Wednesday, November 30, 2005

Again with the Blue-Sky


Again with the Blue-Sky


We reported in our October 17th Report about the possible defence against the "super bug" type illnesses found in the mold of a tree. Oct 17 Blog Entry

Today, Science Daily reports on the discovery another un-likely place to find a medicine: The American Oyster. Recently, The National Sea Grant College Progam announced the discovery of an antimicrobial peptide, "American oyster defensin".

American oyster defensin is an antimicrobal that resists bacterial pathogens, such as Vibrio Vulnificus, that can cause a food-borne illness in humans.

These, and myriad other discoveries and breakthroughs, prove the point of The United Federation Foundation: With no new research, with inadequate funding, there can be no new breakthroughs.

Please help us, The U.F.F., to help humanity, and therefore help our World.

Again with the Blue-Sky


We reported in our October 17th Report about the possible defence against the "super bug" type illnesses found in the mold of a tree. Oct 17 Blog Entry

Today, Science Daily reports on the discovery another un-likely place to find a medicine: The American Oyster. Recently, The National Sea Grant College Progam announced the discovery of an antimicrobial peptide, "American oyster defensin".

American oyster defensin is an antimicrobal that resists bacterial pathogens, such as Vibrio Vulnificus, that can cause a food-borne illness in humans.

These, and myriad other discoveries and breakthroughs, prove the point of The United Federation Foundation: With no new research, with inadequate funding, there can be no new breakthroughs.

Please help us, The U.F.F., to help humanity, and therefore help our World.

Thursday, November 17, 2005

Another great reason for large computer array studies.

One of the projects that The United Federation Foundation endorses and assists is the Climate Predictor, found here: Climatepredictor.net . Using and amalgam of 12 climate studies from 165 different locations, United States Geological Survey has been getting a clearer picture of global water availability in the coming years.

A report on their findings can be found here: Link

Another research project that The U.F.F. is conscidering for endorsement has recently announced that it has just completed 200,000 year's worth of calculations in less than 1 year's time!

This is a brilliant example of why we should both donate and encourage the donation of spare computer time. Our computers wont miss the time, it costs us very little, and so much good can be achieved.

Tuesday, November 15, 2005


The time is NOW

At this moment, right now, we stand both in the center of infinity, and in the middle
of eternity. There's nothing mystical about, nor is there magic in, that statement.
Forever is always, and infinity is everything and everywhere.
Having said that, here we are: holding fast in our place as the future rushes at us.
The future, and the changes it brings will buffet us as long as we exist. Change is
the only constant that we can be assured of.

Consider these two facts: The store of human knowledge doubles every five years;
Children born today could live to see the 22nd century.

The students of the 70's and 80's could find an abacus in their classrooms. The
students of the 80's and 90's would use calculators. The students of the 90's and the
new millenium have laptops.

If we nourish innovation and cut red tape, these children, these citizens of the new
century could cure a dred disease, pioneer new industry, even touch a new horizon
we have yet to imagine. These children could create a world fuled by a new prosperity, with new opportunities, and breakthrough discoveries.

All we have to do is care enough to see the potential, and prepare ourselves and our
progeny. The future will not wait. It IS coming. The only question is: Have we
matured enough to outgrow our past and allow humanity to be all of the wonderfull
things the word "human" suggests?

Thursday, November 10, 2005

Yet another discovery illustrates the importance of the protien research (among other projects) the United Federation Foundation advocates.

Source: Queen's University


KINGSTON, Ont. -- Queen’s researchers may have opened the door to more effective treatment of a deadly strain of the E. coli bacteria with the discovery of a previously unknown protein.

A team led by biochemistry researcher Zongchao Jia and graduate student Michael Suits has identified a protein that allows the bacterial strain known as E. coli 0157:H7 to obtain the iron it needs for survival in the body.

Iron is a catalyst for bacterial growth, so when a human body detects bacterial invasion, it naturally produces proteins that bind tightly to and restrict iron to limit bacterial growth. In response, bacteria have evolved other methods to acquire iron including detecting and using human heme within proteins such as hemoglobin that transports oxygen from our lungs.

The newly discovered protein breaks down heme, releasing the iron atom stored there for use by the deadly bacteria.

“This discovery opens the door for studying the function of heme iron in this strain of E. coli, and may lead to an understanding of how to therapeutically isolate the protein to keep the bacteria from thriving,” says Dr. Jia.

