Posts about medical research

Using Diatom Algae to Deliver Chemotherapy Drugs Directly to Cancer Cells

I am thankful for scientists doing the time consuming and important research to find new ways to fight disease. Here is an interesting webcast discussing how chemotherapy is used to fight cancer and how scientists are looking to algae to deliver the chemotherapy drugs to better target cancer cells (while not savaging our health cells).

I am also thankful to the funding sources that pay for this research (and for cool explanations of science, like SciShow).

Read more about the genetically engineered algae kills 90% of cancer cells without harming healthy ones. The algae are a diatom and many diatoms look very cool.

Sadly the actual research paper (by government funded university professors) is published by a closed science publisher (when are we finally going to stop this practice that was outdated over a decade ago?). Thankfully those responsible for SciShow are much more interested in promoting science than maintaining outdated business models (in direct contrast to so many science journal publishers).

Related post on cool delivery methods for life saving drugs: Using Bacteria to Carry Nanoparticles Into CellsSelf-Assembling Cubes Could Deliver Medicine (2006)Nanoparticles With Scorpion Venom Slow Cancer SpreadNASA Biocapsules Deliver Medical Interventions Based Upon What They Detect in the Body

200,000 People Die Every Year in Europe from Adverse Drug Effects – How Can We Improve?

A new integrated computational method helps predicting adverse drug reaction more reliably than with traditional computing methods. This improved ability to foresee the possible adverse effects of drugs may entail saving many lives in the future.

Most computer tools employed today to detect possible adverse effects of compounds that are candidates for new medicines are based on detecting labile fragments in the drug’s structure. These fragments can potentially transform to form reactive metabolites, which can have toxic properties. This is what is known as idiosyncratic toxicity and is a big headache for the pharmaceutical industry, as it tends to be detected in late development stages of the drug and even when it is already on the market, often causing the drug to be withdrawn.

Jordi Mestres, coordinator of the IMIM and UPF research group on Systems Pharmacology at the Biomedical Informatics Program (GRIB) states ‘With this study we have contributed to complementing the detection of these quite unstable fragments, with information on the mechanism of action of the drug, based on three aspects: similarity to other medicines, prediction of their pharmacological profile, and interference with specific biological pathways. The optimal integration of these four aspects results in a clear improvement of our ability to anticipate adverse effects with higher confidence, which entails an extremely positive impact on society’.

In Europe, nearly 200,000 people die every year from adverse drug reactions, seven times more than in traffic accidents. An estimated 5% of hospitalisations are due to adverse effects and they are the fifth most common cause of hospital death. In addition, elderly people tend to take more than one drug at the same time, which multiplies the chances of suffering from adverse effects due to potential drug-drug interactions. In an increasingly aging society, this problem is becoming much more serious.

I think interactions is a hugely important area that needs a great deal more research. Doing so is very complex, which means it isn’t surprising so much more work is needed. The work of my father (and George Box and others) on multi-factorial experimentation is a powerful tool to aid this work (and that connection is likely one of the reasons I find the area of interactions so interesting – along with the realization there is so much benefit possible if we focus in that area more). Previous post on this Curious Cat Science and Engineering blog: Introduction to Fractional Factorial Designed Experiments.

The human and financial costs of adverse effects are very high. That is why the discovery of new medicines is increasingly focused more on predicting possible adverse effects at the initial stages of developing a new drug. This work hopes to contribute to setting the path toward a new generation of more reliable computational tools with regard to predicting the adverse effects of therapeutically-relevant small molecules. Advancing large-scale predictive safety at the pre-clinical phase is now becoming closer than ever, with expectations to lead to safer drugs for the entire population.

The research is published in closed science journal so I don’t link to it. I happily link to open science publications. Read the full press release which includes a link to the closed science journal.

