Reading this report I flash on Ramez Naam's very intriguing Nexus science fiction novel about nanomachines closely integrated into human brains. This is how it begins: biological transistors that can be placed in cells.
And now a team of Stanford University bioengineers has taken computing beyond mechanics and electronics into the living realm of biology. In a paper published March 28 in Science, the team details a biological transistor made from genetic material — DNA and RNA — in place of gears or electrons. The team calls its biological transistor the “transcriptor."
“Transcriptors are the key component behind amplifying genetic logic — akin to the transistor and electronics,” said Jerome Bonnet, PhD, a postdoctoral scholar in bioengineering and the paper’s lead author.
The creation of the transcriptor allows engineers to compute inside living cells to record, for instance, when cells have been exposed to certain external stimuli or environmental factors, or even to turn on and off cell reproduction as needed.
What we need: complex logic that can detect whether a cell has gone cancerous. A really complex nanodevice that can detect and selectively kill cancer cells would be a boon. The "improve cellular therapeutics" should involve reprogramming DNA in order to fix underlying disease causes.
“Biological computers can be used to study and reprogram living systems, monitor environments and improve cellular therapeutics,” said Drew Endy, PhD, assistant professor of bioengineering and the paper’s senior author.
Reprogram living systems: The biggest need is for repair of aged cells, especially in the brain. We will be able to grow new organs in 10 to 20 years. But the brain has to be repaired. We need advanced gene therapy to fix accumulated mutational damage. We also need the ability to remove accumulated damaged garbage molecules that accumulate in cells.
One of many studies showing a link between telomere length and health. Shorter telomeres are a sign of faster aging.
An international team of scientists including researchers from Imperial College London has found new evidence that links ageing of DNA molecules to the risk of developing several age-related diseases - including heart disease, multiple sclerosis and various cancers.
Telomeres – sections of DNA at the ends of our chromosomes – shorten each time a cell divides, so their length can be interpreted as a measure of biological ageing. However, it has not been clear whether the shortening of telomeres is responsible for causing disease, and whether people with shorter telomeres have a higher risk of diseases
But if telomeres really protect against cancer by hobbling the ability of cancer cells to divide many times will longer telomeres really lengthen life expectancy? The answer might depend on the presence or absence of genetic risk factors for cancer.
Dr Jess Buxton, from the Department of Medicine at Imperial analysed samples from over 5,500 of the study participants belonging to the Northern Finland Birth Cohort study. “We’ve shown that some people have genetic variants that mean they have shorter telomeres and are at higher risk of age-related disease,” she said.
I want stem cell therapy using cells selected for absence of dangerous genetic mutations and then genetically tweaked to have long telomeres. Down with diseases. Up with youthful stem cells that fix whatever ails you.
The research team looked at DNA from over 48,000 people and identified seven genetic variants that were associated with telomere length. They then examined whether these genetic variants also affected risk of various diseases. The scientists found that the variants were linked to risk of several types of cancer, including bowel cancer, as well as diseases like multiple sclerosis and celiac disease. The seven variants they identified were collectively associated with risk of coronary artery disease, which can lead to heart attacks.
I find the bowel cancer link curious. What I wonder: do short telomeres boost risk of some forms of cancer by reducing the immune system's ability to respond to and kill early stage cancer cells?
You need youthful stem cells to replace aging vasculature, turn into new heart muscle cells, and turn into other cells needed for a healthy cardiovascular system.
A drug widely used to treat Parkinson's Disease can help to reverse age-related impairments in decision making in some older people, a study from researchers at the Wellcome Trust Centre for Neuroimaging has shown.
The study, published today in the journal Nature Neuroscience, also describes changes in the patterns of brain activity of adults in their seventies that help to explain why they are worse at making decisions than younger people.
Poorer decision-making is a natural part of the ageing process that stems from a decline in our brains' ability to learn from our experiences. Part of the decision-making process involves learning to predict the likelihood of getting a reward from the choices that we make.
