Think of it as interval training for the dinner table.University of Florida Health researchers have found that putting people on a feast-or-famine diet may mimic some of the benefits of fasting, and that adding antioxidant supplements may counteract those benefits.
Fasting has been shown in mice to extend lifespan and to improve age-related diseases. But fasting every day, which could entail skipping meals or simply reducing overall caloric intake, can be hard to maintain.
“People don’t want to just under-eat for their whole lives,” said Martin Wegman, an M.D.-Ph.D. student at the UF College of Medicine and co-author of the paper recently published in the journal Rejuvenation Research. “We started thinking about the concept of intermittent fasting.”
Michael Guo, a UF M.D.-Ph.D. student who is pursuing the Ph.D. portion of the program in genetics at Harvard Medical School, said the group measured the participants’ changes in weight, blood pressure, heart rate, glucose levels, cholesterol, markers of inflammation and genes involved in protective cell responses over 10 weeks.
“We found that intermittent fasting caused a slight increase to SIRT 3, a well-known gene that promotes longevity and is involved in protective cell responses,” Guo said.
The SIRT3 gene encodes a protein also called SIRT3. The protein SIRT3 belongs to a class of proteins called sirtuins. Sirtuins, if increased in mice, can extend their lifespans, Guo said. Researchers think proteins such as SIRT3 are activated by oxidative stress, which is triggered when there are more free radicals produced in the body than the body can neutralize with antioxidants. However, small levels of free radicals can be beneficial: When the body undergoes stress — which happens during fasting — small levels of oxidative stress can trigger protective pathways, Guo said.
“The hypothesis is that if the body is intermittently exposed to low levels of oxidative stress, it can build a better response to it,” Wegman said.
The researchers found that the intermittent fasting decreased insulin levels in the participants, which means the diet could have an anti-diabetic effect as well.
The group recruited 24 study participants in the double-blinded, randomized clinical trial. During a three-week period, the participants alternated one day of eating 25 percent of their daily caloric intake with one day of eating 175 percent of their daily caloric intake. For the average man’s diet, a male participant would have eaten 650 calories on the fasting days and 4,550 calories on the feasting days. To test antioxidant supplements, the participants repeated the diet but also included vitamin C and vitamin E.
At the end of the three weeks, the researchers tested the same health parameters. They found that the beneficial sirtuin proteins such as SIRT 3 and another, SIRT1, tended to increase as a result of the diet. However, when antioxidants were supplemented on top of the diet, some of these increases disappeared. This is in line with some research that indicates flooding the system with supplemental antioxidants may counteract the effects of fasting or exercise, said Christiaan Leeuwenburgh, Ph.D., co-author of the paper and chief of the division of biology of aging in the department of aging and geriatric research.
“You need some pain, some inflammation, some oxidative stress for some regeneration or repair,” Leeuwenburgh said. “These young investigators were intrigued by the question of whether some antioxidants could blunt the healthy effects of normal fasting.”
On the study participants’ fasting days, they ate foods such as roast beef and gravy, mashed potatoes, Oreo cookies and orange sherbet — but they ate only one meal. On the feasting days, the participants ate bagels with cream cheese, oatmeal sweetened with honey and raisins, turkey sandwiches, apple sauce, spaghetti with chicken, yogurt and soda — and lemon pound cake, Snickers bars and vanilla ice cream.
“Most of the participants found that fasting was easier than the feasting day, which was a little bit surprising to me,” Guo said. “On the feasting days, we had some trouble giving them enough calories.”
Leeuwenburgh said future studies should examine a larger cohort of participants and should include studying a larger number of genes in the participants as well as examining muscle and fat tissue.
- Martin P Wegman, Michael Guo, Douglas M Bennion, Meena N Shankar, Stephen M Chrzanowski, Leslie A Goldberg, Jinze Xu, Tiffany A Williams, Xiaomin Lu, Stephen I Hsu, Stephen D Anton, Christiaan Leeuwenburgh, Mark L Brantly.Practicality of Intermittent Fasting in Humans and its Effect on Oxidative Stress and Genes Related to Aging and Metabolism.Rejuvenation Research, 2014; 141229080855001 DOI: 1089/rej.2014.1624
Seventeen years after losing the use of his hand in a motorcycle crash, Marcus Kemeter volunteered to have it amputated and replaced with a bionic version.
