Your exposure to air pollution could be much higher than your neighbour’s – here’s why


Each year, tens of thousands of people in the UK die early due to air pollution, which is linked to asthma, heart disease and lung cancer. The health risk presented by air pollution depends on how much dirty air we breathe over time. Pollution levels in UK cities regularly exceed the limits set by the World Health Organisation. But people’s exposure to pollution can vary greatly between people living on the same street, or even the same house.

Currently, health authorities estimate exposure to air pollution based on outdoor pollution at a person’s home address. But we don’t just sit outside our front doors all day – we each follow our personal daily schedules. The environment at home, in transit and at work or school all affect our exposure to pollution. Knowing this can help governments to create more effective policies and provide better advice to the public on how to reduce their exposure.

By equipping volunteers with portable pollution sensors, scientists have shown that exposure to air pollution during the day can vary substantially. For example, commuting during peak hour can account for a significant proportion of the pollution we’re exposed to – even though commuting only takes up a small part of our day.

By contrast, being indoors is often associated with lower exposure to pollution, because buildings provide some protection against outdoor pollutants. But gas cookers, wood burners and household cleaning products can also create high levels of indoor pollution.

How habits influence exposure

With all these different sources and levels of pollution around us, our daily activities and habits have a big influence on how much polluted air we breathe. Even couples who live together can have different exposures: a person who stays at home may experience up to 30% less pollution than their partner who commutes to work.

A 24-hour measurement of a person’s pollution exposure, which varies throughout the day. McCreddin et al., CC BY-SA

Small changes in our daily routines can significantly reduce our exposure to air pollution. In a study in London, participants were able to decrease their exposure during commuting by 25% to 90% by choosing alternative routes or modes of transport. Active commuters who walk or cycle are usually less exposed to pollution than people travelling by car or bus – this might be because vehicles travel in a queue, so air pollution from the vehicle directly in front gets drawn in through ventilation systems and trapped inside. The air is also much cleaner on overground trains than on the underground.

Displaying public information about pollution hot spots and ways to avoid them can help. The Wellbeing Walk is a signposted backstreet walking route taking ten to 15 minutes between London’s Euston and King’s Cross stations, which exposes walkers to 50% less pollution than the main road. Since its launch in 2015, the number of people taking the healthier path has tripled. There need to be many more initiatives like this in cities.

Modelling human movements

Being able to tell when and where people are most exposed to pollution makes it possible to compare the benefits of different solutions. That’s why scientists have created computer models to simulate different scenarios. By combining information on outdoor pollution, pollution on transport and people’s travel routes, these models help us understand how people’s movements contribute to their personal exposure.

Computer exposure models for cities, including London, Leicester and Hong Kong among others, are beginning to give us a better picture of how people are exposed to harmful pollution. But the answers they provide are often complicated.

Commuting: the shorter the better. Harry Green/Shutterstock.

For example, the model for London suggests that on average citizens are exposed to less pollution than previously estimated. But many individuals still experience extremely high pollution during long periods on transport – so a lengthy commute by car, bus or underground could mean you’re among the most affected.

What’s more, the model does not yet account for pollution created indoors through cooking or wood burning. Including these additional sources of pollution may well shake up the results.

More data, please

The UK’s clean air strategy aims to halve the number of people exposed to particulate pollution above World Health Organisation guidelines by 2025. But surprisingly little is known about pollution levels inside our homes, schools and workplaces. If the strategy is to meet its goal, the government will need more data and better methods to estimate people’s exposure to air pollution.

Any model needs to be confirmed using actual measurements, to ensure we can trust what the model predicts about our exposure. Although the technology is advancing, portable pollution sensors are still bulky and heavy. Recruiting volunteers to carry these sensors wherever they go can be difficult. Phone-integrated sensors could make this easier in the future, but their reliability is still debated among scientists.

Improving outdoor air quality is currently a top priority in cities across Europe – and rightly so. But measurements and computer models are indicating that our exposure to pollution is much more varied and complex than currently estimated. We should build on this knowledge to develop measures that deliver the greatest reduction in human exposure and empower citizens to make healthier choices in their daily routines.

Your exposure to air pollution could be much higher than your neighbour’s – here’s why


Each year, tens of thousands of people in the UK die early due to air pollution, which is linked to asthma, heart disease and lung cancer. The health risk presented by air pollution depends on how much dirty air we breathe over time. Pollution levels in UK cities regularly exceed the limits set by the World Health Organisation. But people’s exposure to pollution can vary greatly between people living on the same street, or even the same house.

Currently, health authorities estimate exposure to air pollution based on outdoor pollution at a person’s home address. But we don’t just sit outside our front doors all day – we each follow our personal daily schedules. The environment at home, in transit and at work or school all affect our exposure to pollution. Knowing this can help governments to create more effective policies and provide better advice to the public on how to reduce their exposure.

By equipping volunteers with portable pollution sensors, scientists have shown that exposure to air pollution during the day can vary substantially. For example, commuting during peak hour can account for a significant proportion of the pollution we’re exposed to – even though commuting only takes up a small part of our day.

By contrast, being indoors is often associated with lower exposure to pollution, because buildings provide some protection against outdoor pollutants. But gas cookers, wood burners and household cleaning products can also create high levels of indoor pollution.

How habits influence exposure

With all these different sources and levels of pollution around us, our daily activities and habits have a big influence on how much polluted air we breathe. Even couples who live together can have different exposures: a person who stays at home may experience up to 30% less pollution than their partner who commutes to work.

A 24-hour measurement of a person’s pollution exposure, which varies throughout the day. McCreddin et al., CC BY-SA

Small changes in our daily routines can significantly reduce our exposure to air pollution. In a study in London, participants were able to decrease their exposure during commuting by 25% to 90% by choosing alternative routes or modes of transport. Active commuters who walk or cycle are usually less exposed to pollution than people travelling by car or bus – this might be because vehicles travel in a queue, so air pollution from the vehicle directly in front gets drawn in through ventilation systems and trapped inside. The air is also much cleaner on overground trains than on the underground.

