New Melanoma Treatment In Minnesota Has Success

(KARE) Clinical trials of a new treatment for the deadliest form of skin cancer are underway in the Twin Cities. The trials are offering hope for patients who have tried other treatments with recurring cancers.

The treatment is an “oncolytic immunotherapy” or V-Tec, for short. It involves injecting a live, genetically-altered Herpes Simplex Type A virus (normally associated with cold sores) directly into the melanoma tumors.

“What is different about it is that it is a virus that kills cancer,” explained Dr. Thomas Amatruda, Minnesota Oconology, who is one of the key researchers. “It is a virus that is designed to grow selectively in cancer cells and not in normal tissues. It grows in the cells and pops them.”

Amatruda said the treatment is particularly useful in Stage 3 melanoma patients who have had recurring tumors. One of his clinical trial patients is Gary Neilson, 73, of Plymouth.

“It will be six years in July,” said Neilson, referring to his initial Melanoma diagnosis. “They wanted to take the melanoma off my back immediately.”

The melanoma was removed, but treatment after treatment, the tumors returned.

“We were running out of options for him,” said Amatruda. Neilson entered the V-tec trial in May, 2014. At first, Amatruda said the treatment was not what some expected.

“His melanomas got larger and in three months, they were larger than when we started,” said Amatruda,” but we know that immune therapies can take a while to work. So, after three months, he continued treatment and they began to shrink. Now they are shrinking everywhere. We have had areas that have completely gone away.”

“This is the first thing that has really worked,” said an ecstatic Neilson. “I am pretty excited and Dr. Amatruda is pretty excited, too.”

The V-Tec works in two ways, according to Amatruda. First, it attacks the tumors, but secondly, it creates an immune reaction through the entire body.

“In cancer treatement, the problem is not what you see,” said Amatruda. “It is what you cannot see. So, if we could inject everything we saw, we still would be missing cancer cells hiding in the body, but the immune system goes all through the body and it is hard for cells to hide from the immune system.”

Amatruda and Neilson agreed that often there is an initial strong reaction to the injected virus. Neilson suffered fevers and chills, but after three or four treatments, the side effects disappeared.

“Now,” said Neilson, “I go in, have the injections, and walk out.”

Amatruda said they have used the treatment on patients in their 80’s and 90’s with little trouble.

The melanoma clinical trials are still recruiting viable candidates for treatment. The Virginia Piper Cancer Institute can be reached at 763-236-5619. The treatment is only available in clinical trials. It has not been approved by the FDA, as yet. Dr. Amatruda said the FDA has favorably reviewed the trials, but there is not time frame for approval and wider application.

Apple iPhone bug can also affect Twitter

If you’re a victim of Apple’s text messaging bug and have suffered an iPhone crash, there is more shock in store.

The bug that can strike with simple text, also affects Twitter and permanently breaks Snapchat text chat.

The malware causes Apple’s text handling system to choke on certain characters from Arabic, Marathi and Chinese and crashes the iPhone, iPad, Apple Watch or Mac. It also affects apps running on iOS, The Guardian reported.

The malware message can be sent over Twitter either using direct messages or public mentions.

If the recipient uses an iPhone and has notifications turned on, a message will instantly crash their smartphone.

When sent a text chat with the offending string, it permanently crashes the iPhone when the user attempts to read it.

The bug means that the user cannot open their chat history with the person who sent the message without crashing their iPhone.

The message cannot be cleared, but other messages can be sent to and received from other contacts.

Apple issued recovery instructions for its Messages app, which involves using Siri to reply to a message allowing users to then delete that conversation.

A similar recovery method can use the Photos app to send a picture to a contact and gain access to the message history so it can be deleted.

The company said that a fix for the bug via a software update will be provided.

You can disable notifications to protect your device from the mischievous text, but that will not prevent Snapchat and other third-party apps from being disabled.



5 Ways Google’s Brillo OS Will Transform Home Automation

Brillo In The Home

Google on Thursday unveiled Brillo, its new operating system that will give smart capabilities to devices in consumers’ houses.

The announcement, made at the Google I/O developer’s conference, pushes Google further into the Internet of Things market.

