No more sweet tooth? Scientists switch off pleasure from food in brains of mice


Altering activity in brain’s emotion center can eliminate the natural craving for sweet; findings could inform treatments for eating disorders

New research in mice has revealed that the brain’s underlying desire for sweet, and its distaste for bitter, can be erased by manipulating neurons in the amygdala, the emotion center of the brain. The research points to new strategies for understanding and treating eating disorders including obesity and anorexia nervosa.

Brain illustration

New research in mice has revealed that the brain’s underlying desire for sweet, and its distaste for bitter, can be erased by manipulating neurons in the amygdala, the emotion center of the brain.

The study showed that removing an animal’s capacity to crave or despise a taste had no impact on its ability to identify it. The findings suggest that the brain’s complex taste system — which produces an array of thoughts, memories and emotions when tasting food — are actually discrete units that can be individually isolated, modified or removed all together. The research points to new strategies for understanding and treating eating disorders including obesity and anorexia nervosa.

The research was published today in Nature.

“When our brain senses a taste it not only identifies its quality, it choreographs a wonderful symphony of neuronal signals that link that experience to its context, hedonic value, memories, emotions and the other senses, to produce a coherent response,” said Charles S. Zuker, PhD, a principal investigator at Columbia’s Mortimer B. Zuckerman Mind Brain Behavior Institute and the paper’s senior author.

Today’s study builds upon earlier work by Dr. Zuker and his team to map the brain’s taste system. Previously, the researchers revealed that when the tongue encounters one of the five tastes — sweet, bitter, salty, sour or umami — specialized cells on the tongue send signals to specialized regions of the brain so as to identify the taste, and trigger the appropriate actions and behaviors.

To shed light on that experience, the scientists focused on sweet and bitter taste and the amygdala, a brain region known to be important for making value judgments about sensory information. Previous research by Dr. Zuker, a professor of biochemistry and molecular biophysics and of neuroscience and a Howard Hughes Medical Institute Investigator at Columbia University Irving Medical Center, and others showed that the amygdala connects directly to the taste cortex.

“Our earlier work revealed a clear divide between the sweet and bitter regions of the taste cortex,” said Li Wang, PhD, a postdoctoral research scientist in the Zuker lab and the paper’s first author. “This new study showed that same division continued all the way into the amygdala. This segregation between sweet and bitter regions in both the taste cortex and amygdala meant we could independently manipulate these brain regions and monitor any resulting changes in behavior.”

The scientists performed several experiments in which the sweet or bitter connections to the amygdala were artificially switched on, like flicking a series of light switches. When the sweet connections were turned on, the animals responded to water just as if it were sugar. And by manipulating the same types of connections, the researchers could even change the perceived quality of a taste, turning sweet into an aversive taste, or bitter into an attractive one.

In contrast, when the researchers instead turned off the amygdala connections but left the taste cortex untouched, the mice could still recognize and distinguish sweet from bitter, but now lacked the basic emotional reactions, like preference for sugar or aversion to bitter.

“It would be like taking a bite of your favorite chocolate cake but not deriving any enjoyment from doing so,” said Dr. Wang. “After a few bites, you may stop eating, whereas otherwise you would have scarfed it down.”

Usually, the identity of a food and the pleasure one feels when eating it are intertwined. But the researchers showed that these components can be isolated from each other, and then manipulated separately. This suggests that the amygdala could be a promising area of focus when looking for strategies to treat eating disorders.

In the immediate future, Drs. Zuker and Wang are investigating additional brain regions that serve critical roles in the taste system. For example, the taste cortex also links directly to regions involved in motor actions, learning and memory.

“Our goal is to piece together how those regions add meaning and context to taste,” said Dr. Wang. “We hope our investigations will help to decipher how the brain processes sensory information and brings richness to our sensory experiences.”

For all book lovers please visit my friend’s website.
URL: http://www.romancewithbooks.com

Diet may influence the spread of a deadly type of breast cancer, study finds


Diet may influence the spread of a deadly type of breast cancer, study finds
Three-dimensional cell culture of breast cancer cells.

A single protein building block commonly found in food may hold a key to preventing the spread of an often-deadly type of breast cancer, according to a new multicenter study published today in the medical journal Nature.

Investigators found that by limiting an amino acid called asparagine in laboratory mice with triple-negative breast cancer, they could dramatically reduce the ability of the cancer to travel to distant sites in the body. Among other techniques, the team used dietary restrictions to limit asparagine.