Displaying public information about pollution hot spots and ways to avoid them can help. The Wellbeing Walk is a signposted backstreet walking route taking ten to 15 minutes between London’s Euston and King’s Cross stations, which exposes walkers to 50% less pollution than the main road. Since its launch in 2015, the number of people taking the healthier path has tripled. There need to be many more initiatives like this in cities.

Modelling human movements

Being able to tell when and where people are most exposed to pollution makes it possible to compare the benefits of different solutions. That’s why scientists have created computer models to simulate different scenarios. By combining information on outdoor pollution, pollution on transport and people’s travel routes, these models help us understand how people’s movements contribute to their personal exposure.

Computer exposure models for cities, including London, Leicester and Hong Kong among others, are beginning to give us a better picture of how people are exposed to harmful pollution. But the answers they provide are often complicated.

Commuting: the shorter the better. Harry Green/Shutterstock.

For example, the model for London suggests that on average citizens are exposed to less pollution than previously estimated. But many individuals still experience extremely high pollution during long periods on transport – so a lengthy commute by car, bus or underground could mean you’re among the most affected.

What’s more, the model does not yet account for pollution created indoors through cooking or wood burning. Including these additional sources of pollution may well shake up the results.

More data, please

The UK’s clean air strategy aims to halve the number of people exposed to particulate pollution above World Health Organisation guidelines by 2025. But surprisingly little is known about pollution levels inside our homes, schools and workplaces. If the strategy is to meet its goal, the government will need more data and better methods to estimate people’s exposure to air pollution.

Any model needs to be confirmed using actual measurements, to ensure we can trust what the model predicts about our exposure. Although the technology is advancing, portable pollution sensors are still bulky and heavy. Recruiting volunteers to carry these sensors wherever they go can be difficult. Phone-integrated sensors could make this easier in the future, but their reliability is still debated among scientists.

Improving outdoor air quality is currently a top priority in cities across Europe – and rightly so. But measurements and computer models are indicating that our exposure to pollution is much more varied and complex than currently estimated. We should build on this knowledge to develop measures that deliver the greatest reduction in human exposure and empower citizens to make healthier choices in their daily routines.

Big Pharma Returning to U.S. Price Hikes in January After Pause


Novartis AG and Bayer AG are among nearly 30 drugmakers that have taken steps to raise the U.S. prices of their medicines in January, ending a self-declared halt to increases made by a pharma industry under pressure from the Trump administration, according to documents seen by Reuters.

Other drugmakers set to raise prices at the start of 2019 include Allergan Plc, GlaxoSmithKline Plc, Amgen Inc, AstraZeneca Plc and Biogen Inc, the documents show.

The hikes will pose a new challenge to President Donald Trump’s pledge to lower the costs of prescription medications in the world’s most expensive pharmaceutical market.

The U.S. Department of Health and Human Services (HHS) has proposed a slew of policies aimed at lowering prices and passing more of the discounts negotiated by health insurers on to patients. Those measures are not expected to provide relief to consumers in the short-term, however, and fall short of giving government health agencies direct authority to negotiate or regulate drug prices.

Twenty-eight drugmakers filed notifications with California agencies in early November disclosing that they planned to raise prices in 60 days or longer. Under a state law passed last year, companies are required to notify payers in California if they intend to raise the U.S. list price on any drug by more than 16 percent over a two-year period.

The details were provided to Reuters in response to a public records request to California Correctional Health Care Services, which provides healthcare services to the state’s corrections department. The department spends more than $3 billion annually on drugs for inmates, more than any other state.

“Requests and public shaming haven’t worked” to lower drug prices, said Michael Rea, chief executive of RX Savings Solutions, which helps health plans and employers seek lower cost prescription medicines. “We expect the number of 2019 increases to be even greater than in past years.”

Pfizer Inc rolled back planned price increases in July after President Trump said in a tweet that the drugmaker “should be ashamed” and that his administration would respond to the hikes.

Pfizer said it would defer hikes until January 2019 to support the administration as it pursued its new pricing policies. Pfizer’s move prompted many of its industry peers, including Bayer, Novartis, Allergan, AstraZeneca and Amgen, to follow suit.

Drug price increases implemented by the 20 biggest drugmakers did slow down during the second half of 2018, with those companies raising prices on just over half the number of drugs as in 2017, according to data compiled by consultancy RX Savings Solutions.

Pfizer has already announced plans to hike prices on 41 of its drugs in mid-January.

60-DAY NOTICE

The California corrections department documents indicate that the companies plan to increase prices as early as Jan. 1. Most do not detail for which drugs or by how much, but specific details were given in the case of Novartis and Bayer.

Novartis is planning to raise prices on more than 100 indications of over 30 different drugs in January, the documents show, with increases ranging from 4.5 percent to 9.9 percent. Drugs on the list are expected to account for more than $20 billion of Novartis’ revenue this year and include multiple sclerosis drug Gilenya (fingolimod), psoriatic arthritis treatment Cosentyx (secukinumab), and leukemia treatment Tasigna (nilotinib).

The list also includes Diovan, the brand name version of blood pressure treatment valsartan, generic versions of which are currently in shortage after a potential carcinogen was detected in active ingredients made in China, prompting widespread recalls.

Novartis spokesman Eric Althoff said the company plans to raise U.S. list prices on 14 percent of the medicines it sells in the country in 2019, for an average increase of 4.7 percent on those drugs.

“Our rebates and discounts, however, continue to grow even faster,” Althoff said. As a result, the company expects a net price decrease of nearly 5 percent across the whole U.S. portfolio, he said.

Over the last three years, net price decreases for its U.S. business have ranged from 2 percent to 2.6 percent, the company said.

Bayer filed notifications with California agencies to increase prices on six of its drugs in January, many of which are birth control products. Most of these price increases are 5 percent.