In 2014, the company first dipped into the home automation market by acquiring Nest, a home automation company that designs and manufactures Wi-Fi-enabled, programmable home features like thermostats and smoke detectors.

In addition to Brillo, Google released other mobility-related news Thursday, like upgrades to its intelligent personal assistant, Google Now, and its Photos app. Google also introduced its newest OS, Android M, which will succeed Android Lollipop.

Following are five features of Brillo.

5. It Enables Devices To Talk To Each Other, And To Your Phone

Brillo promotes connectivity for various home devices, so that the devices will be able to communicate through a common language.

According to Google Senior Vice President Sundar Pichai (pictured), the operating system is a stripped-down low-power version of Android’s mobile operating system.

The software also ensures that devices will be connected to the user’s phone, so that users can control products like thermostats, stoves and refrigerators.

4. It Includes Weave, To Smooth Communications

As part of Brillo, Google introduced Weave, Brillo’s common standards communications layer that defines certain devices.

Weave uses a common language that enables the platform’s sensors and devices to communicate in a streamlined process through the cloud. This solves the problem of fragmentation in home automation, as connected devices may communicate in several ways and use differing software.

3. It’s Coming Soon

According to Pichai, Google has been partnering with Google’s Nest, Android’s mobile unit and the Chrome Web browser business to develop the platform.

Brillo’s developer preview will be ready in the third quarter, and the operating system will be released in the fourth quarter.

Meanwhile, the full-stack feature of Weave will come out in the fourth quarter of this year. According to Google, Weave is cross-platform and will be able to be used across other Internet of Things operating systems.

2. It Won’t Devour Power

Brillo, which manages and stores data collected in device sensors, is meant to run on connected devices with low memory and small processors.

According to Google, in addition to Wi-Fi- and Bluetooth low energy, Brillo uses minimum system requirements.

This emphasis on low power ensures that smaller home appliances and devices, like door locks, can connect into the system. According to The Verge, the software is reportedly designed for devices that have as little as 32 MBs of RAM.

1. It Joins Other Players In The IoT Space

Google’s Brillo is the latest development in the competitive Internet of Things space.

Last week, Huawei announced LiteOS, a lightweight operating system for the Internet of Things that includes an IoT gateway and controller.

Also this month, Samsung trumpeted its Artik chipsets, which are chips intended for connected devices like wearables and connected home appliances, in addition to its Tizen Internet of Things operating system.


wrp103 links to the BBC’s report of a newly engineered alloy that returns to its original shape after deformation even after 10 million cycles more than 10 million times. From the article: “Memory shape alloys” like this have many potential uses, but present incarnations are prone to wearing out.The new material — made from nickel, titanium and copper — shatters previous records and is so resilient it could be useful in artificial heart valves, aircraft components or a new generation of solid-state refrigerators.” (Original article in Science Magazine.)

A 99% biodegradable computer chip

May 29, 2015

University of Wisconsin-Madison and U.S. Department of Agriculture Forest Products Laboratory (FPL) researchers have jointly developed a wood chip in an effort to alleviate the environmental burden* of electronic devices.

Well, actually, a wood-substrate-based semiconductor chip. They replaced the silicon substrate portion in a conventional chip with environment-friendly cellulose nanofibril (CNF). CNF is a flexible, biodegradable material made from wood, as the researchers note in an open-access paper published May 26 in the journal Nature Communications.

“[More than 99%] of the material in a chip is support,” said Zhiyong Cai, project leader of an engineering composite science research group at FPL. With the new substrate, the chips are “so safe you can put them in the forest and fungus will degrade it. They become as safe as fertilizer.”

The new material is especially important for microwave chips (such as those used in mobile phones) made with gallium arsenide, which is especially difficult to fabricate on foreign substrates. That’s because of the small feature sizes and high temperature processes required for high performance.

Cai’s group addressed two key barriers to using wood-derived materials in an electronics setting: surface roughness and thermal expansion. “You don’t want it to expand or shrink too much. Wood is a natural hydroscopic [water-absorbing] material and could attract moisture from the air and expand,” Cai says. “With an epoxy coating on the surface of the CNF, we solved both [problems].”

