Tag Archives: cure

HPV vaccine will also be administered to boys in the UK, preventing thousands of cancers

In a new programme aimed to protect boys from the risk of HPV-associated cancers, British boys will now also receive the HPV shot, which is estimated to prevent 100,000 cancers by 2058.

HPV-infected cells (bottom right). Image credits: Ed Uthman.

What’s HPV

The Human papillomavirus (HPV) is the most common sexually transmitted infection in most parts of the world. In the US, it’s estimated that 79 million people (most of them in their teens or early 20s) are infected with the virus. You can get HPV by having vaginal, anal, or oral sex with someone who has the virus.

Even if they exhibit no symptoms at all, they can still pass the virus. Sometimes it takes years for symptoms to develop, which makes it difficult to assess when the first infection took place.

In most cases, HPV goes away on its own. There’s a good chance you might have had it at some point in your life and not even realized it. But when HPV doesn’t go away, it can cause

An estimated 561,200 new cancer cases worldwide (5.2% of all new cancers) were attributable to HPV in 2002, although in recent years, vaccination campaigns have brought that rate down somewhat. The vast majority of them were cervical or throat cancers — the latter of which can affect both men and women. HPV can also cause cancers in the vulva, vagina, penis, or anus.

HPV vaccination

Three vaccines of different types of HPV exist on the market, and they have proven extremely effective in protecting against HPV cancers. However, most campaigns focus on girls, since the main target is eradicating cervical cancer. Now, the UK will administer the vaccine to boys also, which is expected to prevent thousands of cancer cases every year.

The best time for vaccination is around 11-13 years old. It is recommended that the vaccine is administered before the recipient has started a sexual life. In the UK, boys aged 12 and 13 will be offered the vaccine in secondary schools as of the next term. Boys who are 14-18 can also get a jab, but they will need to pay for it.

This move has been hailed by the science and medical community. In Australia, the vaccine has been implemented for girls since 2007 and for boys since 2013. This resulted in the HPV rate for young women dropping from 22% to 1% — and similar trends are being reported in boys.

There is a realistic chance of eradicating most HPV-associated cancers for both men, and women, says David Elliman, immunization expert for the Royal College of Paediatrics and Child Health.

“In time, this will lead to a significant reduction in cancers of the anus, penis and head and neck,” he said.

“The latter is currently increasing in incidence, but this trend will be turned around as the vaccination programme takes effect in the future.”

Data recently published in the Lancet shows that HPV infections could be essentially wiped out from developed countries within decades. Data recently published in The Lancet showed an 83% reduction in infections in 15- to 19-year-old girls over five to eight years, with researchers finding “compelling evidence of the substantial impact of HPV vaccination programmes on HPV infections”. Australia, which was the first country to introduce a nationwide HPV vaccination programme in 2007, is on track to eliminate it within 20 years. A recent statement published in the British Medical Journal supports this higher vaccine coverage, emphasizing that it can eliminate cervical cancer, and substantially reduce a number of other cancers.

Unfortunately, there is still a stigma associated with HPV infections, as is the case with other sexually transmitted infections. This is why it’s so important to set up a universal vaccination programme and make sure that nobody is left out.

HIV budding.

Scientists tie antibody escorts on white blood cells’ access points to stop HIV dead in its tracks

Researchers have developed a new technique that could provide long-term defense, possibly even a cure, for HIV patients. The method calls for HIV-antibodies to be anchored to immune cells, creating a population of resistant cells which can then take the fight to the virus.

HIV budding.

HIV budding (spherical growth on the left) in a cultured white blood cell.
Image credits C. Goldsmith / CDC.

Scientists at the Scripps Research Institute (TSRI) may have found a way to hit HIV where it hurts it the most — by taking away the virus’ ability to infect white blood cells. The work is remarkable for its shift in the way antibodies are deployed against HIV. Instead of launching a full-body (but low density) flood of antibodies which float freely in the bloodstream, TSRI researchers led by study senior author Richard Lerner, M.D., Lita Annenberg Hazen Professor of Immunochemistry at the institute, have developed a way in which antibodies can be piggybacked directly on white cells. These active compounds will be tied to the same receptors HIV uses to enter the cells, making out immune system finally immune from the dreaded virus.

“This protection would be long term,” said Jia Xie, senior staff scientist at TSRI and first author of the study.

It comes down to something Xie calls the “neighbor effect.” As the old adage goes, one antibody in hand is worth a hundred five capillaries away. Ok, I may have taken some liberty with that but the underlying idea is that concentrating antibodies to first and foremost defend white cells allows our bodies to join in on the fight — regular treatments can’t do that, and they’re left with a lonely uphill battle against HIV. Even worse, in case HIV is flushed out of the system but the patient gets infected again, his or her immune system will be just as abysmal at fighting off the virus.

