 2019 video review of the first generation of Focals by North.

Intel was working on basic AR smartglasses that could replace simple smartwatch features and notifications. North acquired those patents back in 2018. In fact, they acquired 650 patents in total. That’s a lot of Intellectual Property protecting their AR smartglasses that Google is now owner of if the acquisition goes through.

It’s always interesting to see what the competition is up to as it provides us with a superior image as to what could be coming to market in the future. That along with Apple’s plethora of patents on future AR Glasses and HMDs  that seems to we  expanding monthly,  we’re able to get the bigger picture at the technology that will drive these new mobile devices. Knowing about North’s Focals allows us to see that fitting technology into the frames of smartglasses is much closer to market than most think. 

In someways we can understand why Apple is diving deeper into health features for the Apple Watch, as smartglasses will be able to provide basic apps likely as good or better than a simple smartwatch. Why look at a watch when changing your focus slightly south could provide the time and date reminder much faster.

In the end, Apple, Facebook Google and Huawei at minimum are working hard to find that right blend of features and technologies that could make smartglasses a natural choice as a mobile smart device, if not a user’s first choice as a mobile device.

Google was first with ‘Glass‘ and I’m sure that they want back into this market that they first envisioned. Today’s news that they’ve likely acquired North shows us just how much they want back in.

The gut shields the liver from fructose-induced damage

Date:June 29, 2020Source:University of Pennsylvania School of MedicineSummary:After one consumes food or a beverage containing fructose, the gastrointestinal system, or gut, helps to shield the liver from damage by breaking down the sugar before it reaches the liver, according to a new multi-center study. However, the consumption of too much fructose — particularly in a short period of time — can overwhelm the gut, causing fructose to ‘spill over’ into the liver, where it wreaks havoc and causes fatty liver, researchers discovered.

After one consumes food or a beverage containing fructose, the gastrointestinal system, or gut, helps to shield the liver from damage by breaking down the sugar before it reaches the liver, according to a new multi-center study led by researchers in the Perelman School of Medicine at the University of Pennsylvania. However, the consumption of too much fructose — particularly in a short period of time — can overwhelm the gut, causing fructose to “spill over” into the liver, where it wreaks havoc and causes fatty liver, researchers discovered.

The findings, in mice, help to unravel longstanding questions about how the body metabolizes fructose — a form of sugar often found in fruits, vegetables, and honey, as well as most processed foods in the form of high fructose corn syrup. Consumption of fructose has increased 100-fold over the last century, even as studies have shown that excessive consumption, particularly sweet drinks, are linked to non-alcoholic fatty liver disease, obesity and diabetes. The findings were published in Nature Metabolism.

“What we discovered and show here is that, after you eat or drink fructose, the gut actually consumes the fructose first — helping to protect the liver from fructose-induced damage,” said the study’s corresponding author Zoltan Arany, MD, PhD, a professor of Cardiovascular Medicine at Penn. “Importantly, we also show that consuming the food or beverage slowly over a long meal, rather than in one gulp, can mitigate the adverse consequences.”

Studies have shown that the excessive consumption of fructose can be toxic to the liver. When large quantities of fructose reach the liver, the liver uses excess fructose to create fat, a process called lipogenesis. Eventually, people who consume too much fructose can develop nonalcoholic fatty liver disease, a condition in which too much fat is stored in the liver cells.

Until now, it hasn’t been clear whether the gut’s role in processing the fructose prevents or contributes to fructose-induced lipogenesis and the development of liver diseases. For this study, the team of researchers, including Princeton University’s Joshua Rabinowitz, MD, PhD, studied a key enzyme, called ketohexokinase, that controls how fast fructose is consumed. They showed, by genetically engineering mice, that lowering the levels of this enzyme in the gut led to fatty livers in the mice. Conversely, the team showed that increasing the level of ketohexokinase in the gut protected from fatty liver. Thus, the researchers found the breakdown of fructose in the gut mitigates the development of extra fat in liver cells in mice. They discovered that the rate at which the intestine can clear fructose determines the rate at which fructose can be safely ingested.

In addition, the team showed the same amount of fructose is more likely to result in the development of fatty liver when its consumed via a beverage versus food. Similarly, one faces an increased likelihood of developing fatty liver when consuming fructose in a single setting compared to several doses spread over 45 minutes.

“Collectively, our findings show fructose induces lipogenesis when the intake rate exceeds the gut’s capacity to process fructose and protect the liver,” Arany said. “In the modern context of excessive availability and consumption of processed foods, it is easy to see how the resulting fructose spillover would drive metabolic syndrome.”

Researchers noted that more work is needed to determine the extent to which these findings in mice extend to humans. Additional Penn authors include Shogo Wada, Steven Yang and Bridget Gosis.

