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Cross posted from Next big future

Since a journal article was submitted to the Royal Society of Chemistry, the U of Alberta researchers have already made the processor and unit smaller and have brought the cost of building a portable unit for genetic testing down to about $100 Cdn. In addition, these systems are also portable and even faster (they take only minutes). Backhouse, Elliott and McMullin are now demonstrating prototypes of a USB key-like system that may ultimately be as inexpensive as standard USB memory keys that are in common use – only tens of dollars. It can help with pandemic control and detecting and control tainted water supplies.

This development fits in with my belief that there should be widespread inexpensive blood, biomarker and genetic tests to help catch disease early and to develop an understanding of biomarker changes to track disease and aging development. We can also create adaptive clinical trials to shorten the development and approval process for new medical procedures


The device is now much smaller than size of a shoe-box (USB stick size) with the optics and supporting electronics filling the space around the microchip

Canadian scientists have succeeded in building the least expensive portable device for rapid genetic testing ever made. The cost of carrying out a single genetic test currently varies from hundreds to thousands of pounds, and the wait for results can take weeks. Now a group led by Christopher Backhouse, University of Alberta, Edmonton, have developed a reusable microchip-based system that costs just 500 (pounds) to build, is small enough to be portable, and can be used for point-of-care medical testing.

To keep costs down, ‘instead of using the very expensive confocal optics systems currently used in these types of devices we used a consumer-grade digital camera’, Backhouse explained.

The device can be adapted for used in many different genetic tests. ‘By making small changes to the system you could test for a person’s predisposition to cancer, carry out pharmacogenetic tests for adverse drug reactions or even test for pathogens in a water supply,’ said Backhouse.

The heart of the unit, the ‘chip,’ looks like a standard microscope slide etched with fine silver and gold lines. That microfabricated chip applies nano-biotechnologies within tiny volumes, sometimes working with only a few molecules of sample. Because of this highly integrated chip (containing microfluidics and microscale devices), the remainder of the system is inexpensive ($1,000) and fast.

There are many possible uses for such a portable genetic testing unit:

Backhouse notes that adverse drug reactions are a major problem in health care. By running a quick genetic test on a cancer patient, for example, doctors might pinpoint the type of cancer and determine the best drug and correct dosage for the individual.

Or health-care professionals can easily look for the genetic signature for a virus or E. coli – also making it useful for testing water quality.

“From a public health point of view, it would be wonderful during an epidemic to be able to do a quick test on a patient when they walk into an emergency room and be able to say, ‘you have SARS, you need to go into that (isolation) room immediately.’ ”

A family doctor might determine a person’s genetic predisposition to an illness during an office visit and advise the patient on preventative lifestyle changes.

FURTHER READING
Microfabrication technologies research at the University of Alberta

Rapid genetic analysis

In collaboration with the Glerum Lab we have been developing microchip based implementations of genetic amplification (PCR — the polymerase chain reaction) and capillary electrophoresis (CE) that are extremely fast.

- Cancer diagnostics

- Cell manipulation on a chip

- On chip PCR (polymerase chain reaction)

- Single cell PCR

- DNA Sequencing

According to ScienceDaily:

The British-American biotech company Acambis reports the successful conclusion of Phase I trials of the universal flu vaccine in humans. The universal influenza vaccine has been pioneered by researchers from VIB and Ghent University. This vaccine is intended to provide protection against all ‘A’ strains of the virus that causes human influenza, including pandemic strains. Therefore, this vaccine will not need to be renewed annually.

InfluenzaWhat would make this new vaccine different from the ones already available is that it would target M2e, a conserved region of influenza “A” strains. Since that part doesn’t constantly mutate and about 2/3 of seasonal epidemics and all pandemics are due to type “A” strains, it could be a very efficient weapon against repeats of the “Spanish Flu” (1918−1919) that killed at least 50 million people worldwide. Only the future will tell if phase II and III trials are successful.

You can learn more about the Lifeboat Foundation BioShield program here.

Reposted from Next Big Future which was advancednano.

A 582,970 base pair sequence of DNA has been synthesized.

It’s the first time a genome the size of a bacterium has chemically been synthesized that’s about 20 times longer than [any DNA molecule] synthesized before.

This is a huge increase in capability. It has broad implications for DNA nanotechnology and synthetic biology.

It is particularly relevant for the lifeboat foundation bioshield project

This means that the Venter Institute is on the brink of sythesizing a new bacterial life.

