Tag Archives: medical research

Bionic Vision

Micro Machines and Opto-Electronics on a Contact Lense

Fiction now meets reality with prototype contact lenses developed by Babak Parviz at the University of Washington, in Seattle. Dr. Parviz’s prototype lenses can be used as biosensors to display body chemistry or as a heads up display (HUD). Powered by radio waves and 330 microwatts of power from a loop antenna that picks up power beamed from nearby radio sources, future versions will also be able to harvest power from a cell phone.

In his early 2008 lab tests, rabbits safely wore contact lenses with metal connectors for electronic circuits. The prototype lenses contained an electric circuit as well as red light-emitting diodes for a display. The lenses were tested on rabbits for up to 20 minutes and the animals showed no adverse effects.
…
Contact lenses as replacements for smart phone displays — even to monitor blood glucose levels — might best be done while not operating heavy equipment. “The true promise of this research is not just the actual system we end up making, whether it’s a display, a biosensor, or both,” comments Dr. Parviz. “We already see a future in which the humble contact lens becomes a real platform, like the iPhone is today, with lots of developers contributing their ideas and inventions. As far as we’re concerned, the possibilities extend as far as the eye can see, and beyond.”

The Only Known Cancerless Animal

Unlike any other mammal, naked mole rate communities consist of queens and workers more reminiscent of bees than rodents. Naked mole rats can live up to 30 years, which is exceptionally long for a small rodent. Despite large numbers of naked mole-rats under observation, there has never been a single recorded case of a mole rat contracting cancer, says Gorbunova. Adding to their mystery is the fact that mole rats appear to age very little until the very end of their lives.

The mole rat’s cells express p16, a gene that makes the cells “claustrophobic,” stopping the cells’ proliferation when too many of them crowd together, cutting off runaway growth before it can start. The effect of p16 is so pronounced that when researchers mutated the cells to induce a tumor, the cells’ growth barely changed, whereas regular mouse cells became fully cancerous.

“It’s very early to speculate about the implications, but if the effect of p16 can be simulated in humans we might have a way to halt cancer before it starts.” says Vera Gorbunova, associate professor of biology at the University of Rochester and lead investigator on the discovery.

In 2006, Gorbunova discovered that telomerase—an enzyme that can lengthen the lives of cells, but can also increase the rate of cancer—is highly active in small rodents, but not in large ones.

Until Gorbunova and Seluanov’s research, the prevailing wisdom had assumed that an animal that lived as long as we humans do needed to suppress telomerase activity to guard against cancer. Telomerase helps cells reproduce, and cancer is essentially runaway cellular reproduction, so an animal living for 70 years has a lot of chances for its cells to mutate into cancer, says Gorbunova. A mouse’s life expectancy is shortened by other factors in nature, such as predation, so it was thought the mouse could afford the slim cancer risk to benefit from telomerase’s ability to speed healing.

While the findings were a surprise, they revealed another question: What about small animals like the common grey squirrel that live for 24 years or more? With telomerase fully active over such a long period, why isn’t cancer rampant in these creatures?

2009 Nobel Prize in Physiology or Medicine

This year’s Nobel Prize in Physiology or Medicine is awarded to three scientists who have solved a major problem in biology: how the chromosomes can be copied in a complete way during cell divisions and how they are protected against degradation. The Nobel Laureates have shown that the solution is to be found in the ends of the chromosomes – the telomeres – and in an enzyme that forms them – telomerase.

The long, thread-like DNA molecules that carry our genes are packed into chromosomes, the telomeres being the caps on their ends. Elizabeth Blackburn and Jack Szostak discovered that a unique DNA sequence in the telomeres protects the chromosomes from degradation. Carol Greider and Elizabeth Blackburn identified telomerase, the enzyme that makes telomere DNA. These discoveries explained how the ends of the chromosomes are protected by the telomeres and that they are built by telomerase.