Safety first, advances second

Before tailoring the technique against HIV, the team worked with rhinovirus (the bug responsible for most common colds) as a test subject. A lentivirus was used as a vector to deliver a set of genes to a culture of human cells, instructing them to manufacture antibodies and bind these to the receptor rhinovirus ties to (ICAM-1). The rhinovirus was then unleashed upon the culture, but with no access point inside the cells it shouldn’t infect most of them, the theory goes.

That ‘most’ is exactly why they didn’t start testing off the bat with HIV. Gene delivery systems are basically dumbed down viruses with edited genomes, which have to infect cells and paste their genetic data inside the host’s genome. But no system can reach all cells, so the culture became a mix of edited (immune) and non-edited (vulnerable) cells. The point of the experiment was to see how the colony as a whole would fare.

It actually went pretty good. There was an initial shock of about two days when the majority of cells died off. Control cultures, which held only unedited cells, never recovered after the infection. Mixed cultures, however, got back to about the same numbers as prior to infection after about 125 hours — only this time, they were all descendants of the most resistant cells. In essence, the team forced the cultures to go through an evolutionary crash course in the lab dish. All the vulnerable cells were consumed in the infection and the resistant cells multiplied and passed off their anti-rhinovirus genes along.

“This is really a form of cellular vaccination,” said Lerner.

HI virion structure.

The best thing about this study is that HIV is technically a lentivirus. Nothing beats a dash of irony to go with your scientific win.
Image credits Thomas Splettstoesser.

Next, they used the same system against HIV. The team tested a number of antibodies to find one which could protect the CD4 receptor (the one HIV uses) on immune cells, copied the corresponding genes in the lentivirus, then let them loose upon the culture. And again, it worked. They further showed that these tethered antibodies worked more efficiently at blocking HIV than free-floating antibodies in another experiment led by study co-authors Devin Sok of the International AIDS Vaccine Initiative (IAVI) and TSRI Professor Dennis Burton.

TSRI now plans to collaborate with researchers at City of Hope’s Center for Gene Therapy to get early efficiency and safety testing done prior to human trials, as per federal regulations.

“We at TSRI are honored to be able to collaborate with physicians and scientists at City of Hope, whose expertise in transplantation in HIV patients should hopefully allow this therapy to be used in people,” Lerner added.

The paper “Immunochemical engineering of cell surfaces to generate virus resistance” has been published in the journal Proceedings of the National Academy of Sciences.

Drugs clear HIV from British patient’s system, offering hope for a cure

A new treatment has shown “remarkable” progress in fighting HIV, doctors report. The work is being carried out by five of Britain’s top universities — Oxford, Cambridge, Imperial College London, University College London and King’s College London — coordinated by the NHS.

Scanning electromicrograph of an HIV-infected H9 T cell.
Image credits NIAID / flickr.

A 44-year-old British man could become the first ever patient to be cured by HIV using a treatment developed by five UK universities working together. The man (who has asked to remain anonymous) is one of 50 trial patients for a new drug that can attack the virus even in its dormant form, the team reports.

The man’s blood has been tested clean of HIV, the scientists told The Sunday Times, although that could be the effect of regular treatments. The catch with the virus — and what’s made it so tricky to cure in the past — is that it can infect white T-cells, splicing itself into their DNA. Not only does this make the cells ignore the virus, but after the drugs clear a patient’s system, they actually produce more of the virus. If these infected cells were cleared out, it could prove to be the first real cure for HIV — and that’s what the team has been working on.

“This is one of the first serious attempts at a full cure for HIV,” said managing director of the National Institute for Health Research Office for Clinical Research Infrastructure Mark Samuels.

“We are exploring the real possibility of curing HIV. This is a huge challenge and it’s still early days but the progress has been remarkable.”

Currently, the most efficient treatment we have against HIV are anti-retroviral therapies (Art), which work pretty well at destroying the virus but they can’t spot the infected T-cells. The new treatment uses a two-pronged attack. First, a vaccine teaches the body how to identify HIV-infected cells so our immune system can clear them out. Secondly, a drug called Vorinostat is used to activate the dormant T-cells which start producing HIV-specific proteins, turning them into huge targets for healthy white cells.

Imperial College London consultant physician Professor Sarah Fidler said the treatment worked in the laboratory and there was “good evidence” it will work in patients. She also stressed out that just because a drug worked once doesn’t make it a treatment yet — “We are still a long way from any actual therapy,” she said.

The anonymous patient, a social worker from London, is understandably excited about the results:

“It would be great if a cure has happened. My last blood test was a couple of weeks ago and there is no detectable virus.”

“I took part in the trial to help others as well as myself. It would be a massive achievement if, after all these years, something is found to cure people of this disease. The fact that I was a part of that would be incredible.”