The process to synthesize and assemble the synthetic version of the M. genitalium chromosome

began first by resequencing the native M. genitalium genome to ensure that the team was starting with an error free sequence. After obtaining this correct version of the native genome, the team specially designed fragments of chemically synthesized DNA to build 101 “cassettes” of 5,000 to 7,000 base pairs of genetic code. As a measure to differentiate the synthetic genome versus the native genome, the team created “watermarks” in the synthetic genome. These are short inserted or substituted sequences that encode information not typically found in nature. Other changes the team made to the synthetic genome included disrupting a gene to block infectivity. To obtain the cassettes the JCVI team worked primarily with the DNA synthesis company Blue Heron Technology, as well as DNA 2.0 and GENEART.

From here, the team devised a five stage assembly process where the cassettes were joined together in subassemblies to make larger and larger pieces that would eventually be combined to build the whole synthetic M. genitalium genome. In the first step, sets of four cassettes were joined to create 25 subassemblies, each about 24,000 base pairs (24kb). These 24kb fragments were cloned into the bacterium Escherichia coli to produce sufficient DNA for the next steps, and for DNA sequence validation.

The next step involved combining three 24kb fragments together to create 8 assembled blocks, each about 72,000 base pairs. These 1/8th fragments of the whole genome were again cloned into E. coli for DNA production and DNA sequencing. Step three involved combining two 1/8th fragments together to produce large fragments approximately 144,000 base pairs or 1/4th of the whole genome.

At this stage the team could not obtain half genome clones in E. coli, so the team experimented with yeast and found that it tolerated the large foreign DNA molecules well, and that they were able to assemble the fragments together by homologous recombination. This process was used to assemble the last cassettes, from 1/4 genome fragments to the final genome of more than 580,000 base pairs. The final chromosome was again sequenced in order to validate the complete accurate chemical structure.

The synthetic M. genitalium has a molecular weight of 360,110 kilodaltons (kDa). Printed in 10 point font, the letters of the M. genitalium JCVI-1.0 genome span 147 pages.

The New York Times is reporting today that the continued acceleration of the rate at which the Greenland ice sheets are melting has scientists scrambling for answers. In particular, a combination of changes has the glaciologists particularly concerned. They say the accumulation of meltwater on the surface of the ice in the form of ponds and streams absorbs as much as four times more heat than the lighter-colored ice, thereby accelerating the surface’s rate of melting.

Additionally, this meltwater eventually finds its way to bedrock, where it appears to slightly lubricate the surface between ice and rock, facilitating more rapid ice shifting towards the ocean. A third factor in the trifecta is the breakup of substantial semi-submerged clots of ice that typically block narrow fjords. As these blockages break up, the flow of the frozen glacial rivers accelerates.

While there is still a tremendous amount about this cycle that remains undiscovered, what is clear is that the best estimates to date have fallen far short in terms of the speed at which these rare environments are changing. Although questions remain about how much of these changes are cyclical and how much is due precisely to man-originated global warming, we must gain a more complete understanding of these events so that we can take whatever steps we must to ameliorate any damage we’ve caused before the situation becomes so critical that massive changes come about as a result of our negligent handling of our environment.

Planning for the first Lifeboat Foundation conference has begun. This FREE conference will be held in Second Life to keep costs down and ensure that you won’t have to worry about missing work or school.

While an exact date has not yet been set, we intend to offer you an exciting line up of speakers on a day in the late spring or early summer of 2008.

Several members of Lifeboat’s Scientific Advisory Board (SAB) have already expressed interest in presenting. However, potential speakers need not be Lifeboat Foundation members.

If you’re interested in speaking, want to help, or you just want to learn more, please contact me at [email protected].

(Source: Wikipedia)

Full name: Convention on the Prohibition of the Development, Production and Stockpiling of Bacteriological (Biological) and Toxin Weapons and on their Destruction

Short name: Biological Weapons Convention (BWC)
Open for signature: April 10, 1972
Entered into force: March 26, 1975
Member states: 158
Map of member states:

Summary:

Article I: Never under any circumstances to acquire or retain biological weapons.
Article II: To destroy or divert to peaceful purposes biological weapons and associated resources prior to joining.
Article III: Not to transfer, or in any way assist, encourage or induce anyone else to acquire or retain biological weapons.
Article IV: To take any national measures necessary to implement the provisions of the BWC domestically.
Article V: To consult bilaterally and multilaterally to solve any problems with the implementation of the BWC.
Article VI: To request the UN Security Council to investigate alleged breaches of the BWC and to comply with its subsequent decisions.
Article VII: To assist States which have been exposed to a danger as a result of a violation of the BWC.
Article X: To do all of the above in a way that encourages the peaceful uses of biological science and technology.

Determining the structure of a protein called hemagglutinin on the surface of influenza B is giving researchers at Baylor College of Medicine and Rice University in Houston clues as to what kinds of mutations could spark the next flu pandemic.

This is interesting research and progress in understanding and possibly blocking changes that would lead to pandemics.