Foods rich in asparagine include dairy, whey, beef, poultry, eggs, fish, seafood, asparagus, potatoes, legumes, nuts, seeds, soy and whole grains. Foods low in asparagine include most fruits and vegetables.

“Our study adds to a growing body of evidence that suggests diet can influence the course of the disease,” said Simon Knott, PhD, associate director of the Center for Bioinformatics and Functional Genomics at Cedars-Sinai and one of two first authors of the study. The research was conducted at more than a dozen institutions.

If further research confirms the findings in human cells, limiting the amount of asparagine cancer patients ingest could be a potential strategy to augment existing therapies and to prevent the spread of breast cancer, Knott added.

The researchers studied triple-negative breast cancer cells, which grow and spread faster than most other types of cancer cells. It is called triple negative because it lacks receptors for the hormones estrogen and progesterone and makes little of a protein called HER2. As a result, it resists common treatments—which target these factors and has a higher-than-average mortality rate.

Research from past studies found that most tumor cells remain in the primary breast site, but a subset of cells leaves the breast and enters the bloodstream. Those cells colonize in the lungs, brain and liver, where they proliferate. The study team wanted to understand the particular traits of the tumor cells circulating in the blood and in the sites where the cancer has spread.

The researchers discovered that the appearance of asparagine synthetase—the enzyme cells used to make asparagine—in a primary tumor was strongly associated with later cancer spread.

The researchers also found that metastasis was greatly limited by reducing asparagine synthetase, treatment with the chemotherapy drug L-asparaginase, or dietary restriction. When the lab mice were given food rich in asparagine, the cancer cells spread more rapidly.

“The study results are extremely suggestive that changes in diet might impact both how an individual responds to primary therapy and their chances of lethal disease spreading later in life,” said the study’s senior author, Gregory J. Hannon, PhD, professor of Cancer Molecular Biology and director, Cancer Research UK Cambridge Institute, University of Cambridge in England.

Investigators now are considering conducting an early-phase clinical trial in which healthy participants would consume a low-asparagine diet. If the diet results in decreased levels of asparagine, the next scientific step would involve a clinical trial with cancer patients. That trial likely would employ dietary restrictions as well as chemotherapy and immunotherapy, Knott said.

Studying the effects of asparagine also could alter treatments for other types of cancer, investigators say.

“This study may have implications not only for breast cancer, but for many metastatic cancers,” said Ravi Thadhani, MD, MPH, vice dean, Research and Graduate Research Education, at Cedars-Sinai.

New genetic clues for arthritis


Arthritic hands

 

Current treatments relieve the symptoms but not for all patients, and there is no cure

An international team of researchers has found more than 40 new areas in DNA that increase the risk of rheumatoid arthritis.

The work is the largest genetic study ever carried out, involving nearly 30,000 patients.

The investigators believe new drugs could be developed to target these areas that could one day provide a cure for the disease.

The findings are published in the Journal Nature.

“Start Quote

What this offers in the future is an opportunity to use genetics to discover new medicines for complex diseases like rheumatoid arthritis and to treat or even cure the disease”

Prof Robert PlengeHarvard Medical School

The research team compared the DNA of arthritis patients with those without the disease and found 42 ‘faulty’ areas that were linked with the disease. The hope is that drugs can be developed to compensate for these faults.

The lead researcher Professor Robert Plenge of Harvard Medical School found that one of these areas produced a weakness that was treated by an existing drug that was developed by trial and error, rather than specifically made to correct the genetic problem.

This finding, he says, shows such discoveries could be used to design new drugs.

“What this offers in the future is an opportunity to use genetics to discover new medicines for complex diseases like rheumatoid arthritis to treat or even cure the disease,” he said.

Complex diseases

Some have argued identifying genetic weak areas for complex diseases – known as single nucleotide polymorphisms (SNPs) – is not useful. There is little or no evidence, they argue, that “silencing the SNPs” with drugs will relieve any symptoms.

But Dr Plenge says the fact that he has found an established drug that treats the symptoms that arise from a particular SNP for rheumatoid arthritis validates this genetic approach.

“Start Quote

There are already therapies that have been designed in the cancer field that might open up new opportunities for retargeting drugs”

Prof Jane WorthingtonDirector, Centre for Genetics

“It offers tremendous potential. This approach could be used to identify drug targets for complex diseases, nut just rheumatoid arthritis, but diabetes, Alzheimer’s and coronary heart disease”

Fast track

The study also found SNPs in the rheumatoid arthritis patients that also occur in patients with types of blood cancer.