E. coli 0157:H7 is responsible for the fatal illnesses in the Walkerton tragedy, the illness known as “Hamburger Disease” and the recent evacuation of over a thousand residents from the Kasechewan First Nation reserve. It is most commonly transmitted through undercooked meat, unpasturized milk and infected water sources.

Researchers believe that isolating one of the proteins E. coli 0157:H7 needs for survival will not be enough, however, since the bacteria will migrate to surrounding proteins as iron sources.

Ongoing research is required to examine the functions of several different proteins to find an effective treatment for E. coli 0157:H7, similar to the cocktail used to treat other severe bacterial infections.


We ask you to please consider joining the United Federation Foundation team at Berkley's BOINC Research Project. Protien Predictor link and or Rosetta @ Home .

Monday, November 07, 2005

THIS is why we ask our Membership to participate in projects like The Protien Predictor and Rosetta at Home. Even if we do not do the actual hands-on research, the power of multi-computer arrays can provide tremendous computing power at minimum cost to reseachers.

The Human Genome Project was completed in a fraction of the time first predicted.

Just a bit of computer time donated by a large group of concerned people can, and often does, produce remarkable results. Imagine how much sooner we could have read the following release from The Howard Huges Medical Institute, and other medical researchers, if we could get a few more people assisting these scientists in their efforts.

Technique Offers New View of Dynamic Biological Landscape


Source:
Howard Huges Medical Institute

A new technique for analyzing the network of genetic interactions promises to change how researchers study the dynamic biological landscape of the cell. The technology, which is called epistatic mini array profiles (E-MAP), has already been used to assign new functions to known genes, to uncover the roles of previously uncharacterized proteins, and to define how biochemical pathways and proteins interact with one another.

E-MAP will enable new understanding of how genes and proteins function in the cell, said Jonathan S. Weissman, a Howard Hughes Medical Institute (HHMI) investigator at the University of California, San Francisco (UCSF) and leader of the team that developed the technique. For example, E-MAPs of human gene interactions could enable researchers to optimize drug treatments to patients' genetic backgrounds. It might also be possible to use E-MAP to develop effective combinations of antiviral drugs that target proteins produced by interacting genes. Such a strategy would help to prevent these genes from acting together to compensate for an attack on just one protein, said Weissman.

The researchers, led by Weissman, Maya Schuldiner, a post-doctoral fellow working in his lab, and Nevan Krogan at the University of Toronto, described initial studies of E-MAP in yeast in the November 4, 2005, issue of the journal Cell. Weissman and his colleagues at UCSF collaborated on the studies with researchers at the University of Toronto.

Previous techniques for analyzing epistatic interactions — how the activity of one gene affects that of another — involved altering single genes and analyzing their impact on growth in combination with all other genes in the yeast genome. "The one-to-one method has been an extremely powerful way of studying biological systems,” said Weissman. “But we wanted to approach such analyses in a systematic way and to use the new generation of high-throughput technology to quantitatively explore large numbers of epistatic genetic interactions at once."

The E-MAP technique consists of selectively "dialing down" the activity of a multitude of gene pairs and comparing the effects of those changes to those that result when each gene is dialed down individually. Many genes' activity could be reduced by eliminating them entirely, but for the subset of genes that are essential for yeast growth — whose complete deletion would kill the cell — the researchers invented a high throughput technique to manipulate the half-life of their messenger RNA (mRNA). Since mRNA is a genetic intermediate during the conversion of a gene to protein, reducing its lifespan by mutating the mRNA message lowers the amount of protein the cell can produce. The group called this approach “decreased abundance by mRNA perturbation” (DAmP).

"The DAmP technique gave us a way of lowering the abundance of a target gene's messenger RNA while maintaining its natural regulation," said Weissman. "Most of the mRNAs in yeast have half-lives of ten minutes or so, but our alterations destabilized them to have only a half-life of a couple of minutes. Consequently, they produce five- to ten-fold less protein," he said.

In developing E-MAP, the researchers faced a significant hurdle: Even yeast's relatively modest 6,000 genes would generate nearly 20 million possible gene pairs that would need to be tested. To narrow the number of possible interactions, they adopted a strategy called neighborhood clustering, which restricts analysis to genes that have related functions and that also cluster in one place in the cell. In the Cell paper, they applied the E-MAP technique to a "mini array" of 442 yeast genes that define a biological pathway called the early secretory pathway. This compartmentalized, interconnected pathway synthesizes and regulates lipids and secreted proteins in yeast.

