Showing posts with label HEALTH AND MEDICINE. Show all posts
Showing posts with label HEALTH AND MEDICINE. Show all posts
When enough people are vaccinated against a contagious disease they will create protection for those who aren't vaccinated, in an effect known as "herd immunity".
This effect can eventually lead to the eradication of diseases and also helps those who are not able to receive vaccinations due to medical reasons, such as immunosuppressed children or those going through chemotherapy. But does it mean it's a good idea to ride on the back of the vaccinations of others? Here’s why it's important to keep vaccination rates as high as possible.
Redditor theotheredmund has created a GIF that shows how a contagious disease passes through different populations with varying percentages of its people vaccinated. The simulated data was based on research from a study published in Epidemiologic Reviews in 1993.
The 6-second animation clearly shows how populations with fewer people vaccinated allow the disease to spread significantly quicker and further through the chain of humans. On the other hand, if there is any outbreak in a population with widespread vaccination, the disease struggles to spread and the chains to others are cut. However, the effect of herd immunity is significantly dampened at each level of declining vaccination rates.
"Once you read a high enough level of vaccination, the disease gets effectively roadblocked. It can't spread fast enough because it encounters too many vaccinated individuals, and so the majority of the population (even the unvaccinated people) are protected," the creator explains on Imgur.
An experimental Ebola vaccine being trialled in Guinea has shown to be 100% successful in protecting people from contracting the disease, according to preliminary results announced today. This is the first evidence that a vaccine could shield people from getting the disease, and offers hope that it could be used to finally conquer the ongoing outbreak in West Africa, and any future one that might spring up.
“This is an extremely promising development,” announced Dr. Margaret Chan, director general of the World Health Organization. “The credit goes to the Guinean Government, the people living in the communities and our partners in this project. An effective vaccine will be another very important tool for both current and future Ebola outbreaks.”
The trial was based on the smallpox eradication strategy, using what’s known as a “ring” vaccination technique. After a patient is diagnosed with Ebola, a person’s friends and families are all vaccinated to try and break the main routes of transmission, and stop it spreading further. The trial of this approach in Guinea involved over 4,000 people, and while these initial results show 100% efficacy, the researchers predict that this might fall to between 75 and 100% when larger trials are conducted.
Due to the ethical implications of giving people a placebo vaccination, the researchers instead went for a trial design in which one group of subjects were vaccinated soon after their relative was diagnosed with Ebola, while the second group waited three weeks before vaccination. They found that no one contracted the disease in the first group within the 10-day infection window, but 16 were diagnosed with Ebola in the second group during that same period.
The results, published in The Lancet, have been so successful that from now on the delayed vaccination group will be abandoned and all people who have come into contact with an Ebola patient will receive the vaccination. The trial also only focused on adults, and so now it looks likely that adolescents and children will receive the vaccination too.
The vaccine itself was created using an attenuated livestock virus that has been engineered to produce a particular Ebola protein called rVSV-ZEBOV. The production of the vaccine has been hailed as remarkable due to the unprecedented speed at which it has been developed; rather than taking decades, it has only been 12 months.
“This is a remarkable result which shows the power of equitable international partnerships and flexibility,” said Jeremy Farrar, director of the Wellcome Trust, which was one of the funders of the trial. “This partnership also shows that such critical work is possible in the midst of a terrible epidemic. It should change how the world responds to such emerging infectious disease threats. We, and all our partners, remain fully committed to giving the world a safe and effective vaccine.”
While the vaccine has been shown to work “very well” for three weeks, now the researchers want to find out for exactly how long it offers protection.
There can be nothing more satisfying or refreshing than diving into a glistening lake or river to cool off, but in certain, exceedingly rare circumstances, this can prove to be a fatal mistake, thanks to a freshwater-dwelling amoeba. This has already been demonstrated once this summer, and saddeningly perhaps twice, as two cases of infection with this “brain-eating” parasite have already been reported in the U.S.
The organism blamed in both of these situations is a free-living, single-celled amoeba called Naegleria fowleri. It’s ubiquitous in the environment, meaning it’s found pretty much everywhere, but it’s heat-loving (thermophilic) and often found in warm freshwater, like lakes or hot springs. People are therefore often exposed to this organism and nothing comes of it, but in rare circumstances it can cause a serious brain infection called primary amoebic meningoencephalitis (PAM).
