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Physicists Just Discovered a Way to Track Unobserved Quantum Particles
The numbers are mind-boggling, but the way each individual nerve cell contributes to the brain’s functions is still an area of contention. A new study has overturned a hundred-year-old assumption on what exactly makes a neuron ‘fire’, posing new mechanisms behind certain neurological disorders.
A team of physicists from Bar-Ilan University in Israel conducted experiments on rat neurons grown in a culture to determine exactly how a neuron responds to the signals it receives from other cells.
To understand why this is important, we need to go back to 1907 when a French neuroscientist named Louis Lapicque proposed a model to describe how the voltage of a nerve cell’s membrane increases as a current is applied.
Once reaching a certain threshold, the neuron reacts with a spike of activity, after which the membrane’s voltage resets.
What this means is a neuron won’t send a message unless it collects a strong enough signal.
Lapique’s equations weren’t the last word on the matter, not by far. But the basic principle of his integrate-and-fire model has remained relatively unchallenged in subsequent descriptions, today forming the foundation of most neuronal computational schemes.
According to the researchers, the lengthy history of the idea has meant few have bothered to question whether it’s accurate.
“We reached this conclusion using a new experimental setup, but in principle these results could have been discovered using technology that has existed since the 1980s,” says lead researcher Ido Kanter.
“The belief that has been rooted in the scientific world for 100 years resulted in this delay of several decades.”
The experiments approached the question from two angles – one exploring the nature of the activity spike based on exactly where the current was applied to a neuron, the other looking at the effect multiple inputs had on a nerve’s firing.
Their results suggest the direction of a received signal can make all the difference in how a neuron responds.
A weak signal from the left arriving with a weak signal from the right won’t combine to build a voltage that kicks off a spike of activity. But a single strong signal from a particular direction can result in a message.
This potentially new way of describing what’s known as spatial summation could lead to a novel method of categorising neurons, one that sorts them based on how they compute incoming signals or how fine their resolution is, based on a particular direction.
Better yet, it could even lead to discoveries that explain certain neurological disorders.
It’s important not to throw out a century of wisdom on the topic on the back of a single study. The researchers also admit they’ve only looked at a type of nerve cell called pyramidal neurons, leaving plenty of room for future experiments.
But fine-tuning our understanding of how individual units combine to produce complex behaviours could spread into other areas of research. With neural networks inspiring future computational technology, identifying any new talents in brain cells could have some rather interesting applications.
The lab made mosquitos will be released on the unsuspecting populace of Fresno, California, a city with over half a million people.
Sometimes you have to think that scientists don’t ever read science fiction, and thus have not even contemplated all the things that could go wrong when they do something like creating 20 million mosquitos in a laboratory, infecting them with a bacteria, and then releasing those mosquitos in Fresno, California.
First of all, did you even know that Google had a bio-lab? They do and it’s called Verily. Which, I dunno, sounds rather biblical. “Verily, I say unto you…we are the purveyors of all that is The Truth.”
But I digress.
Verily plans to create 20 million mosquitoes and infect them with a bacteria in their laboratories. Then, the mosquitos will be released on the unsuspecting populace of Fresno, California, a city with over half a million people.
Why? Because, Zika.
Remember last year’s Zika scare that prompted the government to spray harmful chemicals all over citizens in Florida? That terrified a whole bunch of pregnant women and made them worry that their babies would be born with microcephaly?
Apparently, the Aedes aegypti mosquito that is thought to carry the Zika virus is prevalent in Fresno. However prevalent these mosquitos may be, there is only one confirmed case of Zika, and this woman’s partner had been traveling.
So, anyway, in a project wittily named DeBug, Verily has “created” a whole bunch of mosquitos and infected the males with a bacteria called Wolbachia. When the male mate with female mosquitos, the resulting eggs can’t hatch. And by the way, they did a smaller release of franken-mosquitos last year in Fresno. (See? says Verily soothingly. We already did this once without you knowing about it and nothing bad happened. Don’t worry, you silly mortal.)
