Department of Bioscience & Bioengineering

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When somatosensory cortex (S1) is deprived of some of its inputs after section of ascending afferents in the dorsal columns of the spinal cord, it reorganizes to overrepresent the surviving inputs. As somatosensory cortex provides guiding sensory information to motor cortex, such sensory loss and representational reorganization could affect the development of the motor map in primary motor cortex (M1), especially if the sensory loss occurs early in development. To address this possibility, the dorsal columns of the spinal cord were sectioned between cervical levels (C3-5) 3-12 days after birth in five macaque monkeys. After 3-5 years of maturation (young adults), we determined how movements were represented in M1 contralateral to the lesion by using microelectrodes to electrically stimulate sites in M1 to evoke movements. Although the details of the motor maps in these five monkeys varied, the forelimb motor maps were abnormal. The representations of digit movements were reduced and abnormally arranged. Current levels for evoking movements from the forelimb region of M1 were in the normal range, but the lowest mean stimulation thresholds were for wrist or elbow instead of digit movements. Incomplete lesions and bilateral lesions produced fewer abnormalities. The results suggest that the development of normal motor cortex maps in M1 depends on sensory feedback from somatosensory maps.

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Proceedings of the National Academy of Sciences of the United States of America

Functional organization of motor cortex of adult macaque monkeys is altered by sensory loss in infancy

Background: Several highly pathogenic avian influenza (AI) outbreaks have been reported over the past decade. South Korea recently faced AI outbreaks whose economic impact was estimated to be 6.3 billion dollars, equivalent to nearly 50% of the profit generated by the poultry-related industries in 2008. In addition, AI is threatening to cause a human pandemic of potentially devastating proportions. Several studies show that a stochastic simulation model can be used to plan an efficient containment strategy on an emerging influenza. Efficient control of AI outbreaks based on such simulation studies could be an important strategy in minimizing its adverse economic and public health impacts.Methods: We constructed a spatio-temporal multi-agent model of chickens and ducks in poultry farms in South Korea. The spatial domain, comprised of 76 (37.5 km × 37.5 km) unit squares, approximated the size and scale of South Korea. In this spatial domain, we introduced 3,039 poultry flocks (corresponding to 2,231 flocks of chickens and 808 flocks of ducks) whose spatial distribution was proportional to the number of birds in each province. The model parameterizes the properties and dynamic behaviors of birds in poultry farms and quarantine plans and included infection probability, incubation period, interactions among birds, and quarantine region.Results: We conducted sensitivity analysis for the different parameters in the model. Our study shows that the quarantine plan with well-chosen values of parameters is critical for minimize loss of poultry flocks in an AI outbreak. Specifically, the aggressive culling plan of infected poultry farms over 18.75 km radius range is unlikely to be effective, resulting in higher fractions of unnecessarily culled poultry flocks and the weak culling plan is also unlikely to be effective, resulting in higher fractions of infected poultry flocks.Conclusions: Our results show that a prepared response with targeted quarantine protocols would have a high probability of containing the disease. The containment plan with an aggressive culling plan is not necessarily efficient, causing a higher fraction of unnecessarily culled poultry farms. Instead, it is necessary to balance culling with other important factors involved in AI spreading. Better estimations for the containment of AI spreading with this model offer the potential to reduce the loss of poultry and minimize economic impact on the poultry industry. © 2010 Kim et al; licensee BioMed Central Ltd.

BMC Infectious Diseases

Multi-agent modeling of the South Korean avian influenza epidemic

For biomedical applications, emerging nanostructures requires stringent evaluations for their biocompatibility. Core/shell iron/carbon nanoparticles (Fe@CNPs) are nanomaterials that have potential applications in magnetic resonance imaging (MRI), magnetic hyperthermia and drug delivery. However, their interactions with biological systems are totally unknown. To evaluate their potential cellular perturbations and explore the relationships between their biocompatibility and surface chemistry, we synthesized polymer grafted Fe@CNPs with diverse chemistry modifications on surface and investigated their dynamic cellular responses, cell uptake, oxidative stress and their effects on cell apoptosis and cell cycle. The results show that biocompatibility of Fe@CNPs is both surface chemistry dependent and cell type specific. Except for the carboxyl modified Fe@CNPs, all other Fe@CNPs present low toxicity and can be used for further functionalization and in a wide range of biomedical applications. © 2010 Elsevier Ltd.