This usually only happens when the organism is forced up the nose, for example during recreational activities such as swimming or diving, which gives it an opportunity to breach the nasal cavity and subsequently make its way up the olfactory nerve – needed for smell perception – and into the brain.
From here, it feeds on nervous tissue using sucker-like structures, triggering an inflammatory immune response that causes a severe increase in pressure in the skull, ultimately killing the infected individual about 97% of the time.
The latest cases experienced in the U.S. have both been reported in the last month. The first was a 21-year-old woman from Central California, whose infection was confirmed by the Centers for Disease Control and Prevention (CDC), CBS News reports. After waking up on June 16 with nausea that had not resolved itself a day later, the victim was admitted to Northern Inyo Hospital where she was diagnosed with meningitis, which presents itself similarly. Her condition worsened and she later died after being transferred to a different hospital in Nevada.
It’s extremely difficult to ascertain where she contracted the amoeba, but according to CBS News, officials said it’s likely that she became infected on a private property that is inaccessible to the public. But even if it were an area commonly used by the public, panic would not be warranted as PAM is very rare.
The second case, however, is even more out of the ordinary. As reported by the Minnesota Department of Health, an ongoing investigation is taking place for a suspected case of PAM in a 14-year-old boy who is currently critically ill. Officials in the department established that he became infected in Lake Minnewaska, Pope County, marking the third infection to be witnessed in Minnesota in the past five years.
These three cases are interesting because the majority of U.S. infections have occurred in warmer southern states like Florida and Texas, and before 2010 it had never been reported above Missouri. This indicates that the organism is spreading northward, which could possibly be attributable to climate change given N. fowleri’s preference for warmer waters. But this doesn’t necessarily indicate a future rise in cases; between 2002 and 2011 only 32 infections were reported in the U.S., so they're still extremely rare.
Simply adding a low-cost hormone to the therapy of women suffering from breast cancer could slow tumor growth in about half of them, according to a new study released inNature. After treating the cancer with progesterone in combination with the hormonal drug Tamoxifen, researchers found that tumors were half the size of those treated with just the drug alone.
“This important research helps explain why some breast cancer patients have a better prognosis,” explains Dr. Jason Carroll from the University of Cambridge, who co-led the study. “Crucially, it has provided a strong case for a clinical trial to investigate the potential benefit of adding progesterone to drugs that target the oestrogen receptor, which could improve treatment for the majority of hormone-driven breast cancer.”
Scientists have already shown that by blocking the hormone estrogen from attaching to certain types of tumor cells that express estrogen receptors, it is possible to slow the cancer's growth. This is in effect what the drug Tamoxifen does, putting a brake on the cell division within the tumor.
But what they didn’t know was why those women who had tumors that express not only estrogen receptors, but also progesterone receptors – known as “double positive” cancers – have a far better chance of survival. It turns out that when progesterone binds to the tumor cell, it also alters the receptor for estrogen, changing its activity and basically putting a second brake on cell growth.
“We used state-of-the-art DNA reading technology to create maps showing where the estrogen receptor attaches to DNA to switch on genes,” says Carroll. “We then compared these maps in breast cancer cells grown with and without progesterone. This revealed how the 'switched on' progesterone receptor redirects the estrogen receptor to different DNA regions – switching on a different set of genes that slow down cell growth.”
With around 1.7 million women diagnosed with breast cancer each year, it’s thought that the new treatment – which is simply adding the cheap and easily available progesterone to Tamoxifen – could benefit up to half of them. But first, it needs to go through a clinical trial.
This research was only possible because researchers at the University of Adelaide were able to “rescue” tumor cells removed from participating patients, and use them to test new forms of therapy. They hope that in the future, this technique could even be used to provide personalized treatment for women by testing out different therapies on the cells in the lab before giving them to the patient.
photo credit: Micro life. Wyss Institute at Harvard University, Author provided
One of the greatest challenges to our healthcare system today is creating effective new drugs. Despite ever-increasing investments in research and development, the number of drugs that win approval for clinical use each year has steadily decreased over the past 50 years. It now costs of more than $2.5bn (£1.6bn) to bring a single compound from the bench to patients. Because many have to be developed to find one that works, drug costs have become exorbitant.
