Antibiotic Resistance Could Spell End Of Modern Medicine, Says Chief Medic.

England’s chief medical officer has repeated her warning of a “post-antibiotic apocalypse” as she urged world leaders to address the growing threat of antibiotic resistance.

Prof Dame Sally Davies said that if antibiotics lose their effectiveness it would spell “the end of modern medicine”. Without the drugs used to fight infections, common medical interventions such as caesarean sections, cancer treatments and hip replacements would become incredibly risky and transplant medicine would be a thing of the past, she said.

“We really are facing – if we don’t take action now – a dreadful post-antibiotic apocalypse. I don’t want to say to my children that I didn’t do my best to protect them and their children,” Davies said.

Health experts have previously said resistance to antimicrobial drugs could cause a bigger threat to mankind than cancer. In recent years, the UK has led a drive to raise global awareness of the threat posed to modern medicine by antimicrobial resistance (AMR).

Each year about 700,000 people around the world die due to drug-resistant infections including tuberculosis, HIV and malaria. If no action is taken, it has been estimated that drug-resistant infections will kill 10 million people a year by 2050.

The UK government and the Wellcome Trust, along with others, have organised a call to action meeting for health officials from around the world. At the meeting in Berlin, the government will announce a new project that will map the spread of death and disease caused by drug-resistant superbugs.

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England’s chief medical officer has renewed her warning about what she’s described as a “post-antibiotic apocalypse” #r4todaypic.twitter.com/3EAUvmOTAv

October 13, 2017

Davies said: “This AMR is with us now, killing people. This is a serious issue that is with us now, causing deaths. If it was anything else, people would be up in arms about it. But because it is hidden they just let it pass.

“It does not really have a ‘face’ because most people who die of drug-resistant infections, their families just think they died of an uncontrolled infection. It will only get worse unless we take strong action everywhere across the globe. We need some real work on the ground to make a difference or we risk the end of modern medicine.”

She added: “Not to be able to effectively treat infections means that caesarean sections, hip replacements, modern surgery, is risky. Modern cancer treatment is risky and transplant medicine becomes a thing of the past.”

Davies said that if the global community did not act then the progress that had been made in Britain may be undermined.

She estimated that about one in three or one in four prescriptions in UK primary care were probably not needed. “But other countries use vastly more antibiotics in the community and they need to start doing as we are, which is reducing usage,” she said. “Our latest data shows that we have reduced human consumption by 4.3% in 2014-15 from the year before.”

DNA Surgery on Embryos Removes Disease

Original Article

By James Gallagher

Precise “chemical surgery” has been performed on human embryos to remove disease in a world first, Chinese researchers have told the BBC.

The team at Sun Yat-sen University used a technique called base editing to correct a single error out of the three billion “letters” of our genetic code.

They altered lab-made embryos to remove the disease beta-thalassemia. The embryos were not implanted.

The team says the approach may one day treat a range of inherited diseases.

Base editing alters the fundamental building blocks of DNA: the four bases adenine, cytosine, guanine and thymine.

They are commonly known by their respective letters, A, C, G and T.

All the instructions for building and running the human body are encoded in combinations of those four bases.

DNAImage copyrightGETTY IMAGES

The potentially life-threatening blood disorder beta-thalassemia is caused by a change to a single base in the genetic code – known as a point mutation.

The team in China edited it back.

They scanned DNA for the error then converted a G to an A, correcting the fault.

Junjiu Huang, one of the researchers, told the BBC News website: “We are the first to demonstrate the feasibility of curing genetic disease in human embryos by base editor system.”

He said their study opens new avenues for treating patients and preventing babies being born with beta-thalassemia, “and even other inherited diseases”.

The experiments were performed in tissues taken from a patient with the blood disorder and in human embryos made through cloning.

Genetics revolution

Base editing is an advance on a form of gene-editing known as Crispr, that is already revolutionising science.

Crispr breaks DNA. When the body tries to repair the break, it deactivates a set of instructions called a gene. It is also an opportunity to insert new genetic information.

Base editing works on the DNA bases themselves to convert one into another.