Bayer said that the U.S. wholesale price of its products are not representative of what most consumers pay and that “list price increases are expected to be offset by higher rebates and discounts paid to insurance companies and pharmacy benefit managers.”

Amgen did not respond to requests for comment. AstraZeneca and Biogen declined to comment for this story.

GSK would not give details about its specific price increases, which are set to take effect on or around Jan. 1 and could change before then. Allergan said that all of its price increases will be aligned with its pledge made in 2016 to limit drug price increases on its products to less than 10 percent annually.

The United States, which leaves drug pricing to market competition, has higher drug prices than in other countries where governments directly or indirectly control the costs, making it the world’s most lucrative market for manufacturers.

Lowering prescription drug prices was a top priority in Republican Trump’s 2016 presidential campaign. Rival Democrats are expected to step up congressional scrutiny of drug price hikes next year after gaining control of the U.S. House of Representatives in elections in November.

“Drug companies raising their prices and offsetting them with higher rebates benefits everyone but the consumer,” HHS spokeswoman Caitlin Oakley said in a statement.

Trump and HHS Secretary Alex Azar “remain committed to lowering drug prices and reducing out of pocket costs, and will continue to take bold action to restructure this broken market,” she said.

Researchers use DNA nanomachines to discover subgroups of lysosomes


Clockwise from top left: UChicago scientists Anand Saminathan, Kasturi Chakraborty, Yamuna Krishnan and KaHo Leung examine results from a new DNA nano-machine to track lysosome activity in cells.

The story of the lysosome is a classic smear campaign. Once dismissed as the garbage disposal of the cell—it does break down unneeded cell debris—it is now valued by scientists who realized all that dirty work also controls survival, metabolism, longevity and even neurodegenerative diseases.

An innovative tool invented by University of Chicago scientists will give us a new window into the lysosome’s inner workings. Two studies led by Professor of Chemistry Yamuna Krishnan built to tease out clues about lysosomes, including whether they actually come in two or more related types—which may help us understand lysosome-related disorders.

“Both scientists studying the cell and doctors treating patients for lysosome disorders need better diagnostics, so this is a very good step forward,” said graduate student Kasturi Chakraborty, the co-first author for both papers.

Scientists want the ability to watch live footage of what’s going on in a cell, but its inner workings are hard to catch in action. It’s tiny, and what’s more, it’s a harsh environment; lysosomes in particular are highly acidic—not good for cameras. “Most sensors will just stop functioning if the acidity is that high,” Chakraborty said.

To address this issue, Krishnan’s group uses DNA as their to make flashlights and sensors to peer inside. It’s already adapted to life in a cell, and it comes in a handy puzzle-piece format, perfect for building tiny nano-machines that catalogue life inside a living cell.

They designed the nanomachines to measure both pH and the particular ions floating around the lysosome—either calcium or chloride—that are the basis for how lysosomes communicate and carry out their tasks. Through them, can see how lysosomes work—and tease out what’s going on when they’re not working, in certain diseases or hereditary conditions.

One of the most interesting things they found using the new probes was evidence there are actually at least two different kinds of lysosomes.

Scientists had suspected lysosomes came in distinct types with different functions, but it had never been confirmed, Chakraborty said. They don’t yet know exactly how the two kinds of lysosomes differ in function, but they do know one kind is missing in people with a certain lysosome disorder called Niemann-Pick disease.

The key was designing a sensor that could measure two kinds of ions simultaneously. “You absolutely need two independent chemical signatures to discriminate between lysosomes,” Chakraborty said.

“It’s interesting because lysosomes are well-recognized as a multifunctional organelle, and so til now we considered that it was a single type of performing multiple functions,” said Krishnan, corresponding author for both studies. “Our studies reveal that there might actually be different sub-types of lysosomes designated for different functions.”

Scientists have a blast with aluminum nanoparticles


Ciew of native aluminum particles at 150,000 magnification. Credit: ARL

Army scientists proved a decades-old prediction that mixing TNT and novel aluminum nanoparticles can significantly enhance energetic performance. This explosive discovery is expected to extend the reach of U.S. Army firepower in battle.

Researchers from the U.S. Army Research Laboratory and Texas Tech University demonstrated up to 30-percent enhancement in the detonation velocity of the explosive TNT by adding novel aluminum in which the native alumina shell has been replaced with an oxidizing salt called AIH, or aluminum iodate hexahydrate.

The structure of the AIH-coated aluminum nanoparticles was revealed for the very first time through high resolution transmission electron (TEM) microscopy performed by ARL’s Dr. Chi-Chin Wu, a materials researcher who leads the plasma research for the lab’s Energetic Materials Science Branch in the Lethality Division of Weapons and Materials Research Directorate.

Wu said this revolutionary research offers the potential for the exploitation of aluminum and potentially other metallic nanoparticles in explosive formulations to extend the range and destructive power of Army weapons systems, a key objective of the Army’s “Long Range Precision Fires” modernization priority.

“We believe these results show tremendous promise for enhancing the detonation performance of conventional military explosives with aluminum nanoparticles for the first time,” said ARL’s Dr. Jennifer Gottfried, a physical chemist who collaborated on the research.

Single nanoparticle extracted out from a view of native aluminum particles at 150,000 magnification. The image highlights the amorphous oxide shell surrounding the crystalline core. Credit: ARL

“It is very exciting to advance science to a point where we can harness more chemical energy from metal particles at faster timescales. This is an exciting time for transforming energy generation technology,” said Dr. Michelle L. Pantoya, the J. W. Wright Regents Chair in Mechanical Engineering and Professor at Texas Tech University.Details of this breakthrough work are described in the team’s May 28 published paper “Improving the Explosive Performance of Aluminum Nanoparticles with Aluminum Iodate Hexahydrate (AIH)” by Jennifer L. Gottfried, Dylan K. Smith, Chi-Chin Wu, and Michelle L. Pantoya in the high-impact journal Scientific Reports.