Part of the problem is that the animal models we use to test potential therapeutics often fail to predict results in humans. Very simply, a guinea pig is not a human. To overcome this limitation, drug companies have tried to use human cell cultures to test drugs in the laboratory. But these too are poor predictors of how drugs will work in patients because they fail to accurately replicate the complexity of human organs. As a result, there has been a search for more accurate ways to mimic human organ functions outside the body.
We recognised part of the problem is that human cells are usually cultured on rigid plastic dishes in a static pool of medium, and in isolation from other cell types. In contrast, living organs are composed of two or more different types of tissues that interact with one another physically and chemically. These organs depend on flow of blood and other body fluids for their survival and function. They also experience dynamic physical motions, such as breathing in the lung and peristalsis (the movement of food using muscle contractions) in the intestine, which clinicians know to be crucial for normal physiology.
Knowing this, we distilled down the essence of organ design into three fundamental principles. First, the establishment of a tissue-tissue interface where organ-specific cells and blood vessel lining cells come together. Second, the provision of fluid flow to mimic blood flow. And third, reconstitution of physiological mechanical motions, such as rhythmic expansion and contraction of the air sacs in our lungs or peristalsis in our intestines.
Inspired by these key biodesign principles, we adapted manufacturing techniques from the computer microchip industry that allow the creation of cell-sized features to create artificial human “organs-on-chips”. These computer memory stick-sized devices are made of crystal-clear, flexible rubber and contain a central hollow channel. This channel is thinner than the width of a pencil lead and is separated into an upper and lower channel by a thin flexible porous membrane.
Lung on a Chip
To make a lung-on-a-chip, for example, living human cells from the lung’s air sacs are cultured on the top of the membrane, while cells from human blood capillaries are placed on its lower surface. This replicates the normal tissue-tissue interface that mediates the gas exchange and the inflammatory response to infections in the lungs.
Air is then placed over the lung cells and a nutrient medium or whole blood containing human white blood cells is flowed through the lower channel. Finally, applying suction to the flexible tube’s side chambers causes the interfaced tissues to repeatedly stretch and relax. The result is a tiny replication of the process of breathing in and out that occurs in the lung.
When we introduced living bacteria into the air space of the lung chip, we triggered an infection within the chip. The white blood cells flowing through the vascular channel responded by migrating into the air space where they engulfed the invading germs, just as they do inside living lungs.
Six millimetre man Wyss Institute at Harvard University, Author provided
The lung chip also has been used to mimic diseases, such pulmonary edema or “fluid on the lungs”, and to identify new drug candidates that prevent this condition. Since then, we have fabricated many other organ chips, including a “gut-on-a-chip” that mimics the peristalsis movements that push food through the digestive tract. And our kidney chipfaithfully mimics drug toxicities that occur in humans, but not in animal models. We have even started to link different types of organ chips by their channels to begin to create a human body-on-chips that can help analyse the way that drugs are absorbed, metabolised and cleared as they move throughout the body.
Given that it is now possible to create stem cells from normal cells taken from any individual, patient-specific organs-on-chips may one day be used to test how a drug might affect a particular person. However, the game-changer is how this technology could transform drug development. Most pharmaceutical companies carry out huge clinical trials that usually fail, and then they sift through the data searching for a subgroup of patients who might have responded better than others. They then initiate a new clinical trial on this small group of patients.
But by creating organs-on-chips populated by cells from a known patient subpopulation, we might be able to develop drugs specifically for this group, and then execute a small clinical trial with these same patients. This could revolutionise drug development by shortening timelines, drastically reducing costs, and greatly increasing the likelihood of success.
In a quite unusual turn of events, our human organs on chips were recently honored with the 2015 Design of the Year Award from the London Design Museum. Perhaps this is because simplicity combined with impact is the true essence of design.
Hailed as a “breakthrough” at the time, research conducted by a scientist in the U.S. led us to believe that a vaccine for HIV could be well within our grasps. But raised hopes quickly came crashing down when, a few years ago, it was realized that the promising findings were the result of spiked samples and data fiddling.
Now, the scientist behind the multi-million dollar scam, Dong-Pyou Han, has received his punishment for the crime, and it’s much more than a slap on the wrist: He will serve more than four and a half years behind bars and cough up $7.2 million to cover the federal funding he received for the research.