An area of the brain called the nucleus accumbens is responsible for interpreting the difference between the reward that we're expecting to get from a decision and the reward that is actually received. These so called 'prediction errors', reported by a brain chemical called dopamine, help us to learn from our actions and modify our behaviour to make better choices the next time.
What I predict from this result: Future stem cell therapies that reverse Parkinson's Disease will also reverse aging in the nucleus accumbens and improve brain performance. Parkinson's Disease is one of many diseases of old age whose cure will necessarily be a rejuvenation therapy.
Dr Rumana Chowdhury, who led the study at the Wellcome Trust Centre for Neuroimaging at UCL, said: "We know that dopamine decline is part of the normal aging process so we wanted to see whether it had any effect on reward-based decision making. We found that when we treated older people who were particularly bad at making decisions with a drug that increases dopamine in the brain, their ability to learn from rewards improved to a level comparable to somebody in their twenties and enabled them to make better decisions."
Brain scans show which older brains have more decay in dopamine pathways.
The team then looked at brain activity in the participants as they played the game using functional Magnetic Resonance Imaging (fMRI), and measured connections between areas of the brain that are involved in reward prediction using a technique called Diffusor Tensor Imaging (DTI).
The findings reveal that the older adults who performed best in the gambling game before drug treatment had greater integrity of their dopamine pathways. Older adults who performed poorly before drug treatment were not able to adequately signal reward expectation in the brain – this was corrected by L-DOPA and their performance improved on the drug.
We need neural stem cell therapies to reverse brain aging. What else would help: gene therapies to fix mitochondrial DNA mutations. Also, stem cell therapies for the vascular system will improve brain circulation and therapies to rejuvenate the immune system will enhance the immune system's ability to carry away the extra-cellular trash that accumulates. Throw in some other gene therapies and cell therapies for glial cells that support neurons and gene or cell therapies to restore deteriorated myelin nerve insulation.
Rejuvenated brains will substantially boost economic activity by making aging brains much more productive.
More than 200 million years ago, a massive extinction decimated 76 percent of marine and terrestrial species, marking the end of the Triassic period and the onset of the Jurassic. This devastating event cleared the way for dinosaurs to dominate Earth for the next 135 million years, taking over ecological niches formerly occupied by other marine and terrestrial species.
It’s not entirely clear what caused the end-Triassic extinction, although most scientists agree on a likely scenario: Over a relatively short period of time, massive volcanic eruptions from a large region known as the Central Atlantic Magmatic Province (CAMP) spewed forth huge amounts of lava and gas, including carbon dioxide, sulfur and methane. This sudden release of gases into the atmosphere may have created intense global warming and acidification of the oceans that ultimately killed off thousands of plant and animal species.
Now researchers at MIT, Columbia University and elsewhere have determined that these eruptions occurred precisely when the extinction began, providing strong evidence that volcanic activity did indeed trigger the end-Triassic extinction. Their results are published in the journal Science.
If you knew it was coming how would you prepare for a really really massive volcanic eruption? It took place in repeated bursts over 40,000 years.
From its measurements, the team reconstructed the region’s volcanic activity 201 million years ago, discovering that the eruption of magma — along with carbon dioxide, sulfur and methane — occurred in repeated bursts over a period of 40,000 years, a relatively short span in geologic time.
Suppose we knew the massive multi-year eruption was coming and it was going to be thousands of miles away from where you live. What to do? Dig large underground communities with sophisticated air filtration systems. Also, build large covered surface areas. It would be like building a base on another planet that is hostile to life. Except you'd already be there and with a lead time during which the planet was not hostile.
Lots of species could be saved from extinction with some planning and preparation. Could we save any large bodies of inland water from the sulfur and carbon dioxide impacts and acidification? If one could build large arrays of mirrors in space could localized heating of ocean to produce steam provide any benefit in terms of atmospheric cleansing? How to do geoengineering to reduce the impact of an eruption that spanned hundreds or thousands of miles?