If the telomeres are shortened, cells age. Conversely, if telomerase activity is high, telomere length is maintained, and cellular senescence is delayed. This is the case in cancer cells, which can be considered to have eternal life. Certain inherited diseases, in contrast, are characterized by a defective telomerase, resulting in damaged cells. The award of the Nobel Prize recognizes the discovery of a fundamental mechanism in the cell, a discovery that has stimulated the development of new therapeutic strategies.

Scientists began to investigate what roles the telomere might play in the cell. Szostak’s group identified yeast cells with mutations that led to a gradual shortening of the telomeres. Such cells grew poorly and eventually stopped dividing. Blackburn and her co-workers made mutations in the RNA of the telomerase and observed similar effects in Tetrahymena. In both cases, this led to premature cellular ageing – senescence. In contrast, functional telomeres instead prevent chromosomal damage and delay cellular senescence. Later on, Greider’s group showed that the senescence of human cells is also delayed by telomerase. Research in this area has been intense and it is now known that the DNA sequence in the telomere attracts proteins that form a protective cap around the fragile ends of the DNA strands.

Many scientists speculated that telomere shortening could be the reason for ageing, not only in the individual cells but also in the organism as a whole. But the ageing process has turned out to be complex and it is now thought to depend on several different factors, the telomere being one of them. Research in this area remains intense.

The 3 awardees are citizens of the USA; two were born elsewhere.
Read more about their research at the Nobel Prize web site.

Molecular biologist Elizabeth Blackburn–one of Time magazine’s 100 “Most Influential People in the World” in 2007–made headlines in 2004 when she was dismissed from the President’s Council on Bioethics after objecting to the council’s call for a moratorium on stem cell research and protesting the suppression of relevant scientific evidence in its final report.

Webcast of Dr. Elizabeth Blackburn speaking at Google:
Continue reading →

Engineer Tried to Save His Sister and Invented a Breakthrough Medical Device

Here is another remarkable example of the great benefit engineers provide society.

How a software engineer tried to save his sister and invented a breakthrough medical device

I wanted to help my sister as much as I could. I went to Medline, where there are hundreds of thousands of documents describing clinical studies, to see what I could find.

There are billions of dollars spent every year on clinical studies. I was surprised to discover that there were sometimes clinical studies of treatments for which there were no clinical applications. The trials would show successful results but no clinical applications.

I found a 1987 Italian funded set of clinical studies that showed successful treatment of tumors by the application of chemotherapy directly into the tumors. But I could find nothing since then.
…
It took us two years to do the engineering. And it has taken the FDA seven years and two months to approve the product for sale. We were able to shorten the FDA process a little by saying that it was similar to other devices that had already been approved.

Great stuff.

Merck and Elsevier Publish Phony Peer-Review Journal

Elsevier is one of those publishers fighting open science. They try to claim that the government publishing government funded research in an open way will tarnish science. The argument makes no sense to me. Here is another crazy action on their part: they published a “journal” funded by Merck to promote Merck products. Merck Makes Phony Peer-Review Journal:

Merck cooked up a phony, but real sounding, peer reviewed journal and published favorably looking data for its products in them. Merck paid Elsevier to publish such a tome, which neither appears in MEDLINE or has a website, according to The Scientist.
…
What’s sad is that I’m sure many a primary care physician was given literature from Merck that said, “As published in Australasian Journal of Bone and Joint Medicine, Fosamax outperforms all other medications….” Said doctor, or even the average researcher wouldn’t know that the journal is bogus. In fact, knowing that the journal is published by Elsevier gives it credibility!

As I have said the journals fighting open science should have their credibility questioned. They are putting their outdated business model above science. We should not see organizations that are focused on closing science research through deceptive publicity efforts and lobbying efforts as credible.

Nanoparticles With Scorpion Venom Slow Cancer Spread

In a, chlorotoxin molecules, colored blue and green, attach themselves to a central nanoparticle. In b, each nanoprobe offers many chlorotoxin molecules that can simultaneously latch on to many MMP-2s, depicted here in yellow, which are thought to help tumor cells travel through the body. In c, over time nanoprobes draw more and more of the MMP-2 surface proteins into the cell, slowing the tumor’s spread. Image from the University of Washington.

