Education Planet

'Noise And Sound Assault Us All The Time'
~ Dada Vaswani

Several disciples had gathered around the one day, eager to hear his sermon. But the Buddha chose to remain utterly silent, only holding out a lotus flower. What did this silence mean?Only Mahakashyapa, gazed intently at the flower, and realised the inexpressible meaning of the Buddha’s gesture. He had obtained inspiration directly from the Buddha’s gaze, and the flower that the Master had held. He smiled at the Buddha in gratitude, and the Buddha smiled back in recognition of his disciple’s subtle sense of insight.

Thus was born a new school of Buddhism, Zen, in which experiential wisdom took precedence over sermons and scriptures; and in which revealed transmission bypassed the need for words and rituals. To this day, Zen Masters do not use words to transmit their wisdom, relying instead, on intuitive thought processes and the grasp of unspoken truths. It is believed that Bodhidharma, the South Indian Pallava prince-turned-monk, first brought Zen to China; he was perhaps in the direct lineage of the disciples of Mahakashyapa.

The essence of Zen philosophy is expressed in the Bloodstream Sermon attributed to him. “Buddhas don’t save Buddhas. As long as you look for a Buddha somewhere else, you will never see that your own mind is the Buddha. Don’t use a Buddha to worship a Buddha. And don’t use the mind to invoke a Buddha. Buddhas don’t recite sutras. Buddhas don’t keep precepts. And Buddhas don’t break precepts. Buddhas don’t do good or evil. To find a Buddha, you have to see your nature. ”Silence is looking within to find out your true nature.

Our workaday world has the tendency to drown us in a tsunami of noise! Incessant (and often mindless) chatter, blaring music, non-stop TV, constant telephone calls, endless meetings and lengthy presentations, and at times, heated arguments, hurt our eardrums and our hearts: noise and sounds assault us all the time. The demands and distractions of modern life only take us away from ourselves. This is why Indic philosophy and culture insist on silence, withdrawal, stillness and meditation whereby you can discover the Divine within yourself.

“The more a man finds his sources of pleasure in himself, the happier he will be,” writes the philosopher Schopenhauer. “… The highest, the most varied and lasting pleasures are those of the mind…”Truly, if we cannot find our sense of self-worth, our true happiness and contentment within, it is useless to seek it elsewhere! This is exactly what silence helps us to do!The best part of silence is that the ego is switched off at least for a while, and we are focusing our attention inwards.

If any of you have voluntarily or compulsorily sat in silence even for a few minutes, you will know that the mind is energised, recharged by this experience. Not only Zen; most other ancient faiths set great store by the sadhana of silence. Dhyana and yoga are based on silencing the mind and emotions as well as speech. Of Shiva, who is worshipped as the ultimate guru, Dakshinamurthy, scriptures say this: “Thou art He who imparts instruction in utter silence. Thou art He that observes the vow of taciturnity, for Thou instructest in silence.

” For it is said that He brought the four learned Sanakati Munis -- Brahma’s intellectual offspring -- to the state of Self-realisation by the power of His silence. .

Beating Type 2 Diabetes Into Remission ~

Recognising and accurately coding reversal of type 2 diabetes is key to improving outcomes and reducing healthcare costs, argue Louise McCombie and colleagues

Type 2 diabetes, generally perceived as progressive and incurable, now affects 5-10% of the population, about 3.2 million people in the UK. Until complications develop, most patients are managed entirely within primary care, with diabetes comprising a major part of general practice activity. About 10% of total UK NHS expenditure goes on treating diabetes, and international figures suggest that medical costs for people with diabetes are twofold to threefold greater than the average for age and s*x matched people without diabetes.

Application of current clinical guidelines to reduce glycated haemoglobin (HbA1c) levels and cardiovascular risks, primarily with drugs and generic lifestyle advice, has improved clinical outcomes, but many patients still develop vascular complications, and life expectancy remains up to six years shorter than in people without diabetes. The diagnosis carries important social and financial penalties for individuals, as well as poor health prospects.