Related: Lifestyle Drugs and RiskRoot Cause, Interactions, Robustness and Design of ExperimentsOne factor at a time (OFAT) Versus Factorial DesignsThe Purpose of Mulit-Factorial Designed Experiments11 Year Old Using Design of ExperimentsOver-reliance on Prescription Drugs to Aid Children’s Sleep?

Youyou Tu: The First Chinese Woman to Win a Nobel Prize

The Nobel Prize in Physiology or Medicine 2015 was divided, one half jointly to William C. Campbell (born Ireland, now USA) and Satoshi Ōmura (Japan) “for their discoveries concerning a novel therapy against infections caused by roundworm parasites” and the other half to Youyou Tu (China) “for her discoveries concerning a novel therapy against Malaria”.

Youyou Tu is the first Chinese woman to win a Nobel Prize.

Diseases caused by parasites have plagued humankind for millennia and constitute a major global health problem. In particular, parasitic diseases affect the world’s poorest populations and represent a huge barrier to improving human health and wellbeing. This year’s Nobel Laureates have developed therapies that have revolutionized the treatment of some of the most devastating parasitic diseases.

William C. Campbell and Satoshi Ōmura discovered a new drug, Avermectin, the derivatives of which have radically lowered the incidence of River Blindness and Lymphatic Filariasis, as well as showing efficacy against an expanding number of other parasitic diseases. Youyou Tu discovered Artemisinin, a drug that has significantly reduced the mortality rates for patients suffering from Malaria.

These two discoveries have provided humankind with powerful new means to combat these debilitating diseases that affect hundreds of millions of people annually. The consequences in terms of improved human health and reduced suffering are immeasurable.

image of Artemisinin

via Noble Prize website

Malaria was traditionally treated by chloroquine or quinine, but with declining success. By the late 1960s, efforts to eradicate Malaria had failed and the disease was on the rise. At that time, Youyou Tu in China turned to traditional herbal medicine to tackle the challenge of developing novel Malaria therapies. From a large-scale screen of herbal remedies in Malaria-infected animals, an extract from the plant Artemisia annua emerged as an interesting candidate.

However, the results were inconsistent, so Tu revisited the ancient literature and discovered clues that guided her in her quest to successfully extract the active component from Artemisia annua. Tu was the first to show that this component, later called Artemisinin, was highly effective against the Malaria parasite, both in infected animals and in humans. Artemisinin represents a new class of antimalarial agents that rapidly kill the Malaria parasites at an early stage of their development, which explains its unprecedented potency in the treatment of severe Malaria.

Youyou Tu was born in 1930 in China and is a Chinese citizen. She graduated from the Pharmacy Department at Beijing Medical University in 1955. From 1965-1978 she was Assistant Professor at the China Academy of Traditional Chinese Medicine, from 1979-1984 Associate Professor and from 1985 Professor at the same Institute. From 2000, Tu has been Chief Professor at the China Academy of Traditional Chinese Medicine. She doesn’t have a doctorate, very rare for a Nobel Prize winner in the sciences.

Read the full press release

Related: Nobel Prize in Physiology or Medicine 2012 for Reprogramming Cells to be PluripotentNobel Prize in Physiology or Medicine 2008Parasites in the Gut Help Develop a Healthy Immune System2011 Nobel Prize in Physiology or MedicineVideo showing malaria breaking into cell

Cancer Rates Consistent Across Species Instead of Increasing Due to Body Mass

It would seem sensible to think cancer should be more prevalent in species with a huge number of cells, and thus more cells to become cancerous. But cancer risk doesn’t increase in this way. This interesting, open source paper, sheds some light on what is behind this.

Solutions to Peto’s paradox revealed by mathematical modelling and cross-species cancer gene analysis

Whales have 1000-fold more cells than humans and mice have 1000-fold fewer; however, cancer risk across species does not increase with the number of somatic cells and the lifespan of the organism. This observation is known as Peto’s paradox. How much would evolution have to change the parameters of somatic evolution in order to equalize the cancer risk between species that differ by orders of magnitude in size? Analysis of previously published models of colorectal cancer suggests that a two- to three-fold decrease in the mutation rate or stem cell division rate is enough to reduce a whale’s cancer risk to that of a human. Similarly, the addition of one to two required tumour-suppressor gene mutations would also be sufficient.