Only two other people have ever been cured of HIV. One is Timothy Brown, also known as The Berlin Patient, who received a stem cell transplant from a patient with natural immunity to HIV in 2008. The other, a Mississippi newborn, seemed to have been cured through anti-retroviral therapy in 2013, an undoubtedly unique case.

Hopefully, they’re just the first in what’s to become a very long list of successes.

An antibody that clears Alzheimer’s patients’ brains of plaque could be the treatment we’ve been waiting for

A recent breakthrough has left scientists “trying not to get too excited” as a new antibody cleared all visible signs of Alzheimer’s disease from human subjects’ brains.

Brain scans of Alzheimer’s patients, showing how different doses of the drug reduced the number of amyloid plaques, in red, over a year. Image credits Sevigny et al.

A novel drug based on immune cells harvested from elderly patients aged up to 100 who show no signs of Alzheimer’s could finally allow us to treat the degenerative brain condition. Small-scale human trials led by scientists at pharmaceutical companies Biogen and Neurimmune showed that the drug aducanumab can completely clear the visible signs of Alzheimer’s from the brain.

The team scanned the brains of patients as they were undergoing treatment with the drug. They found that after a year, almost all of the toxic amyloid plaques that build up in their brains were cleared in patients given the highest antibody dose. The scientists also said the patients showed signs that the rate of their cognitive decline had slowed.

Amyloid is a protein found throughout the body but for unknown reasons, in Alzheimer’s patients, it divides imperfectly, creating beta amyloids which are toxic to brain cells and accumulate as plaques on the outside of neurons. The trial’s results suggest that these plaques aren’t a simple byproduct of the condition, but are at least part of what cause it.

The team is understandably very excited about the results.

“Compared to other studies published in the past, the effect size of this drug is unprecedented,” Zurich University Professor and co-author of the paper Roger Nitsch told The Independent.

As part of the trial, different participants received different doses of the drug and a control group which received a placebo treatment.

“One year later, the images of the placebo group are basically unchanged. In the three doses groups, a very clear reduction in amyloid plaques is shown – the higher the dose, the larger the degree of reduction,” Nitsch said.

For the 10mg group, which received the highest dose, the amyloid plaque was almost completely removed.

It’s crucial however that we don’t jump ahead of ourselves here. Aducanumab has been seen to work, but only in a small-scale study. Until the results are reproduced at a larger scale, the drug’s effectiveness is still unproven. If the results are confirmed in larger trials, the drug could become out best tool to cure the condition. Until then, however, as Arizona University Professor Eric Reiman commented in a separate article in Nature:

“Although the authors’ additional cognitive findings are encouraging, they are not definitive. It would be prudent to withhold judgement about aducanumab’s cognitive benefit until results from the larger trials are in.”

However, he shares the enthusiasm of the team for their findings.

“Confirmation that an anti-amyloid plaque treatment slows cognitive decline would be a game-changer for how we understand, treat and prevent Alzheimer’s disease. Now is the time to find out.”

Other experts in the field also have high hopes for the drug but try to keep an objective outlook on the trials. For example, Dr Tara Spires-Jones, interim director of Edinburgh University’s Centre for Cognitive and Neural Systems, said the research showed that the antibody “robustly reduced amyloid pathology in a small group of people in very early stages of the disease”. She said she’s optimistic about the treatment but is trying “not to get too excited” as many drugs that seem promising in small-scale tests fail when scaled up.

Dr James Pickett, head of research at the Alzheimer’s Society, said that the “results are the most detailed and promising that we’ve seen for a drug that aims to modify the underlying causes of Alzheimer’s disease”.

“The study showed that the drug was first able to remove clumps of amyloid – a toxic protein associated with Alzheimer’s – from the brain of mice and also, excitingly, in people. What is most compelling is that more amyloid was cleared when people took higher doses of the drug,” he added.

“No existing treatments for Alzheimer’s directly interfere with the disease process – and so a drug that actually slows the progress of the disease by clearing amyloid would be a significant step.”

He noted that there is evidence of side-effects such as headaches associated with the drug and that the initial trial had not been designed to measure whether the drug slowed the decline in memory and thinking. Pickett too is waiting for the results of larger trials — some already underway in the Uk — to better understand if and how the drug works.

Gordon Wilcock, emeritus professor of geratology at Oxford University, hopes that the trials will bear fruit despite the fact that similar strategies have previously failed to pan out.

“We have already had previous trials of various anti-amyloid strategies, especially the monoclonal antibodies, that have failed to deliver at phase three.

“Nevertheless these trials are justified by the data and I hope they are successful, despite my feelings of déjà vu!”

The full paper, titled “The antibody aducanumab reduces Aβ plaques in Alzheimer’s disease” was published in the journal Nature.