Prof David Liu, who pioneered base editing at Harvard University, describes the approach as “chemical surgery”.

He says the technique is more efficient and has fewer unwanted side-effects than Crispr.

He told the BBC: “About two-thirds of known human genetic variants associated with disease are point mutations.

“So base editing has the potential to directly correct, or reproduce for research purposes, many pathogenic [mutations].”

EmbryoImage copyrightGETTY IMAGES

The research group at Sun Yat-sen University in Guangzhou hit the headlines before when they were the first to use Crispr on human embryos.

Prof Robin Lovell-Badge, from the Francis Crick Institute in London, described parts of their latest study as “ingenious”.

But he also questioned why they did not do more animal research before jumping to human embryos and said the rules on embryo research in other countries would have been “more exacting”.

The study, published in Protein and Cell, is the latest example of the rapidly growing ability of scientists to manipulate human DNA.

It is provoking deep ethical and societal debate about what is and is not acceptable in efforts to prevent disease.

Prof Lovell-Badge said these approaches are unlikely to be used clinically anytime soon.

“There would need to be far more debate, covering the ethics, and how these approaches should be regulated.

“And in many countries, including China, there needs to be more robust mechanisms established for regulation, oversight, and long-term follow-up.”

New Antibody Attacks 99% of HIV Strains

Original Article

By James Gallagher

HIVImage copyright SPL

Scientists have engineered an antibody that attacks 99% of HIV strains and can prevent infection in primates.

It is built to attack three critical parts of the virus – making it harder for HIV to resist its effects.

The work is a collaboration between the US National Institutes of Health and the pharmaceutical company Sanofi.

The International Aids Society said it was an “exciting breakthrough”. Human trials will start in 2018 to see if it can prevent or treat infection.

Our bodies struggle to fight HIV because of the virus’ incredible ability to mutate and change its appearance.

These varieties of HIV – or strains – in a single patient are comparable to those of influenza during a worldwide flu season.

So the immune system finds itself in a fight against an insurmountable number of strains of HIV.

Super-antibodies

But after years of infection, a small number of patients develop powerful weapons called “broadly neutralising antibodies” that attack something fundamental to HIV and can kill large swathes of HIV strains.

Researchers have been trying to use broadly neutralising antibodies as a way to treat HIV, or prevent infection in the first place.

The study, published in the journal Science, combines three such antibodies into an even more powerful “tri-specific antibody”.

Dr Gary Nabel, the chief scientific officer at Sanofi and one of the report authors, told the BBC News website: “They are more potent and have greater breadth than any single naturally occurring antibody that’s been discovered.”

The best naturally occurring antibodies will target 90% of HIV strains.

“We’re getting 99% coverage, and getting coverage at very low concentrations of the antibody,” said Dr Nabel.

Experiments on 24 monkeys showed none of those given the tri-specific antibody developed an infection when they were later injected with the virus.

Dr Nabel said: “It was quite an impressive degree of protection.”

The work included scientists at Harvard Medical School, The Scripps Research Institute, and the Massachusetts Institute of Technology.

‘Exciting’

Clinical trials to test the antibody in people will start next year.

Prof Linda-Gail Bekker, the president of the International Aids Society, told the BBC: “This paper reports an exciting breakthrough.

“These super-engineered antibodies seem to go beyond the natural and could have more applications than we have imagined to date.

“It’s early days yet, and as a scientist I look forward to seeing the first trials get off the ground in 2018.

“As a doctor in Africa, I feel the urgency to confirm these findings in humans as soon as possible.”

Dr Anthony Fauci, the director of the US National Institute of Allergy and Infectious Diseases, said it was an intriguing approach.

He added: “Combinations of antibodies that each bind to a distinct site on HIV may best overcome the defences of the virus in the effort to achieve effective antibody-based treatment and prevention.”

Poliovirus Kills Off Cancer Cells Stops Tumor Regrowth

Original Article

By Ana Sandoiu

Researchers from Duke University in Durham, NC, may have discovered a new way of killing off cancer cells.

The team was jointly led by Dr. Matthias Gromeier, a professor in the Department of Neurosurgery, and Prof. Smita Nair, who is an immunologist in the Department of Surgery.