We surveyed mammalian genomes and did not find a positive correlation of tumour-suppressor genes with increasing body mass and longevity. However, we found evidence of the amplification of TP53 in elephants, MAL in horses and FBXO31 in microbats, which might explain Peto’s paradox in those species. Exploring parameters that evolution may have fine-tuned in large, long-lived organisms will help guide future experiments to reveal the underlying biology responsible for Peto’s paradox and guide cancer prevention in humans.

Elephants in Kenya

Elephants in Kenya by John Hunter. See more photos from my trip to Kenya.

In another way it would make sense that large animals would have hugely increased risks of cancer. As they evolved, extremely high cancer rates would be a much bigger problem for them. Therefore it wouldn’t be surprising to find they have evolved a way of reducing cancer risks.

Despite these limitations, we found genes that have been dramatically amplified in specific mammalian genomes, the most interesting of which is the discovery of 12 TP53 copies in the genome of the African elephant. We subsequently cloned those genes and identified 19 distinct copies of TP53 in African elephants and 15–20 in Asian elephants [1]. Another potential lead for solving Peto’s paradox is MAL, which is found to have eight copies in the horse genome and two in microbat. This could be an example of convergent evolution where a large animal (horse) and a small, long-lived animal (microbat) both evolved extra copies of the same gene to overcome their increased risk of cancer. Further analysis and experimentation would need to be performed to determine the function of these copies and whether or not they provide enhanced suppression of carcinogenesis.

The researchers have found an interesting potential explanation for how that has been accomplished.

Related: The Only Known Cancerless Animal (the naked mole rat)Webcast of a T-cell Killing a Cancerous CellResearchers Find Switch That Allows Cancer Cells to SpreadCancer Vaccines

Teixobactin – New Antibiotic Attacks Ability of Bacteria to Build Cell Walls

New class of antibiotic could turn the tables in battle against superbugs

The antibiotic, called teixobactin, kills a wide range of drug-resistant bacteria, including MRSA and bugs that cause TB and a host of other life-threatening infections.

It could become a powerful weapon in the battle against antimicrobial resistance, because it kills microbes by blocking their capacity to build their cell walls, making it extremely difficult for bacteria to evolve resistance.

It would be great if the exciting results carried through to real world results similar to the hope. Medical research is full of promising initial results that fail to deliver, however. We are at great risk if some new miracle anti-biotic isn’t found. Many people are investigating potential solutions.

Most antibiotics are isolated from bacteria or fungi that churn out lethal compounds to keep other microbes at bay. But scientists have checked only a tiny fraction of bugs for their ability to produce potential antibiotics because 99% cannot be grown in laboratories.

Lewis’s group found a way around the problem by developing a device called an iChip that cultures bacteria in their natural habitat. The device sandwiches the bugs between two permeable sheets. It is then pushed back into the ground where the microbes grow into colonies.

Working with a Massachusetts-based company, NovoBiotic, and researchers at the University of Bonn, [Kim] Lewis’s group screened 10,000 soil bacteria for antibiotics and discovered 25 new compounds. Of these, teixobactin was the most promising.

Though promising, Lewis said that years more work lie ahead before the drug could be available. Human clinical trials could begin within two years to check its safety and efficacy, but more development would follow that.

It is wonderful to read about the great work so many scientists are making in researching potential life saving drugs. Hopefully this antibiotic will save us from what will be catastrophic harm if some new antibiotic is not available soon.