Scientists move closer to world’s first Alzheimer’s disease vaccine

A team of researchers from the United States and Australia has made a breakthrough in the creation of a vaccine that can target the abnormal beta-amyloid and tau proteins that are involved in the development of Alzheimer’s disease.

Image credit Pixabay

Image credit Pixabay

Each year, 7.5 million people develop Alzheimer’s and it is quickly becoming one of the biggest costs to healthcare systems worldwide. Despite ongoing research, scientists have yet to discover a cure for the disease. However, the recent findings published in Scientific Reports suggest that an effective vaccine might be on the horizon.

“If we are successful in pre-clinical trials, in three to five years we could be well on the way to one of the most important developments in recent medical history,” said Nikolai Petrovsky of the Flinders University School of Medicine and co-author of the study.

Petrovsky highlights the necessity of a vaccine by pointing to the increase in type 2 diabetes cases in the West, which fuels the rise in dementia, as well as our rapidly aging populations.

The team used a combination of anti-amyloid-beta and anti-tau vaccines and an adjuvant technology called Advax to create a vaccine that generates antibodies that effectively bind to the amyloid and tau molecules in brain tissue obtained from patients with Alzheimer’s disease. Thus far, the vaccine has not shown any negative effects on immune system response.

“This study suggests that we can immunize patients at the early stages of AD, or even healthy people at risk for AD, using our anti-amyloid-beta vaccine, and, if the disease progresses, then vaccinate with another anti-tau vaccine to increase effectiveness,” said Anahit Ghochikyan of the Institute of Molecular Medicine (IMM) Department of Molecular Immunology and co-author of the study.

As of now, the team is working on non-clinical safety-toxicology studies to ensure that the vaccine meets government safety standards. After these pre-clinical studies are completed, they plan to move on to human trials.

Journal Reference: Alzheimer’s disease AdvaxCpG- adjuvanted MultiTEP-based dual and single vaccines induce high-titer antibodies against various forms of tau and Aβ pathological molecules. 22 June 2016. 10.1038/srep28912

Malaria protein that kills cancer to begin human trials in 2019

Scientists have in the past toyed with the idea of using a disease to fight cancer. Now, after identifying a malaria protein that binds to cancer cells and kills 95% of tumor types, human trials are expected to start within four years.

Malaria protein (green) binding to cancer cells. Image via Futuretimeline.

I doesn’t seem like it’s happening fast, but it is, in medical terms. Clinical trials take a lot of time, and there are several stages through which any proposed treatment has to pass – and even clinical trials have several stages which can take a lot of time. But this treatment promises to go through them quite fast, especially given its potential.

The researchers from the University of British Columbia (UBC), Vancouver Coastal Health and the BC Cancer Agency initially discovered that a protein from malaria halted cancer spread in mice. Interestingly, the hints for this discovery were initially offered by scientists from the University of Copenhagen, where they were studying why pregnant women are so susceptible to malaria. They found that the mosquito-borne parasite produces a protein that binds to a particular type of sugar molecule in the placenta. You can read all about their find here.

This finding led to another: that same sugar molecule is also found in most cancers. This makes quite a lot of sense, because both cancers and placentas grow fast, pushing other processes out of their way. The researchers then thought that targeting this molecule can work against cancer – eliminating its growth fuel, and stopping cancer growth.

“Scientists have spent decades trying to find the biochemical similarities between placenta tissue and cancer, but we just didn’t have the technology to find it,” said project leader Mads Daugaard, an assistant professor at UBC. “When my colleagues discovered how malaria uses VAR2CSA to embed itself in the placenta, we immediately saw its potential to deliver cancer drugs in a precise, controlled way to tumours.”

The drug was already tested on mice that were implanted with three types of human tumours, and the results were very encouraging.

“This is an extraordinary finding that paves the way for targeting sugar molecules in pediatric and adulthood human cancer, and our groups are vigorously pursuing this possibility together,” said UBC professor Poul Sorensen, co-senior investigator on the study.

“There is some irony that a disease as destructive as malaria might be exploited to treat another dreaded disease,” said Ali Salanti, a professor of immunology and microbiology at the University of Copenhagen. “The biggest questions are whether it’ll work in the human body, and if the human body can tolerate the doses needed without developing side effects. But we’re optimistic, because the protein appears to only attach itself to a carbohydrate that is only found in the placenta and in cancer tumours in humans.”

At the very latest, human trials  will start in 2019. It may be a very big year.

Study bolsters hope for lung cancer pill

A much anticipated and highly expected drug could come from Pfizer Inc, the biggest drug company in the world; the drug appears to double survival over standard approved drugs, but only against lung tumours with a certain mutation. The drug, called crizotinib, would be the first targeted treatment for the roughly 50,000 people who get this cancer each year worldwide, and it would also greatly benefit the pharmaceutical company, producing an annual revenue of over $2 billion.