According to Prof Jane Worthington, director of the centre for genetics in Manchester, this observation suggests that drugs that are being used to treat the cancer could be effective against rheumatoid arthritis and so should be fast tracked into clinical trials.

“There are already therapies that have been designed in the cancer field that might open up new opportunities for retargeting drugs,” she told BBC News.

“It might allow us a straightforward way to add therapies we have to treat patients with rheumatoid arthritis”.

Nobel winner declares boycott of top science journals.


  • Randy Schekman
Randy Schekman, centre, at a Nobel prize ceremony in Stockholm. Photograph: Rob Schoenbaum/Zuma Press/Corbis

Leading academic journals are distorting the scientific process and represent a “tyranny” that must be broken, according to a Nobel prize winner who has declared a boycott on the publications.

Randy Schekman, a US biologist who won the Nobel prize in physiology or medicine this year and receives his prize in Stockholm on Tuesday, said his lab would no longer send research papers to the top-tier journals, Nature, Cell and Science.

Schekman said pressure to publish in “luxury” journals encouraged researchers to cut corners and pursue trendy fields of science instead of doing more important work. The problem was exacerbated, he said, by editors who were not active scientists but professionals who favoured studies that were likely to make a splash.

The prestige of appearing in the major journals has led the Chinese Academy of Sciences to pay successful authors the equivalent of $30,000 (£18,000). Some researchers made half of their income through such “bribes”, Schekman said in an interview.

Writing in the Guardian, Schekman raises serious concerns over the journals’ practices and calls on others in the scientific community to take action.

“I have published in the big brands, including papers that won me a Nobel prize. But no longer,” he writes. “Just as Wall Street needs to break the hold of bonus culture, so science must break the tyranny of the luxury journals.”

Schekman is the editor of eLife, an online journal set up by the Wellcome Trust. Articles submitted to the journal – a competitor to Nature, Cell and Science – are discussed by reviewers who are working scientists and accepted if all agree. The papers are free for anyone to read.

Schekman criticises Nature, Cell and Science for artificially restricting the number of papers they accept, a policy he says stokes demand “like fashion designers who create limited-edition handbags.” He also attacks a widespread metric called an “impact factor”, used by many top-tier journals in their marketing.

A journal’s impact factor is a measure of how often its papers are cited, and is used as a proxy for quality. But Schekman said it was “toxic influence” on science that “introduced a distortion”. He writes: “A paper can become highly cited because it is good science – or because it is eye-catching, provocative, or wrong.”

Daniel Sirkis, a postdoc in Schekman’s lab, said many scientists wasted a lot of time trying to get their work into Cell, Science and Nature. “It’s true I could have a harder time getting my foot in the door of certain elite institutions without papers in these journals during my postdoc, but I don’t think I’d want to do science at a place that had this as one of their most important criteria for hiring anyway,” he told the Guardian.

Sebastian Springer, a biochemist at Jacobs University in Bremen, who worked with Schekman at the University of California, Berkeley, said he agreed there were major problems in scientific publishing, but no better model yet existed. “The system is not meritocratic. You don’t necessarily see the best papers published in those journals. The editors are not professional scientists, they are journalists which isn’t necessarily the greatest problem, but they emphasise novelty over solid work,” he said.

Springer said it was not enough for individual scientists to take a stand. Scientists are hired and awarded grants and fellowships on the basis of which journals they publish in. “The hiring committees all around the world need to acknowledge this issue,” he said.

Philip Campbell, editor-in-chief at Nature, said the journal had worked with the scientific community for more than 140 years and the support it had from authors and reviewers was validation that it served their needs.

“We select research for publication in Nature on the basis of scientific significance. That in turn may lead to citation impact and media coverage, but Nature editors aren’t driven by those considerations, and couldn’t predict them even if they wished to do so,” he said.

“The research community tends towards an over-reliance in assessing research by the journal in which it appears, or the impact factor of that journal. In a survey Nature Publishing Group conducted this year of over 20,000 scientists, the three most important factors in choosing a journal to submit to were: the reputation of the journal; the relevance of the journal content to their discipline; and the journal’s impact factor. My colleagues and I have expressed concerns about over-reliance on impact factors many times over the years, both in the pages of Nature and elsewhere.”