A US Department of Homeland Security 1.6 billion round ammo purchase signals that DHS takes seriously the threat of a massive zombie outbreak? That was my first hope on reading about the big bullet buy. The 1.6 billion rounds to kill a few hundred million zombies sounds about right due to lots of likely misses when trying to do head shots. You've got to shoot the zombies in the brain or they'll just keep coming. Or at least that's what I've learned from a few zombie novels.
It was quite gratifying to think that the US government was at least preparing for one possible type of massive disaster. But my relief was short lived. A Military Times article points out DHS has a lot of law enforcement officers who go thru a lot of ammunition to stay proficient at shooting guns. So those bullet buys get used up pretty fast for target practice. Also, the purchases are over several years. DHS is probably not amassing the sort of stockpile needed to deal with a major zombie outbreak. Pity that.
What I'd like to know: with the practice bullets they go thru every year how efficient are federal law enforcement agents at making the head shots that are so necessary to stop a zombie outbreak? Will all their target practice result in much lower levels of missed head shots? Do you want to stay near your local DEA or Border Patrol agent neighbor come the Zombie Apocalypse? Maybe stock several hundred rounds for him to use?
Or do you want to hang out with hunters? Or will local cops have good aim? I'm thinking military sharp shooters will do best. But I don't know any of them and don't live near Marine or Army base.
My other practical thought along these lines: Put up really strong metal fence or concrete wall around your yard that can withstand large numbers of zombies leaning against it. Make the top of the fence about 5 feet high so that only heads will stick up. Then you can shoot them at close range and get really good kill ratios. Come the zombie outbreak get all your gunner friends with all their ammo over to your place and kill all the zombies in the neighborhood. You'd better have thousands or tens of thousands of rounds though.
One worry: as the inert zombie bodies pile up the undead will be able to stand on them. Then eventually they'll be able to climb over your wall and you'll be overrun unless you live somewhere rural with few people around who can become zombies. So the whole "killing fields for zombies" idea still needs improvement. But that's got to be the way we defeat them.
Another thought: domestic drones are going to be able to identify civilians packing heat. Well, if drones can detect guns on people they also ought to be able to detect the undead. Infrared signatures have gotta be way different. Plus, the gait of an undead is distinct as well. So can the drones be armed with high powered rifles that can kill large numbers of zombies? If so, they'd at least provide an upside to living in a society where the government is patrolling the nation with Skynet UAVs that all set to go Terminator when Skynet develops AI capabilities.
The research team recruited 34 healthy young women to participate in the project. Each woman was asked to give a speech about her candidacy for a job to two interviewers in white laboratory coats, who listened with stone-faced expressions, Zoccola said.
Half of the group was asked to contemplate their performance in the public speaking task, while the other half was asked to think about neutral images and activities, such as sailing ships or grocery store trips.
Sailing ships. I mean, why not. But how about dogs or cross country skiing? What's the weirdest thing you do that relieves stress?
If you don't distract yourself the body's stress reaction will be greater and last longer.
The researchers drew blood samples that showed that the levels of C-reactive protein were significantly higher in the subjects who were asked to dwell on the speech, Zoccola reported.
For these participants, the levels of the inflammatory marker continued to rise for at least one hour after the speech. During the same time period, the marker returned to starting levels in the subjects who had been asked to focus on other thoughts.
Go read escapist fantasy. Or futurism blogs (which are pretty much the same thing).
Mountain View, Calif. – March 14, 2013 – In the largest ever genome-wide association study on myopia, 23andMe, the leading personal genetics company, identified 20 new genetic associations for myopia, or nearsightedness. The company also replicated two known associations in the study, which was specific to individuals of European ancestry. The study included an analysis of genetic data and survey responses from more than 50,000 23andMe customers and demonstrates that the genetic basis of myopia is complex and affected by multiple genes.
I think it is great that people are paying to get themselves genetically tested, filling in some online forms about their physical attributes, and thereby enabling original discoveries about human DNA. Crowd sourcing could do much more to enable biomedically useful discoveries about human health.