Remission of diabetes (no longer having diabetes, at least for a period) is clearly attainable for some, possibly many, patients but is currently very rarely achieved or recorded. Greater awareness, documentation, and surveillance of remissions should improve health outcomes and reduce healthcare costs.

Beating type 2 diabetes into remission Recognising and accurately coding reversal of type 2 diabetes is key to improving outcomes and reducing healthcare costs, argue Louise McCombie and colleagues Type 2 diabetes, generally perceived as progressive and incurable, now affects 5-10% of the population, about 3.2 million people in the UK.1…

Hyperloop pod breaks own high-speed record

Elon Musk and hyperloop tunnel

Tests of the futuristic hyperloop transport system have managed to propel one of its pods at 355km/h (220mph).

The tests establish a new record for the technology only days after a separate prototype hit 324km/h.

Hyperloop puts pods in an airless tunnel and seeks to accelerate them to very high speeds to cut travel times for freight and passengers.
Backers of the hyperloop idea claim that eventually the pods will travel at speeds of about 1,000 km/h.

Speed racer

The idea for the version of the hyperloop transportation system currently being developed was floated in 2013 by Tesla boss Elon Musk. This week saw the first tests of prototype carriages or pods on a one mile long test track near Los Angeles. A pod made by a German student team came top in this competition.

In an Instagram post, Mr Musk said that once the prototype competition was finished, the hyperloop team let a "pusher pod" travel by itself on the tunnel test track.
The pusher pod was used to get some of the prototypes moving down the track during the tests.

Running by itself, the pusher pod set the new record before things started burning, wrote Mr Musk. He described the spectacle of the pod racing down the track as "...kind of like racing with a tugboat".

Improvements to the test track might mean the pods hit 500 km/h next month, he said.
The series of tests this week suggest the technology is close to the top speed at which existing terrestrial transport technology can travel.

Earlier this month, China started letting its high-speed "Fuxing" trains travel at speeds of about 350 km/h (217mph).
It is also looking into ways to upgrade high-speed tracks to let them go faster - perhaps at speeds approaching 400km/h.

Prehabilitation: preparing patients for surgery

Major surgery is like running a marathon—and both require training

The impact of surgery leads to significant homeostatic disturbance. The surgical stress response is characterised by catabolism and increased oxygen demand. The extent and duration of the stress response is proportionate to the magnitude of surgery and the associated risk of developing postoperative complications.

Patients who experience postoperative complications within 30 days of surgery have a reduced long term survival rate. Even in the absence of complications there is a 20-40% reduction in postoperative physical function and a significant deterioration in quality of life after major surgery.

The demand for surgical services is increasing as a result of an expanding, ageing population. Added to which, patients are becoming more “high risk” as they are often elderly, frail, and obese. These factors are not only associated with adverse postoperative outcomes but may negatively impact on decision making and, consequently, fair access to surgery.

Google has released the latest version of its Android mobile operating system (OS), which is named after Oreo chocolate biscuits.
It adds a new "picture-in-picture" mode that lets some apps run in a small corner of the screen.

Google's own Nexus and Pixel phones are expected to be the first to receive the software update.
New versions of Android can be slow to roll out, and just 14% of Android devices run the previous OS, Nougat.
Android Oreo introduces measures to help people manage the volume of notifications on their devices, which has been described as "notification diarrhoea".
App developers will now be able to split notifications into categories, so people can block some types of alert while still receiving others.
Previously, Android users could only allow all or block all notifications from each app.

Android Oreo lets some video calls appear as a "picture-in-picture"

Other new features include:
"smart copy-and-paste", which highlights an entire address, telephone number or web addresses when people try to copy it
limiting how many system resources apps can use while they are running in the background, to reduce memory use and battery use
Instant Apps, which lets some services invoke parts of their Android apps, even if people have not installed them
a redesigned set of emojis, which look more like the ones seen on Apple's iOS
The picture-in-picture mode will let people watch YouTube videos in a corner of the screen while they use other apps, as long as they have paid for the YouTube Red subscription service.

However, people using Android Nougat can already watch YouTube videos in split-screen mode for free.