The team found that the crystalline aluminum core was effectively protected against unwanted oxidation by the AIH shell, which appears as protruding nodules on the aluminum surface. The enhanced reactivity due to this unique morphological feature and novel core-shell structure was demonstrated by laser-induced air shock from energetic materials experiments, an innovative laboratory-scale energetic testing method developed by Gottfried. This technique involves impacting the sample with a high-energy, focused laser pulse to violently break apart the explosive molecules. The interaction of the laser with the material forms a laser-induced plasma and produces a shock wave that expands into the surrounding air. The energy released from an explosive sample can then be experimentally determined by measuring the laser-induced shock velocity with a high-speed camera.

It was predicted decades ago that aluminum nanoparticles have the potential to enhance the energetic performance of explosives and propellants because of their high energy content and potential for rapid burning. This is because they have exceptionally large surface areas compared to their total volume and a very large heat of reaction. However, the surface of the aluminum nanoparticles is naturally oxidized in air to form a thick alumina shell, typically 20% by weight, which not only lowers the energy content of the nanoparticles by reducing the amount of active aluminum, it also slows the rate of energy release because it acts as a barrier to the reaction of the aluminum with the explosive. Therefore, replacing the oxide shell, as successfully achieved by TTU, can significantly improve the explosive performance.

An AIH-salt crystal found at 400,000 magnification. The background is the carbon support film on the specimen grid. Credit: U.S. Army

These preliminary joint efforts have also led to a formal research collaboration under an ARL Director’s Research Award, the fiscal 2018 External Collaboration Initiative between Wu and TTU.

After publishing two papers in high-impact scientific journals in the past year, the team is poised to pursue additional energetics research with nanoparticles by working with the U.S. Army Research, Development and Engineering Command at Picatinny Arsenal, New Jersey, and the Air Force Research Laboratory.

Read more at: https://phys.org/news/2018-06-scientists-blast-aluminum-nanoparticles.html#jCp

New Study Reveals Harmful Effects of Dim Light Exposure During Sleep


Story at-a-glance

  • Exposure to very dim light during sleep — even if it does not noticeably impair your sleep — may affect your brain function and cognition during the day
  • Sleeping under 10 lux light conditions decreased activation in a brain region involved in response inhibition, attentional control and the detection of relevant cues when performing a task the following day
  • Animal research found that nighttime exposure to 5 lux for three weeks in a row produced depression-like symptoms and impaired cognition

By Dr. Mercola

Inside the suprachiasmatic nucleus (SCN) of your brain, which is part of your hypothalamus, resides your master biological clock. Based on signals of light and darkness, your SCN tells your pineal gland when it’s time to secrete melatonin, and when to turn it off.

Your melatonin level inversely rises and falls with light and darkness, and both your physical and mental health is intricately tied to this rhythm of light and dark.

When it’s dark, your melatonin levels increase, which is why you may feel tired when the sun starts to set. Conversely, when you’re exposed to bright artificial lighting at night, including blue light emitted from TVs and electronic screens, you may have trouble falling asleep due to suppressed melatonin levels.

Many sleep problems can be resolved by making sure you avoid blue light exposure after sunset and sleep in total darkness.

Interestingly, being exposed to very dim light during sleep — even if it does not noticeably seem to impair your sleep — may also affect your brain function and cognition during the day.

Minute Amounts of Light During Sleep Can Affect Cognition

I’ve been a long-time advocate of sleeping in TOTAL darkness, and an interesting study1 published in Scientific Reports highlights the importance of this recommendation — not just for solid sleep, but also for cognitive health.

In this study, 20 healthy men slept in a laboratory shrouded in complete darkness for two nights in a row. On the third night, they were exposed to a dim light of either 5 or 10 lux while sleeping.

To get an idea of how dim a light intensity of 5 or 10 lux is, 1 lux is equal to the brightness of a surface illuminated by one candle, placed 1 meter (3.28 feet) away from the surface. Twilight is just below 11 lux, whereas an object illuminated by the light of the full moon is about one-tenth of a lux.2

After the second and third nights, the participants performed working memory tests (so-called n-back tests) while undergoing functional magnetic resonance imaging (fMRI). The goal was to evaluate the effects of dim light exposure during sleep on functional brain activation during a working memory task the next day.

When sleeping under 10 lux light conditions, there was decreased activation in the right inferior frontal gyrus, an area of your brain involved in response inhibition, attentional control and the detection of relevant cues when performing a task.3

Exposure to 5-lux light had no statistically significant effect on the participants’ brain activity. In other words, past a certain point of very dim light, nighttime light exposure can have a direct influence on your brain function, specifically your cognition and working memory.

Nighttime Light — A Hazardous ‘Pollutant’

According to the authors of this study:

“Nighttime light is now considered to be one of the fastest growing pollutants, and the invasion of artificial light into previously unlit areas is threatening the soundness of human health and sleep.

Nighttime artificial lighting in cities is divided into three types: sky glow, trespass and glow. Light trespass refers to unwanted direct lighting of an area, and it occurs when unwanted light spills over into another property or dwelling and causes sleep interference, negative influence on one’s well-being …

Several studies have also shown that light pollution and shift work are tentative risk factors for cardiovascular disease, breast cancer, ovarian cancer, gastrointestinal disease and metabolic syndrome …”

Fortunately, the detrimental effects of nighttime light pollution are starting to gain recognition, and some countries have even adopted regulations to reduce nighttime light in residential areas.

Guidelines issued by the Commission Internationale de l’Eclairage (CIE), Illuminating Engineering Society of North America (IESNA) and Institution of Lighting Engineers (ILE), have an upper brightness limit for light trespass of 2, 3 and 5 lux in in residential areas respectively.

Advertisement

Liposomal Vitamin C


Chronic Exposure to Light During Sleep May Cause Pronounced Effects on Cognition

The study in question was done to investigate whether these limits are sufficient to reduce sleep and cognitive problems associated with nighttime light pollution.