Myopia is the most common eye disorder worldwide. In the United States, an estimated 30 to 40 percent of the adult population is nearsighted. Myopia is a refractive error that results primarily from increased axial length of the eye. The increased physical length of the eye relative to optical length causes images to be focused in front of the retina, resulting in blurred distance vision.
The study, titled "Genome-Wide Analysis Points to Roles for Extracellular Matrix Remodeling, the Visual Cycle, and Neuronal Development in Myopia" was published on February 28, 2013 in PLOS Genetics, an open-access, peer-reviewed journal.
As the genetic test technology advances and generates more genetic data per test run the amount of information available for studies such as this one will explode. The flow of new genetic testing and sequencing results is going to rise by more orders of magnitude.
Clicking thru from the 23andMe site to the Illumina site (23andMe uses Illumina gene chips for testing) I found it interesting that these chips also detect copy number variations. So the chips can detect when a person has variations in the number of copies of genes. This is an important form of genetic variation.
Work groups at Technische Universität München (TUM) under Prof. Peter Schieberle and at the University of Vienna under Prof. Veronika Somoza studied four different edible fats and oils: Lard, butterfat, rapeseed oil and olive oil. Over a period of three months, the study participants ate 500 grams of low-fat yoghurt enriched with one of the four fats or oils every day – as a supplement to their normal diet.
“Olive oil had the biggest satiety effect,” reports Prof. Peter Schieberle, Head of the TUM Chair of Food Chemistry and Director of the German Research Center for Food Chemistry. “The olive oil group showed a higher concentration of the satiety hormone serotonin in their blood. Subjectively speaking, these participants also reported that they found the olive oil yoghurt very filling.” During the study period, no member of this group recorded an increase in their body fat percentage or their weight.
Aroma compounds in olive oil are key in reducing appetite. Try out olive oils to find ones that have a strong scent.
“The findings surprised us,” admits Schieberle, “because rapeseed oil and olive oil contain similar fatty acids.” The researchers decided to turn their attention to a completely different type of substance – the aroma compounds in olive oil. In the second part of the study, one group was given yoghurt with olive oil aroma extracts and a control group was given plain yoghurt.
The results were conclusive: The olive oil group’s calorie intake remained the same, but the control group had been consuming an extra 176 kilocalories per day. Schieberle explains: “The aroma group adapted their eating habits – but the control group participants were obviously not able to do likewise. We also found that in comparison to the other group, the control group had less of the satiety hormone serotonin in their blood.”
Not all olive oils have the same amount of the aroma chemicals.
The researchers used olive oils from Spain, Greece, Italy and Australia for their study. The research team managed to identify two substances that reduce the absorption of glucose from the blood in liver cells: Hexanal and E2-Hexenal. They also discovered that Italian olive oil contained larger amounts of the two aroma compounds.
I've noticed differences in the smell of olive oils. I already prefer the ones with stronger aromas.
Evolutionary psychologist Geoffrey Miller comments when offspring genetic engineering becomes possible the Chinese are going to embrace it with alacrity.
We have ideological biases that say, “Well, this could be troubling, we shouldn’t be meddling with nature, we shouldn’t be meddling with God.” I just attended a debate in New York a few weeks ago about whether or not we should outlaw genetic engineering in babies and the audience was pretty split. In China, 95 percent of an audience would say, “Obviously you should make babies genetically healthier, happier, and brighter!” There’s a big cultural difference.
Western countries have been ascendant for centuries. China is going to give the West its first real competition in a really long time. I think this is very healthy and constructive. The Westerners had better get ready to improve genome quality or get left in the dust.
One way to make better babies: get rid of the very low frequency mutations. The vast majority are harmful or neutral in effect. The many harmful mutations we all carry are known as genetic load. Cut down the genetic load and the result will be super babies. One of the benefits of cheap full genome sequencing is going to be the identification of these many lower frequency mutations. Better we do this to humans first before someone tries to use many Neanderthal genomes to basically vote on which genetic variants to keep in order to create a Neanderthal baby. Greg Cochran asks his readers what the problem is in doing this. The likely result of such an exercise: super Neanderthal. If a large number of Neanderthal genomes can be discovered and sequenced then that'll enable more reduction of genetic load.