Monica Bradford, executive editor at Science, said: “We have a large circulation and printing additional papers has a real economic cost … Our editorial staff is dedicated to ensuring a thorough and professional peer review upon which they determine which papers to select for inclusion in our journal. There is nothing artificial about the acceptance rate. It reflects the scope and mission of our journal.”

Emilie Marcus, editor of Cell, said: “Since its launch nearly 40 years ago, Cell has focused on providing strong editorial vision, best-in-class author service with informed and responsive professional editors, rapid and rigorous peer-review from leading academic researchers, and sophisticated production quality. Cell’s raison d’etre is to serve science and scientists and if we fail to offer value for both our authors and readers, the journal will not flourish; for us doing so is a founding principle, not a luxury.”

• This article was amended on 10 December 2013 to include a response from Cell editor Emilie Marcus, which arrived after the initial publication deadline.

Brain may play key role in blood sugar metabolism and diabetes development.


A growing body of evidence suggests that the brain plays a key role in glucose regulation and the development of type 2 diabetes, researchers write in the Nov. 7 ssue of the journal Nature. If the hypothesis is correct, it may open the door to entirely new ways to prevent and treat this disease, which is projected to affect one in three adults in the United States by 2050.

In the paper, lead author Dr. Michael W. Schwartz, UW professor of medicine and director of the Diabetes and Obesity Center of Excellence, and his colleagues from the universities of Cincinnati, Michigan, and Munich,  note that the brain was originally thought to play an important role in maintaining normal glucose metabolism  With the discovery of insulin in the 1920s, the focus of research and diabetes care shifted to almost exclusively to insulin. Today, almost all treatments for diabetes seek to either increase insulin levels or increase the body’s sensitivity to insulin.

“These drugs,” the researchers write, “enjoy wide use and are effective in controlling hyperglycemia [high blood sugar levels], the hallmark of type 2 diabetes, but they address the consequence of diabetes more than the underlying causes, and thus control rather than cure the disease.”

New research, they write, suggests that normal glucose regulation depends on a partnership between the insulin-producing cells of the pancreas, the pancreatic islet cells, and neuronal circuits in the hypothalamus and other brain areas that are intimately involved in maintaining normal glucose levels. The development of diabetes type 2, the authors argue, requires a failure of both the islet-cell system and this brain-centered system for regulating blood sugar levels .

In their paper, the researchers review both animal and human studies that indicate the powerful effect this brain-centered regulatory system has on blood glucose levels independent of the action of insulin. One such mechanism by which the system promotes glucose uptake by tissues is by stimulating what is called “glucose effectiveness.” As this process accounts for almost 50 percent of normal glucose uptake, it rivals the impact of insulin-dependent mechanisms driven by the islet cells in the pancreas.

The findings lead the researchers to propose a two-system model of regulating blood sugar levels composed of the islet-cell system, which responds to a rise in glucose levels by primarily by releasing insulin, and the brain-centered system that enhances insulin-mediated glucose metabolism while also stimulating glucose effectiveness.

The development of type 2 diabetes appears to involve the failure of both systems, the researchers say. Impairment of the brain-centered system is common, and it places an increased burden on the islet-centered system. For a time, the islet-centered system can compensate, but if it begins to fail, the brain-centered system may decompensate further, causing a vicious cycle that ends in diabetes.

Boosting insulin levels alone will lower glucose levels, but only addresses half the problem. To restore normal glucose regulation requires addressing the failures of the brain-centered system as well. Approaches that target both systems may not only achieve better blood glucose control, but could actually cause diabetes to go into remission, they write.

The Drugs of Work-Performance Enhancement .


My morning writer’s ritual is as predictable as it is contemporary: Walk the dog. Down a cup of coffee. Eat my shredded wheat. And, twice a week—sometimes three times—I flip open my vial of Adderall, tip out one of the 15-milligram peach tabs, and break it in half. For a moment the bitterness burns my tongue, and then down it goes.

The Adderall addition to my routine started three years ago, after I happened upon 60 Minutes one evening and caught a segment titled “Boosting Brain Power.” It was an examination of the Adderall epidemic on college campuses nationwide, and I found myself quickly drawn into it.

By the end of the story, the conclusion was inescapable: Adderall makes everything easier to understand; it makes you more alert and focused. Some college students scarf them like M&Ms and think they’re more effective at cognitive enhancement than energy drinks and safer than a smoke or a beer. A Harvard professor admitted he regularly devoured Adderall to help make a book deadline.