“It wasn’t hard for me to decide to do the operation,” said Kemeter, 35, a used-car dealer in Austria. “I couldn’t do anything with my hand. The prosthesis doesn’t replace a full hand, but I can do a lot of stuff.”
Kemeter’s artificial hand was made possible by a new medical procedure developed at the Medical University of Vienna, which combines reconstructive surgery with advances in prosthetics and months of training and rehabilitation, according to an article published Wednesday in the Lancet, a U.K. medical journal. The researchers performed the procedure on three Austrian men from 2011 to 2014.
The technique, called bionic reconstruction, offers hope for patients like Kemeter who have brachial plexus injuries, which can result in severe nerve damage and the loss of function in the arms.
The nerves of the brachial plexus start in the neck and branch out to control shoulder, arms and hands. They can be damaged in collisions from car and motorcycle accidents, and in sports like football and rugby. In the past, surgical reconstruction for brachial plexus patients could restore some function in their arms but not hands.
The injuries result in an “inner amputation,” permanently separating the hands from neural control, said Oskar Aszmann, a professor of plastic and reconstructive surgery at the Vienna university who is the lead author of the Lancet study.
The damaged limbs “are a biologic wasteland,” Aszmann said in a telephone interview. The solution is transplanting nerves and muscles from the legs into the arm, creating new avenues for signals from the brain.
“We can establish a new signal and we can use these signals to drive a prosthetic hand,” he said.
The process represents a significant step for patients with brachial plexus injuries, said Levi Hargrove, a researcher in prosthetics at the Rehabilitation Institute of Chicago.
“It provides them with an option,” he said. “As mechanical prosthesis become more advanced and more functional, this should only improve.”
The ultimate success of the procedure won’t be known for years and will depend on how often patients use their new hands, said Simon Kay and Daniel Wilks in a Lancet article accompanying the study. Kay is a hand surgeon at the Leeds Teaching Hospital, while Wilks is at The Royal Children’s Hospital in Melbourne.
“Compliance declines with time for all prostheses, and motorized prostheses are heavy, need power and are often noisy,” they wrote.
Kemeter, who lives in the Lower Austrian town of Hollabrunn, damaged his shoulder in a 1996 motorcycle accident. That year, he had surgery that grafted new nerves to his arm, which restored some function to his shoulder and elbow. Over the next decade and a half, his arm withered and atrophied, with his fingers permanently clenched.
“I could feel everything but I couldn’t do anything with the hand,” he said.
In 2011, Aszmann transplanted Kemeter’s nerves from his lower leg and muscle from his thigh to his injured forearm. After waiting three months for the nerves to grow back, Kemeter’s arm was connected to a computer, where he could practice manipulating a virtual hand.
“The brain has forgotten to use the hand,” Aszmann said. “We have to retrain them.”
The next step was connecting the prosthesis to the new nerves, with Kemeter’s biological hand still in place, to train him to use the device. That helps patients with the decision to amputate, Aszmann said.
“When it’s obvious this mechatronic hand can be of great use to them, then the decision to have the hand amputated is a very easy one,” he said. “If I have to convince someone, they’re not a good patient.”
Finally, after the amputation wounds healed and the prosthesis was fitted, the adjustment to the new appendage took only a few days.
“I can do much more than before,” Kemeter said. “Carrying big things, for example, wasn’t possible with only one hand. Now I can do it.”
Related News and Information: Bionic Hands Move Close to Human Control With Sensation of Touch Innovative Prosthetic Arm From Segway Inventor Cleared by U.S. First Bionic Leg to Harness Nerves Allows Mind Control Movement.
»Anyone who knows me also knows that I have a huge sweet tooth. I always have. My friend and fellow graduate student Andrew is equally afflicted, and living in Hershey, Pennsylvania – the “Chocolate Capital of the World” – doesn’t help either of us.
But Andrew is braver than I am. Last year, he gave up sweets for Lent. I can’t say that I’m following in his footsteps this year, but if you are abstaining from sweets for Lent this year, here’s what you can expect over the next 40 days.
Sugar: natural reward, unnatural fix
In neuroscience, food is something we call a “natural reward.” In order for us to survive as a species, things like eating, having sex and nurturing others must be pleasurable to the brain so that these behaviours are reinforced and repeated.