In 2016, CMAD and MosquitoMate piloted the first-ever U.S. release of male Aedes aegypti mosquitoes with Wolbachia in Fresno County. Our 2017 collaboration represents a more than 25x increase in the release efforts, with a total of one million non-biting sterile male mosquitoes released weekly, made possible by the automated mass rearing and sex-sorting processes developed at Verily. Additionally, our software algorithms and on-the-ground release devices will allow us to distribute the sterile male mosquitoes in an even and targeted way throughout Fresno’s mosquito season. We believe that these advancements could have a meaningful impact on what is traditionally a very labor-intensive process and could reduce the number of biting Aedes aegypti in Fresno County.
Theoretically, the Wolbachia virus is harmless to humans, male mosquitos don’t bite, and whether Fresno residents like it or not, they’ll be subject to the release of a million of these franken-mosquitoes per week for the next 20 weeks.
The project, which has already rather quietly begun, is turning the area into a test facility without the consent of residents. Trucks will be driving through the city releasing swarms of millions of infected male mosquitos in Fresno.
For the Debug team at Verily, moving our work from the laboratory to the field is not only an important milestone for our group of biologists, engineers, and automation experts, but it’s also a critical step in bringing our long-term vision to reality. Field studies allow us to test our discoveries and technologies in challenging, real-world conditions and collect the necessary evidence to bring them to a broader scale. We hope to demonstrate success with Debug Fresno that will benefit the local communities working with us on this study and later other communities globally where Zika, dengue, and chikungunya are endemic. We are excited to take the first step in that journey today by bringing these technologies to the field. (source)
Here’s some more information about the project in this
propaganda informational video.
Does anyone else think that this sounds like the first chapter in a novel by the likes of Michael Crichton or Stephen King? (For information about protecting yourself from mosquitos that doesn’t include the potential for some kind of mosquito apocalypse, read this.)
I can see quite a lot of potential unfavorable variables here. Just off the top of my head, here are just some of the things that could go wrong:
- What if the mosquitos are sorted incorrectly? Do you really think that out of 20 million mosquitos, nary a biting female will get through the sorting process?
- What if the Wolbachia mutates? Something that is not harmful now could morph into something far worse than Zika.
- What if scientists believe that this gives them innate permission to conduct “field studies” of other things? Oh…wait. Apparently, they already feel they don’t require our permission to turn our neighborhoods into test facilities.
It’s like they don’t even consider these things. Or, if they do, then the risks are worth taking. Maybe this will be harmless, but the fact remains that this city is being turned into a “controlled environment” for Verily without the consent of citizens.
And that is not okay.
More men than ever are developing type 2 diabetes. I knew my weight put me at risk, but I needed a nudge from my friends before I changed.
Men, be warned. It seems we are not taking very good care of ourselves. Many of us are overweight and we are paying the price with poorer health. Research by charity the Men’s Health Forum found men were over 25% more likely to develop type 2 diabetes than women. Shockingly, almost one in 10 men are now suffering from this disease.
The research also found that men were more than twice as likely to have a major amputation. Almost 70% of people presenting with a foot ulcer caused by type 2 diabetes are men. It gets grimmer. Untreated, type 2 diabetes kills, and it is now killing proportionately more men than ever, according to the study.
We can’t ignore the facts that health messages are not getting through to many men. We are developing problems such as type 2 diabetes through a combination of obesity – apparently the UK is the sixth fattest nation in the world – and a woeful lack of exercise. In March, the NHS’s annual review of obesity said one in four adults in England took less than 30 minutes of moderate exercise a week, compared to the recommended 150 minutes.
Is being overweight suddenly socially acceptable for men? Without the social stigma, is it now OK to be obese? Worryingly, Men’s Health Forum says that more than half of overweight men think their weight is fine.
We are all too familiar with the social pressures on girls and women to be slim (and beautiful), and how this causes crippling anxiety leading to terrible eating disorders and self-harm. Surely, men can choose a healthy menu that avoids obesity, leading to poor health, without a diet of weight obsession leading to sickness?
What the report didn’t reveal was information relating to men’s ages or social backgrounds. It strikes me the vital missing ingredient is the extent to which our attitudes to health and weight depend on our friendship groups, ages and jobs. A friend I train with at the gym plays weekly five-a-side football with his mates and says they’re all fit and take their health and fitness seriously. None are overweight.