In a report that goes online today in the Proceedings of the National Academy of Sciences (PNAS), Drs. Qinghua Wang, assistant professor of biochemistry and molecular biology at BCM, and Jianpeng Ma, associate professor in the same department and their colleagues describe the actual structure of influenza B virus hemagglutinin and compare it to a similar protein on influenza A virus. That comparison may be key to understanding the changes that will have to occur before avian flu (which is a form of influenza A virus) mutates to a form that can easily infect humans, said Ma, who holds a joint appointment at Rice. He and Wang have identified a particular residue or portion of the protein that may play a role in how different types of hemagglutinin bind to human cells.

“What would it take for the bird flu to mutate and start killing people” That’s the next part of our work,” said Ma. Understanding that change may give scientists a handle on how to stymie it.

There are two main forms of influenza virus – A and B. Influenza B virus infects only people while influenza A infects people and birds. In the past, influenza A has been the source of major worldwide epidemics (called pandemics) of flu that have swept the globe, killing millions of people. The most famous of these was the Pandemic of 1918–1919, which is believed to have killed between 20 and 40 million people worldwide. It killed more people than World War I, which directly preceded it.

The Asian flu pandemic of 1957–1958 is believed to have killed as many as 1.5 million people worldwide, and the so-called Hong Kong flu pandemic of 1968–1969 is credited with as many as 1 million deaths. Each scourge was accompanied by a major change in the proteins on the surface of the virus.

The Lifeboat Foundation has the bioshield project

A new biosensor developed at the Georgia Tech Research Institute (GTRI) can detect avian influenza in just minutes. In addition to being a rapid test, the biosensor is economical, field-deployable, sensitive to different viral strains and requires no labels or reagents.

This kind of technology could be applied to real time monitoring of other diseases as well.


Photograph of the optical biosensor that is approximately 16 millimeters by 33 millimeters in size. The horizontal purple lines are the channels on the waveguide. Credit: Gary Meek

“We can do real-time monitoring of avian influenza infections on the farm, in live-bird markets or in poultry processing facilities,” said Jie Xu, a research scientist in GTRI’s Electro-Optical Systems Laboratory (EOSL)

The biosensor is coated with antibodies specifically designed to capture a protein located on the surface of the viral particle. For this study, the researchers evaluated the sensitivity of three unique antibodies to detect avian influenza virus.

The sensor utilizes the interference of light waves, a concept called interferometry, to precisely determine how many virus particles attach to the sensor’s surface. More specifically, light from a laser diode is coupled into an optical waveguide through a grating and travels under one sensing channel and one reference channel.

Researchers coat the sensing channel with the specific antibodies and coat the reference channel with non-specific antibodies. Having the reference channel minimizes the impact of non-specific interactions, as well as changes in temperature, pH and mechanical motion. Non-specific binding should occur equally to both the test and reference channels and thus not affect the test results.

An electromagnetic field associated with the light beams extends above the waveguides and is very sensitive to the changes caused by antibody-antigen interactions on the waveguide surface. When a liquid sample passes over the waveguides, any binding that occurs on the top of a waveguide because of viral particle attachment causes water molecules to be displaced. This causes a change in the velocity of the light traveling through the waveguide.

Five evolutionary stages of pathogen progression from animals to human transmission have been identified A proposed monitoring system of viral chatter has been proposed to provide warning of new diseases before they spread to humans.

In 1999, Wolfe began field work in the jungles of Cameroon to track “viral chatter,” or the regular transmission of diseases from animals to people, usually without further spread among humans. By monitoring the habits and the blood pathologies of bushmeat hunters and their kills, Wolfe and his team have identified at least three previously unknown retroviruses from the same family as HIV, as well as promoted safe practices for handling animals and animal carcasses.

“The Cameroon project demonstrated that it’s possible to collect information on viral transmission under very difficult circumstances from these highly exposed people,” Wolfe said.

With Cameroon as a prototype and a $2.5 million National Institutes of Health Pioneer Award as seed money, Wolfe has gone on to create a network of virus-discovery projects that monitor hunters, butchers, and wildlife trade and zoo workers in some of the world’s most remote viral hotspots. The network of a dozen sites in China, the Democratic Republic of Congo, Malaysia, Laos, Madagascar and Paraguay include source locations for such emerging diseases as SARS, avian flu, Nipah, Ebola and monkeypox.

There are more details of the five stages and a proposed study of the detailed origins of disease.

Wolfe and his colleagues begin by identifying five intermediate stages through which a pathogen exclusively infecting animals must travel before exclusively infecting humans. The research team identifies no inevitable progression of microbes from Stage 1 to Stage 5 and notes that many microbes remain stuck at a specific stage. The journey is arduous, and pathogens rarely climb through all five stages:

Stage 1. Agent only in animals: A microbe that is present in animals but not detected in humans under natural conditions. Examples include most malarial plasmodia.