The software was released at 19:50 BST to coincide with a solar eclipse visible on the east coast of the United States.
It is now up to phone manufacturers to decide whether to make the new software available on their existing devices, although many do pre-install it on their new releases.

Google unveiled an Oreo-themed version of its mascot at an event in a New York park
"Google's challenge with new versions of Android is that it's only immediately available to a small number of smartphone users," said Ian Fogg, of IHS Markit consultancy.
"Android typically needs to be adapted and approved by each handset maker and mobile operator, so it takes months for new versions of Android to reach a significant number of users.

"One key change in Android Oreo is in the architecture: to make it easier in the future for phone manufacturers to make their changes, but still push out new versions of the operating system to users.
"That's probably the most significant change."

🔰Dream On, But Sleep Is Very Important, Too ~

Everybody dreams. Some remember their dreams; others don’t. The brain never sleeps; neural pathways are always active, whether mediated by ego during waking state or without it, as happens during sleep. Activation of neural pathways produces dreams. During sleep, we go through 4-5 cycles of deep sleep and dreaming episodes, each of roughly 90 minutes’ duration. Electro-encephalography (EEG) studies done on the human brain during sleep, show that deep sleep is characterised by production of low frequency (1-4 Hz) Delta waves, known to help produce life and mood-enhancing chemicals.

At this stage, we are totally unaware of our surroundings. But, dreaming episodes characterised by rapid eye movement (REM), are of light sleep kind, from which one can be woken up quite easily. Dreams are both internal and external. Since ego, the director, is absent during sleep, neural pathways have free run. Thus, day-long experiences or existing memories are the driving force for internal dreams. When there is sanyam or tremendous thinking activity on a particular thought during waking time, it leads sometimes to solution-dreams.

Several great inventions and discoveries have come through such dreaming process. Externality of dreams comes because brain is both receiver and transmitter of human thought. Hence during sleep, memories or signals from knowledge-space impinge on the brain and may modify neural pathways. This can give rise to strange dreams of events and places never visited or interacted with. This is also the mechanism of getting prophetic dreams of which there are many instances. Why don’t we remember dreams? Brain scientists say part of it is to do with creating long-term memory.

But it is dreams we remember that make life interesting. We still don’t know why we dream. A possible answer may lie in how synapses behave during sleep. Synapses are connections between two neurons; they allow the transfer of information through passage of neurochemicals across the synaptic cleft, the distance (about 0. 02 micron) between neuron and synapse that exchanges neurochemicals. Scientists have found that during deep sleep, the synaptic cleft widens by about 20 per cent. Perhaps it helps in allowing the cerebrospinal fluid to flow through it and to remove toxins from the brain.

The more we dream during the night, the less restful is the sleep. A really restful sleep is deep sleep without dreams. This helps in flushing out toxic material from major part of the brain. Besides this, the increase of synaptic cleft may also help in explaining the dreaming process. During sleep, neural pathways are active without ego, so circuit production is quite random. But only those pathways produce circuits in which neural connections are still strong. Thus “loosened” synapses or those with increased synaptic cleft might not take part in the information transfer and hence, in the dreaming process.

So dreams could be random in nature. Besides, this loosening of neural pathways may also explain the removal of some memories of day-long experiences. Sleep is therefore necessary to remove clutter or irrelevant information from the brain. Too often, we have dreams connected with our suppressed desires; most are based on unfulfilled emotional needs and psychological knots based on strong memories that do not get loosened during sleep and cause recurring dreams. Resolution of these knots through wisdom allows the loosening of strong memories and helps in brain detoxification, producing dreamless sleep.

🔰The Antibiotic Course Has Had Its Day ~

With little evidence that failing to complete a prescribed antibiotic course contributes to antibiotic resistance, it’s time for policy makers, educators, and doctors to drop this message.

Antibiotics are vital to modern medicine and antibiotic resistance is a global, urgent threat to human health. The relation between antibiotic exposure and antibiotic resistance is unambiguous both at the population level and in individual patients. Reducing unnecessary antibiotic use is therefore essential to mitigate antibiotic resistance.