Related: Search for Antibiotic Solutions Continues: Killing Sleeper Bacteria Cells (2013)New Family of Antibacterial Agents Discovered (2009)Potential Antibiotic Alternative to Treat Infection Without Resistance (2012)

Apples Increase the Growth of Beneficial Bacteria in Our Guts, Which Improves Our Health

Science provides some very clear knowledge that is easy for us to apply (the value of vaccines, materials to use in solar panels, support needed to build a bridge, dangers of consuming small amounts of lead…). But much of our knowledge about nutrition and human health is a bit unclear. This is one of the struggles we face is using our judgement to decide how to eat and live based on what we know and what seems to be so.

Eating more fruit and vegetables than most in the USA eat is pretty clearly beneficial to our health. but exactly how much, how beneficial, how it is beneficial are questions with only varying degrees of good answers so far. Apple’s Scientists at Washington State University have concluded that nondigestible compounds in apples – specifically, Granny Smith apples – may help prevent disorders associated with obesity.

“We know that, in general, apples are a good source of these nondigestible compounds but there are differences in varieties,” said food scientist Giuliana Noratto, the study’s lead researcher. “Results from this study will help consumers to discriminate between apple varieties that can aid in the fight against obesity.”

The tart green Granny Smith apples benefit the growth of friendly bacteria in the colon due to their high content of non-digestible compounds, including dietary fiber and polyphenols, and low content of available carbohydrates. The non-digestible compounds are fermented by bacteria in the colon, which benefits the growth of friendly bacteria in the gut.

The study showed that Granny Smith apples surpass Braeburn, Fuji, Gala, Golden Delicious, McIntosh and Red Delicious in the amount of nondigestible compounds they contain.

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Massive Blast of Measles Vaccine Wiped Out Cancer In Study

Unfortunately these stories are not uncommon but the hoped for follow through of practical solutions that work at all are rare. But we keep learning and while the breakthroughs based on these news stories is rare we do keep finding new and better methods to cope with health issues.

Mayo Clinic trial: Massive blast of measles vaccine wipes out cancer

Stacy Erholtz was out of conventional treatment options for blood cancer last June when she underwent an experimental trial at the Mayo Clinic that injected her with enough measles vaccine to inoculate 10 million people.

The 50-year-old Pequot Lakes mother is now part of medical history.

The cancer, which had spread widely through her body, went into complete remission and was undetectable in Erholtz’s body after just one dose of the measles vaccine, which has an uncanny affinity for certain kinds of tumors.

Erholtz was one of just two subjects in the experiment and the only one to achieve complete remission. But the experiment provides the “proof of concept” that a single, massive dose of intravenous viral therapy can kill cancer by overwhelming its natural defenses, according to Dr. Stephen Russell, a professor of molecular medicine who spearheaded the research at Mayo.

Researchers have known for decades that viruses can be used to destroy cancer. They bind to tumors and use them as hosts to replicate their own genetic material; the cancer cells eventually explode and release the virus. Antiviral vaccines that have been rendered safe can produce the same effects and can also be modified to carry radioactive molecules to help destroy cancer cells without causing widespread damage to healthy cells around the tumors. The body’s immune system then attacks any remaining cancer that carries remnants of the vaccine’s genetic imprint.

Mayo started out giving patients 1 million infectious units and gradually cranked up the dosage — but it didn’t work until Erholtz and another patient were injected with 100 billion infectious units, he said.

While the treatment worked in Erholtz, whose tumors were primarily in her bone marrow, the results weren’t sustained in the second patient, whose tumors were largely confined to her leg muscles. Russell said researchers need to study how the nature of the tumor affects the lethality of the virus.

One challenge of health research on fatal health conditions is that the experimentation with people is usually limited to people that have no available options left from the approved treatments. So, in general they are very sick. And the great complexity of dealing with human immune systems, the variation in the disease and in people create a very difficult research environment. Thankfully we have many great scientists dedicated to finding new treatments.

Related: Virus Kills Breast Cancer Cells in LaboratoryVirus Engineered To Kill Deadly Brain TumorsUsing Bacteria to Carry Nanoparticles Into CellsWebcast of a T-cell Killing a Cancerous Cell

Study After Study Find No Benefits to Multivitamins

The largest study of its kind concludes that long-term multivitamin use has no impact on the risk of common cancers, cardiovascular disease or overall mortality in postmenopausal women.