The twice-a-day pill showed very promising results in studies, ensuring that 3 out of every 4 patients with advanced lung cancer lived past the first year, and over half of them lived after the second year; this, even if it is sad to say, are indeed very promising results.

Dr. Alice Shaw, a Mass. General oncologist who was also the lead researcher in this project explained how this treatment works by basically turning off an enzyme which stimulates the growth and mantains the survival of the cancer cells; without that enzyme, the cancer dramatically slows down, allowing the body to regain strength, and there are even hopes of total remission.

Lung cancer is responsible for 1.3 million deaths anually; in the US alone, some 30.000 people are diagnosed with lung cancer each year, and out of them, about 14 percent live past the five year mark. Of course, smoking is the main cause of the disease, accounting for over three quarters of the victims.

Algae gene therapy could cure blindness

Researchers have managed to restore light perception to mice through gene therapy, by inserting algae genes into the retina. The treatment has succeeded in restoring the ability to sense light and dark to blind mice, and clinical trials in humans could begin in as little as two years.

“The idea is to develop a treatment for blindness,” says Alan Horsager, a neuroscientist at the Institute of Genetic Medicine at the University of Southern California, Los Angeles, who leads the research. “We introduce a gene that encodes a light-sensitive protein, and we target the expression of that gene to a subset of retinal cells.”

It is estimated that over 15 million people worldwide suffer from one form or another of blindness, like the most common retinitis pigmentosa (RP) or age-related macular degeneration (AMD). Most affections relate to the photoreceptors in the retina, which transform light hitting the eye into electrical impulses, this way preventing the brain from receiving image information.

Scientists based their very creative gene therapy on the Channelrhodopsin-2 (ChR2), a photosensitive protein used by unicellular algae to help them move towards light, which they injected into the mice retina via a “domesticated” virus. The procedure was conducted on three groups of mice: one with normal vision, and two groups of mouse strains that naturally become blind with age in a similar way to people with RP and AMD. One of hte blind groups was subjected to gene therapy.

After dissection, treated mice reveled in their retinas that the  ChR2 protein was being indeed expressed by the bipolar cells. The biggest revealing data which poised researchers to believe their on the right track is their maze experiment in with blind and treated mice alike were put in the middle of a 6 corridor maze, with only one possible exit which was lighten. Scientist found that treated mice managed to find the exit on average 2.5 times faster than untreated blind mice.

“It’s a good paper, and it’s clear that they are heading towards a clinical trial with the information they are gathering,” says Pete Coffey of the department of ophthalmology at University College London. But he points out that although there is a statistical difference between the performance of the treated and untreated mice, that difference is small.

Even though this particular research, published in Molecular Therapy, might only render human patients to experience light/dark discrimination, it’s still some sort of progress, different from current non-commercial stem cell treatments, and in my opinion provides a definite step forward to curing what’s maybe one of the most tragic, yet common, affections of humanity.


Photograph of nanobots killing off cancer


Take a really good look at this picture; you may just be looking at the very thing that will defeat cancer. The black dots are nanobots, practically delivering a killing blow to the cancerous cells, and only to those cells. According to Mark Davis, head of the research team that created the nanobot anti-cancer army at the California Institute of Technology, the above mentioned technology “sneaks in, evades the immune system, delivers the siRNA, and the disassembled components exit out”.

According to the study published in Nature, you can use as many of these nanobots as you wish, and they’ll keep on raiding and killing the cancerous cells and stoping tumours.

“The more [they] put in, the more ends up where they are supposed to be, in tumour cells.”

The technology has its roots on RNA interference, a discovery that brought Andrew Fire and Craig Mello the Nobel Prize in 2006.

“RNAi is a new way to stop the production of proteins,” says Davis. “What makes it such a potentially powerful tool, he adds, is the fact that its target is not a protein. The vulnerable areas of a protein may be hidden within its three-dimensional folds, making it difficult for many therapeutics to reach them. In contrast, RNA interference targets the messenger RNA (mRNA) that encodes the information needed to make a protein in the first place. In principle,” says Davis, “that means every protein now is druggable because its inhibition is accomplished by destroying the mRNA. And we can go after mRNAs in a very designed way given all the genomic data that are and will become available.”

This is just the first demonstration CalTech performed, but it went on perfectly, and the results are quite promising. We will hold our fingers crossed.

Bacteria wouldn’t go for a swine flu shot

swine-flu-vaccineJust like many categories of people, I’ve recently been (insistently) offered a free flu shot. I said no. Without going into the reasons that determined me to do this, let’s look at what would determine the average bacteria to do the same thing, at least according to Tel Aviv University bacteria expert Prof. Eshel Ben-Jacob.