Those of us already born by reducing genetic load from many parts of our bodies. First we need the ability to grow replacement organs. We then need (and will soon have) massive amounts of full genome sequencing information to identify the harmful genetic mutations. Next, we need gene therapy that can fix pieces of our DNA in cells removed from our body and grown in culture. Basically, replace the harmful genetic letters and make cell lines immunologically compatible but superior. Then use one or more of these cell lines as starting points to grow replacement organs. Then we'll be able to replace our body parts with new parts that are both younger and higher functioning.
Athens, Ga. - Students who date in middle school have significantly worse study skills, are four times more likely to drop out of school and report twice as much alcohol, tobacco and marijuana use than their single classmates, according to new research from the University of Georgia.
My guess: both genetic and dietary differences cause earlier age of puberty, greater attraction to the opposite sex, and therefore early romance. If you are going crazy about the hottie sitting next to you in class of course it is hard to concentrate.
Drugs to delay the onset of puberty would likely improve educational outcomes. The rare or never daters did best in school. The instinct to reproduce gets in the way of learning.
The Healthy Teens Longitudinal Study included schools from six school districts in northeast Georgia. Investigators used two indicators of students' school success: high school dropout rates and yearly teacher-rated study skills. The results of the study were recently published in the Journal of Research on Adolescence.
"In our study, we found four distinct trajectories," Orpinas said. "Some students never or hardly ever reported dating from middle to high school, and these students had consistently the best study skills according to their teachers. Other students dated infrequently in middle school but increased the frequency of dating in high school. We also saw a large number of students who reported dating since sixth grade."
Modest proposal: kids should have to pass a test in solving quadratic equations before a switch that could be installed in their hormonal system gets flipped to start sexual maturation. No puberty before mathematical competence.
A medical first: Livers can be kept alive outside the body while getting transported for a liver recipient. A pump replicates of function of the heart and an oxygenator replicates the function of the lungs with the liver maintained at body temperature. Donor organ quality will improve. Used at King's College London to do liver transplants.
This is a big step in the direction of a much more ambitious goal: grow new livers outside the body. I especially like biomedical technologies developed to achieve smaller goals that are also steps toward achieving full body rejuvenation. If we can grow organs outside the body we will eventually be able to replace old worn out organs with new young organs.
This Oxford device only keeps a liver alive 24 hours.
All of our cells are ticking down to senescence. One notable aging biomarker is the telomere, a cap found on every chromosome. This report reminds a recent report that found shorter telomeres on immune cells predict susceptibility to the common cold starting at age 22. Yes, your decay really does start that early. Telomere length in the immune CD8CD28-T cells predicted odds of getting rhinovirus 39 (one of the main viruses that cause colds) as well as severity of infection.
Analysis indicated that only telomere length in the CD8CD28- subset was associated with risk for clinical illness, with shorter telomere length associated with increased risk. Among participants with the shortest telomeres, 26 percent became clinically ill. The rate for clinical illness was 13 percent for those in the group with the longest telomeres.
The reason I bring this up: There's continuum of difficulty for growing different types of cells and organs outside the body. The hardest will be organs with really complex 3-D structures such as kidneys and hearts. Livers are more amorphous and therefore growth of livers outside the body should prove easier than growth of lungs, hearts, or kidneys.
I'm guessing growth of youthful immune cells outside the body should be easier still. That's good because the immune system serves many functions aside from killing pathogens. e.g. regulate and dispose of red blood cells, clear the plaque associated with Alzheimer's disease, and regulate neurons.
I'm betting we will get replacement immune cells and stem cells before we get replacement organs grown outside the body.
Why do people learn less as they get older? It could be that higher levels a gene called Nogo Receptor 1 reduce formation of synaptic connections. The blocking of Nogo Receptor 1 made old mouse brains recover from brain injury as rapidly as adolescent mice.