Stage 2. Primary infection: Animal pathogens that are transmitted from animals to humans as a primary infection but not transmitted among humans. Examples include anthrax, rabies and West Nile virus.

Stage 3. Limited outbreak: Animal pathogens that undergo only a few cycles of secondary transmission among humans so that occasional human outbreaks triggered by a primary infection soon die out. Examples include the Ebola, Marburg and monkeypox viruses.

Stage 4. Long outbreak: A disease that exists in animals and has a natural cycle of infecting humans by primary transmission from the animal host but that also undergoes long sequences of secondary transmission between humans without involvement of animals. Examples include Chagas disease, yellow fever, dengue fever, influenza A, cholera, typhus and West African sleeping sickness.

Stage 5. Exclusive human agent: A pathogen exclusive to humans that involves either an ancestral pathogen present in a common ancestor of chimps and humans or involves a more recent pathogen that evolved into a specialized human pathogen. Examples include HIV, measles, mumps, rubella, smallpox and syphilis.

In addition, the team examines 25 diseases of important historic consequence to humans. Of the 25 diseases, 17 impose the heaviest world burden today: hepatitis B, influenza A, measles, pertussis, rotavirus A, syphilis, tetanus, tuberculosis, AIDS, Chagas disease, cholera, dengue hemorrhagic fever, East and West African sleeping sicknesses, falciparum and vivax malarias, and visceral leishmaniasis.

Eight more imposed heavy burdens in the past but have been reined in or eradicated thanks to modern medicine and public health practices: temperate diphtheria, mumps, plague, rubella, smallpox, typhoid, typhus and tropical yellow fever. Except for AIDS, dengue fever and cholera, most of the 25 have been important for more than two centuries.

The research team considered the varied pathologies of diseases originating in temperate (15) versus tropical (10) regions, as well as differing pathogen and geographic origins. Among the conclusions:

– Most of the temperate diseases, but none of the tropical diseases, are so-called “crowd epidemic diseases,” occurring locally as a brief epidemic and capable of persisting regionally only in large human populations. Most of the diseases originating in temperate climates convey long-lasting immunity.

– Eight of the 15 temperate diseases probably or possibly reached humans from domestic animals, three more from apes or rodents, and the other four came from still unknown sources. Thus the rise of agriculture, starting 11,000 years ago, plays multiple roles in the evolution of animal pathogens into human pathogens.

– Most tropical diseases have originated in wild, non-human primates. These animals are most closely related to humans and thus pose the weakest species barriers to pathogen transfer.

– Animal-derived human pathogens virtually all arose from pathogens of other warm-blooded vertebrates plus, in two cases, birds.

– Nearly all of the 25 major human pathogens originated in the Old Word (Africa, Europe and Asia), facilitating the conquest of the New World. Chagas disease is the only one of the 25 that clearly originated in the New World, while the debate is unresolved for syphilis and tuberculosis.

–Far more temperate diseases arose in the Old World because far more animals that furnish ancestral pathogens were domesticated there. Far fewer tropical diseases arose in the New World because the genetic distance is greater between humans and primates in this part of the globe.

The conclusions of the review illustrate large gaps in the understanding of the origins of even established major infectious diseases. Almost all studies reviewed were based on specimens collected from domestic animals, plus a few wild animal species.

The researchers propose an “origins initiative” aimed at identifying the origins of a dozen of the most important human infectious diseases as well as a global early warning system to monitor pathogens emerging from animals to humans.

This work is relevant to the lifeboat bioshield

If humanity ever meets lifeforms beyond Earth (or discovers our solitude in our galaxy) one thing will be sure–galactic historians will remark how interesting it must have been living in the nuclear age that “we now enjoy” (assuming we survive of course).

Speaking of nuclear, it seems that some scientists are utilizing a new drug that is showing major promises of fighting against radiation exposure, ensuring that victims not only survive, but remain “semi-healthy” as well.

(Space War) But now researchers at Washington University School of Medicine in St. Louis report they have developed an agent that protects cells from the lethal effects of radiation, regardless of whether it is given before or after exposure.

Using this agent in mice, the investigators found that the treatment helped shield rapidly dividing cells that are most vulnerable to radiation-induced death, providing proof in principle that it is possible to fend off radiation damage, according to a study published in the April issue of Biochemical and Biophysical Research Communications.

The interesting aspect of this drug is that it can be applied not only before a potential radiation calamity, but afterwards as well. Despite the fact that this drug is intended for those living on our home world, this anti-radiation drug could enable us to actually live upon the lunar and Martian surface.

Although this drug is not a “cure all” for all of our radiation woes, it could represent the first step of us actually living upon other worlds.