Automated Segmentation Of Multiple Sclerosis Lesions By Model Outlier Detection
Van Leemput K, Maes F, Vandermeulen D, Colchester A, Suetens P
IEEE Trans Med Imaging 2001 Aug;20(8):677-88
Univ Hospital Gasthuisberg, Medical Image Computing, Faculties of Medicine and Engineering, Leuven, Belgium
PMID: 11513020; UI# 21403924
This paper presents a fully automated algorithm for segmentation of Multiple Sclerosis (MS) lesions from MultiSpectral Magnetic Resonance (MR) images.
The method performs intensity-based tissue classification using a stochastic model for normal Brain images and simultaneously detects MS lesions as outliers that are not well explained by the model.
It corrects for MR field inhomogeneities, estimates tissue-specific intensity models from the data itself, and incorporates contextual information in the classification using a Markov random field.
The results of the automated method are compared with lesion delineations by human experts, showing a high total lesion load correlation.
When the degree of spatial correspondence between segmentations is taken into account, considerable disagreement is found.
Both between expert segmentations, and between expert and automatic measurements.
Caserta MT, Mock DJ, Dewhurst S
Clin Infect Dis 2001 Sep 15;33(6):829-33
Univ of Rochester Medical Center, Dept of Pediatrics, Rochester, NY, USA
PMID# 11512088; UI# 21402456
The development of techniques for the culture of Lymphoid Cells and the isolation of Viruses that infect these cells led to the discovery of human HerpesVirus (HHV) 6 in 1986.
At the time, HHV-6 was the first new human HerpesVirus to be discovered in roughly a quarter of a century.
And its isolation marked the beginning of an era of discovery in HerpesVirology, with the identification of HHV-7 and HHV-8 (Kaposi's Sarcoma-associated HerpesVirus) during the following decade.
Like most Human HerpesViruses, HHV-6 is ubiquitous and capable of establishing a lifelong, latent infection of its host.
HHV-6 is particularly efficient at infecting infants and young children, and primary infection with the Virus is associated with Roseola Infantum (Exanthem Subitum) and, most commonly, an undifferentiated febrile illness.
Viral reactivation in the ImmunoCompromized host has been linked to a variety of diseases, including Encephalitis, and HHV-6 has been tentatively associated with Multiple Sclerosis.
This article discusses the major properties of HHV-6, its association with human disease, and the PathoBiological significance of Viral reactivation.
Astrocytes, Not Microglia, Are The Main Cells Responsible For Viral Persistence In Theiler's Murine EncephaloMyelitis Virus Infection Leading To DeMyelination
Zheng L, Calenoff MA, Dal Canto MC
J Neuroimmunol 2001 Aug 30;118(2):256-67
Northwestern Univ, Medical School, Division of NeuroPathology, Dept of Pathology, 60611, Chicago, IL, USA
PMID# 11498260; UI# 21389405
The BeAn strain of Theiler's Murine EncephaloMyelitis Virus (TMEV) persists in the CNS and produces a chronic inflammatory DeMyelinating Disease that is an animal model for human Multiple Sclerosis (MS).
The mechanisms leading to TMEV-induced DeMyelination are still under study but most likely involve both Immune-mediated and Virus induced damage to cells in the CNS.
Both depending on Viral persistence. It is therefore important to identify the cells in which continued Virus production is permitted.
In this study, we looked at Virus infection in primary Astrocytes, Microglia and Oligodendrocytes, derived from Brains of neonatal susceptible SJL/J mice.
As evidenced by Western blots and ImmunoCytoChemistry, we were able to detect Viral Antigens in all these Brain-derived cells.
In addition, we extended the study to Spinal Cord tissues from mice suffering TMEV-induced disease.
ImmunoHistoChemistry staining with anti-TMEV Sera and Antibodies to specific cell markers detected Viral Antigens in all these cells.
We then asked the question whether Viral Antigen present in these cells, particularly in Microglia/Macrophages, represented true Viral replication or not.
By using different techniques, including ImmunoPrecipitation experiments and the very sensitive method of negative RNA detection through RNase protection assay, we show that both Astrocytes and Oligodendroglia permit de novo Viral replication.
And Viral protein synthesis but with only minimal cytopathic effects. Of these two cell types, Astrocytes carry the brunt of Viral replication.
In Microglia, on the other hand, Viral replication is restricted since only minimal amounts of negative RNA copies can be demonstrated, while there are clear signs that some of these cells undergo Apoptosis.
These findings show that the main cell for Viral replication is the Astrocyte, rather than the Microglia/Macrophage.
Most of the Viral Antigen present in Macrophages, therefore, is probably the result of Phagocytosis, rather than actual Viral replication.
In view of the demonstrated presence of Viral replication in Astrocytes and of great amounts of Viral Antigens in Microglia/Macrophages.
It is possible that both types of cells act as Antigen Presenting Cells during this ImmunoPathological Disease.
Genetic Polymorphisms Of IL-1ß And IL-1 Receptor Antagonist In Association With Multiple Sclerosis In Japanese
Niino M, Kikuchi S, Fukazawa T, Yabe I, Sasaki H, Tashiro K
J Neuroimmunol 2001 Aug 30;118(2):295-9
Hokkaido UnivGraduate School of Medicine, Dept of Neurology, Kita-15 Nishi-7, Kita-ku, 060-8638, Sapporo, Japan
PMID# 11498264; UI# 21389409
In the present study, we have investigated the association of specific polymorphisms of the InterLeukin-1ß (IL-1ß) and IL-1 receptor antagonist (ra) Gene.
With both the susceptibility to and the clinical characteristics of Multiple Sclerosis (MS) in Japanese patients.
We collected and analyzed DNA from 98 MS patients and 104 healthy controls for distribution of IL-1ß or IL-1ra polymorphisms.
Our results show no significant differences in the distribution of the polymorphisms between MS patients and controls.
Furthermore, no association was observed between IL-1ß or IL-1ra polymorphisms and clinical characteristics, such as age at disease onset, clinical course and severity.
Together, our findings suggest that IL-1ß or IL-1ra Gene polymorphisms may not be relevant in the susceptibility to MS or the clinical characteristics of Japanese patients with MS.