This is not only an extremely rare occurrence in research, with only a handful of scientistshaving been sent to prison for scientific misconduct so far, but also a significant step up from the telling off he originally received. After his research institution, Iowa State University, concluded that he had been fabricating data back in 2013, he was forced to admit his guilt and resign. He was also given a three-year ban on receiving federal research funds, and his university had to pay back half a million dollars to the National Institutes of Health to cover the salary he was given.
Unfortunately for Han, his case caught the eye of Iowa Senator Charles Grassley, who has investigated similar cases before, meaning that the repercussions from his criminal actions were far from over. “This seems like a very light penalty for a doctor who purposely tampered with a research trial and directly caused millions of taxpayer dollars to be wasted on fraudulent studies,” Grassley wrote in a letter to the office that hands out punishments for scientific misconduct.
Following a storm in the media, charges were pressed in 2014 and his case was later presented to a grand jury, in which he pled guilty. It might be unusual for cases to go this far, but that doesn’t mean he is undeserving of his sentence: He spent years flushing hard-to-come-by funds down the drain and deceived people into thinking we could be close to a desperately needed HIV vaccine. According to the Washington Post, here’s how he did it.
Seven years ago, Han was working in the lab of Professor Michael Cho, who at the time was based at Case Western Reserve University. His team began injecting an experimental HIV vaccine into rabbits to see if it could evoke an appropriate immune response, and remarkably it seemed to work. Antibodies were discovered in the blood samples, suggesting the animals were starting to tackle the virus. Of course, Cho was ecstatic about the finding and requested more money to continue the research.
Little did he know that the antibodies were actually the result of a mix up with samples that contained human antibodies. But rather than coming clean of the supposedly accidental error, Han continued to lace samples with human antibodies, making it look more and more convincing that the candidate could be the groundbreaking vaccine everyone had been yearning for.
While repeatability is critical in scientific research, Han had obviously failed to take this into consideration and, of course, other groups later tried to replicate the findings. After requesting a sample from Cho’s lab to assist their investigation, Harvard researchers were a tad surprised to find human antibodies in a rabbit blood sample. An investigation was launched, and Han had no choice but to admit what he had done.
While scientists should not be immune to the law, some have questioned whether jail time will achieve anything, although such a harsh sentence may serve as a deterrent from future acts.
Doctors have started treating stroke patients with a tiny new device that grabs blood clots blocking arteries within the brain.
The procedure, called mechanical thrombectomy, involves threading a catheter tube through an artery in the groin up to the clot that’s blocking oxygen from reaching the brain. Once there, the tiny, wire mesh cage snatches up the clot, traps it, and the device is pulled back out. The thrombectomy should be performed within six hours of acute stroke symptoms and only after the patient first receives a clot-busting drug called tissue plasminogen activator, or tPA.
Earlier this week, the American Heart Association and the American Stroke Association issued guidelines that urged doctors to use this approach for treating the worst kinds of strokes. The recommendation comes after five studies were published in New England Journal of Medicine over the last six months showing how the treatment improves the chances that certain stroke patients will not only survive but also function normally again.
The clot-busting drug tPA, which was approved by the U.S. Food and Drug Administration back in 1996, is effective when given intravenously within 4.5 hours. But it doesn’t completely dissolve clots in larger arteries. While these cases occur in only a fraction of the 690,000 Americans who suffer a clot-induced stroke every year, the larger clots are often the most deadly and disabling.
At least two of these so-called stent retrievers (or “stentrievers”) have been FDA-approved since 2012: Solitaire by Medtronic and Trevo by Stryker. These newer stents are safer and more effective than older devices, which resembled a corkscrew.
“Everything is different than it was a year ago,” William Powers from the University of North Carolina at Chapel Hill says in a statement. He led the panel that wrote the new guidelines. Stent retrievers are already being used across the U.S., and up to 13,000 thrombectomies were performed in the country last year.
According to the American Stroke Association, the telltale warning signs of stroke include: face drooping, arm weakness, and speech difficulty. Patient showing these symptoms should be rushed to a hospital in order to receive tPA. “Once that’s done,” Powers adds, “the question we should all now be asking is, will the patient benefit from this additional treatment?”