Weissman and his colleagues also needed a way to quantify the epistatic effects of interacting mutant genes on the cells' viability. Since yeast form round colonies when grown in culture dishes, they could measure the mutant cells' colony size in an automated fashion and use that to calculate their growth rates. To determine epistatic effects, they compared the growth rate for each cell containing mutations in two genes with the growth rate of mutant cells carrying mutations in only one of those genes.

"The analysis of these epistatic interactions gave us a unique and coherent perspective on the function and structure of this network in yeast," Weissman explained. "And it also proved a great way to find new gene functions or to figure out how known genes were functioning and the processes they were likely to be involved in. But on top of that, we could identify groups of genes that were acting in a coherent way, to produce protein complexes. And then on a more global level, we could see how the different processes were interacting with each other.

"By contrast, in classical genetics, you begin with a process you're interested in — for example secretion — and look for all the genes that affect secretion. It's a productive approach, but it's very process oriented,” he said. “You might find a given gene that's involved in secretion, but it doesn't tell you about the many other processes it could be involved in.

With the E-MAP approach, however, the researchers start with the gene and ask about all the processes that it affects. “It gives you a less hypothesis-biased, more objective way of looking at the structure of biological systems," Weissman said.

In future studies, Weissman and his colleagues plan to develop better quantitative measures of the effects of epistatic interactions and to extend their technique to other organisms, ultimately to humans.

In addition to offering important basic insights into the roles of proteins and genes, E-MAPs will also contribute to understanding evolutionary processes. “In evolutionary theory, the structure of epistatic gene interactions is critical,” he said. “To understand how different variations, or alleles, of a gene affect an organism's evolution, you have to understand for each gene how it's affected by the genetic background in which it operates.”

Moving beyond the theoretical, E-MAPs might also have a role in clinical applications. "In the field of pharmacogenomics, clinicians seek to tailor drug therapies to an individual's genetic makeup,” said Weissman. “They are essentially asking the very questions about epistatic interactions that E-MAPs can answer. They want to know whether if they inhibit a protein — in this case with a drug instead of knocking down the mRNA — how other genes interact with that inhibition.”

Knowing the interactions a target gene participates in could also enable clinicians to predict the variability of effects of a drug among different people. Understanding such interactions could also give pharmaceutical researchers clues to the magnitude of possible side effects of drugs under development.

The development of combination drug therapies, such as for cancer or viruses, could also benefit from the E-MAP approach. “In such cases, clinicians want to know — if drugs that inhibit each of two proteins slow down a cancer or virus — whether the two proteins interact epistatically, such that inhibiting both produces a much greater effect than the sum of the two,” he said.

Tuesday, November 01, 2005


A New Breakthrough for cancer patients



Bionomics today announced that it has been granted a patent in New Zealand for a series of compounds that have shown promise as potential new treatments for cancer.Bionomics is currently developing the compounds as "vascular targeting agents" for the treatment of solid tumours. Vascular targeting agents act by starving tumors of the blood flow they require to grow.

Dr. Bernard Flynn, a co-inventor of the compounds and now VP of Chemistry of Bionomics, stated that, "This patent covers a range of structures that have demonstrated significant efficacy as anticancer agents. These compounds have resulted from application of our MultiCore chemistry platform to vascular targeting, a highly promising new area of anticancer drug discovery. This is a field of intense interest within the industry and our compounds offer the competitive advantages of exceptional potency and superior drug-likeness."

The granted patent was originally licensed to Iliad Chemicals Pty Ltd by the Australian National University and the U.S. Government. Iliad was acquired by Bionomics on 1 July 2005.

Significant progress in Bionomics anticancer program

In announcing the grant of the patent, Bionomics also reported that rapid progress in the vascular targeting agent program has resulted in the identification of six lead candidate compounds. Further testing will enable the selection of a nominated clinical candidate.

Bionomics anticipates that this further work will be completed in the first quarter of 2006. "Following the acquisition of Iliad, we have rolled out a comprehensive integration program to bring together Bionomics' Angene platform in cancer biology with the MultiCore chemistry technology. This effort has already borne fruit in the identification of several promising anticancer leads," stated Dr. Deborah Rathjen, CEO and Managing Director of Bionomics.

At the completion of the acquisition of Iliad Chemicals Pty Ltd earlier this year, a plan for further evaluating in excess of 90 active compounds was implemented. The execution of this plan has enabled Bionomics to select potent vascular targeting compounds with desirable drug-like properties to move forward, prior to commencement of manufacture of drug compound and formal toxicology which will support clinical development of the preferred anticancer vascular targeting compound. Each of the compounds currently under evaluation is proprietary to the Company with both composition of matter and use patent claims under examination.