* In 2007, it was estimated that over 426,000 cell phones (most of them were still functional) and 112,000 computers were discarded every day in the US, totalling 3.2 million tons of electronic waste generated per year, the researcher note in the paper.

Abstract of High-performance green flexible electronics based on biodegradable cellulose nanofibril paper

Today’s consumer electronics, such as cell phones, tablets and other portable electronic devices, are typically made of non-renewable, non-biodegradable, and sometimes potentially toxic (for example, gallium arsenide) materials. These consumer electronics are frequently upgraded or discarded, leading to serious environmental contamination. Thus, electronic systems consisting of renewable and biodegradable materials and minimal amount of potentially toxic materials are desirable. Here we report high-performance flexible microwave and digital electronics that consume the smallest amount of potentially toxic materials on biobased, biodegradable and flexible cellulose nanofibril papers. Furthermore, we demonstrate gallium arsenide microwave devices, the consumer wireless workhorse, in a transferrable thin-film form. Successful fabrication of key electrical components on the flexible cellulose nanofibril paper with comparable performance to their rigid counterparts and clear demonstration of fungal biodegradation of the cellulose-nanofibril-based electronics suggest that it is feasible to fabricate high-performance flexible electronics using ecofriendly materials.

Light electric stimulation of the brain may improve memory for people with schizophrenia

May 29, 2015

Lightly stimulating the brain with transcranial direct current stimulation (tDCS) may improve short-term memory in people with schizophrenia, according to a new study by researchers at the Johns Hopkins University School of Medicine.

The tDCS procedure involves placing sponge-covered electrodes on the head and passing a weak electrical current between them.

David Schretlen, Ph.D., a professor of psychiatry and behavioral sciences at the Johns Hopkins University School of Medicine, reasoned that this type of brain stimulation might ease some of the cognitive difficulties that afflict people with schizophrenia.

A test based on prefrontal cortex stimulation

To test that possibility, Schretlen and Johns Hopkins colleagues targeted a brain region called the left dorsolateral prefrontal cortex, which plays an important role in short-term or working memory and is abnormal in people with schizophrenia, according to Schretlen.

Schretlen recruited 11 participants: five adults with confirmed schizophrenia and six of their close relatives (parents, siblings, and children of people with schizophrenia show some of the same abnormalities to a lesser degree, says Schretlen).

Each participant received two 30-minute treatments — one using a negative electrical charge, which the researchers thought might prove beneficial — and the other using a positive charge as a control. During and after each treatment, participants completed a battery of cognitive tests.

Thinking improvements

There were two notable results:

  • On tests of verbal and visual working memory, participants performed significantly better after receiving a negative charge, and the effects were “surprisingly strong,” says Schretlen.
  • Participants did better at the challenging task of switching between naming categories of items in a supermarket after a negatively charged treatment. The stimulation “was associated with better performance on working memory and subtle changes in word retrieval,” Schretlen says. People with schizophrenia often struggle to find the right words, he says. Because the prefrontal cortex contains a brain region responsible for word retrieval, Schretlen reasoned that transcranial direct current stimulation might help.

Schretlen is now studying transcranial direct current stimulation in a larger sample of patients using repeated sessions of stimulation, which he hopes will induce lasting benefits.

“Cognitive impairment is as ubiquitous as hallucinations in schizophrenia, yet medications only treat the hallucinations,” Schretlen says. “So even with medication, affected individuals often remain very disabled.” His hope is that transcranial direct current stimulation could give people with schizophrenia a shot at leading a more normal life.

Other findings

A related study last year showed that tDCS improved correction of mistakes. But another recent study found that after a repeated IQ test (which is normally expected to show improvements), IQ scores of people who underwent tDCS brain stimulation improved markedly less than did the IQ scores of people in the placebo group.

The tDCS procedure is also being studied by other researchers as a treatment for depression and Alzheimer’s-related memory loss, and to enhance recovery following strokes.

The research is described in a paper published online in Clinical Schizophrenia and Related Psychoses. The study was funded by the Therapeutic Cognitive Neuroscience Professorship; the Therapeutic Cognitive Neuroscience Fund; the Benjamin and Adith Miller Family Endowment on Aging, Alzheimer’s and Autism; and the National Institute on Child and Human Development.