Prior to watching, I had some close friends and relatives with ADHD whose doctors prescribed the amphetamine for completely legitimate reasons. I called them “closet users” since they all seemed ashamed of their diagnosis, not to mention their prescription. Why they felt this stigma I’m not entirely sure. According to the National Institutes of Mental Health, 4.4 percent of the adult U.S. population has ADHD, which if left untreated is associated with significant morbidity, divorce, employment, and substance abuse.

Like all prescription medications, Adderall has risks that are crucial to understand. Buried in the middle of that 60 Minutes segment was a too-short riff on amphetamine’s side effects, which include addiction, psychosis, and cardiovascular problems. I’ve read many of the horrific news stories about lives, especially young people’s lives, destroyed by this drug. Most notably, the tragic tale of Richard Fee, “an athletic, personable college class president and aspiring medical student,” as The New York Times reported earlier this year, who developed a full-fledged addiction, abetted by his doctors who routinely signed off on more meds. He was 24 when he hung himself at home.

Nonetheless, for untold healthy adults (those whom researchers refer to as “mentally competent”) the cognitive-enhancing drug has led to positive changes in their lives. Not surprisingly, the many Adderall “success” stories often go unnoticed in the current debate and climate. Explained one young woman, in her late 20s, on a public bulletin board: “[Adderall] makes me so happy I can be at a family function or out socializing and not get too distracted by other events/conversations around me. I can hear them, but am not taken in by them.”

And this testimonial from an anonymous poster: “Since being on Adderall, I have been insanely productive… I have paid all my outstanding bills and parking tickets (and even renewed my car’s registration before it was due). I’m not late for things anymore… I have not spent a single day lying around my house doing nothing in the past few months. I have a budget, and a scheduler that I actually use.”

The authors of a study published in the journal Nature argue in favor of moderate use: “Cognitive enhancement has more to offer individuals and society, and a proper societal response will involve making enhancements available while managing their risks.”

That spring when I watched the 60 Minutes broadcast I was on a deadline to finish a 400-plus-page book. After viewing the segment, I had a moment of insight. Jumping online, I took a few ADHD screening quizzes and was told I had “possible ADHD.” Such a diagnosis doesn’t place me among the 4.1 percent of U.S. adults with ADHD but it did lead me to promptly make an appointment with my primary care physician. When she asked me why I needed it, I replied just as the college kids had on 60 Minutes: “For focus.”

The first morning I swallowed the whole pill (as prescribed), and within 30 minutes thought I was going to have a stroke. My heart and head were pounding, and I felt as if I were, well, on speed. Which I was—Adderall is, after all, an aggregation of amphetamines. I cut the tabs in half after that and completed my book manuscript by the deadline, with about half my 60-day supply left.

Did it make me smarter? No. Did it make me a faster writer? Yes. Previously, when I’d sit down at my desk, I felt adrift at sea. It was as though my MacBook and research materials, piled high, swayed from left to right and then back again. It was dizzying; I just couldn’t get a grip.

For me, Adderall was like putting my foot on the ground to stop the drunken whirlies. I had a connection. I had control. My metaphoric double vision snapped to mono and I could see and think as clearly as if I’d stepped out of a fog. I’d never had such concentration and it showed in the number of well-written pages I produced daily.

Which isn’t to say that I didn’t experience some side effects. Amphetamines suppress appetite, so I easily lost weight. While the medication did wonders in prompting me to write, it inexplicably interfered with my ability to speak, scrambling my thoughts before they’d come out of my mouth. (I learned never to take a dose if I were to be out in the world anytime in the next four to six hours, otherwise I either spoke too quickly or too garbled.)

From time to time, I witnessed the shadows of depression, which I’ve read that others on the drug sometimes succumb to. Fortunately, I had the wherewithal to know this was a chemically induced darkness—one that reminded me of the sharp mood swings associated with Decadron, a corticosteroid once prescribed to me for a subdural hematoma resulting from a head injury. After two weeks of usage with this steroid, I felt suicidal. My physician had not warned me of this side effect. But with Adderall, I had knowledge aplenty and knew that once I stopped it, my depression would quickly lift. I also know that not everyone has that kind of previous experience or perspective, which is when folks get into deep trouble.

I take other meds, too, which also have their known side effects. The Lexapro I consume daily for anxiety can decrease sex drive; the Lipitor for high cholesterol can cause muscle and liver problems; and the Niaspan, also for cholesterol, can bring flushing and double vision. I’ve read about these side effects, recognize them when they occur, and understand that with the promised benefits of these meds comes risk.