Most of my friends are middle aged like me. As we have got older, we’ve become much more concerned about our weight and general health and fitness. Still, there’s usually some sort of catalyst before embarking on a weight loss and exercise regime. We all knew and understood the health messages, but needed a spur to action before taking them seriously.
For one, for whom diabetes runs in his family, it was coming last in the dads’ race at his son’s school sports day that spurred him to take action. Another friend was prescribed medication for high blood pressure and started to lose weight to help better manage his condition. A friend who freelances for a living said his spur was the need to look youthful and in good physical shape when pitching for projects, in order to radiate vitality and demonstrate capacity to cope with the slog. For another mate, it was simply the approach of a significant birthday, and with it a bit of taking stock.
My catalyst was the kindness of male friends, by which I mean they took the mickey out me for being fat and unfit. In my late 30s and early 40s my weight had increased slowly. By my mid-40s it had jumped from a lithe 12 stone to a porky 15.5, and was showing no signs of stopping there. Long hours at my desk and client networking concentrated around eating and drinking, combined with little routine exercise had caught up with me. A health check at the doctor’s told me I was at risk of type 2 diabetes.
It was really the comments from friends that forced me finally into to action. One of my more kindly mates remarked that I was a little portly. Others were frankly blunter. Bluster and jokes are pretty typical ways that men get serious points over, but behind it I could detect some genuine concern for my welfare.
I found pleasure in a drastic life change. For eight months, out went all booze, bread, pasta, rice and sugary treats such as chocolate, biscuits and cake. In came running, regular trips to the gym with a personal trainer, smaller food portions and lots more fruit and salads. The weight fell off.
We all agree that media messages encouraging us to eat healthily and exercise on the whole have gone in. Yet a catalyst is often needed to turn thought into action.
The enteric nervous system that regulates our gut is often called the body’s “second brain.” Although it can’t compose poetry or solve equations, this extensive network uses the same chemicals and cells as the brain to help us digest and to alert the brain when something is amiss. Gut and brain are in constant communication.
“There is immense crosstalk between these two large nerve centers,” says Braden Kuo, MD, MMSc ’04, co-executive director of the Center for Neurointestinal Health at Massachusetts General Hospital (MGH) and assistant professor of medicine at Harvard Medical School. “This crosstalk affects how we feel and perceive gastrointestinal (GI) symptoms and impacts our quality of life.”
Normally, when we see something tasty, the brain signals the gut to prepare for incoming food. When we feel anxious or stressed, we might experience these as abdominal pain, diarrhea, nausea, or “butterflies.” Messages travel from gut to brain, too. This helps explain why, when we eat something that makes us sick, we instinctively avoid the food and even the place we found it.
These everyday activities can go awry when gut nerves are damaged or malfunction. The Center for Neurointestinal Health treats patients with life-altering conditions such as chronic constipation, extreme bloating, and irritable bowel syndrome (IBS). Center physician-scientists also contribute to the exciting basic, clinical, and translational research happening across HMS to understand the gut-brain connection.
For example, Kuo and colleagues are measuring brain activity in patients with chronic nausea using functional MRI, which detects blood-flow changes. Their discovery that nausea and pain involve similar nerve centers has prompted new treatment plans for certain patients, potentially improving their quality of life.
Center researchers are also investigating how the trillions of bacteria in the gut (the gut microbiome) interact with the enteric nervous system (a component of the autonomic nervous system) and ultimately with the central nervous system, notes center co-leader Allan M. Goldstein, MD ’93, Marshall K. Bartlett Professor of Surgery at HMS and chief of pediatric surgery at MGH. “Increasing evidence is showing that bacteria in the gut, and the byproducts they produce, affect mood, cognition, and behavior.”
HMS Instructor in Medicine Kyle Staller, MD ’09, MPH ’15, is studying how abnormal body image and eating disorders in adolescents influence the likelihood of developing IBS and other GI problems in adulthood. These patients, he says, typically perceive normal digestion sensations, like the gut’s expansion with food and stool, as abnormal and may seek a doctor’s help for bloating.
