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Fletcher told the ABC the guidelines were developed in consultation with people living with autism, researchers and doctors, and had been approved by the National Health and Medical Research Council.

“It does not change what the NDIS does and indeed it may well be that there are people who, today, would not be diagnosed who will be diagnosed,” he said. “That will be a judgment for clinicians and medical profession and the NDIS will continue to do what it does, which is make an assessment of the impairment that somebody suffers as a result of a disability. Is it likely to be permanent and lifelong? Is it significant? What impact does it have on the functioning?”

Dr Wenn Lawson, the co-chair of the Australian Autism Research Council, said a consistent assessment and diagnosis process for autism meant people would be able to access more appropriate supports.

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Some of Allen’s philanthropy has taken a scientific bent: Allen founded the Allen Institute for Brain Science in 2003, pouring $500 million into the non-profit that aims to give scientists the tools and data they need to probe how brain works. One recent project, the Allen Brain Observatory, provides an open-access “catalogue of activity in the mouse’s brain,” Saskia de Vries, senior scientist on the project, said in a video. That kind of data is key to piecing together how the brain processes information.


Microsoft co-founder Paul Allen died today from complications with non-Hodgkin’s lymphoma. He was 65. Allen said earlier this month that he was being treated for the disease.

Allen was a childhood friend of Bill Gates, and together, the two started Microsoft in 1975. He left the company in 1983 while being treated for Hodgkin’s lymphoma and remained a board member with the company through 2000. He was first treated for non-Hodgkin’s lymphoma in 2009, before seeing it go into remission.

In a statement given to ABC News, Gates said he was “heartbroken by the passing of one of my oldest and dearest friends.” He went on to commend his fellow co-founder for his life after Microsoft:

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Speaking from beyond the grave, Professor Stephen Hawking has told a new generation growing up in an increasingly insular world: ‘Remember to look up at the stars and not down at your feet.’

The eminent cosmologist, who had motor neurone disease and died in March, had his final public thoughts broadcast at a special event to launch his last book, Brief Answers To The Big Questions.

Prof Hawking’s words of advice and defiance, echoing from an Imax screen at London’s Science Museum, brought tears to the eyes of his daughter Lucy.

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A peroxide scavenger nanoparticle reduces systemic inflammation in mouse models.

With 19 million cases per year worldwide, sepsis is one of the most life-threatening conditions in the intensive care unit. However, to date, there is no specific and effective treatment. Oxidative stress has been shown to play a major role in sepsis pathogenesis by altering the systemic immune response to infections, which, in turn, may lead to multiorgan dysfunction and cognitive impairment. Here, Rajendrakumar et al. developed a nanoparticle-based peroxide scavenger treatment for reducing oxidative stress during sepsis.

To produce the nanoassembly, the authors first developed a water-soluble nanoparticle core containing an active peroxide scavenger and a protein that stabilizes the scavenger and improves its biocompatibility. The nanoparticle core was then coated with a polymer material conjugated with mannose to help the final nanoassembly target inflammatory immune cells through the mannose receptor on the immune cell surfaces. The authors first confirmed in cell cultures that the nanoassembly can selectively reduce hydrogen peroxide–mediated free radical production with minimal toxicity. In cultures, immune cells demonstrated enhanced intracellular uptake of the particles and reduced production of inflammatory markers during activation. To demonstrate the therapeutic efficacy in vivo, the authors carried out three sets of animal studies. In the first set, the nanoassembly was shown to reduce locally induced tissue inflammation and prevent inflammatory immune cell infiltration.

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![Figure][1]

Coronal section of the neocortex in a juvenile mouse. Double immunostaining shows microglia (green) and inhibitory interneurons (red), whereas nuclear counterstaining is in blue.

IMAGE: PAOLA SQUARZONI

The human brain contains billions of well-connected neurons. Neural neighborhoods perform different tasks: Some coordinate movement, whereas others hum along planning dinner. The mature brain is a complex assembly of networks, structures, and tracts. Like cities and their neighborhoods, however, the brain does not arise fully formed. Rather, operational patterns and developmental constraints guide the proliferating neurons that build the typical adult human brain. Just as cities are governed by both hard and soft infrastructure—e.g.

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Invariant natural killer T cells might lead to cheaper and more effective immunotherapy.


Researchers at the Imperial College London have discovered that specifically employing invariant natural killer T cells, rather than generic T cells, in cancer immunotherapies based on chimeric antigen receptors might lead to significantly more effective, cheaper, and more easily mass-produced treatments [1].

Abstract

Chimeric antigen receptor anti-CD19 (CAR19)-T cell immunotherapy-induced clinical remissions in CD19+ B cell lymphomas are often short lived. We tested whether CAR19-engineering of the CD1d-restricted invariant natural killer T (iNKT) cells would result in enhanced anti-lymphoma activity. CAR19-iNKT cells co-operatively activated by CD1d- and CAR19-CD19-dependent interactions are more effective than CAR19-T cells against CD1d-expressing lymphomas in vitro and in vivo. The swifter in vivo anti-lymphoma activity of CAR19-iNKT cells and their enhanced ability to eradicate brain lymphomas underpinned an improved tumor-free and overall survival. CD1D transcriptional de-repression by all-trans retinoic acid results in further enhanced cytotoxicity of CAR19-iNKT cells against CD19+ chronic lymphocytic leukemia cells. Thus, iNKT cells are a highly efficient platform for CAR-based immunotherapy of lymphomas and possibly other CD1d-expressing cancers.

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Current brain-computer interface (BCI) research helps people who have lost the ability to affect their environment in ways many of us take for granted. Future BCIs may go beyond motor function, perhaps aiding with memory recall, decision-making, and other cognitive functions.


Have you ever studied a foreign language and wished you could upload the vocabulary lists directly into your brain so that you could retain them? Would you like to do mental math with the speed and accuracy of a calculator? Do you want a literal photographic memory? Well, these dreams are still the stuff of science fiction, but the brave new world of brain-computer interfaces, or BCI, is well on its way to making technological miracles of this sort a reality.

The story of BCI begins with the discovery of electrical signals emitted by the brain. In 1924, German scientist Hans Berger recorded the first electroencephalogram, or EEG, by placing electrodes under a person’s scalp. Although his research was at first met with derision, a whole new way to study the brain was born from his work. It is now well accepted that the human brain emits electric signals at a variety of frequencies currently known as brainwaves.

BCI researchers attempt to harness these signals to create some desired effect in the world outside the brain. In other words, BCI seeks to make things happen based on a thought in a person’s head. Actually, humans do this all the time when they decide to do anything. A person thinks, “I’m thirsty; I need a drink,” and then the brain sends a litany of instructions to the extremities that allows the person to pour a glass of water, lift it to their mouth, swallow the water, and so on. Most of us go through our days executing these kinds of actions, which require complex interaction between the body and brain, without giving them a second thought.

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