Evolution has resulted in the mesolimbic pathway, a brain system that deciphers these natural rewards for us. When we do something pleasurable, a bundle of neurons called the ventral tegmental area uses the neurotransmitter dopamine to signal to a part of the brain called the nucleus accumbens. The connection between the nucleus accumbens and our prefrontal cortex dictates our motor movement, such as deciding whether or not to taking another bite of that delicious chocolate cake. The prefrontal cortex also activates hormones that tell our body: “Hey, this cake is really good. And I’m going to remember that for the future.”
Not all foods are equally rewarding, of course. Most of us prefer sweets over sour and bitter foods because, evolutionarily, our mesolimbic pathway reinforces that sweet things provide a healthy source of carbohydrates for our bodies. When our ancestors went scavenging for berries, for example, sour meant “not yet ripe,” while bitter meant “alert – poison!”
Fruit is one thing, but modern diets have taken on a life of their own. A decade ago, it was estimated that the average American consumed 22 teaspoons of added sugar per day, amounting to an extra 350 calories; it may well have risen since then. A few months ago, one expert suggested that the average Briton consumes 238 teaspoons of sugar each week.
Today, with convenience more important than ever in our food selections, it’s almost impossible to come across processed and prepared foods that don’t have added sugars for flavour, preservation, or both.
These added sugars are sneaky – and unbeknown to many of us, we’ve become hooked. In ways that drugs of abuse – such as nicotine, cocaine and heroin – hijack the brain’s reward pathway and make users dependent, increasing neuro-chemical and behavioural evidence suggests that sugar is addictive in the same way, too.
Sugar addiction is real
“The first few days are a little rough,” Andrew told me about his sugar-free adventure last year. “It almost feels like you’re detoxing from drugs. I found myself eating a lot of carbs to compensate for the lack of sugar.”
There are four major components of addiction: bingeing, withdrawal, craving, and cross-sensitisation (the notion that one addictive substance predisposes someone to becoming addicted to another). All of these components have been observed in animal models of addiction – for sugar, as well as drugs of abuse.
A typical experiment goes like this: rats are deprived of food for 12 hours each day, then given 12 hours of access to a sugary solution and regular chow. After a month of following this daily pattern, rats display behaviours similar to those on drugs of abuse. They’ll binge on the sugar solution in a short period of time, much more than their regular food. They also show signs of anxiety and depression during the food deprivation period. Many sugar-treated rats who are later exposed to drugs, such as cocaine and opiates, demonstrate dependent behaviours towards the drugs compared to rats who did not consume sugar beforehand.
Like drugs, sugar spikes dopamine release in the nucleus accumbens. Over the long term, regular sugar consumption actually changes the gene expression and availability of dopamine receptors in both the midbrain and frontal cortex. Specifically, sugar increases the concentration of a type of excitatory receptor called D1, but decreases another receptor type called D2, which is inhibitory. Regular sugar consumption also inhibits the action of the dopamine transporter, a protein which pumps dopamine out of the synapse and back into the neuron after firing.
In short, this means that repeated access to sugar over time leads to prolonged dopamine signalling, greater excitation of the brain’s reward pathways and a need for even more sugar to activate all of the midbrain dopamine receptors like before. The brain becomes tolerant to sugar – and more is needed to attain the same “sugar high.”
Sugar withdrawal is also real
Although these studies were conducted in rodents, it’s not far-fetched to say that the same primitive processes are occurring in the human brain, too. “The cravings never stopped, [but that was] probably psychological,” Andrew told me. “But it got easier after the first week or so.”
In a 2002 study by Carlo Colantuoni and colleagues of Princeton University, rats who had undergone a typical sugar dependence protocol then underwent “sugar withdrawal.” This was facilitated by either food deprivation or treatment with naloxone, a drug used for treating opiate addiction which binds to receptors in the brain’s reward system. Both withdrawal methods led to physical problems, including teeth chattering, paw tremors, and head shaking. Naloxone treatment also appeared to make the rats more anxious, as they spent less time on an elevated apparatus that lacked walls on either side.
Similar withdrawal experiments by others also report behaviour similar to depression in tasks such as the forced swim test. Rats in sugar withdrawal are more likely to show passive behaviours (like floating) than active behaviours (like trying to escape) when placed in water, suggesting feelings of helplessness.