Kuo has also co-led a pilot study that found the “relaxation response,” a state of deep rest induced by practices such as meditation and yoga, helped relieve symptoms in some patients with IBS and inflammatory bowel disease.
With the brain and gut so intertwined, it makes sense for clinicians treating gastrointestinal disorders to include cognitive approaches such as talk therapy, hypnosis, or relaxation response in their recommendations, and for clinicians treating cognitive symptoms to consider what’s happening in the patient’s gut.
Hemophilia is a rare blood disease that usually occurs in males. In fact, it’s extremely rare for women to be born with the condition because of the way it’s passed down genetically. A female would need to inherit two copies of the faulty gene — one from each parent — to develop hemophilia A, B or C. Boys only need to inherit one copy of the faulty gene responsible for hemophilia A and B, but both parents’ faulty gene for hemophilia C.
However, women can be carriers of the disease and may also experience issues with clotting factor. These women often only possess between 30 percent and 70 percent of the clotting factor of someone who isn’t a carrier. This is usually enough to protect from severe bleeds but can lead to problems with heavy menstruation.
Women who do have hemophilia may only be aware of the problem if they have skin that bruises easily and experience symptoms such as excessive and frequent nosebleeds, heavy bleeding after childbirth, heavy periods, or prolonged bleeding following surgical or dental procedures.
Women may also develop acquired hemophilia later in life. Acquired hemophilia usually affects older people and can be a complication of an autoimmune disease such as inflammatory bowel disease or cancer. In very rare cases, women can develop the disease following childbirth.
The first recorded mention of hemophilia came in the second century when a collection of ancient Jewish writings noted that baby boys did not need to be circumcised if two of their older brothers had bled to death following the procedure. Later in the 10th century, an Arabian doctor described cases of male members of the same family dying from excessive bleeding after a trauma according to the National Hemophilia Foundation.
In 1803, Dr. John Conrad Otto from Philadelphia published a paper about a familial bleeding disorder that only affected male members. His research managed to trace the origin of the disease to a female relative who lived in New Hampshire in 1720.
The term hemophilia comes from a student of Zurich University, Friedrich Hopff and his professor, Dr. Schonlein, who came up with the term “haemorrhaphilia” which became “haemophilia” in 1828.
Argentinian physician, Alfredo Pavlovsky discovered there were two types of hemophilia (A and B) in 1947. The different factor deficiencies were distinguished in the 1950s and 1960s.
Until the early 1900s, there was no way to store blood for hemophiliacs so they were generally given a transfusion from a family member if they had suffered a trauma. At this point, the life expectancy for boys with hemophilia was around 13 years old.
Some of the early treatments used for hemophilia included lime, bone marrow, oxygen, thyroid gland, hydrogen peroxide or gelatin. In the 1930s, snake venom was used to help blood clotting. Hospital-based plasma transfusions were common treatments for hemophiliacs in the late 1920s and continued until the 1950s. Hospitals then moved to fresh frozen plasma, although patients needed very large amounts for it to be successful and young boys often sustained crippling joint bleeds. By 1960, the life expectancy of a person with severe hemophilia had risen to just under 20 years old.
In 1965, Dr. Judith Graham Pool from Stanford University discovered that the precipitate (cryoprecipitate) left from thawing plasma was high in factor VIII. This could be infused to control heavy bleeding and blood banks were able to produce and store large amounts for use in surgical procedures for hemophiliacs.
By the 1970s, freeze-dried powder formulas of factor VIII and IX were readily available, which meant hemophiliacs were able to self-administer the factor in their own homes.
The rise of HIV and AIDS in the 1980s led to many people with hemophilia dying of AIDS and becoming HIV positive through contaminated blood products. Hemophiliacs were also at a high risk of contracting hepatitis C until blood screening was introduced in 1992.
In the 1990s, synthetic factor became available and recombinant factors were approved by the FDA. In 1995, prophylaxis started being used as a preventive treatment for children.
New recombinant factors that didn’t contain human or animal plasma were introduced in the early 2000s which lessened the chance of allergic reactions. Currently, researchers are working on ways of correcting the mutated gene using viruses as vehicles to deliver corrected factor IX genes.