University of Washington researchers found they could cut the spread of cancerous cells by 98 percent, compared to 45 percent for the scorpion venom alone, by combining nanoparticles with a scorpion venom compound already being investigated for treating brain cancer.

For more than a decade scientists have looked at using chlorotoxin, a small peptide isolated from scorpion venom, to target and treat cancer cells. Chlorotoxin binds to a surface protein overexpressed by many types of tumors, including brain cancer. Previous research by Miqin Zhang‘s group combined chlorotoxin with nanometer-scale particles of iron oxide, which fluoresce at that size, for both magnetic resonance and optical imaging.

Chlorotoxin also disrupts the spread of invasive tumors — specifically, it slows cell invasion, the ability of the cancerous cell to penetrate the protective matrix surrounding the cell and travel to a different area of the body to start a new cancer. The MMP-2 on the cell’s surface, which is the binding site for chlorotoxin, is hyperactive in highly invasive tumors such as brain cancer. Researchers believe MMP-2 helps the cancerous cell break through the protective matrix to invade new regions of the body. But when chlorotoxin binds to MMP-2, both get drawn into the cancerous cell.

Research showed that the cells containing nanoparticles plus chlorotoxin were unable to elongate, whereas cells containing only nanoparticles or only chlorotoxin could stretch out. This suggests that the nanoparticle-plus-chlorotoxin disabled the machinery on the cell’s surface that allows cells to change shape, yet another step required for a tumor cell to slip through the body.

So far most cancer research has combined nanoparticles either with chemotherapy that kills cancer cells, or therapy seeking to disrupt the genetic activity of a cancerous cell. This is the first time that nanoparticles have been combined with a therapy that physically stops cancer’s spread.

Full press release

Image of the Common Cold Virus

image created by Dr. Jean-Yves Sgro, Institute for Molecular Virology, University of Wisconsin-Madison, from published X-ray data. larger image

Sequences capture the code of the common cold

Conducted by teams at the University of Maryland School of Medicine, UW-Madison and the J. Craig Venter Institute, the work to sequence and analyze the cold virus genomes lays a foundation for understanding the virus, its evolution and three-dimensional structure and, most importantly, for exposing vulnerabilities that could lead to the first effective cold remedies.

“We’ve had bits and pieces of these things for a long time,” says Ann Palmenberg, of UW-Madison’s Institute for Molecular Virology and the lead author of the new study. “Now, we have the full genome sequences and we can put them into evolutionary perspective.”

As its name implies, the common cold is an inescapable, highly contagious pathogen. Humans are constantly exposed to cold viruses, and each year adults may endure two to four infections, while schoolchildren can catch as many as 10 colds.

“We know a lot about the common cold virus,” Palmenberg explains, “but we didn’t know how their genomes encoded all that information. Now we do, and all kinds of new things are falling out.”
…
The newly sequenced viruses also show, says Palmenberg, why it is unlikely we will ever have an effective, all-purpose cold vaccine: The existing reservoir of viruses worldwide is huge and, according to the new study, they have a tendency to swap genetic sequences when cells are infected by more than one virus, a phenomenon that can lead to new virus strains and clinical manifestations.
…
The ability of different cold virus strains to swap genes and make entirely new strains was thought to be impossible, notes Claire M. Fraser-Liggett, a co-author of the new study and director of the Institute for Genome Sciences and professor of medicine and microbiology at the University of Maryland School of Medicine. “There is the possibility that this could lead to the emergence of a new rhinovirus strain with fairly dramatic properties,” says Fraser-Liggett.

Value of Prostate Cancer Screening Questioned by Two Studies

Ben Goldacre, in his bad science blog, again takes on journalist’s articles of health research in: Venal, misleading, pathetic, dangerous, stupid, and busted

1410 men would need to be screened to prevent one death. For each death prevented, 48 people would need to be treated: and prostate cancer treatment has a high risk of very serious side effects like impotence and incontinence. These figures are not hard to find: they are in the summary of the research paper.

