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December 18, 2014
Blood protein may indicate brain lesions in trauma patients
A team of researchers from Florida, Virginia, and Texas demonstrated how a protein found in the blood may be an indicator for whether traumatic brain injury patients have sustained cranial lesions, as published in the Journal of Neurotrauma. This study may be particularly important given the increasing amount of attention focused on concussions from sports, accidents, and other incidents.
For their research, the study authors enrolled 397 general trauma patients, 209 of whom had mild to moderate traumatic brain injuries. The researchers collected human blood specimens and measured the levels of two proteins: glial fibrillary acidic protein (GFAP) and S100ß. Both of these proteins are found in glial cells and released into the blood after a brain injury. However, S100ß may be problematic because bones also release it after a fracture.
Results from this study illustrated how S100ß levels increase after a fracture regardless of whether a brain injury occurred, while levels of GFAP do not change in the presence of broken bones.
"This study convincingly demonstrates the efficacy and brain-specific nature of GFAP and its ability to detect traumatic intracranial lesions while also calling into question the overall utility of S100ß in the same patient population," John Povlishock, Ph.D., editor-in-chief of the Journal of Neurotrauma, said in a statement.
X-chromosome testing uncovers clues about disease
The difference in the number of X-chromosomes between males and females accounts for a range of genetic diseases, and researchers continue to study the impact of these chromosomes. One team of scientists from the Translational Genomics Research Institute (TGen) was able to use sequencing technology to discover an X-linked neurobehavioral disorder in a pre-teen girl, as published in the journal PLOS ONE.
The case study involved a pre-teen girl whose parents brought her to TGen with an undiagnosed neurobehavioral condition. Researchers at the center sequenced both DNA and RNA biospecimens collected from the girl, her mother, and her father. In theory, both parents should have contributed to half the number of X-chromosomes in the girls' cells.
What the scientists discovered was that the X-chromosome from the father had abnormalities that were associated with neurobehavioral problems. However, more of the active X-chromosomes came from the mother, which likely led to a mild, less harsh form of the X-linked condition.
"With just a small bio sample, we are now able to provide a comprehensive evaluation of the effects that genetic variation has on patients, leading to highly personalized treatment options, while at the same time providing researchers with insights into the underlying molecular processes," lead author Szabolcs Szelinger said in a statement.
Loss of protein function linked to fat cell accumulation
Researchers from the University of Rochester Medical Center (URMC) in New York asserted that the loss of functional Thy1 proteins from primitive cells is what leads them to develop into fat cells, as published in the FASEB Journal. The discovery may be pivotal to tackling the obesity epidemic in the U.S., in which about 60 million individuals in the country are considered clinically obese.
The protein Thy1 had been discovered about 40 years ago, but its function in cells had not been well understood. The URMC team had been investigating the protein since 1989. In the most recent research, they observed the behavior of Thy1 in both rodents and human fat cells harvested from human tissues from eyes and abdomens. In the animal studies, the researchers fed two groups of mice a similar high-fat diet. One group of mice lacked functional Thy1 proteins in their cells, while the other was normal. Results showed that those missing Thy1 gained more weight. Similar results were seen in the human cells.
Eventually, the URMC team wants to market an anti-obesity drug that contains a Thy1 peptide.
Blood proteins may prevent inflammatory response to nanoparticles
Although nanomedicine has shown great promise, the potential for nanoparticles to cause inflammatory reactions poses a significant obstacle. However, one team of scientists from Brunel University London discovered that proteins in the blood may help disguise nanoparticles in a way that makes them benign to the immune system, as published in the Journal of Biomedical Nanotechnology.
In their experiments, the researchers observed that carbon nanotubes coated in proteins from the immune complement system are more easily tolerated by the immune system. If this continues to be borne out in studies, the scientists may have found a way to use nanoparticles to treat inflammatory diseases, such as Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis.
"By using a protein recognized by the immune system to effectively disguise carbon nanoparticles, we will be able to deploy these tiny particles to target hard-to-reach [human tissue] areas without damaging side effects to the patient," researcher Uday Kishore said in a statement. "This is a big step forward. It is like understanding how to use penicillin safely and could be as revolutionary to modern medicine as its twentieth century predecessor."
Currently, data from these experiments are informing tests to use carbon nanoparticles coated in genetically engineered proteins to treat glioblastoma.