“Dietary supplements are used by more than half of all Americans, who spend more than $20 billion on these products each year. However, scientific data are lacking on the long-term health benefits of supplements,” said lead author Marian L. Neuhouser, Ph.D., an associate member of the Public Health Sciences Division at the Hutchinson Center.

The study focused the effects of multivitamins because they are the most commonly used supplement. “To our surprise, we found that multivitamins did not lower the risk of the most common cancers and also had no impact on heart disease,” she said.

The study assessed multivitamin use among nearly 162,000 women enrolled in the Women’s Health Initiative, one of the largest U.S. prevention studies of its kind designed to address the most common causes of death, disability and impaired quality of life in postmenopausal women. The women were followed for about eight years.

Nearly half of the study participants – 41.5 percent – reported using multivitamins on a regular basis. Multivitamin users were more likely to be white, live in the western United States, have a lower body-mass index, be more physically active and have a college degree or higher as compared to non-users.

The study found no significant differences in risk of cancer, heart disease or death between the multivitamin users and non-users.

These findings are consistent with most previously published results regarding the lack of health benefits of multivitamins, Neuhouser said, but this study provides definitive evidence. Since the study did not include men, Neuhouser cautions that the results may not apply to them.

So what advice do Neuhouser and colleagues offer to women who want to make sure they’re getting optimal nutrition? “Get nutrients from food,” she said. “Whole foods are better than dietary supplements. Getting a wide variety of fruits, vegetables and whole grains is particularly important.”

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Search for Antibiotic Solutions Continues: Killing Sleeper Bacteria Cells

Killing Sleeper Cells and Superbugs with Assassin Janitors

Discovered in 2005 by scientists from Bayer Healthcare in Germany, ADEP4 killed a variety of different bacteria and cured lethal infections in mice and rats.

Here’s how it works. Proteins need to fold into very precise shapes to do their jobs, and misfolded proteins are wastes of space. Bacteria dispose of these useless molecules with ClpP—a janitorial protein that digests other proteins. It works with a partner, which recognises misfolded proteins, unfolds them, and threads them through a hole in the middle of ClpP so they can be broken down. But ADEP4 opens ClpP up so it no longer needs its partner. The janitor now becomes an assassin, running amok and chopping up any protein it comes across, misfolded or not.

The Bayer scientists showed that ADEP4 can force fast-growing cells to self-destruct, but Lewis suspected that it would do the same to persisters. Afterall, ClpP’s partner requires energy to do its job, but ClpP itself doesn’t. Once ADEP4 opens it up, it should go about its fatal business even in a dormant cell.

Lewis’ team found that ADEP4 did effectively kills persister populations of Staphylococcus aureus, but the bacteria bounce back. ClpP isn’t essential, so the bacteria just inactivated it to evolve their way around ADEP4. This, says Lewis, is why Bayer stopped working on the drug.

His solution was to pair ADEP4 with another antibiotic called rifampycin. ADEP4 would kill off the majority of the persisters, and if any of the rest started growing again, rifampycin would finish them off. He predicted that the double-whammy would leave very few survivors, maybe just a thousand cells or so.

“That’s not what we saw,” he says. “What we saw was complete sterilisation.”

This is a very nice effort. As our efforts fail to find “magic bullet” antibiotics fail and antibiotic resistance increases combo drug solutions offer some hope. While this is good news, the overall state of our ability to treat bacterial infections continues to decline as our misuse of antibiotics has greatly increased the speed at which antibiotic resistance has developed in bacteria.

This solution only works on gram positive antibiotics. ADEP4 is too big to pass through the extra outer layers of the gram-negative bacteria like ecoli and salmonella.