But it’s different when it comes to Adderall; the most notable distinction is the “Black Box” warning on all amphetamines:

“AMPHETAMINES HAVE A HIGH POTENTIAL FOR ABUSE. ADMINISTRATION OF AMPHETAMINES FOR PROLONGED PERIODS OF TIME MAY LEAD TO DRUG DEPENDENCE AND MUST BE AVOIDED. MISUSE OF AMPHETAMINE MAY CAUSE SUDDEN DEATH AND SERIOUS CARDIOVASCULAR ADVERSE EVENTS.”

Still, according to the National Institutes of Health: “Under medical supervision, stimulant medications are considered safe.” I’d add, as the Nature authors did, especially for “mentally competent adults.”

I know some will say I’m lacking in discipline or that I’m abusing. I don’t think that’s the case, a belief that is buttressed every time I approach my desk to see the swaying stacks of research materials or my laptop levitating. On Adderall I function better and get immediate relief from the chaos—not to mention meet my deadlines. Certainly, like anything and everything in life, it’s not for everybody and the risk for abuse is very real. But as an educated patient, who measures risks and benefits every time a doctor hands me a prescription, I feel confident I’m making an informed choice for myself. And on those mornings when my routine includes half a peach tab, I know it will be a good work day.

Bat virus clues to origins of Sars.


Researchers have found strong evidence that the Sars virus originated in bats.

Two novel Sars-like coronaviruses were found in Chinese horseshoe bats which are closely related to the pathogen that infects humans.

Chinese horseshoe bat      Dr. Libiao Zhang, Guangdong Entomological Institute/South China Institute of Endangered Animals

Critically, the viruses infect human cells in the same way, binding to a receptor called ACE2.

This suggests coronaviruses could transfer directly from bats to humans, rather than via an intermediate species like civets as was previously thought.

The results are reported in the journal Nature.

According to Gary Crameri, virologist at CSIRO and an author on the paper, this research “is the key to resolving the continued speculation around bats as the origin of the Sars outbreaks”.

This Sars-like coronavirus is around 95% genetically similar to the Sars virus in humans, the research shows. And they say it could be used to develop new vaccines and drugs to combat the pathogen.

Sars
The viruses use the same basic route into human cells as Sars

The Sars outbreak between November 2002 and July 2003 resulted in more than 8,000 worldwide cases and more than 770 deaths. This, along with the ongoing endemic of the Mers-coronavirus demonstrates the threat to humans from novel coronaviruses.

Dr Peter Daszak is the president of the EcoHealth Alliance and an author on the paper published in Nature. He said: “Coronaviruses evolve very rapidly. The ones we are seeing are exquisitely evolved to jump from one species to another, which is quite unusual for a virus. So the big question is why are they emerging now?”

At wildlife markets in China other animals and humans come into close proximity with bats, creating an ideal environment for the virus to jump between species. Also, those hunting in or living near bat caves have a significant risk of infection from such viruses, which are excreted in bat faeces.

Understanding the origins of infectious diseases like Sars could help scientists tackle future infectious viruses before they emerge, through knowing where they are likely to arise and which families of virus we are most vulnerable to, and taking action to prevent initial infection.

Dr Daszak said it would cost “about $1.5bn to discover all the viruses in mammals. I think that would be a great investment because once you have done it, you can develop vaccines and get ready with test kits to find the first stage of emergence and stop it.”

Common Blue Pigment Could Help Make A Quantum Computer.


Sometimes you just have to look around. A new analysis of a common blue pigment—it’s used in the British five-pound note—found it has some unusual properties that make it a candidate semiconductor for quantum computers.

Researchers from the U.K. and Canada found molecules of copper phthalocyanine are able to hold the superimposed state of a quantum bit for as long as, or longer than, other materials being studied for quantum computers. Unlike ordinary bits, which must take on one of two states—for example, 0 or 1—quantum bits must hold two states at once. If a material is able to hold quantum states long enough, engineers could get them to store and pass on information.

Researchers are interested in building computers with quantum bits because such machines could work much faster than computers today. Some quantum computers already exist, but they’re still experimental and often aren’t able to solve practical problems.

Copper phthalocyanine has one other property that makes it a good prospect for a quantum semiconductor, the researchers wrote in a paper they published yesterday in the journal Nature. The researchers were able to produce it as a thin film, which is convenient for putting into electronic devices.

Scientists unveil energy-generating window.