While limits of 5 lux or less appear sufficient, they discovered that exposure to 10 lux may produce adverse brain effects even if there are no subjective, outward symptoms of impairment. As noted by the authors:

“This study is meaningful because it is the first to scientifically identify the effect of the dim light at night on human brain function and cognition. It is noteworthy that the brain activation was altered after only a single night of light exposure.

This suggests that the chronic exposure to the light at night for many nights might have caused more pronounced effects on the brain and cognition … The interesting finding in the 10 lux group … was the discrepancy between the n-back task and fMRI results.

The decrease of the brain activation in fMRI in the frontal lobe without significant finding in the n-back task of 10 lux group suggests that the absence of evidence of subjective or objective cognitive dysfunction does not necessarily mean that the brain is functioning normally.

This indicates that certain exposure to dim light might influence brain function for cognition even if there is no significant impairment in subjective symptoms (or even in an objective neurocognitive function test).” 

Lack of Symptoms Does Not Mean You’re Unaffected

In other words, what they discovered is that while you might not notice a problem, your brain is still not working normally or optimally. The reason for this is not entirely clear. One possibility is that the decrease in brain activity is related to a reduction in deep sleep, most likely brought on by disrupted melatonin secretion.

Another possibility is that light exposure at night somehow directly induces cognitive dysfunction (opposed to indirectly, via sleep disturbance). One mouse study found that aberrant light exposure caused learning impairments and mood disturbances by directly affecting melanopsin-expressing neurons.

These melanopsin-expressing neurons, also known as photosensitive retinal ganglion cells, found in the retina of the eye, are not involved in vision. Instead, they play a role in circadian rhythm synchronization and the suppression or release of melatonin.

These retinal cells are also linked to the hypothalamus and the limbic regions, including the amygdala. Other researchers have suggested dim light at night could have a direct influence on brain function via some process related to these photosensitive retinal ganglion cells.

Even 5 Lux Could Potentially Contribute to Depressed Mood

In one study, hamsters exposed to 5 lux at night for four weeks altered their neuronal structure, which in turn caused the hamsters to exhibit symptoms of depression. Another animal study also found that nighttime exposure to 5 lux — this time for three weeks in a row — produced both depression-like symptoms and impaired cognition.

Neurons in the hippocampus also shrunk in length, an effect primarily attributed to a decrease in brain-derived neurotrophic factor (BDNF).

BDNF is a remarkable rejuvenator in several respects. Not only does it preserve existing brain cells, it also activates brain stem cells to convert into new neurons, effectively making your brain grow larger.

The study in question basically showed that nighttime light exposure of just 5 lux effectively inhibited this important brain rejuvenator, causing neuronal shrinkage in the hippocampus, a brain region involved in both long-term memory storage and the regulation of emotions.

In light of such evidence (no pun intended), it would certainly be prudent to evaluate your nighttime light exposure if you “feel blue” or struggle with any kind of depression. Even a seemingly insignificant amount of light could be interfering with your melatonin and/or BDNF production, causing a mood imbalance.

Even the display on your alarm clock could be causing you trouble without you realizing it. I used to recommend covering up digital alarm clocks but know from personal experience how inconvenient that can be, especially if you have blackout drapes and sleep in pitch blackness like I do. I finally discovered a perfect solution — an alarm clock for blind people. It has a very large button that is easy to find, and when you tap it, it audibly tells you the time.

Light-Sensing Pigment in Your Eyes Help Direct Waking/Sleeping Cycles

The wavelength of light also matters to your health, not just the brightness itself. The wavelength gives light its color. Red and orange light have longer wavelengths while green and blue are shorter. The influence of varying wavelengths of light on brain function was demonstrated in a 2014 Belgian study,4 which showed that orange light serves as a powerful “wake-up call” for your entire body.

Again, the influence of light wavelengths has to do with the photosensitive retinal ganglion cells in your eye, which produce a light-sensing pigment called melanopsin. This pigment plays an important role in directing your waking and sleeping cycles. As reported by New Scientist:5

“To find out how melanopsin wakes up the brain, Gilles Vandewalle at the University of Liege, Belgium, and his team gave 16 people a 10-minute blast of blue or orange light while they performed a memory test in an fMRI scanner. They were then blindfolded for 70 minutes, before being retested under a green light.

People initially exposed to orange light had greater brain activity in several regions related to alertness and cognition when they were retested, compared with those pre-exposed to blue light. Vandewalle thinks that melanopsin is acting as a kind of switch, sending different signals to the brain depending on its state.

Orange light, which has the longer wavelength, is known to make the pigment more light-sensitive, but blue light has the opposite effect. Green light lies somewhere in the middle. The findings suggest that pre-exposure to orange light pushes the balance towards the more light-sensitive form of melanopsin, enhancing the response in the brain.”

This kind of information becomes particularly important if you work the night shift. By carefully selecting the type of artificial light you expose yourself to at different times, you can ameliorate at least some of the adverse effects associated with shift work. For more details, please see my previous article, “How to Counteract the Ill Effects of Working the Night Shift.”

How to Make Digital Screens Healthier

In addition to reducing the light in your sleeping environment it is also helpful to eliminate blue light from artificial sources like watching TV at night. You can do this be picking up a $9 pair of UVEX blue blockers on Amazon.  It is far more convenient, though, to use blue light blocking software on your computer monitor after sunset.

Many use f.lux to do this, but I have a great surprise for you as I have found a FAR better alternative that was created by Daniel Georgiev, a 22-year-old Bulgarian programmer that Ben Greenfield introduced to me.

He is one of the rare people that already knew most of the information in this article. He was using f.lux but was very frustrated with the controls. He attempted to contact the f.lux programmers but they never got back to him. So, he created a massively superior alternative called Iris. It is free, but you’ll want to pay the $2 and reward Daniel with the donation. You can purchase the $2 Iris software here.

Iris is better because it has three levels of blue blocking below f.lux: dim incandescent, candle and ember. I have been using ember after sunset and measured the spectrum and it blocked nearly all light below 550 nanometers (nm), which is spectacular, as you can see in the image below when I measured it on my monitor in the ember setting.