Abstract of Can Transcranial Direct Current Stimulation Improve Cognitive Functioning in Adults with Schizophrenia?

Cognitive impairment is nearly ubiquitous in schizophrenia. First-degree relatives of persons with schizophrenia often show similar but milder deficits. Current methods for the treatment of schizophrenia are often ineffective in cognitive remediation. Since transcranial direct current stimulation (tDCS) can enhance cognitive functioning in healthy adults, it might provide a viable option to enhance cognition in schizophrenia. We sought to explore whether tDCS can be tolerated by persons with schizophrenia and potentially improve their cognitive functioning. We examined the effects of anodal versus cathodal tDCS on working memory and other cognitive tasks in five outpatients with schizophrenia and six first-degree relatives of persons with schizophrenia. Each participant completed tasks thought to be mediated by the prefrontal cortex during two 30-minute sessions of tDCS to the left and right dorsolateral prefrontal cortex (DLPFC). Anodal stimulation over the left DLPFC improved performance relative to cathodal stimulation on measures of working memory and aspects of verbal fluency relevant to word retrieval. The patient group showed differential changes in novel design production without alteration of overall productivity, suggesting that tDCS might be capable of altering selfmonitoring and executive control. All participants tolerated tDCS well. None withdrew from the study or experienced any adverse reaction. We conclude that adults with schizophrenia can tolerate tDCS while engaging in cognitive tasks and that tDCS can alter their performance.

Scientists recover ‘lost’ memories using brain stimulation by blue light

Amnesia is a fixable result of retrieval impairment, not damage
May 29, 2015

MIT researchers have found they were able to reactivate memories in mice that could not otherwise be retrieved, using optogenetics — in which proteins are added to neurons to allow them to be activated with light.

The breakthrough finding, in a paper published Thursday (May 28) in the journal Science, appears to answer a longstanding question in neuroscience regarding amnesia.

Damaged or blocked memory?

Neuroscience researchers have for many years debated whether retrograde amnesia — which follows traumatic injury, stress, or diseases such as Alzheimer’s — is caused by damage to specific brain cells, meaning a memory cannot be stored, or if access to that memory is somehow blocked, preventing its recall.

The answer, according to Susumu Tonegawa, the Picower Professor in MIT’s Department of Biology and director of the RIKEN-MIT Center at the Picower Institute for Learning and Memory: “Amnesia is a problem of retrieval impairment.”

Memory researchers have previously speculated that somewhere in the brain network is a population of neurons that are activated during the process of acquiring a memory, causing enduring physical or chemical changes.

If these groups of neurons are subsequently reactivated by a trigger such as a particular sight or smell, for example, the entire memory is recalled. These neurons are known as “memory engram cells.”

Blocking, then activating memories with light

Until now, no one has been able to show that these groups of neurons undergo enduring chemical changes, in a process known as memory consolidation. One such change, known as “long-term potentiation” (LTP), involves the strengthening of synapses, the structures that allow groups of neurons to send signals to each other, as a result of learning and experience.

To find out if these chemical changes do indeed take place, the researchers first identified a group of engram cells in the hippocampus that, when activated using optogenetic tools, were able to express a memory.

When they then recorded the activity of this particular group of cells, they found that the synapses connecting them had been strengthened. “We were able to demonstrate for the first time that these specific cells — a small group of cells in the hippocampus — had undergone this augmentation of synaptic strength,” Tonegawa says.

The researchers then attempted to discover what happens to memories without this consolidation process. By administering a compound called anisomycin, which blocks protein synthesis within neurons, immediately after mice had formed a new memory, the researchers were able to prevent the synapses from strengthening.

When they returned one day later and attempted to reactivate the memory using an emotional trigger, they could find no trace of it. “So even though the engram cells are there, without protein synthesis those cell synapses are not strengthened, and the memory is lost,” Tonegawa says.

But startlingly, when the researchers then reactivated the protein synthesis-blocked engram cells using optogenetic tools, they found that the mice exhibited all the signs of recalling the memory in full.

“If you test memory recall with natural recall triggers in an anisomycin-treated animal, it will be amnesiac, you cannot induce memory recall,” Tonegawa says. “But if you go directly to the putative engram-bearing cells and activate them with light, you can restore the memory, despite the fact that there has been no LTP.”