Avoiding overuse requires healthcare professionals and the public to be well informed about antibiotic treatment, as set out in the first objective of the World Health Organization Global Action Plan. Public communication about antibiotics often emphasises that patients who fail to complete prescribed antibiotic courses put themselves and others at risk of antibiotic resistance. For example, in materials supporting Antibiotic Awareness Week 2016 WHO advised patients to “always complete the full prescription, even if you feel better, because stopping treatment early promotes the growth of drug-resistant bacteria.”

Similar advice appears in national campaigns in Australia,5 Canada,6 the United States,7and Europe.8 And in the United Kingdom it is included as fact in the curriculum for secondary school children.9

However, the idea that stopping antibiotic treatment early encourages antibiotic resistance is not supported by evidence, while taking antibiotics for longer than necessary increases the risk of resistance. Without explicitly contradicting previous advice, current public information materials from the US Centers for Disease Control and Prevention (CDC) and Public Health England have replaced “complete the course” with messages advocating taking antibiotics “exactly as prescribed.”

We explore the evidence for antibiotic duration, clinical effectiveness, and resistance, and encourage policy makers, educators, and doctors to stop advocating “complete the course” when communicating with the public. Further, they should publicly and actively state that this was not evidence-based and is incorrect.

🔰Origin of the idea
Concern that giving too little antibiotic treatment could select for antibiotic resistance can be traced back to the dawn of the antibiotic era. When Howard Florey’s team treated Albert Alexander’s staphylococcal sepsis with penicillin in 1941 they eked out all the penicillin they had (around 4 g, less than one day’s worth with modern dosing) over four days by repeatedly recovering the drug from his urine. When the drug ran out, the clinical improvement they had noted reversed and he subsequently succumbed to his infection. There was no evidence that this was because of resistance, but the experience may have planted the idea that prolonged therapy was needed to avoid treatment failure.

Fleming’s early work showed that sensitive bacteria could be “acclimatised” to penicillin in the laboratory. In his 1945 Nobel prize acceptance speech, Fleming painted a vivid clinical vignette in which an imagined patient with a streptococcal throat infection who takes insufficient penicillin, transmits the infection—now in resistant form—to his wife, and is thus responsible for her subsequent death from antibiotic resistant disease. Fleming advised, “If you use penicillin, use enough!” Ironically, Streptococcus pyogenes has never developed resistance to penicillin, and we now know that for most forms of antibiotic resistance that currently threaten patients, selection of resistance in the bacteria being treated is of limited importance.

Antibiotic treatment drives resistance
The scenario envisaged by Fleming was of target selected resistance. Infections typically begin when a small population of microorganisms gain access to the host and replicate. Genetic mutations conferring antibiotic resistance may arise spontaneously during replication and be selected for during treatment. Target selected resistance can occur with inadequate antimicrobial dosing or with monotherapy for infections for which spontaneous resistant mutations arise on treatment, such as tuberculosis, gonorrhoea, and HIV.

Early trials of tuberculosis treatment showed resistance emerging during monotherapy and underpin the need for combination therapy for this disease. Transmission of such pathogens during or following inadequate treatment may allow resistant strains to spread from person to person.

However, most of the bacterial species now posing the greatest problems do not develop resistance through target selection. The clinical threat comes mainly from species such as Escherichia coli and the so called ESKAPE organisms (Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter spp, Pseudomonas spp, Enterobacter spp), which are all found harmlessly in us, on us, or in our environment. They can also act as “opportunistic” pathogens.

When a patient takes antibiotics for any reason, antibiotic sensitive species and strains present among commensal flora on their skin or gut or in the environment are replaced by resistant species and strains ready to cause infection in the future. This collateral selection is the predominant driver of the important forms of antibiotic resistance affecting patients today. The longer the antibiotic exposure these opportunist bacteria are subjected to, the greater the pressure to select for antibiotic resistance.