The research was supported, in part, by a grant from the DRC Regional Metabolomics Core (P30 DK19525), National Institutes of Health (1DP1DK113643 and DK107667).

Story Source:

Materials provided by University of Pennsylvania School of MedicineNote: Content may be edited for style and length.

Journal Reference:

  1. Cholsoon Jang, Shogo Wada, Steven Yang, Bridget Gosis, Xianfeng Zeng, Zhaoyue Zhang, Yihui Shen, Gina Lee, Zoltan Arany, Joshua D. Rabinowitz. The small intestine shields the liver from fructose-induced steatosisNature Metabolism, 2020; DOI: 10.1038/s42255-020-0222-9

Cite This Page:

University of Pennsylvania School of Medicine. “The gut shields the liver from fructose-induced damage.” ScienceDaily. ScienceDaily, 29 June 2020. <>.

Ford Mustang Mach-E To Gets Performance Boost Prior To Launch

JUN 30, 2020 at 1:55PM4+

Mark Kane

By: Mark Kane

Ford: “The all-electric Mustang Mach-E isn’t a Mustang in name only – and we’ll let the horses do the talking.”

Ford has officially announced today that the final version of the Mustang Mach-E will get slightly higher horsepower and torque than initially estimated.

The increase of up to several percent (already shown two weeks ago) is an additional incentive for the reservation holders to trigger orders, as in the U.S. order banks are open.

  • Extended-range all-wheel-drive Mach-E will deliver 346 horsepower/258 kilowatts and 428 lb.-ft. of torque, up from previous estimates of 332 horsepower/240 kilowatts and 417 lb.-ft., right out of the gate – with a targeted 0-60-mph time in the mid-5-second range*
  • Extended-range rear-wheel-drive models will produce 290 horsepower/216 kilowatts and 317 lb.-ft., up from 282 horsepower/210 kilowatts and 306 lb.-ft.*
  • Standard-range all-wheel-drive models will pump out 266 horsepower/198 kilowatts and 428 lb.-ft., up from 255 horsepower/190 kilowatts and 417 lb.-ft.*
  • Standard-range rear-wheel-drive models will deliver 266 horsepower/198 kilowatts and 317 lb.-ft., up from 255 horsepower/190 kilowatts and 306 lb.-ft.*

The * means that the peak performance of the powertrain depends on available peak battery power as usually, at a lower state-of-charge, performance is noticeably limited (mainly acceleration).

More about Ford Mustang Mach-E

 Official 2021 Ford Mustang Mach-E Price List With MSRP And Invoice Ford Mustang Mach-E: Dealers Reportedly Adding $15,000 Markup Over MSRP

Ron Heiser, Mustang Mach-E chief program engineer said:

“We remain dedicated to delivering on the promise of the Mustang name. These better-than-estimated performance figures show that our team is squeezing every last bit of performance out of this vehicle so that it not only delivers Mustang style but Mustang soul as well.”

Let’s take a look at the latest set of trims on Ford’s website (details for the top of the line GT version will be confirmed “soon”):


Ford Mustang Mach-E launch:

  • initial target: late 2020, at least in some markets delayed until early 2021
  • several versions and trims, including a limited quantity First Edition and a special GT Performance Edition (Spring 2021)
  • $500 refundable reservation deposit

Ford Mustang Mach-E specs (U.S.):

  • Range depends version (EPA-estimated):
    SR, RWD: 230 miles (370 km)
    SR, AWD: 210 miles (338 km)
    ER, RWD: 300 miles (483 km)
    ER, AWD: 270 miles (434 km)
    GT with Optional Equipment: 235 miles (378 km)
    * SR (standard range battery), ER (extended range battery)
  • Battery capacity:
    SR: 75.7 kWh (288 lithium-ion cells); 68 kWh usable
    ER: 98.8 kWh (376 lithium-ion cells); 88 kWh usable
    * batteries are liquid-cooled
  • 0-60 mph acceleration (target):
    SR, RWD: in the low six second range
    SR, AWD: in the mid five second range
    ER, RWD: in the mid six second range
    ER, AWD: in the mid five second range
    GT: in 4 seconds
    GT Performance Edition: in the mid-3-second range
  • Powertrain (target):
    SR, RWD: 198 kW/266 HP and  317 lb-ft (up from 190 kW/255 HP and 306 lb.-ft.)
    SR, AWD: 198 kW​/266 HP and 428 lb-ft (up from 190 kW/255 HP and 417 lb.-ft.)
    ER, RWD: 216 kW​/290 HP and 317 lb-ft (up from 210 kW/282 HP and 306 lb.-ft.)
    ER, AWD: 258 kW/346 HP and 428 lb-ft (up from 240 kW/332 HP and 417 lb.-ft. of torque)
    GT: estimated 342 kW/459 HP and 830 Nm (612 lb.-ft.) of torque
    GT Performance Edition: 342 kW/459 HP and 830 Nm (612 lb.-ft.) of torque
  • Charging:
    AC charging
    DC fast charging 10-80% in about 38-45 minutes(peak charging rate of 150 kW; 115 kW in entry-level trims)
  • Seating: 5
  • Cargo Space
    Cargo Space (Behind Rear Seat): 29 cu ft/822 liters,
    Cargo Space (Behind First Row): 59.6 cu ft/1689 liters,
    Front Trunk: 4.8 cu ft/139.5 liter
  • Overall length: 186 in, Overall width: 74 in, Overall height: 63 in, Wheelbase: 117 in
  • Warranty: 8 years/100,000 miles (160,000 km)