The flip of a single molecular switch helps create the mature neuronal connections that allow the brain to bridge the gap between adolescent impressionability and adult stability. Now Yale School of Medicine researchers have reversed the process, recreating a youthful brain that facilitated both learning and healing in the adult mouse.
Brain rejuvenation won't be as easy as suppressing one gene. Lots of things go wrong in brain cells (and all cells) as we age. But it seems possible that development of drugs targeted at key brain genes could boost the performance of older minds. I am also hoping for the development of gene therapies that will restore the mitochondria that are the energy generators of cells.
By monitoring the synapses in living mice over weeks and months, Yale researchers have identified the key genetic switch for brain maturation a study released March 6 in the journal Neuron. The Nogo Receptor 1 gene is required to suppress high levels of plasticity in the adolescent brain and create the relatively quiescent levels of plasticity in adulthood. In mice without this gene, juvenile levels of brain plasticity persist throughout adulthood. When researchers blocked the function of this gene in old mice, they reset the old brain to adolescent levels of plasticity.
The ability to inhibit Nogo Receptor 1 could provide great benefit for stroke victims.
Rehabilitation after brain injuries like strokes requires that patients re-learn tasks such as moving a hand. Researchers found that adult mice lacking Nogo Receptor recovered from injury as quickly as adolescent mice and mastered new, complex motor tasks more quickly than adults with the receptor.
We are approaching the era when cells become very manipulable. The many genes and their functions are being identified orders of magnitude faster than they used to be. In 20 years time major feats of tissue engineering, gene therapy, and cell therapy will be commonplace. Our bodies will become far more moldable and repairable. I just want it to happen sooner. As Glenn Reynolds likes to say: Faster please!
Barcelona, 7 March 2013. The study, led by the Vall d'Hebron Institute of Oncology (VHIO), has managed to eliminate mouse lung tumours by inhibiting Myc, a protein that plays a key role in the development of many different tumours. The results, to be published in the journal Genes & Development, confirm that repeated, long-term treatment does not cause side effects. Even more importantly, no resistance to treatment has been encountered, which is one of the biggest concerns with anticancer therapies. These results show that anticancer therapies based on Myc inhibition are a safe, effective therapeutic option in new drug development.
One of the major potential ways to really cure cancer is to send in genes that counteract the effect of the mutant genes that cause cancer. Gene therapy is like a software patch sent in to fix a bug. DNA is like a really complex piece of software. Once we can rewrite the genetic software to cancel out the effects of cancer-causing mutations we will be able to cure cancer.
The work conducted by the Mouse Models of Cancer Therapy group at the VHIO, led by Dr Laura Soucek, shows that Myc can be controlled and inhibited through a mutant called Omomyc that hijacks Myc and prevents it from acting. "Even if we clearly identify a mechanism behind tumour development, it is still extremely complex to pinpoint how to intervene in cells' internal machinery or modify genetic processes," explained Dr Soucek. "We have found a way to inhibit Myc through Omomyc," she continued. "We induced Omomyc expression in mice through gene therapy and managed to activate and deactivate it by administering an antibiotic to the mice in their drinking water."
In the study, multiple lung tumours were induced in the mouse (up to 200 tumours in each individual) and Myc inhibition episodes were achieved by activating Omomyc expression for 4-weeks, followed by 4-week rest periods. This therapy - known as metronomic therapy - was maintained for more than a year, regularly checking tumour progress in each mouse. All mice became tumour free after the first inhibition period, but 63% of cases then relapsed. After the second Myc inhibition period, only 11% of the initial tumours reappeared. According to Dr Soucek, "the most important finding was that there were no signs of resistance to treatment. This is one of the biggest disadvantages of many anticancer therapies: the disease develops resistance and can return even more aggressively."
One of the challenges with gene therapy is to get it into every cancer cell. Another challenge is to do it in a way that does not mess up the genes of normal cells. Since both problems are hard I am surprised these researchers have gotten this far.
The Economist Babbage column has a good write-up on the better prospects for lithium air batteries to eventually replace gasoline. The energy density is much higher but lithium air has longevity problems. IBM, Toyota and PolyPlus are among the companies competing to make a workable lithium air battery.