Scientists in China said Thursday they had designed a “smart” window that can both save and generate energy, and may ultimately reduce heating and cooling costs for buildings.

Scientists unveil energy-generating window

While allowing us to feel close to the outside world, windows cause heat to escape from buildings in winter and let the Sun‘s unwanted rays enter in summer.

This has sparked a quest for “smart” windows that can adapt to weather conditions outside.

Today’s  are limited to regulating light and heat from the sun, allowing a lot of potential  to escape, study co-author Yanfeng Gao of the Chinese Academy of Sciences told AFP.

“The main innovation of this work is that it developed a concept smart window device for simultaneous generation and saving of energy.”

Engineers have long battled to incorporate energy-generating solar cells into window panes without affecting their transparency.

Gao’s team discovered that a material called  (VO2) can be used as a transparent coating to regulate infrared radiation from the Sun.

VO2 changes its properties based on temperature. Below a certain level it is insulating and lets through infrared light, while at another temperature it becomes reflective.

A window in which VO2 was used could regulate the amount of Sun energy entering a building, but also scatter light to  the team had placed around their glass panels, where it was used to generate energy with which to light a lamp, for example.

“This smart window combines energy-saving and generation in one device, and offers potential to intelligently regulate and utilise solar radiation in an efficient manner,” the study authors wrote in the journal Nature Scientific Reports.



Probiotics may save patients from deadly chemotherapy.


If you or someone you love is facing the possibility of cancer or chemotherapy, make sure they read this story. Breakthrough new science conducted at the University of Michigan and about to be published in the journal Nature reveals that intestinal health is the key to surviving chemotherapy.

 

The study itself is very difficult for laypeople to parse, however, so I’m going to translate into everyday language while also offering additional interpretations of the research that the original study author is likely unable to state due to the nutritional censorship of medical journals and universities, both of which have an anti-nutrition bias.

The upshot is this: A clinical study gave mice lethal injections of chemotherapy that would, pound for pound, kill most adult human beings, too. The study authors openly admit: “All tumors from different tissues and organs can be killed by high doses of chemotherapy and radiation, but the current challenge for treating the later-staged metastasized cancer is that you actually kill the [patient] before you kill the tumor.” (See sources below.)

Chemotherapy is deadly. It is the No. 1 cause of death for cancer patients in America, and the No. 1 side effect of chemo is more cancer. But certain mice in the study managed to survive the lethal doses of chemo. How did they do that? They were injected with a molecule that your own body produces naturally. It’s production is engineered right into your genes, and given the right gene expression in an environment of good nutrition (meaning the cellular environment), you can generate this substance all by yourself, 24 hours a day.

The substance is called “Rspo1″ or “R-spondon1.” It activates stem cell production within your own intestinal walls, and these stem cells are like super tissue regeneration machines that rebuild damaged tissues faster than the chemotherapy can destroy them, thereby allowing the patient to survive an otherwise deadly does of chemo poison.

As the study showed, 50 – 75 percent of the mice who were given R-spondon1 survived the fatal chemotherapy dose!

The cancer industry needs to find a way to stop killing all their customers

The problem with the cancer industry today is that all the conventional cancer treatments keep killing the patients. This is bad for business. So the purpose of research like the R-spondon1 research mentioned here — which was funded by a government grant — is to find ways to keep giving patients deadly doses of high-profit chemotherapy without actually killing them. You slap a patient with a dose of R-spondon1 (sold at $50,000 a dose as a patented “drug,” of course), dose ‘em up with a fatal injection of chemotherapy, and then thanks to the R-spondon1 you get a repeat cancer customers instead of a corpse.

That’s called “good business practices” in the cancer industry, which is so far best known for turning patients into body bags rather than actually curing cancer.

(Yes, there is a reason why most oncologists would never undergo chemotherapy themselves. They know it doesn’t work on 98% of all cancers.)

Probiotics are likely the key to generating your own R-spondon1

Before I discuss why these findings are so important for followers of natural health and nutrition, let me first offer a disclaimer. The research mentioned here was conducted on mice, not humans, so it isn’t full proof that the same mechanism works in humans. Nevertheless, the reason mice are used for such research is because they are nearly identical to humans in terms of biology, gene expression, endocrine system function and more.

Furthermore, even though this study used an injection of R-spondon1 as the “activator” of gene expression in endothelial cells of the intestinal lining, in truth your cells already possess the blueprint to produce R-spondon1 on their own. In fact, human intestines are coated with a layer of epithelial cells that are regenerated every 4-5 days in a healthy person. This is only possible through the activation and continued operation of intestinal stem cells, a normal function for a healthy human.