For complex risk decisions like screening, it has been shown in three separate studies that patients, doctors, and NHS purchasing panels make more rational decisions about treatments and screening programmes when they are given the figures as real numbers, as I did above, instead of percentages. I’m not saying that PSA screening is either good or bad: I am saying that people deserve the figures in the clearest form possible so they can make their own mind up.
…
So newspapers ignore one half of the evidence, and they fail to explain the other half properly.
…
They can also link directly and transparently to scientific papers, which mainstream media still refuses to do. Journalists insist that we need professionals to mediate and explain science. From today’s story, their self belief seems truly laughable.

He also says some journalists got it right including the Washington Post in, Prostate Cancer Screening May Not Reduce Deaths:

The PSA blood test, which millions of men undergo each year, did not lower the death toll from the disease in the first decade of a U.S. government-funded study involving more than 76,000 men, researchers reported yesterday. The second study, released simultaneously, was a European trial involving more than 162,000 men that did find fewer deaths among those tested. But the reduction was relatively modest and the study showed that the tests resulted in a large number of men undergoing needless, often harmful treatment.

I think it is true that most people need help having science mediated to some extent. But he is also right that those doing so need to do better. And also everyone needs to learn about science to understand the choices they personally and politically (for policy issues) need to make decisions on. Being scientifically illiterate is dangerous.

Scientists Target Bacteria Where They Live

Scientists Learning to Target Bacteria Where They Live

Scientists have learned that bacteria that are vulnerable when floating around as individual cells in what is known as their “planktonic state” are much tougher to combat once they get established in a suitable place — whether the hull of a ship or inside the lungs — and come together in tightly bound biofilms. In that state, they can activate mechanisms like tiny pumps to expel antibiotics, share genes that confer protection against drugs, slow down their metabolism or become dormant, making them harder to kill.

The answer, say researchers, is to find substances that will break up biofilms.
…
Melander said “a throwaway sentence in an obscure journal” — the Bulletin of the Chemical Society of Japan — gave them another clue. They isolated a compound from the sponge that disperses biofilms and figured out how to synthesize it quickly and cheaply.
…
But dispersing biofilms without understanding all the ramifications could be a “double-edged sword,” Romeo warned, because some bacteria in a biofilm could wreak worse havoc once they disperse.

“Simply inducing biofilm dispersion without understanding exactly how it will impact the bacterium and host could be very dangerous, as it might lead to spread of a more damaging acute infection,” he said.

Monoclonal Antibodies Found That Stop All Flu Types

Universal Flu Drug Stops All Flu Types

A new kind of drug cocktail kills all types of flu bugs and could protect against pandemic or seasonal flu. “I certainly believe that a therapy for all kinds of influenza may be within our grasp,” study researcher Robert Liddington, DPhil, director of infectious diseases at the Burnham Institute in La Jolla, Calif., said at a news conference announcing the finding.

The treatment is based on new monoclonal antibodies that attack flu viruses in a shared Achilles heel. Of the many different subtypes of flu, there are only two basic patterns for this vulnerable, essential part of the flu virus.

And despite heroic efforts, researchers could not breed a flu strain resistant to the treatment — suggesting that there’s only a very small chance that mutated viruses could render the treatment obsolete. The breakthrough finding is a joint effort from labs at the Burnham Institute; Dana-Farber Cancer Institute in Boston; and the CDC in Atlanta.

Like many breakthroughs, the finding was partly accidental. The researchers were, at first, trying only to create a treatment to stop the H5N1 bird flu virus, the most likely candidate for igniting the next worldwide flu pandemic.
…
While monoclonal antibodies against flu are new, a wide range of drugs are based on this technology. That means the new, fully human anti-flu antibodies could become new human drugs relatively quickly…

“We hope these antibodies are in clinical trials during the 2011-2012 flu season — maybe earlier,” Marasco said. “This really is an important advance in the field of antiviral therapy. The possibility of having a universal therapy for flu is made more real and possible because of these discoveries.”