A new study published by Victor Mangabeira and colleagues in this month’s Physiology & Behavior reports that sugar withdrawal is also linked to impulsive behaviour. Initially, rats were trained to receive water by pushing a lever. After training, the animals returned to their home cages and had access to a sugar solution and water, or just water alone. After 30 days, when rats were again given the opportunity to press a lever for water, those who had become dependent on sugar pressed the lever significantly more times than control animals, suggesting impulsive behaviour.
These are extreme experiments, of course. We humans aren’t depriving ourselves of food for 12 hours and then allowing ourselves to binge on soda and doughnuts at the end of the day. But these rodent studies certainly give us insight into the neuro-chemical underpinnings of sugar dependence, withdrawal, and behaviour.
Through decades of diet programmes and best-selling books, we’ve toyed with the notion of “sugar addiction” for a long time. There are accounts of those in “sugar withdrawal” describing food cravings, which can trigger relapse and impulsive eating. There are also countless articles and books about the boundless energy and new-found happiness in those who have sworn off sugar for good. But despite the ubiquity of sugar in our diets, the notion of sugar addiction is still a rather taboo topic.
Are you still motivated to give up sugar for Lent? You might wonder how long it will take until you’re free of cravings and side-effects, but there’s no answer – everyone is different and no human studies have been done on this. But after 40 days, it’s clear that Andrew had overcome the worst, likely even reversing some of his altered dopamine signalling. “I remember eating my first sweet and thinking it was too sweet,” he said. “I had to rebuild my tolerance.”
And as regulars of a local bakery in Hershey – I can assure you, readers, that he has done just that.«
Given the deadly global rampage that HIV has been on for the past few decades, you’re all probably familiar with the virus. But you may not be aware that there are two types of HIV—HIV-1 and HIV-2—with the former being significantly more prevalent worldwide. The most common type of HIV-1 is then further divided into distinct subtypes, some of which are associated with a more rapid progression to AIDS. If these different viruses meet in an infected person, for example if someone infected with one subtype is exposed to a different one, they can exchange bits of their genetic material to create a new virus.
One of these so called “circulating recombinant forms” is currently spreading through Cuba, and it’s unfortunately extremely aggressive. Individuals infected with this hybrid virus, which is a mix of three different HIV-1 subtypes, progress to AIDS more than three times faster than average. Now, scientists have scrutinized this particularly pathogenic strain, which has yielded insight into the traits that have bestowed it with this deadly efficiency. The findings have been published in EBioMedicine.
Before HIV can get inside our cells, it first needs to bind to receptors on the surface called CD4. While this is an essential first step, it’s insufficient to get the virus inside. This is where anchoring points, called coreceptors, come in, which HIV also has to latch onto to gain entry. There are two coreceptors, CCR5 and CXCR4, and around 90% of newly transmitted HIV uses the former.
CXCR4-using viruses emerge in around 50% of individuals, but this usually takes around five years from infection. These viruses are associated with a more pronounced depletion of immune cells, but whether this shift in coreceptor preference is a cause or consequence of disease progression is unknown. Interestingly, however, the aggressive recombinant currently spreading through Cuba starts to use CXCR4 very early on in infection, and researchers think this is likely contributing to the observed rapid progression to AIDS.
To find this out, researchers examined 73 recently infected patients in Cuba, 52 who had rapidly progressed to AIDS within three years and 21 without AIDS. Then, they compared the blood of these individuals with 22 patients who had progressed to AIDS after the period typically expected, which is around 10-15 years without treatment.
They found that all those who had progressed to AIDS within three years of infection were infected with a recombinant called CRF19, which is a mixture of subtypes A, D and G. Interestingly, infection with A/D recombinants has previously been reported to result in rapid progression to AIDS, but no CRFs had been exclusively associated with rapid progression. Furthermore, those infected with CRF19 had abnormally high levels of an immune response molecule called RANTES, which acts by binding to CCR5. Without this coreceptor available for binding, CRF19 may have been forced to bypass that anchor point and go straight for CXCR4. Since the switch to CXCR4 usage is associated with progression to AIDS, this could explain why those infected with CRF19 developed AIDS so early on.
Another reason that CRF19 might be so pathogenic is that it has an enzyme, called protease, from subtype D, which is known to be very efficient. This enzyme helps the virus form mature particles, which is an essential stage in the virus life cycle.
It might seem like science fiction but a new implant which attaches directly to the spine could help paralysed people walk again
Paralysed patients have been given new hope of recovery after rats with severe spinal injuries walked again through a ‘groundbreaking’ new cyborg-style implant.