When I measured the f.lux at its lowest setting of incandescent it showed loads of blue light coming through, all the way down to as you can clearly see in the images below.

So, if you are serious about protecting your vision you will abandon f.lux software and switch to Iris. I have been using it for about three months now, and even though I have very good vision at the age of 62 and don’t require reading glasses, my visual acuity seems to have dramatically increased. I believe this is because I am not exposing my retina to the damaging effects of blue light after sunset.

Iris Software:

F.lux Software:

Nighttime LED Light Pollution May Be Particularly Harmful

As detailed in my interview with Dr. Alexander Wunsch, a world class expert on photobiology, lighting is an important health consideration. Natural sunlight simply cannot be beat, but unless you spend a majority of your time outside, you’ll need to give some serious consideration to the kind of artificial lighting you use at home and at work.

Light-emitting diodes (LEDs) have now become a standard indoor light source, thanks to their energy efficiency. However, the price society will have to pay in terms of health could end up being enormous. If you missed this interview, I strongly recommend taking the time to listen to it, and read through the accompanying article, “How LED Lighting May Compromise Your Health.” It’s a really crucial issue.

In summary, light-emitting diode (LED) lighting may promote age-related macular degeneration (AMD), the leading cause of blindness, and exacerbate health problems rooted in mitochondrial dysfunction, including obesity, diabetes, heart disease and cancer. For this reason, LEDs are best avoided.

One rare exception is if you work the night shift. In this case, to help establish a new circadian rhythm you’ll want a small amount (just 15 to 30 minutes’ worth) of blue light exposure first thing upon waking (which if you work nights will typically be in the evening, when it’s dark out), along with incandescent light for the longer wavelengths, which include near-infrared. I describe all of this in more detail in the shift work article hyperlinked above. For all others, LED lighting is simply not a good idea.

Environmental Near-Infrared Light Exposure Is Important for Health

As explained by Wunsch, the vast majority of the energy your body needs to maintain systemic equilibrium actually comes from environmental infrared light exposure. The near-infrared range of light found not only in natural sunlight but also in incandescent light bulbs and halogens benefit your health in a number of important ways, including priming the cells in your retina for repair and regeneration.

LEDs emit primarily blue light, which reduces melatonin production in both your pineal gland and in your retina. In your retina, melatonin helps with regeneration, which is why LEDs are so harmful to your vision. Blue light also creates reactive oxygen species (ROS) that, when generated in excess, cause damage. So, when using LEDs, you end up with increased damage and decreased repair and regeneration throughout your body, not just in your eyes.

LED light exposure that is not balanced with full sunlight loaded with the red parts of the spectrum is always damaging to your biology, but even more so at night. Hence lighting your living room, kitchen and dining room — any room where you spend most of your evening — is best done using good old-fashioned incandescent light bulbs, halogens and candles.

Save the energy-saving LEDs for your garage, closets and hallways where exposure is minimal. More detailed information on how to identify the healthiest light bulbs can be found in “How LED Lighting May Compromise Your Health.”

To Optimize Your Sleep and Protect Your Brain Health, Sleep in Total Darkness

When your circadian rhythm is disrupted, your body produces less melatonin, which means it has less ability to fight cancer, and less protection against free radicals that may accelerate aging and disease. So if you’re having even slight trouble sleeping, I suggest you review my 33 Secrets to a Good Night’s Sleep for more guidance on how to improve your sleep-wake cycle.

Even if you think you’re sleeping OK, but know you have light pollution entering your room at night, consider taking steps to block it, since being asymptomatic does not mean your brain is unaffected and functioning normally. Also consider cleaning up the lighting sources in your home and office to avoid unnecessary harm.

As mentioned, AMD is a very real and serious side effect of being chronically exposed to LED lighting, especially if you’re also getting very little natural sunlight exposure.

Effects of platinum and palladium nanocolloid on macrophage polarization in relevance to repigmentation of vitiligo


Abstract

Background

Elevated oxidative stress is accepted to be the initial event in vitiligo leading to the final pathological regulation of immune systems known as autoimmune reaction, which destroys melanin‐forming cells, melanocytes. Recently, we reported an efficient topical use of PAPLAL, nanocolloid of platinum and palladium, having intense catalase‐like activity to vitiligo patients. In addition, we found that PAPLAL has dual effects on the AhR and Nrf‐2 pathways in keratinocytes, and suggested its contribution to the recovery of immune state in vitiligo. The precise mechanism developing autoimmune reaction in vitiligo, however, remains to be clarified. It is important to clarify what kinds of cells play an essential role in the development of vitiligo.

Objective

To further understand the effective mechanisms of PAPLAL on immunity of skin, and to confirm a role of autoimmunity in vitiligo development, we studied the effect of PAPLAL on macrophage polarization and its activities which are recognized to play a pivotal role in immune and inflammatory reactions in many organs.

Methods

Rat and human macrophages were cultured and stimulated in vitro with both LPS and IFN‐γ for M1 polarization and IL‐4 and IL‐13 for M2 polarization with or without PAPLAL. Expression of typical M1 and M2 markers was determined at mRNA and protein levels.

Results

Simultaneous treatment with PAPLAL suppressed remarkably the production of M1 markers, iNOS, and TNF‐α; further, PAPLAL also suppressed M2 markers, mannose receptor (Man R), Chitinase 3‐like 3 (YM‐1), and iron regulatory protein‐1 (IRP‐1), at mRNA and protein levels, but less effectively compared to those of M1. PAPLAL, however, did not suppress phagocytic activity of M0, M1, and M2 cells.

Conclusion

These results indicate that macrophages may be involved in the therapeutic potential of PAPAL by altering immunological environment disturbed in skin, with the delicate shift of the M1‐M2 polarization, but without affecting on phagocytic activity.