The new research – which is published in the journal Science Translational Medicine – shows how a modified poliovirus enables the body to use its own resources to fight off cancer. The modified virus bears the name of recombinant oncolytic poliovirus (PVS-RIPO).

PVS-RIPO has been in clinical trials since 2011 and preliminary results have offered hope to patients with one of the most aggressive forms of brain tumor: recurrent glioblastoma. So, the researchers set out to investigate more deeply how exactly PVS-RIPO works.

Explaining the rationale behind their research endeavor, Dr. Gromeier says, “Knowing the steps that occur to generate an immune response will enable us to rationally decide whether and what other therapies make sense in combination with poliovirus to improve patient survival.”

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Poliovirus attacks tumors, inhibits regrowth

The researchers examined the behavior of the poliovirus in two human cell lines: melanomaand triple-negative breast cancer. They observed that the poliovirus attaches itself to cancerous cells. These cells have an excess of the CD155 protein, which acts as a receptor for the poliovirus.

Then, the poliovirus starts to attack the malignant cells, triggering the release of antigens from the tumorAntigens are toxic substances that the body does not recognize, therefore setting off an immune attack against them.

So, when the tumor cells release antigens, this alerts the body’s immune system to start attacking. At the same time, the poliovirus infects the dendritic cells and macrophages.

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Dendritic cells are cells whose role it is to process antigens and “present” them to T cells, which are a type of immune cell. Macrophages are another type of immune cell – namely, large white blood cells whose main role is to rid our bodies of debris and toxic substances.

The cell culture results – which the researchers then verified in mouse models – showed that once PVS-RIPO infects the dendritic cells, these cells “tell” T cells to start the immune attack.

Once started, this process seems to be continuously successful. The cancer cells continue to be vulnerable to the immune system’s attack over a longer period of time, which appears to stop the tumor from regrowing.

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As Prof. Nair explains, “Not only is poliovirus killing tumor cells, it is also infecting the antigen-presenting cells, which allows them to function in such a way that they can now raise a T cell response that can recognize and infiltrate a tumor.”

“This is an encouraging finding, because it means the poliovirus stimulates an innate inflammatory response.”

Prof. Smita Nair

Speaking to Medical News Today about the clinical implications of the findings and the scientists’ directions for future research, Dr. Gromeier said, “Our findings provide clear rationales for moving forward with clinical trials in breast cancer, prostate cancer, and malignant melanoma.”

“This includes novel combination treatments that we will pursue,” he added.

More specifically, he explains, because the study revealed that after treatment with the poliovirus “immune checkpoints are increased on immune cells,” a future strategy the researchers plan to explore is “[oncolytic] poliovirus combined with immune checkpoint blockade.”

Studies of Pregnant Mice Highlight Link Between Immune Response and Autism

Original Article

A century ago, a largely forgotten, worldwide epidemic that would kill nearly a million people was beginning to take hold. Labelled as sleepy sickness — or more properly encephalitis lethargica — the disease caused a number of bizarre mental and physical symptoms and frequently left people in a catatonic state, sometimes for decades. (Oliver Sacks described his successful treatment of some of them in 1969, in the book Awakenings.) The cause has never been officially pinned down, but the most common suggestion is that some kind of infectious agent triggered an autoimmune response, which targeted and inflamed part of the brain.

The role of the immune system in mental disorders is subject to much important research at the moment. The onset of conditions from depression and psychosis to obsessive–compulsive disorder has been linked to the abrupt changes in biology and physiology that occur when the body responds to infection, especially in childhood. And some researchers have traced the possible chain of events back a generation. Studies have highlighted that pregnant women could react to infection in a way that influences their baby’s developing brain, which could lead to cognitive and neurodevelopmental problems in the child.

One consequence of this ‘maternal immune activation’ (MIA) in some women could be to increase the risk of autism in their children. And two papers published online this week in Nature (S. Kim et alNaturehttp://dx.doi.org/10.1038/nature23910; 2017 and Y. S. Yim et al. Naturehttp://dx.doi.org/10.1038/nature23909; 2017) use animal models to examine how this might happen, as well as suggest some possible strategies to reduce the risk.