Memories are stored in a circuit of groups of cells in multiple brain areas, not synapses

Further studies carried out by Tonegawa’s group demonstrated that memories are stored not in synapses strengthened by protein synthesis in individual engram cells, but in a circuit, or “pathway” of multiple groups of engram cells and the connections between them.

“We are proposing a new concept, in which there is an engram cell ensemble pathway, or circuit, for each memory,” he says. “This circuit encompasses multiple brain areas and the engram cell ensembles in these areas are connected specifically for a particular memory.”

The research dissociates the mechanisms used in memory storage from those of memory retrieval, according to Ryan. “The strengthening of engram synapses is crucial for the brain’s ability to access or retrieve those specific memories, while the connectivity pathways between engram cells allows the encoding and storage of the memory information itself,” he says.

Changes in synaptic strength and in spine properties have long been associated with learning and memory, according to Alcino Silva, director of the Integrative Center for Learning and Memory at the University of California at Los Angeles.

“This groundbreaking paper suggests that these changes may not be as critical for memory as once thought, since under certain conditions, it seems to be possible to disrupt these changes and still preserve memory,” he says. “Instead, it appears that these changes may be needed for memory retrieval, a mysterious process that has so far evaded neuroscientists.”

Abstract of Engram cells retain memory under retrograde amnesia

Memory consolidation is the process by which a newly formed and unstable memory transforms into a stable long-term memory. It is unknown whether the process of memory consolidation occurs exclusively through the stabilization of memory engrams. By using learning-dependent cell labeling, we identified an increase of synaptic strength and dendritic spine density specifically in consolidated memory engram cells. Although these properties are lacking in engram cells under protein synthesis inhibitor–induced amnesia, direct optogenetic activation of these cells results in memory retrieval, and this correlates with retained engram cell–specific connectivity. We propose that a specific pattern of connectivity of engram cells may be crucial for memory information storage and that strengthened synapses in these cells critically contribute to the memory retrieval process.

Opening a new front in the war on cancer

The Great War on Cancer began in 1970, when US President Richard Nixon vowed to spend whatever it took to rid humanity of this most pernicious disease – one which kills by turning the body against itself.

Back then we had already made great strides against the ancient scourges of infectious disease. Antibiotics and vaccines had, in a couple of generations, tamed or even eradicated illnesses such as polio,smallpox and diphtheria. Surely cancer would now go the same way.

Since Nixon made his pledge, the US federal government alone has spent more than $100 billion fighting this menace. With most advanced nations boasting well-funded cancer research programmes, plus the tens of billions spent by private pharmaceutical firms, humanity has thrown the best part of a trillion dollars into the fight. This week we learn of a new front opening up in the war, an elegant treatment that uses a virus to trigger an immune response that destroys the renegade cells of the tumour.

More on this breakthrough below. First, it is important to realise that with some exceptions (childhood leukemia, breast cancer, some brain cancers) the war on cancer has been a dismal failure.

In the US, the death rates for all kinds of cancer dropped by only 5 per cent in the period 1950-2005, according to the National Center for Health Statistics. Even if you strip out confounding variables such as age (more people are living long enough to get cancer) and better diagnosis, the blunt fact is that, with most kinds of cancer, your chances in 2015 are not much better than they were in 1975.

In many cases, your treatment will be pretty much the same. Doctors will use knives to hack the cancer out, hoping they do not leave any bits behind, flood your body with poisons in the hope they will kill the tumour before it (or the poisons) kill you, or blast you with radiation. One eminent oncologist once described modern cancer treatment to me as “medieval barbarism”.

Sometimes this brutality works; but with a whole suite of cancers it usually does not. Get lung, liver, bladder or many kinds of brain cancers then your prognosis is poor. No wonder many doctors privately admit that were they to be diagnosed with some of the most common forms of cancer they would eschew the unpleasant treatments on offer and let the disease take its course, buffering its worst effects with painkillers.