In technology which could have come straight out of a science fiction novel or Hollywood movie, French scientists have created a thin prosthetic ribbon, embedded with electrodes, which lies along the spinal cord and delivers electrical impulses and drugs.
The prosthetic, described by British experts as ‘quite remarkable’, is soft enough to bend with tissue surrounding the backbone to avoid discomfort.
Paralysed rats who were fitted with the implant were able to walk on their own again after just a few weeks of training.
Researchers at the Ecole Polytechnique Fédérale de Lausanne are hoping to move to clinical trials in humans soon. They believe that a device could last 10 years in humans before needing to be replaced.
The implant, called ‘e-Dura’, is so effective because it mimics the soft tissue around the spine – known as the dura mater – so that the body does not reject its presence.
“Our e-Dura implant can remain for a long period of time on the spinal cord or cortex,” said Professor Stéphanie Lacour.
“This opens up new therapeutic possibilities for patients suffering from neurological trauma or disorders, particularly individuals who have become paralyzed following spinal cord injury.”
Previous experiments had shown that chemicals and electrodes implanted in the spine could take on the role of the brain and stimulate nerves, causing the rats’ legs to move involuntarily when they were placed on a treadmill.
But this is the first study to show a simple gadget can help rats walk again and be tolerated by the body.
Scientists have struggled to find a device which will sit next to the spine or brain because both are surrounded by a protective envelope of tissue which the hard surface of implants can rub against, causing inflammation and scar tissue
However the new gadget is flexible and stretchy enough that it can be placed directly onto the spinal cord. It closely imitates the mechanical properties of living tissue, and can simultaneously deliver electric impulses and drugs which activate cells.
The implant is made of silicon and covered with gold electric conducting tracks that can be pulled and stretched. The electrodes are made of silicon and platinum microbeads which can also bend in any direction without breaking.
Writing in the journal Science, where the results were published, science writer Robert Service said: “Soft flexible nerves connected to unyielding silicon and metal – the combination has spawned many a Hollywood cyborg.
“The implants Lacour’s team created still have to be wired to the outside world to operate, but she and her colleagues are designing wireless versions of the technology. Watch out, Hollywood, reality is catching up.”
The research was praised by British scientists.
“The work described here is a groundbreaking achievement of technology, which could open a door to a new era in treatment of neuronal damage,” said Dr Duško Ilić, Reader in Stem Cell Science at King’s College London.
“Until now, the most advanced prostheses in intimate contact with the spinal cord caused quite substantial damage to tissue in just one week due to their stiffness.
“There is still a long way to go before we may see any practical use of such neuroprostheses in humans. But it may be that it is something that could potentially be developed for use in humans in the foreseeable future.”
Prof John Hunt, Head of Unit of Clinical Engineering, University of Liverpool, added: “This study in rats is an interesting one and it could have the potential to be quite promising in terms of being applicable to people with spinal injuries.”
The implant has been primarily tested in cases of spinal cord injury in paralyzed rats but researchers believe it could eventually be used in epilepsy, Parkinson’s disease and pain management.
The scientists are planning to move towards clinical trials in humans within the next few years.
The research was published in the journal Science.
A new class of antibiotic has been discovered thanks to a new technique that could yield more of the same – an incredible boon in our fight against antimicrobial resistance.
Scientists in the US have discovered a new class of antibiotic that has been shown to kill Staph and Strep throat infections in mice. They say the way it kills bacteria will make it very difficult for them to evolve resistance in response to the attacks.
Last month, a report chaired by US economist Jim O’Neill predicted that 300 million people will die prematurely by the year 2050 thanks to antimicrobial resistance, if nothing is done to solve the problem. The report went on to add that our global GDP would dip by 0.5 percent by 2020 and will end up 1.4 percent smaller by 2030, purely due to the steady march of resistant bacteria.
In 2013, the chief medical officer of the UK, Sally Davies, announced that antimicrobial resistance would be put on the government’s national risk register of civil emergencies, to join the equally serious threats of terrorism, the pandemic flu, and major flooding.
Antimicrobial resistance is a huge problem, but we might finally have the upper hand in this power struggle between man and bug – a new antibiotic called teixobactin, which has been shown to kill a wide range of drug-resistant bacteria in lab mice, including those responsible for tuberculosis and septicaemia, plus Clostridium difficile colitis (C. dif) – the most common gut bug infection.