Bacteria have inhabited this planet for some 4 billion years before we did, and they’ll probably be here long after we’re gone. At the very least, it’s safe to say we have something to learn from them; and if you’d look at them carefully, you’ll find that the average bacteria would just say no to the swine flu vaccine. In his latest research, professor Ben-Jacob studies the decision-making process of bacteria as analogue to game theory and creates a truly fascinating model to support his case.

“Unlike our health authorities, bacteria would never panic,” he says. “Bacteria don’t follow the media or watch cable news. Instead, they send chemical messages to each other –– in a colony 100 times larger than the earth’s human population –– to make their decisions. And based on what we’ve seen in bacterial colonies, I know they would be suspicious committing to swine flu shots. They wouldn’t opt for a colony wide vaccination,” Prof. Ben Jacob concludes.

His research, done in collaboration with Dr. Daniel Schultz, a postdoctoral fellow at TAU, and Profs. José Onuchic and Peter Wolynes at the University of California/San Diego looks at a variety of things we can learn from these microscopic creatures, such as a way to deal better with health related mass emergencies or giving investors some clues as to how to deal with the stock portfolio (which we’re not gonna go into here).

bacteriaIt’s a well known fact by now that bacteria ‘communicate’ via chemical signals, but the above mentioned scientists found that they reach a common decision in very sophisticated ways, using a network of chemical signals, proteins and genes to calculate odds, just like in the game theory. Basically, when put in a life or death situation, the bacteria use more advanced tactics than previously thought; they don’t use the prisoner’s dilemma (in case you don’t know: two prisoners are given the choice to betray each other or remain silent. If one betrays the other and the other remains silent, the betrayer goes free and the other one gets 10 years in prison. If they both remain silent, they both get just 1 year of prison; and if they both betray, they both get 5 years in prison. Of course they aren’t allowed to speak to one another. The temptation would be of course to betray and not risk 10 years in jail, but you could get 4 extra years, it all depends on how you mentally collaborate with your fellow prisoner).

When it comes to bacteria, there are not two put in the approximate situation, but rather two hundred billions that have to decide whether to all turn into spores or not. Each has to decide whether to participate in this or not, and tell the other what they will do. In real (bacteria) life, there’s also a clock ticking, so the decision has to be taken quickly. The thing about them is that they don’t lie… usually. Prof. Ben Jacob explains that the ones with a bigger chance of surviving won’t cheat to postpone the decision of the others. The model they elaborated analyzes how they calculate the risks that naturally come with either decision.

Though it’s a bit of a stretch, mankind could be put in the situation of the prisoner’s dilemma; on one hand, you could think that if everybody (or almost everybody, at least with a high infection risk) takes the vaccine (which, in my humble opinion, is impossible) the virus will be wiped out or contained easily and then eradicated. But perhaps it’s better not to take it, because if everybody takes it, it will be wiped out before it reaches me, and I’m free from the risks that come with such a vaccine.

“The simple rule we learned from bacteria is that anybody who has to make an important decision — especially one of life and death at times of stress — should wait to see the trend of changes, process the risks and odds in depth, and only then decide,” says Prof. Ben-Jacob.

He imagines what a bacteria would say if you asked it about the flu shot:

“They might suggest that only people who have widespread and intense contact with many others, such as business travellers and teachers, should get the shot. Those who are most likely to spread the virus should be vaccinated. Bacteria don’t take risks like we do and the results have paid off. They are super-successful, more than any creature on earth. They wouldn’t abuse the stock market, and would never invest beyond their means. I am also pretty sure most would not rush to get the flu shot, if given the choice,” he concludes. “They know how to keep a delicate balance.”

Fighting against soot – more important than ever

Most of the talk about global warming revolves around carbon dioxide, sometimes giving the false impression that it alone is responsible for global warming and all its implications. However, numerous studies have revealed a new enemy, one almost as dangerous as carbon dioxide: soot.


The black powdery pollutant is responsible for numerous climatic shifts, especially in the areas between the tropics. The main difference however, is that soot can be relatively very easy ‘defeated’. Soot, generally called black carbon by climatologists, originates mostly from power plants, diesel engines and activities mostly related with developing countries (burning the fields or open cooking stoves, for example).

What happens is that as it drifts into the atmosphere, soot attracts a lot of sunlight and heat, warms up and then radiates heat; it can do the same thing on the ground too. Changing pollution trends have affected the way it manifests, and for the worst. Until recently, soot was generally mixed with sulfate particles that reflected sunlight. However, the mix of sulfate and soot produces new particles that have an even greater ability of absorbing sunlight.

“That actually enhances the effect,” says Mark Jacobson, a Stanford University atmospheric scientist. “It can double the warming.”

There are still many things researchers have been unable to assess, but one thing’s for sure: at least in the Northern Hemisphere, soot has caused some dramatic changes. The thing is that unlike greenhouse gases that quickly disperse in the atmosphere, soot congregates above and stays there. Here’s what Al Gore says:

“A new understanding is emerging of soot. Black carbon is settling in the Himalayas. The air pollution levels in the upper Himalayas are now similar to those in Los Angeles.”, and he’s right.