To date, many of the “new” treatments for cancer have consisted of hugely expensive drugs that may prolong the life of sufferers by a few weeks. For example, the drug Abiraterone can both reduce pain and extend the life of men suffering advanced prostate cancer by an average of four months, at a cost of around GBP 3,000 per patient per month.

Many would argue that GBP 12,000 is a small price to pay to give a father and husband an extra 12 weeks with his family, but the reality is that if lots of drugs like this were to become freely available, any universal state-funded health care system would quickly go bankrupt.

So what about the new treatment? More than 400 patients in Britain, the US, Canada and South Africa took part in an international effort to determine the efficacy of using a genetically modified cold sore virus to treat inoperable malignant melanoma, a lethal form of skin cancer.

The viruses were injected into the tumours, where they began a two-pronged attack on the cancer cells. First, they released chemicals that attacked the tumour directly. And secondly, they stimulated a localised immune response that marshalled the body’s own defence system to recognise the cancer as an alien in its midst and launch an attack. The results, published in the Journal of Clinical Onclogy, indicated that the treatment could lengthen survival by years.

Similar immunotherapy treatments are already available – the technology moved from lab to hospitals in the late Nineties, with the FDA approval of Tituximab to treat follicular lymphoma. It is probable that modifying the body’s immune response to enable it to attack tumours in situ may turn out to be a far more effective way of dealing with a disease that will affect one in three of us in our lifetimes.

Still, nearly half a century into the war on cancer, for millions these advances are too little and too late. They demonstrate the sheer complexity of a “disease” which in truth is not a single illness but a whole suite of conditions.

Some scientists say that we need to rethink our whole idea of what cancer is to stand any chance of defeating it properly. At Arizona State University in Phoenix, a small team headed by the British physicist and cosmologist Paul Davies has been tasked with doing just that. “I told them: ‘I’m a cosmologist – I don’t know anything about cancer’,” he said to me after the programme was set up. “They replied, ‘exactly!’?”

This is blue-sky thinking and it is too early to say if it will yield clinical breakthroughs, but the fact that money is being given to people whose job it is to study stars and galaxies to see if they can help fight cancer shows just how far we have to go till the battle is won.

Man-made virus can ‘cure’ skin cancer


Man-made virus can 'cure' skin cancer
A skin lesion, diagnosed as a melanoma, in a file photo.

HO-University of Pittsburgh Department of Dermatology / THE CANADIAN PRESS



A genetically engineered virus has been shown to “cure” patients of skin cancer, raising hopes of an end to chemotherapy.

In a worldwide study led by The Institute of Cancer Research in the UK, scientists showed that the new treatment allowed some patients with melanoma to live for more than three years – the benchmark many oncologists use to define a cure.

The therapy, called T-VEC, works by infecting and killing cancer cells while also kicking the immune system into action against tumours.

Charities said the development was exciting and offered new hope to many patients. “Patients showing responses beyond three years is something that up until now, we could only have imagined,” said Gillian Nuttall, the founder of Melanoma UK.

Malignant melanoma is the fifth most common cancer in the UK, with more than 13,000 cases diagnosed each year. It kills more than 2,000 people each year.

Prof Paul Workman, the chief executive of The Institute of Cancer Research, London, said: “We may normally think of viruses as the enemies of mankind, but it’s their very ability to specifically infect and kill human cells that can make them such promising cancer treatments.

“In this case, we are harnessing the ability of an engineered virus to kill cancer cells and stimulate an immune response.”

The clinical trials, which have been ongoing for more than three years, have been conducted in 64 centres across the UK, US, Canada and South Africa.

The results show that 163 patients with stage-three and early stage-four melanoma who were treated with T-VEC lived for an average of 41 months.

That was compared with an average survival of 21.5 months for the patients who were given the current best immunotherapy drugs.

The response was most pronounced in patients with less advanced cancers, underlining the potential benefit as a first-line treatment for metastatic cancers, which have spread to other parts of the body and cannot be surgically removed.

T-VEC is a modified form of herpes virus which multiplies inside cancer cells and bursts them from within. It has been genetically engineered to produce a molecule called GM-CSF, which stimulates the immune system to attack and destroy the tumour.

