vCJD Families Protest outside Downing Street, London

The government has recorded 168 deaths due to variant CJD - caught from infected bovine material - but this figure is contested as being inaccurate by the families of victims because many of the families who have lost a loved one to this devastating brain disease say that they were never recorded in the official statistics.

Victims are also recorded as 'sporadic CJD', which was the original and very rare form of CJD that can occur in anybody and is not related to infected cattle.

Some cases, even in people in their teens and twenties, are put down to 'early onset alzheimer's disease'. Those left to nurse their husband's, son's, daughter's and wives through the terminal illness say that this is part of a cover up to protect pharmaceutical industries, who use bovine products widely in medicines and vaccines.

Unsafe Blood Donations

Eighteen UK blood donors later died of vCJD and their blood was used to make vaccines and medicines such as factor 8 which is given to haemophiliacs. Some haemophiliacs have since died of vCJD after being given infected blood. Despite this, the government refuse to screen donated blood. An effective test is available but they will not use it. Why not? Christine Lord, Grahame Bell and other members of the protest think it's maybe because screening people's blood would reveal the true magitude of the problem, which would be a disaster of epic proportions for government, the pharmaceutical and agricultural industries.

UK blood bags have warning labels on them due to being possibly contaminated with vCJD and they are not allowed for donation in any other country in the world apart from the UK.

Individual Fibrin Fibers Distribute Strain Across A Network

A new study shows that when it comes to networks of protein fibers, individual fibers play a substantial role in effectively strengthening an entire network of fibers. The research, published by Cell Press in the April 20th issue of the Biophysical Journal,describes a mechanism that explains how individual fibrin fibers subjected to significant strain can respond by stiffening to resist stretch and helping to equitably distribute the strain load across the network.

Fibrin is a fibrous protein that assembles into a remarkably strong mesh-like network and forms the structural framework of a blood clot. Failure of a clot can have fatal consequences. For example, if a portion of the clot breaks away and is carried downstream by the flowing blood, it can cause a stroke or heart attack. Although previous research has characterized the mechanical properties and behavior of fibrin networks on a macroscopic level, much less is known about the behavior of individual fibrin fibers and the distribution of strain from one fiber to the next.

"We know that network strength is determined in part by the maximum strain individual fibers can withstand, so it is of particular interest to determine how the high strain and failure characteristics of single fibrin fibers affect the overall strength of the network," says senior study author Dr. Michael R. Falvo from the Department of Physics and Astronomy at the University of North Carolina at Chapel Hill. "Further, determining how strain is shared among the constituent fiber segments in a network under imposed stress is crucial to understanding failure modes of networks and their strength."

Dr. Falvo and colleagues used a combined fluorescence/atomic force microscope nanomanipulation system to stretch two dimensional fibrin networks to the point of failure while recording the strain of individual fibers. "Specifically, we observed that as fibers were stretched, they became stiffer than the surrounding fibers at lower strains; this allowed the more strained, stiffer fibers, to distribute the strain load to the less strained fibers and reduce strain concentrations," explains Dr. Falvo. "So in effect, strain stiffening in the individual fibers acts to distribute strain equitably throughout the network and thereby strengthen it."

The strain concentration reduction effect described in this study may be part of an important physiological mechanism to strengthen blood clots under high shear conditions in the blood stream. The authors note that along with this physiological insight, their findings bring about a better understanding of this remarkable strengthening mechanism and may help to guide new design strategies for engineered materials