Army of Nanorobots Successfully Strangles Cancerous Tumors


Nearly 1.7 million new cases of cancer are detected in the United States each year, and each year cancer claims almost 600,000 lives in the U.S. alone, making it the second-leading cause of death nationally. Treatment is sometimes worse than the illness, as invasive surgeries can be traumatic, and chemotherapy can cause off-target effects that wreak havoc on the entire body. But a new technique described in Nature Biotechnology, which uses nanorobots — literally microscopic robots — to specifically target tumors and cut off their blood supply has the potential to change treatment forever.

In the paper, published in February, an international team of scientists demonstrated the effectiveness of using DNA nanorobots to attack tumors in mice and pigs with cancer. These nanometer-sized robots are made of DNA that unfolds itself at precisely the right time and place to deliver a drug to only the exact target in the body. The DNA, folded up like an origami package, held molecules of thrombin, an enzyme that makes blood clot.

DNA origami nanorobot
When this DNA origami nanorobot detects blood vessels associated with tumors, it opens up to deliver thrombin, a clotting factor that chokes off the blood supply to the tumor.

To test whether this novel drug delivery system works, the team of scientists from Arizona State University and the National Center for Nanoscience and Technology of the Chinese Academy of Sciences injected the nanorobots into the bloodstreams of mice with tumors. They found that the treatment effectively targeted tumors, stopping their growth and even initiating tumor death.

Stopping tumor growth isn’t enough to prove the drug works, though, as it must also prove itself safe. So, the researchers also injected the nanorobots into the bloodstreams of Bama miniature pigs, which have been shown to be good models for testing preliminary drug safety for humans. One major concern with nanorobots is that they could get into the brain and cause strokes, but this did not happen with the test subject animals.

The nanorobots open up to deliver thrombin to the blood vessels that feed the tumor.
When they detect proteins associated with cancer cells, the nanorobots open up to deliver thrombin to the blood vessels that feed the tumor.

The precision of the nanorobots, which is what makes their potential for safe cancer treatment so great, is due to their meticulously crafted structure. The drug-holding “package” is made up of DNA sheets, measuring 60 by 90 nanometers, that wrap around thrombin molecules. On the outside of the folded sheets are molecules that zero in on nucleolin, a protein that’s present in the lining of blood vessels associated with growing tumors.

These molecules, called aptamers, both target the proper spot to deliver drugs and actually open up the DNA sheet up to expose the thrombin when the nanorobot finds the right spot. In theory, when the thrombin is released, it clots the blood entering the tumor, thereby starving it of the oxygen it needs to grow. This method, which essentially strangles the tumor, is reminiscent of the class of cancer drugs known as angiogenesis inhibitors, which help inhibit the growth of blood vessels that feed tumors.

These nanorobots show great promise, but they aren’t ready for humans yet. To get there, the researchers are seeking out clinical partners to further develop this treatment pathway. Still, the fact that it seems to work in mice and pigs makes it likely that nanorobots like these will be available as cancer treatments within our lifetimes.

Abstract: Nanoscale robots have potential as intelligent drug delivery systems that respond to molecular triggers. Using DNA origami we constructed an autonomous DNA robot programmed to transport payloads and present them specifically in tumors. Our nanorobot is functionalized on the outside with a DNA aptamer that binds nucleolin, a protein specifically expressed on tumor-associated endothelial cells, and the blood coagulation protease thrombin within its inner cavity. The nucleolin-targeting aptamer serves both as a targeting domain and as a molecular trigger for the mechanical opening of the DNA nanorobot. The thrombin inside is thus exposed and activates coagulation at the tumor site. Using tumor-bearing mouse models, we demonstrate that intravenously injected DNA nanorobots deliver thrombin specifically to tumor-associated blood vessels and induce intravascular thrombosis, resulting in tumor necrosis and inhibition of tumor growth. The nanorobot proved safe and immunologically inert in mice and Bama miniature pigs. Our data show that DNA nanorobots represent a promising strategy for precise drug delivery in cancer therapy.

Scientists Discover Hundreds of 2D Materials That Could Be The Next Graphene


This is so amazing!

Part of what makes graphene so fantastically useful is its amazing thinness – it’s just one atom thick.

Scientists have now found hundreds of other materials that are equally thin, providing a wide selection of new materials with perhaps as much potential as graphene.

The team analysed data in open resources including the Crystallography Open Database, looking for materials with structural similarities to graphene with the help of a custom computer program.

They were looking for materials with strong chemical bonds along one plane – the 2D atom layer – and relatively weak non-chemical action along the perpendicular plane. It’s this combination that lets us peel sheets of graphene from graphite.

Starting off with a pool of over 100,000 crystal structures, the team from the École Polytechnique Fédérale de Lausanne in Switzerland was able to narrow down the selection to 1,825 compounds with the potential to form sheets just a single atom thick.

“Two-dimensional materials provide opportunities to venture into largely unexplored regions of the materials space,” the researchers explain in their study.

“On the one hand, their ultimate thinness makes them extremely promising for applications in electronics. On the other, the physical properties of monolayers often change dramatically from those of their parent 3D materials, providing a new degree of freedom for applications while also unveiling novel physics.”

In the case of graphene and graphite, graphite is held together by a relatively weak electrostatic interaction known as a van der Waals force. Usually this is strong enough to keep the material together, but it does allow graphene to be extracted.

Whether or not that will also be true for the 1,825 materials identified here remains to be seen, but they have been shown to be structurally similar in terms of atom locations and their chemical bonds. A few of the structures have never been seen before.

Based on calculations run on 258 of the less complex chemicals in the final list, the researchers found that 166 turned out to be semiconductors with a variety of voltages. Meanwhile, 92 materials were identified as metallic, with another 56 likely to have unusual magnetic properties.

Even if just a small subsection of these new materials end up functioning like graphene does, that gives us a lot more options for creating materials for specific purposes in electronics and other areas. The next step is to test how these compounds work in both sheet form and in tightly packed layers.

What we do know thanks to this advanced database search is that these materials might just be exfoliable – able to be peeled into super-thin layers just like graphene. It’s going to be exciting to see what happens next with the materials on this list.