“Teixobactin kills exceptionally well. It has the ability to rapidly clear infections,” lead researcher and director of the Antimicrobial Discovery Centre at Northeastern University, Kim Lewis, told Ian Sample at The Guardian.
The secret to Teixobactin’s success is that it prevents microbes from being able to construct their cell walls, and holes in your cell walls means certain death. In fact, the antibiotic ended up killing 100 percent of the bacteria it came into contact with, and no survivors means there’s no one to evolve resistance. “That’s an Achilles’ heel for antibiotic attack,” the researcher who discovered this ability, Tanja Schneider from the University of Bonn, told Sample. “It would take so much energy for the cell to modify this, I think it’s unlikely resistance will appear this way.”
As Kelly Servick explains at Science Magazine, resistance usually occurs when a fraction of a population of microbes somehow survives an antibiotic attack because of a particular mutation, and then those mutated bacteria multiply into a separate resistant population.
“My guess is that if resistance is going to develop against Teixobactin, it will take more than 30 years for that to occur,” Lewis told CBS News.
Not only did Teixobactin kill off 100 percent of the bacteria it came into contact with, including Staphylococcus aureus (Staph infection) and Streptococcus pneumoniae (Strep throat), but it cleared these infections without any side-effects.
Which is all great, but perhaps even more exciting is how the antibiotic was discovered. “Most antibiotics are isolated from bacteria or fungi that churn out lethal compounds to keep other microbes at bay,” says Sample at The Guardian. “But scientists have checked only a tiny fraction of bugs for their ability to produce potential antibiotics because 99 percent cannot be grown in laboratories.”
Since the first antibiotic, Penicillin, was discovered by accident in 1928 by Alexander Fleming, scientists haven’t had a particularly efficient way of finding more. But recently, Kim Lewis’s team developed a device they’re calling the iChip, which can culture bacteria in their natural habitat – in this case, dirt. Bacteria are inserted into the device between two permeable sheets and dug into the ground, where the bacteria are free to grow into colonies as they would in the wild, except for the fact that they’re confined to their iChip chambers.
After two weeks, the researchers retrieved their iChip and were able to test the colonies that had grown in their natural habitat. “To do this, they covered the top of the iChip with layers of pathogens,” says Sample. “Bugs that produced natural antibiotics revealed themselves by killing the pathogens above them.”
The team paired up with NovoBiotic, a Massachusetts-based pharmaceuticals start-up, and researchers at the University of Bonn, and screened 10,000 different types of soil bacteria – cultured in the iChip – for antibiotics. They found 25 new antibiotic compounds, teixobactin being the most high-achieving of the lot. They published their results in Nature today.
Servick reports at Science Magazine that Teixobactin was so effective, it also outperformed Vancomycin – the antibiotic we currently rely on to treat methicillin-resistant Staphylococcus aureus (MRSA) – by a factor of 100. “In mice infected with MRSA, injections of teixobactin led to a 100 percent survival rate at lower doses than vancomycin,” she says.
It’s exciting stuff, but it’s still going to be a while before people can be treated with the antibiotic. Human trials are set to begin in about two years, and if they go well, development for the market will follow.
“Another shortcoming of Teixobactin is that it only works against bacteria that lack outer cell walls, known as Gram-positive bacteria, such as MRSA, Streptococcus and TB,” says Sample at The Guardian. “It doesn’t work against Gram-negative bacteria, which include some of the most worrying antibiotic-resistant pathogens, such as Klebsiella, E. coli and Pseudomonas.”
But hopefully that’s something Lewis’s team’s new iChip method will help solve.
“Any report of a new antibiotic is auspicious, but what most excites me about the paper is the tantalising prospect that this discovery is just the tip of the iceberg. Most antibiotics are natural products derived from microbes in the soil. The ones we have discovered so far come from a tiny subset of the rich diversity of microbes that live there.
Lewis et al. have found a way to look for antibiotics in other kinds of microbe, part of the so-called microbial ‘dark matter’ that is very difficult to study.”
The WordPress.com stats helper monkeys prepared a 2014 annual report for this blog.
Here’s an excerpt:
The concert hall at the Sydney Opera House holds 2,700 people. This blog was viewed about 10,000 times in 2014. If it were a concert at Sydney Opera House, it would take about 4 sold-out performances for that many people to see it.