Importantly for these opportunistic pathogens, resistant strains are transmitted between asymptomatic carriers rather than people with disease. Furthermore, many resistance conferring genes can pass easily between bacterial strains or species. Thus antibiotic selection may drive outbreaks of resistant infections independently of transmission of a specific strain or species.

From fear of undertreatment to harm from overtreatment.

Traditionally, antibiotics are prescribed for recommended durations or courses. Fundamental to the concept of an antibiotic course is the notion that shorter treatment will be inferior. There is, however, little evidence that currently recommended durations are minimums, below which patients will be at increased risk of treatment failure.

The key argument for changing how we discuss antibiotic courses with patients is that shorter treatment is clearly better for individual patients. Not only does an individual patient’s risk of resistant infection depend on their previous antibiotic exposure but reducing that exposure by shorter treatment is associated with reduced risk of resistant infection and better clinical outcome. In hospital acquired pneumonia, for example, randomised controlled trial data indicate that short treatment strategies have equivalent clinical outcomes to longer courses and are associated with lower rates of infection recurrence and antibiotic resistance.

There are reasons to be optimistic that the public will accept that completing the course to prevent resistance is wrong if the medical profession openly acknowledges that this is so, rather than simply substituting subtle alternatives such as “exactly as prescribed.” Completing the course goes against one of the most fundamental and widespread medication beliefs people have, which is that we should take as little medication as necessary. Concerted and consistent efforts have successfully educated the public that antibiotics do not treat viral infections, for example.

Research is needed to determine the most appropriate simple alternative messages, such as stop when you feel better. Until then, public education about antibiotics should highlight the fact that antibiotic resistance is primarily the result of antibiotic overuse and is not prevented by completing a course. The public should be encouraged to recognise that antibiotics are a precious and finite natural resource that should be conserved. This will allow patient centred decision making about antibiotic treatment, where patients and doctors can balance confidence that a complete and lasting cure will be achieved against a desire to minimise antibiotic exposure unimpeded by the spurious concern that shorter treatment will cause antibiotic resistance.

Gif and image written into the DNA of bacteria :-

An image and short film has been encoded in DNA, using the units of inheritance as a medium for storing information.

Using a genome editing tool known as Crispr, US scientists inserted a gif - five frames of a horse galloping - into the DNA of bacteria.

Then the team sequenced the bacterial DNA to retrieve the gif and the image, verifying that the microbes had indeed incorporated the data as intended.

The results appear in Nature journal.

For their experiments, the team from Harvard University in Cambridge, Massachusetts, used an image of a human hand and five frames of the horse Annie G captured in the late 19th Century by the British photography pioneer Eadweard Muybridge.

In order to insert this information into the genomes of bacteria, the researchers transferred the image and the movie onto nucleotides (building blocks of DNA), producing a code that related to the individual pixels of each image.

The researchers then employed the Crispr platform, in which two proteins are used to insert genetic code into the DNA of target cells - in this case, those of E.coli bacteria.

For the gif, sequences were delivered frame-by-frame over five days to the bacterial cells.

The data were spread across the genomes of multiple bacteria, rather than just one, explained co-author Seth Shipman, from Harvard University in Massachusetts.

"The information is not contained in a single cell, so each individual cell may only see certain bits or pieces of the movie. So what we had to do was reconstruct the whole movie from the different pieces," Dr Shipman told the BBC.

"Maybe a single cell saw a few pixels from frame one and a few pixels from frame four... so we had to look at the relation of all those pieces of information in the genomes of these living cells and say: can we reconstruct the entire movie over time?"

To "read" the information back, the researchers sequenced the bacterial DNA and used custom computer code to unscramble the genetic information, which spits out the images.

The team was able to achieve 90% accuracy: "We were really happy with how it came out," Seth Shipman told me.

Eventually, the team wants to use the technique to create "molecular recorders".

Dr Shipman says these are cells that can "encode information about what's going on in the cell and what's going on in the cell environment by writing that information into their own genome".

This is why the researchers used images and a movie: images because they represent the kind of complex information the team would like to use in future, and movies because they have a timing component.

The timing component is important because it would be useful to track changes in a cell and its environment over time.