It has also been modified to remove two key genes so that it cannot replicate within healthy cells. Normal cells detect and destroy T-VEC before it can cause damage, but it replicates easily in cancer cells because their infection defences are compromised by genetic errors. It is one of a new wave of virus-based drugs to show benefits in cancer trials, and is now the first to do so in a major randomised, controlled phase III trial.

“There is increasing excitement over the use of viral treatments like T-VEC for cancer, because they can launch a two-pronged attack on tumours – both killing cancer cells directly and marshalling the immune system against them,” said Prof Kevin Harrington, professor of biological cancer therapies at The Institute of Cancer Research.

“Because viral treatment can target cancer cells specifically, it tends to have fewer side-effects than traditional chemotherapy or some of the other new immunotherapies.”

Dr Hayley Frend, the science information manager at Cancer Research UK, said: “Using a virus to both kill cancer cells and nudge the immune system into attacking them is exciting.

“Previous studies have shown T-VEC could benefit some people with advanced skin cancer but this is the first study to prove an increase in survival. The next step will be to understand why only some patients respond to T-VEC, in order to help better identify which patients might benefit from it.”

The research was also welcomed by British academics. Prof Leonard Seymour, professor of gene therapies at the University of Oxford, said: “This T-VEC study shows powerful stimulus of an anti-cancer immune response in patients with melanoma skin cancer.

“Increasingly, we understand that cancer is characterised by suppression of the immune system within tumour deposits, meaning that cancer vaccines have struggled to create useful responses. However, T-VEC appears to be able to overcome this suppression. At this stage it’s very promising that this appears to have positive results for melanoma skin cancer.”

Muzlifah Haniff, senior lecturer and honorary consultant dermatologist atNewcastle University, added: “This study reports another treatment strategy based on harnessing the power of our immune system to destroy melanoma, offering new hope to many patients.”

The trial was funded by the manufacturer of T-VEC, Amgen, and is published in theJournal of Clinical Oncology.

Chemists’ Discovery Could Lead To Greatly Improved Energy Storage

The key lies in Nazar's group discovery of the so-called proton phase transfer catalyst. By isolating its role in the battery's discharge and recharge reactions, Nazar and colleagues were not only able to boost the battery's capacity, they achieved a near-perfect recharge of the cell. When the researchers eliminated the catalyst from the system, they found the battery no longer worked. Unlike the traditional solid-state battery design, a metal-oxygen battery uses a gas cathode that takes oxygen and combines it with a metal such as sodium or lithium to form a metal oxide, storing electrons in the process. Applying an electric current reverses the reaction and reverts the metal to its original form. (Image: University of Waterloo)
The key lies in Nazar’s group discovery of the so-called proton phase transfer catalyst. By isolating its role in the battery’s discharge and recharge reactions, Nazar and colleagues were not only able to boost the battery’s capacity, they achieved a near-perfect recharge of the cell. When the researchers eliminated the catalyst from the system, they found the battery no longer worked. Unlike the traditional solid-state battery design, a metal-oxygen battery uses a gas cathode that takes oxygen and combines it with a metal such as sodium or lithium to form a metal oxide, storing electrons in the process. Applying an electric current reverses the reaction and reverts the metal to its original form. (Image: University of Waterloo)

Canadian researchers this week announced the discovery of a battery reaction that could pave the way for the “holy grail of electrochemical energy storage.”

Chemists from the University of Waterloo successfully isolated a substance called the proton phase transfer catalyst, which allowed them to increase the capacity of a sodium-oxygen battery as well as achieve a near-perfect battery recharge.

The researchers said that the same process could eventually be used for lithium-oxygen batteries, potentially resolving the cost and size constraints of the lithium-ion batteries currently used to power everything from cell phones to electric cars.

Lithium-oxygen reactions are too unstable to generate sufficiently long battery life, but the Waterloo scientists said they’re investigating redox mediators in order to enable more efficient charging.

The research, published in the journal Nature Chemistry, could also offer additional applications for sodium-oxygen batteries, which hold less energy than their lithium counterparts but are cheap enough for large-scale storage.

“Our new understanding brings together a lot of different, disconnected bits of a puzzle that have allowed us to assemble the full picture,” Chemistry Professor Linda Nazar said. “These findings will change the way we think about non-aqueous metal-oxygen batteries.”