Ford Mustang Mach-E specs (Europe):

  • target range of up to 600 km (373 miles) under WLTP regulations
  • ER, AWD: targeting 337 PS (248 kW) and 565 Nm of torque
    ER, AWD, Mach-E GT: 465 PS (342 kW) and 830 Nm of torque and 0-to-100 km/h (0-62 mph) in less than 5 seconds
  • rear trunk offers 402 litres of space (and with the rear seats down 1,420 litres of space)

Ford Mustang Mach-E U.S. pricing:

  • Select – $43,895
  • Premium – $50,600
  • California RT. 1 – $52,400
  • First Edition – $59,900
  • GT – $60,500

Gallery: Ford Mustang Mach-E

89 Photos

Ford Mustang Mach-E
Ford Mustang Mach-E
Ford Mustang Mach-E
Ford Mustang Mach-E
Ford Mustang Mach-E
Ford Mustang Mach-E
Ford Mustang Mach-E

A revolutionary new treatment alternative to corneal transplantation

by University of Montreal

Credit: Pixabay/CC0 Public Domain

The team was co-led by May Griffith, a researcher at Maisonneuve-Rosemont Hospital Research Centre, which is affiliated with Université de Montréal and is part of the CIUSSS de l’Est-de-l’Île-de-Montréal.

The results of this multinational project have just been published in the journal Science Advances.

“Our work has led to an effective and accessible solution called LiQD Cornea to treat corneal perforations without the need for transplantation,” said Griffith. She is also a full professor in the Department of Ophthalmology at Université de Montréal.

“This is good news for the many patients who are unable to undergo this operation due to a severe worldwide shortage of donor corneas,” she said.

“Until now, patients on the waiting list have had their perforated corneas sealed with a medical-grade super glue, but this is only a short-term solution because it is often poorly tolerated in the eye, making transplantation necessary.”

A synthetic, biocompatible and adhesive liquid hydrogel, LiQD Cornea, is applied as a liquid, but quickly adheres and gels within the corneal tissue. The LiQD Cornea promotes tissue regeneration, thus treating corneal perforations without the need for transplantation.

Griffith praised the work of her trainees, Christopher McTiernan and Fiona Simpson, and her collaborators from around the world who have helped create a potentially revolutionary treatment to help people with vision loss avoid going blind.

“Vision is the sense that allows us to appreciate how the world around us looks,” said Griffith. “Allowing patients to retain this precious asset is what motivates our actions as researchers every day of the week.”

For Sylvain Lemieux, president and CEO of the CIUSSS de l’Est-de-l’Île-de-Montréal, “this innovative treatment in ophthalmology confirms the level of expertise of the Centre universitaire d’ophtalmologie de l’Université de Montréal (CUO) at the Maisonneuve-Rosemont Hospital (HMR).

“The HMR has one of the largest teams of ophthalmologists in Quebec and one of the best-equipped ophthalmology research laboratories in North America,” he said. “The hard work of our scientists and clinicians contributes daily to best practices and knowledge development.

“The multiple therapeutic possibilities resulting from our fundamental research, particularly in regenerative medicine, benefit and give hope to people suffering from ophthalmological diseases not only in Quebec, but in the rest of the world,” he concluded.

Explore furtherNew study offers added hope for patients awaiting corneal transplants

More information: Christopher D. McTiernan et al, LiQD Cornea: Pro-regeneration collagen mimetics as patches and alternatives to corneal transplantation, Science Advances (2020). DOI: 10.1126/sciadv.aba2187Journal information:Science AdvancesProvided by University of Montreal

For The First Time, Scientists Have Captured Video of Brains Clearing Out Dead Neurons


We already know that our brains have a waste disposal system that keeps dead and toxic neurons from clogging up our biological pathways. Now, scientists have managed to capture a video of the process for the first time, in laboratory tests on mice.

main article image

There’s still a lot we don’t know about how dead neurons are cleared out, and how the brain reacts to them, so the new research could be a significant step forward in figuring some of that out – even if we’ve not yet confirmed that human brains work in the exact same way.