AIDS vaccine shows success for the first time

AIDS is one of the most dangerous diseases nowadays, being a pandemic for many years now, and there’s been quite little development for a cure or a vaccine. However in the past few years researchers have been getting closer and closer to pinning down a solution. Yesterday, a team formed of Thai and US scientists announced that they have found a vaccine combo that reduced the number of HIV infections.


No less than 25 years after the virus responsible for AIDS (HIV) was discovered, it seems scientists have finally been able to make a small but crucial step towards controlling this lethal pandemic. However, the benefits of the vaccine were not spectacular (only 31% less infections), but this is just the first step and can be improved greatly, and shows promise of providing an effective way to control the virus.

“This is a historic day in the 26-year quest to develop an AIDS vaccine,” Dr. Alan Bernstein, executive director of the Global HIV Vaccine Enterprise, who was not involved in the research, said in a statement.

“We now have evidence that it is possible to reduce the risk of HIV infection with a vaccine,” said Mitchell Warren, executive director of the AIDS Vaccine Advocacy Coalition, in his own statement. “There is little doubt that this finding will energize and redirect the AIDS vaccine field as all of us begin the hard work to translate this landmark result into true public health benefit.”

The trial began 6 years ago, and many dispatched it as being a waste of time and money, mostly because each of the two vaccines (separately) were ineffective. However, this study involving more than 16.000 people from Thailand proved them wrong. However, it did not show any results in the 69% that contracted the virus, but with the improvements that will come, it just might be what saves the lives of the 7.500 people that get infected each day.

Devil’s Claw brings new hope for arthritis

devilsclaw03webDeep in one of the warmest places on the planet, in the Kalahari desert, there lies the ‘Devil’s Claw’, a plant that may hold the key to effective treatment to arthritis, tendonitis and numerous related illnesses that affect millions and millions each year. Despite being a ‘desert plant’ the Devil’s Claw doesn’t thrive in extreme drough, like the one the Kalahari desert has seen in the past few years. This lead the plant to the brink of extinction so scientists are trying to find out ways to grow it, or grow other plants that produce the same valuable chemicals, or produce the chemicals in a lab.

Today was the 238th National Meeting of the American Chemical Society (ACS). At that meeting, they described the first successful method of producing the active ingredients in the plant, ingredients that have already made the Devil’s Claw sought after by more and more people who use it as alternative medicine – with amazing results. Researchers hope this will eventually lead to ‘biofactories’ that could produce huge quantities of the needed substances at low costs.

They started studying this plant when they found out that native populations from South Africa have been using it for generations in a number of conditions, from fever and diarrhea to serious blood diseases.

“In Germany, 57 pharmaceutical products based on Devil’s claw, marketed by 46 different companies, have cumulative sales volumes alone worth more than $40 million.”, said Milen I. Georgiev, Ph.D., who delivered the report

“The Devil’s Claw faces significant problems with its natural renewal, especially low rainfall,” Georgiev notes. “These problems are driving efforts to find alternative ways to produce high value compounds from the plant, independent of geographical and climatic factors,” he says.

Another extremely interesting fact (though not directly related) is that 25 percent of ALL medicines prescribed in industrialized countries comes from plants, most of which are endangered, so these biofactories that could ensure fast growth rate and genetic stability for the necessary plants could be crucial.

“Our target aim is to develop such technology, so we are paying attention not only to fundamental scientific tasks, but also to those related to some of the technological problems associated with hairy root biofactories,” Georgiev said. “It is the desire of each scientist is to see the fruits of his work. In the current case, we hope to be able to develop cost-effective laboratory technology for production of these pharmaceutically-important metabolites within the next five years.”

Of Trojan Horses and miracle drugs

When Oscar was diagnosed with a very aggresive form of cancer called anal sac adenocarcinoma, his days seemed numbered – literally. Doctors gave him very little to no chance of living 100 days when they noticed he was unresponsive to chemotherapy and radiation. But things took an unexpected turn, and in two weeks, Oscar was healthy and on his feet again.

Oscar, the miracle dog

His extraordinary recovery made scientists at the 237th National Meeting of the American Chemical Society call him the ‘Miracle dog’. Which is quite true, as he is a Bichon Frise that with the help of a new promising drug managed to keep his tail up and be victorious in the battle with cancer. The drug is called nitrosylcobalamin (NO-Cbl) and it helped three other dogs in a similar situation with Oscar without showing signs of negative side effects, and the way it works is at an elementary level pretty simple: it infiltrates cancer cells the trojan horse way.