“The materials identified are classified into groups of easily or potentially exfoliable compounds, showing that only a very small fraction of possible 2D materials has been considered up to now,” conclude the researchers.

The research has been published in Nature Nanotechnology.

Fighting cancer with nanobodies and computer simulations


Researchers in the Netherlands are hoping to move vaccine therapy from the lab to inside the body.

Stimulating or enhancing someone’s own immune system to fight cancer is not a new concept but scientists are taking it one step further by using nanoscience and computer simulations to improve existing treatments.

Immunotherapy drugs are specifically designed to help the immune system respond to cancerous cells, something that it doesn’t naturally do. That’s because cancer cells are essentially the body’s own cells gone rogue and the immune system is programmed not to target native cells.

 

Now, a new computer simulation that mimics the body’s response when exposed to certain immunotherapy drugs could speed up their development by eliminating any dud ideas at an earlier stage.

Scientists on the EU-funded MODICELL project have developed prototype software that can trial potential recipes for drugs by using a kind of graphic interface called reactive animation to demonstrate the body’s expected response.

With the information gained from the simulation, the scientists can decide whether to pursue developing a potential drug or to go back to the drawing board, without wasting valuable time and resources.

‘We wanted to develop a computerised approach that will allow us to simulate and to make predictions regarding immune responses that could be used to improve therapies against cancer or in-organ transplantations,’ said Dr Nuno Andrade of St. Anna Children’s Cancer Research Institute, Austria, who managed the project.

To improve the accuracy of the simulations, the researchers first of all conducted real-life experiments in the laboratory and collected extensive biological information from published literature.

Computer scientists worked in the lab together with biologists to better understand the behaviour of the immune system, and used the knowledge gained to develop the computer simulation.

‘There is no way that we can keep doing science without computerised approaches.’

Dr Nuno Andrade, St. Anna Children’s Cancer Research Institute, Austria

Dr Andrade says this type of collaboration is likely to continue. ‘Biology is such a complex science. There is no way that we can keep doing science without computerised approaches.’

Vaccines

One drug-based approach to immunotherapy that is currently used to treat cancer is vaccine therapy. Today this involves taking a blood sample from a patient and mixing it with molecules found on the tumour called antigens. A substance known as an adjuvant is then added to help the immune cells in the blood sample respond to these antigens, and these activated immune cells are injected back into the patient’s body.

However, because this takes place in a lab, the process is cumbersome and time-consuming. The EU-funded PRECIOUS project is developing a novel nano-sized vaccine containing nanoparticles packed with both antigens and an adjuvant, which can be injected into the patient to stimulate the immune response inside the body.

Professor Carl Figdor of Radboud University Medical Center, the Netherlands, who leads the project, said that this couldn’t happen without nanoparticles. ‘These particles are so small that you can inject them directly into the bloodstream without harming the patient. If you were to use bigger particles or bigger molecules then you would have all kinds of difficulties, perhaps small blood vessels would clog.’

Advantages include reduced wait times for the patient and a stable vaccine that is not so heavily affected by the individual health concerns of each patient.

‘Here we are going to have a product that is much more stable and of a constant quality, and is cheaper in the end because it can be used in a much wider way for a lot of patients,’ said Prof. Figdor.

Large scale

The idea is to find an efficient process for creating these nanoparticles en masse so that nanovaccines can be manufactured on a large scale. The PRECIOUS team will test their nanoparticles for safety in humans and if successful will move up to trials involving 500 people.

‘There is a lot of gain because you make one product that you can use for a lot of patients, rather than having to take blood from each patient, making an individual vaccine, which is labour intensive and expensive,’ said Prof. Figdor.

Nano-sized particles are also being used to improve a kind of cancer therapy called photodynamic therapy (PDT). PDT involves a photoactive drug, called a photosensitiser, which, when introduced into the body, acts like a ticking bomb – it is safe until it is activated by contact with a particular wavelength of light and then it reacts with oxygen to form a chemical that kills the cells.

It’s not fully understood how or why, but PDT is also thought to activate the immune system to attack the cancer.

Expel

However, the problem with the photosensitisers currently in use is that they stick to all the body’s cells, not only cancer cells. Healthy cells will expel the drug after two to four days, whereas cancer cells find the photosensitisers much more difficult to remove. Patients returning after two to four days are exposed to the type of light which activates the photoactive drug, killing the cancer cells.

Now, scientists on the KILLCANCER project, funded by the EU’s European Research Council, plan to reduce this waiting period to just a couple of hours by developing an approach where small nanobodies – fragments of antibodies – are bound chemically to the photosensitiser. These actively target cancerous cells, but not healthy cells.

‘We expect that we can more efficiently reach cancer cells compared to traditional antibodies,’ said Dr Sabrina Oliveira of Utrecht University, the Netherlands, who leads the work. The project is also investigating how PDT interacts with the immune system response.

The next goal for the research is to progress from mouse studies to larger animals like cats and dogs. In the near future, Dr Oliveira will start working with veterinary centres to offer PDT as a therapy for cats with oral cancer, and can then use the resulting data to produce a body of evidence supporting nanobody-targeted PDT.

The issue

Improving immunotherapy treatments isn’t just about developing better drugs, it’s also about manufacturing those treatments on a large scale so they can be used in the wider population.

To support this, the EU has allocated more than €1.5 billion to research into industrial leadership in the areas of nanotechnologies, advanced materials, biotechnology and advanced manufacturing and processing between 2018 and 2020.

The work includes addressing the regulatory framework and developing an environment that enables high-quality healthcare for Europeans. Nanomedicines that are developed in the EU for use in tumour-targeted treatment strategies are produced at an industrial level that respects the highest possible quality standards.

In 2013, the European Technology Platform on Nanomedicine (ETPN) set up Nano World Cancer Day, which this year takes place on 2 February and is supported by the EU-funded ENATRANS project. There will be simultaneous events in 10 countries to demonstrate the disruptive nanomedicine-based innovations that are being developed to beat cancer.