On the other hand, a group of researchers who have spent a lot of time working on lithium ion have shifted their focus to sodium ion since they see it as an easier problem to solve.
“The big advances in battery technology happen rarely. It’s been more than 200 years and we have maybe five different successful rechargeable batteries,” said George Blomgren, a former senior technology researcher at Eveready and now a private battery consultant. “It’s frustrating.”
Will we see much in the way of EV battery price declines in the next few years? in 1Q 2012 EV battery prices went down, but to a still very high price. I can't find any reports of further EV battery price declines since then. Has any reader come across a more recent report on recent EV battery prices?
An ideal cure for cancer will only kill cancer cells while leaving all other cell types alone. It is quite difficult to develop such a narrowly targeted anti-cancer agent. However, some VPI researchers have genetically modified a virus so that it selectively targets and kills only prostate cancer cells.
A recombinant Newcastle disease virus kills all kinds of prostate cancer cells, including hormone resistant cells, but leaves normal cells unscathed, according to a paper published online ahead of print in the Journal of Virology. A treatment for prostate cancer based on this virus would avoid the adverse side effects typically associated with hormonal treatment for prostate cancer, as well as those associated with cancer chemotherapies generally, says corresponding author Subbiah Elankumaran of Virginia Polytechnic Institute, Blacksburg. The modified virus is now ready to be tested in preclinical animal models, and possibly in phase I human clinical trials.
Viruses have surface fusion proteins which enable viruses to enter cells. The researchers modified the Newcastle virus' fusion protein so it would become activated by the prostate specific antigen found only on prostate cells. So the virus only enters prostate cells.
Newcastle disease virus kills chickens, but does not harm humans. It is an oncolytic virus that hones in on tumors, and has shown promising results in a number of human clinical trials for various forms of cancer. However, successful treatments have required multiple injections of large quantities of virus, because in such trials the virus probably failed to reach solid tumors in sufficient quantities, and spread poorly within the tumors.
The researchers addressed this problem by modifying the virus's fusion protein. Fusion protein fuses the virus envelope to the cell membrane, enabling the virus to enter the host cell. These proteins are activated by being cleaved by any of a number of different cellular proteases. They modified the fusion protein in their construct such that it can be cleaved only by prostate specific antigen (which is a protease). That minimizes off-target losses, because these "retargeted" viruses interact only with prostate cancer cells, thus reducing the amount of virus needed for treatment.
Proteases slice into a protein and can activate or deactivate the protein by doing this depending on where they slice and how the protein is structured. Not all types of cancers are necessarily going to have a cell surface protease that can be harnessed to target just one cell type.
In a University of Washington study people were fed catered organic foods which had no exposure to plastic containers in an attempt to reduce urinary pthalates and bisphenol A (BPA), which are endocrine system disruptors. Surprisingly, the special diet had an effect opposite of what was intended.
The urinary concentration for pthalates were 100-fold higher than the those levels found in the majority of the general population, The comparison comes from a study conducted by the National Health and Nutrition Examination Survey (NHANES), a program of studies managed by the Centers for Disease Control and Prevention and designed to assess the health and nutritional status of adults and children in the United States. The concentrations were also much higher for children as compared to the adults.
The dairy products, cinnamon, and cayenne pepper supplied high concentrations of phthalates. So avoid these foods?
Then, the researchers tested the phthalate concentrations in the food ingredients used in the dietary intervention. Dairy products—butter, cream, milk, and cheese—had concentrations above 440 nanograms/gram. Ground cinnamon and cayenne pepper had concentrations above 700 ng/g, and ground coriander had concentrations of 21,400 ng/g.
"We were extremely surprised to see these results. We expected the concentrations to decrease significantly for the kids and parents in the catered diet group. Chemical contamination of foods can lead to concentrations higher than deemed safe by the U.S. Environmental Protection Agency," said Sathyanarayana.
Readers, do you have any tips on how to cut exposure to endocrine disruptor chemicals?