The top three news stories of the week, as chosen by our resident students. This week’s top three news stories are mad cow disease, advances in microscopy, and squeezing white blood cells; Brought to you by Brooke Lumicisi.
Preparing for the second wave of vCJD
Variant Creutzfeldt-Jakob disease (vCJD) is a neurological disorder caused by infection with the deadly prion protein from bovine spongiform encephalopathy (BSE) or mad cow disease. The UK saw a high-profile outbreak of vCJD in the 1990’s from infected cattle with 177 people diagnosed. The misfolded prion protein is able to bind to and deform the native form of the protein, resulting in dense plaques in the brain causing neural disorders and eventually death. The native form of the protein exists in 2 forms, containing the amino acid methionine or valine at position 177. People can either have only methionine-containing proteins, only valine or a mixture of both. This is where the pathology of this second wave comes in to play. The BSE prion protein is only able to act on the native proteins containing a methionine at 177, and up until now only people that exclusively produced M177 prion proteins had been diagnosed with vCJD.
The number of cases of vCJD had slowed to a trickle after the millennium leading researchers to believe that this particular outbreak had passed. However, the number of cases of regular human CJD, meaning spontaneous infection not caused by exposure to external prions, has actually doubled in the last 2 decades. Now, a 36-year-old man who began to show symptoms in 2014 has been confirmed as a vCJD patient with a mosaic methionine/valine expression of prion protein. This is likely what protected him from developing the symptoms until now. A lower level of methionine 177 containing proteins meant the incubation period prior to him displaying symptoms was significantly longer than the other patients. The experience of this patient coupled with the increase in human CJD cases has lead researchers to believe a second wave of patients may be on their way, and that this second wave has already potentially begun but is being misdiagnosed as spontaneous CJD.
J.J. HAUW/SCIENCE PHOTO LIBRARY
Faster than a speeding bullet, and the speed of light (sort of).
How great would it be to be able to look inside tissues without having to separate out the parts? Pretty great. Well, that’s what Jinyang Liang at Washington University in St Louis and his colleagues thought. However, they just needed to overcome the light scattering properties of 3-dimensional medium. The technique they came up with is called “lossless-encoding compressed ultrafast photography” (LLE-CUP). It captures 100 billion frames per second, allowing it to create a real-time video of scattering light with a single snapshot. In order to image the beam of light, they shot a laser through a tunnel filled with dry ice fog flanked by two silicone rubber panels. Because light travels through silicone more slowly than through fog, the laser pulse left a shock wave trailing behind it in a cone shape. Liang explains “Our camera is different from a common camera where you just take a snapshot and record one image: our camera works by first capturing all the images of a dynamic event into one snapshot. And then we reconstruct them, one by one”. Liang says that this could be coupled with existing cameras and microscopes.
Single-shot real-time imaging of light-scattering dynamics: Representative snapshots acquired by LLE-CUP. A photonic Mach cone is observed.
Leukocytes unpick the endothelial cytoskeleton in order to squeeze through
Leukocytes, or white blood cells, travel around your body in your blood vessels. However, to get where they are needed they must pass through the wall of the vessels by squeezing in between the gaps in the cells that are the bricks in this wall, the endothelial cells. It is known that the leukocytes have a relatively soft nucleus that they push to the front of the cell to help them squeeze through. However, it was proposed that the leukocyte then induced the endothelial cells to contract in order to widen the opening. Researchers at The Weizmann institute of science in Israel are proposing that this is not the case and in fact the leukocyte nuclei must disassemble the thin endothelial actin filaments, that provide the frame for the cell, interlaced between endothelial stress fibres to complete migration. The researchers propose a three step process including: 1. a reversible bending of endothelial stress fibres; 2. disassembly of the thin actin filaments interlaced in between these endothelial stress fibres; and 3. formation of actin rings around the protrusions of the transmigrating leukocyte, strengthening this area. Apparently, the holes left behind by these migrating leukocytes are not a problem and are repaired during normal cell maintenance. This is a novel method of cells moving through tissue structures, and will go some way in helping researchers to further understand the harmful migration of cancer cells out of their primary location
T cell squeezing from Cell Report.
Article was written by Brooke Lumicisi