Kim et al. looked at the impact of MIA on the brains and behaviour of mice. They found that pregnant female animals exposed to circumstances similar to a viral infection have offspring that are more likely to show atypical behaviour, and they unpick some of the cellular and molecular mechanisms responsible. Some of their results confirm what scientists already suspected: pregnancy changes the female mouse’s immune response, specifically, by turning on the production of a protein called interleukin-17a. But the authors also conducted further experiments that give clues about the mechanisms at work.

“It’s tempting to draw parallels with mechanisms that might increase the risk of autism in some people.”

The types of bacteria in the mouse’s gut seem to be important. When the scientists used antibiotics to wipe out common gut microorganisms called segmented filamentous bacteria in female mice, this seemed to protect the animals’ babies from the impact of the simulated infection. The offspring of mice given the antibiotic treatment did not show the unusual behaviours, such as reduced sociability and repetitive actions. Segmented filamentous bacteria are known to encourage cells to produce more interleukin-17a, and an accompanying News & Views article (C. M. Powell Nature http://dx.doi.org/10.1038/nature24139; 2017) discusses one obvious implication: some pregnant women could use diet or drugs to manipulate their gut micro­biome to reduce the risk of harm to their baby if an infection triggers their immune response. Much science still needs to be done before such a course could be recommended — not least further research to confirm and build on these results.

Yim et al. analysed the developing brain of mice born to mothers who showed MIA. They traced the abnormalities to a region called the dysgranular zone of the primary somato-sensory cortex (S1DZ). The authors genetically engineered the mice so that neurons in this region could be activated by light, and they showed that activation of S1DZ induced the same telltale atypical behaviours, even in mice that were born to mothers with no MIA.

It’s unusual to be able to demonstrate such a direct link between the activities of brain regions and specific behaviours — although plenty of work on mental disorders makes a strong theoretical case for linking particular conditions to over- and under-active brain zones and circuitry.

Encephalitis lethargica, for example, has been linked to changes in the deep regions of the basal ganglia, and the disease produces symptoms that are similar to those often seen in autism, including stereotyped and repetitive behaviours. Yim et al.’s study shows that the S1DZ region projects to one of those deep brain regions — the striatum — and that this connection helps to trigger repetitive actions in the animals. But S1DZ also connects to a separate, distinct, region in the cortex, and this is what seems to drive the changes in sociability.

Taking the two studies together, it’s tempting to draw parallels with mechanisms that might increase the risk of autism in some people and explain some of its symptoms. Scientists and others should be cautious about doing so — much can change when results from animal models are applied to human biology. But the studies do offer some intriguing leads.

‘The Orion Bionic Eye’ To Begin Huma Trails. Hopes To Restore Sight of Blind Patients

Original Article

American medical company, ‘Second Sight’ manufacture implantable visual prosthetics to provide vision to people that suffer from a variety of different visual impairments. Their most advanced piece of technology so far is ‘The Argus® II Retinal Prosthesis System’ that can restore some functional vision for people suffering from blindness. Although a very successful product, it only provides a limited about of restored vision to the patient, so the company have been working on it’s successor, ‘The Orion’.

The Argus® II Retinal Prosthesis System

The Orion™ Cortical Visual Prosthesis System

The idea behind The Orion is to convert images captured by a small video camera mounted on a pair of glasses that the patient wears daily, these images are then converted into a series of small electrical impulses.

The Orion would then wirelessly transmit these pulses to an array of electrodes that have been implanted into the patient. The electrodes bypass the retina and optic nerve to directly stimulate the visual cortex. This is the area of the brain that processes visual data, effectively allowing a person to see.

This technology has the potential to essential “cure” all forms of blindness including glaucoma, diabetic retinopathy, and forms of cancer and trauma. The Argus II had been approved for use in Canada, France, Germany, Italy, Russia, Saudi Arabia, South Korea, Spain, Taiwan, Turkey, United Kingdom, and the U.S., so you can expect to see The Orion in the same, if not more countries.

Second Sight’s Argus II Restores Vision to Blind Patient