And what determines the health of those stem cells more than anything else? Their local environment which is predominantly determined by gut bacteria. If your gut bacteria are in balance, the gene expression of your epithelial cells is normal and healthy. If your gut bacteria are out of whack, so to speak, the gene expression of your epithelial cells will be suppressed, thereby slowing or halting the regenerative potential of your intestinal cells. This is why people who have imbalanced intestinal flora also suffer from inflammatory intestinal conditions such as Crohn’s, IBS and so on.

Thus, probiotics are a key determining factor in the ability of your intestines to maintain the appropriate gene expression for the very kind of rapid cellular regeneration that can help your body survive a fatal dose of chemotherapy.

Meat and dairy cause devastating gut flora imbalances that may increase susceptibility to chemotherapy drugs

This may also explain why people who eat large quantities of processed meat, cheese and dead, pasteurized dairy products — especially when combined with starchy carbohydrates and processed sugars — are far more likely to die from chemotherapy than people who eat more plant-based diets. (There isn’t yet a source to substantiate this claim, but it’s something I’ve noted from considerable personal observation. You may have noticed it too among your own family members who have undergone chemotherapy treatments. Those with the worst diets seem to have far higher fatality rates.)

Those who consume processed meat and dead dairy have their intestines filled with fiber-less, difficult-to-digest proteins that are putrefied and sit in the intestines for 2 – 5 days, typically. Dietary sugars and carbohydrates then feed the bacteria fermentation process, resulting in the rapid growth and replication of sugar-feeding bacteria that displace the kind of healthy flora which best protect intestinal wall cells.

This imbalance, I suggest, increases susceptibility to chemotherapy toxicity while simultaneously impairing the ability of the patient to absorb key nutrients that protect healthy cells from the toxicity of chemo drugs. This may explain why patients who heavily consume meat, cheese and dairy diets tend to die so easily when exposed to chemotherapy.

But there’s something even more alarming about all this that everyone needs to know…

Antibiotics may also set you up to be killed by chemo

Although the research did not directly address this question, its findings seem to indicate that the kind of gut bacteria “wipeout” caused by antibiotics could prove fatal to a chemotherapy patient.

This is especially worrisome because many cancer patients are simultaneously prescribed antibiotics as they undergo chemotherapy. This could be a death sentence in disguise. While neither the antibiotics nor the chemo directly kill the patient, the combination of sterilized gut bacteria and highly-toxic chemotherapy drugs could multiply the toxicity and prove fatal. The death certificate, however, will say the patient died from “cancer,” not from the chemotherapy which is usually the actual cause of death.

And yet, every single day in America, patients who are taking antibiotics are subjected to multiple courses of chemotherapy. This may quite literally be a death sentence for those patients.

There’s also a self-fulfilling death spiral at work in all this: following the first round of chemotherapy, many patients suffer from weakened immune system that result in symptomatic infections. Physicians respond to this by prescribing antibiotics, resulting in the patient undergoing subsequent rounds of chemotherapy with “wiped out” gut flora. So the chemo causes the problem in the first place, and then the response to the problem by western doctors makes the next round of chemo fatal. This is a self-fulfilling death spiral of failed medicine.

Oncologists seem to have no awareness whatsoever of the importance of gut bacteria in allowing patients to protect their own healthy cells from the devastating effects of chemotherapy drugs. Many oncologists, in fact, actively discourage their patients from taking any sort of supplements during chemotherapy out of an irrational, anti-scientific fear that such supplements may “interfere” with the chemo and make the treatment fail.

This is one of the many ways in which oncologists get cancer patients killed.

Takeaway points from this article:

• New research shows that a substance generated by intestinal stem cells allows subjects to survive an otherwise fatal dose of toxic chemotherapy.

• Healthy gene expression of intestinal cells allows them to naturally produce protective molecules that support and boost cell regeneration.

• Probiotics may protect and support the intestinal stem cells that help cancer patients survive toxic chemotherapy. (More studies needed to explore this and document the impact.)

• Antibiotics may be a death sentence when followed by chemotherapy.

• Oncologists need to consider the risks and benefits of postponing chemotherapy in patients who are simultaneously taking antibiotics. The combination may be deadly. Conversely, they need to consider the benefits of encouraging chemotherapy patients to take probiotic supplements before beginning chemotherapy treatment.

Source: naturalnews.com