Related: Entirely New Antibiotic Developed, Platensimycin (2006) (2013 update: Platensimycin is a very effective antibiotic in vivo when continuously administered to cells, however this efficacy is reduced when administered by more conventional means. Efforts continue to find a way to create delivery options that are successful in treating people.) – New Family of Antibacterial Agents Discovered (2009)Potential Antibiotic Alternative to Treat Infection (2012)

Medical Study Findings too Often Fail to Provide Us Useful Knowledge

There are big problems with medical research, as we have posted about many times in the past. A very significant part of the problem is health care research is very hard. There are all sorts of interactions that make conclusive results much more difficult than other areas.

But failures in our practices also play a big role. Just poor statistical literacy is part of the problem (especially related to things like interactions, variability, correlation that isn’t evidence of causation…). Large incentives that encourage biased research results are a huge problem.

Lies, Damned Lies, and Medical Science

He discovered that the range of errors being committed was astonishing: from what questions researchers posed, to how they set up the studies, to which patients they recruited for the studies, to which measurements they took, to how they analyzed the data, to how they presented their results, to how particular studies came to be published in medical journals. The systemic failure to do adequate long term studies once we approve drugs, practices and devices are also a big problem.

This array suggested a bigger, underlying dysfunction, and Ioannidis thought he knew what it was. “The studies were biased,” he says. “Sometimes they were overtly biased. Sometimes it was difficult to see the bias, but it was there.” Researchers headed into their studies wanting certain results—and, lo and behold, they were getting them. We think of the scientific process as being objective, rigorous, and even ruthless in separating out what is true from what we merely wish to be true, but in fact it’s easy to manipulate results, even unintentionally or unconsciously. “At every step in the process, there is room to distort results, a way to make a stronger claim or to select what is going to be concluded,” says Ioannidis. “There is an intellectual conflict of interest that pressures researchers to find whatever it is that is most likely to get them funded.”

Another problem is that medical research often doesn’t get the normal scientific inquiry check of confirmation research by other scientists.

Most journal editors don’t even claim to protect against the problems that plague these studies. University and government research overseers rarely step in to directly enforce research quality, and when they do, the science community goes ballistic over the outside interference. The ultimate protection against research error and bias is supposed to come from the way scientists constantly retest each other’s results—except they don’t. Only the most prominent findings are likely to be put to the test, because there’s likely to be publication payoff in firming up the proof, or contradicting it.

Related: Statistical Errors in Medical StudiesMedical Study Integrity (or Lack Thereof)Contradictory Medical Studies (2007)Does Diet Soda Result in Weight Gain?

Exercise Reduces Anxiety While Also Promoting the Growth of New Neurons

Exercise reorganizes the brain to be more resilient to stress

These findings potentially resolve a discrepancy in research related to the effect of exercise on the brain — namely that exercise reduces anxiety while also promoting the growth of new neurons in the ventral hippocampus. Because these young neurons are typically more excitable than their more mature counterparts, exercise should result in more anxiety, not less. The Princeton-led researchers, however, found that exercise also strengthens the mechanisms that prevent these brain cells from firing.

From an evolutionary standpoint, the research also shows that the brain can be extremely adaptive and tailor its own processes to an organism’s lifestyle or surroundings, Gould said. A higher likelihood of anxious behavior may have an adaptive advantage for less physically fit creatures. Anxiety often manifests itself in avoidant behavior and avoiding potentially dangerous situations would increase the likelihood of survival, particularly for those less capable of responding with a “fight or flight” reaction, she said.

The anxiety-reducing effect of exercise was canceled out when the researchers blocked the GABA receptor that calms neuron activity in the ventral hippocampus.

Interesting research (with mice) that explores how exercise makes us more resilient to stress. I know for me, exercise seems to help relieve stress.

Related: Feed your Newborn NeuronsNew Neurons are Needed for New MemoriesRegular Aerobic Exercise for a Faster Brain (2007)Inactivity Leads to 5.3 Million Early Deaths a YearHow Aerobic Exercise Suppresses Appetite

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