“This is the first time the process has ever been seen in a live mammalian brain,” says neurologist Jaime Grutzendler from the Yale School of Medicine in Connecticut.

Further down the line, these findings might even inform treatments for age-related brain decline and neurological disorders – once we know more about how brain clean-up is supposed to work, scientists can better diagnose what happens when something goes wrong.

The team focussed in on the glial cells responsible for doing the clean-up work in the brain; they used a technique called 2Phatal to target a single brain cell for apoptosis (cell death) in a mouse and then followed the route of glial cells using fluorescent markers.

“Rather than hitting the brain with a hammer and causing thousands of deaths, inducing a single cell to die allows us to study what is happening right after the cells start to die and watch the many other cells involved,” says Grutzendler.

“This was not possible before. We are able to show with great clarity what exactly is going on and understand the process.”

Three types of glial cells – microglia, astrocytes, and NG2 cells – were shown to be involved in a highly coordinated cell removal process, which removed both the dead neuron and any connecting pathways to the rest of the brain. The researchers observed one microglia engulf the neuron body and its main branches (dendrites), while astrocytes targeted smaller connecting dendrites for removal. They suspect NG2 may help prevent the dead cell debris from spreading.

The researchers also demonstrated that if one type of glial cell missed the dead neuron for whatever reason, other types of cells would take over their role in the waste removal process – suggesting some sort of communication is occurring between the glial cells.

Another interesting finding from the research was that older mouse brains were less efficient at clearing out dead neural cells, even though the garbage removal cells seemed to be just as aware that a dying cell was there.

This is a good opportunity for future research, and could give experts insight into how older brains start to fail in various ways, as the garbage disposal service starts to slow down or even breaks.

New treatments might one day be developed that can take over this clearing process on the brain’s behalf – not just in elderly people, but also those who have suffered trauma to the head, for example.

“Cell death is very common in diseases of the brain,” says neurologist Eyiyemisi Damisah, from the Yale School of Medicine.

“Understanding the process might yield insights on how to address cell death in an injured brain from head trauma to stroke and other conditions.”

The research has been published in Science Advances.

Learn More

  1. Q&A: Biden Cancer Initiative President Greg Simon Discusses Data Sharing in Precision OncologyPrecision Oncology News, 2019
  2. Transgenic rhesus monkeys carrying the human MCPH1 gene copies show human-like neoteny of brain developmentShi et al., National Science Review
  1. iReceptor Plus Consortium Wants to Improve Immunological Data SharingPrecision Oncology News, 2019
  2. Lipid Removal Sample Prep for Cell Response ApplicationsGenomeWeb

Google has acquired North, the maker of Focals smart glasses

The company says the startup will join its Kitchener-Waterloo office.

Igor Bonifacic@igorbonifacic4h ago 10Comments 86Shares 


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North Focals smartglasses.

After a weekend of rumors, Google confirmed on Tuesday that it’s the new owner of North. Before today, the Canadian startup was best known for its Focals smart glasses. The wearable integrated a holographic display inside a pair of fashion-forward frames.

Google didn’t disclose the terms of the deal. However, the company says the North team will join its office in Kitchener-Waterloo, Canada. “North’s technical expertise will help as we continue to invest in our hardware efforts and ambient computing future,” Google said. What’s more, North is ending support for Focals. “We are winding down Focals 1.0 and we will not be shipping Focals 2.0, but we hope you will continue the journey with us as we start this next chapter,” the startup said on its website.

According to The Globe and Mail, the search giant paid approximately $180 million to buy the startup. Despite a $400 price cut at the start of 2019, North had reportedly sold very few of its Focals smart glasses to consumers, and the Globe says the company was running out of money before the deal came about. In April, North co-founder Stephen Lake teased that North was working on a second-generation model.

With Focals, North thought of a variety of clever solutions to some of the pain points that had come with earlier wearables like Google Glass. For instance, each pair of Focals came with a ring you would wear on your index finger. It featured a small joystick and D-pad to allow you to control the smart glasses without touching them and drawing attention to yourself.

No one could accuse you of being a “glasshole” because Focals were discrete in a way that Google Glass was not. The problem was that they were too expensive. Before North discounted them, a pair of Focals cost $1,000. You also had to get custom fitted for them at a physical retail store. All of those were significant issues for technology that did not feel indispensable.