This biological trojan horse doesn’t only mean good news for dog owners, but for other people too, as researchers are working to modify the drug so that it can work on humans the same way it does on dogs. That probably won’t happen tomorrow, but it definitely shows promise and gives hope in the long run; however, if we’re talking now, it’s good news for dogs.

“We are one of the few research groups that is offering to treat dogs with cancer that otherwise have no hope,” Joseph A. Bauer, Ph.D, said. “With no other options available, most people in this situation opt to euthanize so that their pets don’t go through the pain of disease and trauma of surgery.”

This is a win-win situation, and with millions and millions of dogs getting cancer each year, scientists now have the chance to study cancer in animals other than lab mice and develop further treatments. As Bauer puts it:

“The beauty of using a dog or a cat to test a cancer drug is two-fold. First, the animal can get the benefit of the most up-to-date drug in cancer medicine. Second, the NCI gets data on pets that are exposed to the same environmental factors their owners are. They breathe the same polluted air and drink the same polluted water that you and I do every day. If you can find an agent to treat cancer that occurs in a dog with success, there is a higher likelihood that you can take that to the human population and have a much higher response rate than with mice.”

Despite the fact that it hasn’t been used effectively on more than four dogs, NO-Cbl shows a lot of promise, because the cases varied drastically, all of them showed major improvements and none had any side effect. This “biological Trojan horse technology” have receptors for vitamin B12 on their outer surface, but it’s just recently that scientists managed to find out how to take advantage of this technology that has been studied for more than 50 years, but with little results.

“This is one of the most rewarding things I’ve ever done in my life,” says Bauer, the owner of a two-year old Beagle. “It gets boring working in the lab, but to see the fruits of your labor in a positive outcome like this and to know you’re responsible in some small way, that’s pretty cool.”

New medicine uses light to cure skin cancer

A drug which uses light to cure skin cancer is getting nearer and nearer to being offered to sale in Sweden for the tens of thousands of patients suffering from it in this country. The solution is quite simple, cheap and not at all unpleasant as other ways of treating this disease.

Researcher Leif Eriksson’s team at Örebro University in Sweden, the head of the team, has received from the Swedish Research Council about SEK 4 million for further development and commercialization of the method.

The new drug uses photo-dynamic therapy to cure skin cancer as after its reorganization in the cell, which is caused by light, it triggers chemical reactions that destroy cancer cells in a very efficient way.

This way, about 30000 people who are diagnosed with this skin cancer every year could have access to a simple treatment method, which also applies to its pre-stages, the so-called actinic keratosis.

Leif Eriksson’s drug research has spread to more institutions, now being conducted in collaboration with Professor Lennart Löfgren at the Center for Head and Neck Oncology at Örebro University Hospital and receiving international acclaim.

The researchers have also been working on methods to treat other severe affections such as rheumatism or atherosclerosis using the new concept, which proved to be successful especially as a new method is used for this purpose, the computer modeling.

The research is aimed to describe at a detailed level the way the way the medicines should look like, what should be done so that they will reach their target and what happens if some molecules are altered. Then, after the theory has been settled, numerous tests and experiments follow in collaboration with other institutions.

“This makes the research exciting and dynamic,” says Leif Eriksson

Source: Vetenskapsrådet (The Swedish Research Council)

Potential Alzheimer’s, Parkinson’s Cure Found In Century-old Drug

Every once in a while, you hear about the hardest of problems that have really easy solutions. In numerous cases, cures have been found in most common of substances, or even foods. This time, a study led by researchers at Children’s Hospital & Research Center Oakland showed that in small concentrations, something as common as methylene blue could significantly slow down or even cure Alzheimer’s and Parkinson’s disease.

This substance has been used for more than a century, in various situations, including as a treatment for a cold or a flu. The study was conducted by Hani Atamna, PhD, and a his team at Children’s and it was published in the March 2008 issue of the Federation of American Societies for Experimental Biology (FASEB) Journal.

Their research found that methylene blue can slow down or even prevent the decline of mitochondrial function, which leads to the above diseases.

“The results are very encouraging,” said Dr. Atamna. “We’d eventually like to try to prevent the physical and cognitive decline associated with aging, with a focus on people with Alzheimer’s disease. One of the key aspects of Alzheimer’s disease is mitochondrial dysfunction, specifically complex IV dysfunction, which methylene blue improves. Our findings indicate that methylene blue, by enhancing mitochondrial function, expands the mitochondrial reserve of the brain. Adequate mitochondrial reserve is essential for preventing age-related disorders such as Alzheimer’s disease.”

Methylene blue was first discovered more than 100 years from now, in 1891. It is used also for treating methemoglobinemia, a blood disorder. It is a well known fact that when taken in large quantities, it affects the brain. But what comes out as a surprise, at least to me, is that this fact alone was enough to discourage scientists to experiment with smaller quantities.