Biomaterials

Biocompatibility of polymer grafted core/shell iron/carbon nanoparticles

Journal of Urology

Re: Genetic Polymorphisms of Matrix Metalloproteinases: Susceptibility and Prognostic Implications for Prostate Cancer. S. T. dos Reis, J. Pontes, Jr., F. E. Villanova, P. M. D. Borra, A. A. Antunes, M. F. Dall'oglio, M. Srougi and K. R. M. Leite J Urol 2009; 181: 2320-2325

Friedreich's ataxia (FRDA) is caused by expansion of GAA repeats in the frataxin (FXN) gene on chromosome 9q13-q21.1. We analysed the origin of FRDA in 21 North Indian (NI) and eight South Indian (SI) families using five single nucleotide polymorphisms (SNPs) and a microsatellite marker spanning the GAA repeats. The NI and SI families were derived from Indo-European and Dravidian linguistic backgrounds respectively. The frequency of large normal (LNs) alleles of the GAA repeat correlate with the overall lower prevalence of FRDA in India compared to the European population. All of the expanded alleles in the Indian population share a common core haplotype suggesting a founder effect. The expanded alleles in the NI population demonstrate more similarity to those of Europeans in terms of age of GAA repeat expansion (15975 ± 2850 years) and association of LNs with expanded alleles. FRDA seems to have been introduced recently in the South Indian population since the average estimated age of the mutation in SI is 5425 ± 1750 years and unlike NI some of the haplotypes of LNs are not associated with the expanded alleles. © 2010 IGIB, CSIR, Delhi, India Journal compilation © 2010 Blackwell Publishing Ltd/University College London.

Annals of Human Genetics

North and South Indian Populations Share a Common Ancestral Origin of Friedreich's Ataxia but Vary in Age of GAA Repeat Expansion

National Medical Journal of India

Brain-machine interface: The future is now

Gene selection from microarray data is an important issue for gene expression based classification and to carry out a diagnostic test. In this regard, a rough set based gene selection algorithm is presented. It selects the set of genes by maximizing the relevance and significance of the genes, which are calculated based on the theory of rough sets. Using the predictive accuracy of K-nearest neighbor rule and support vector machine, the performance of the proposed algorithm, along with a comparison with other related methods is studied on five cancer and two arthritis microarray data sets. Promising performance was achieved by the proposed gene selection algorithm with relevant and significant genes from microarray data set in a reasonable time. © 2010 IEEE.

Proceedings of 2010 International Conference on Methods and Models in Computer Science, ICM2CS-2010

Rough set based gene selection algorithm for microarray sample classification

We analyzed subunit interfaces in 315 homodimers with an X-ray structure in the Protein Data Bank, validated by checking the literature for data that indicate that the proteins are dimeric in solution and that, in the case of the "weak" dimers, the homodimer is in equilibrium with the monomer. The interfaces of the 42 weak dimers, which are smaller by a factor of 2.4 on average than in the remainder of the set, are comparable in size with antibody-antigen or protease-inhibitor interfaces. Nevertheless, they are more hydrophobic than in the average transient protein-protein complex and similar in amino acid composition to the other homodimer interfaces. The mean numbers of interface hydrogen bonds and hydration water molecules per unit area are also similar in homodimers and transient complexes. Parameters related to the atomic packing suggest that many of the weak dimer interfaces are loosely packed and we suggest that this contributes to their low stability. To evaluate the evolutionary selection pressure on interface residues, we calculated the Shannon entropy of homologous amino acid sequences at 60% sequence identity. In 93% of the homodimers, the interface residues are better conserved than the residues on the protein surface. The weak dimers display the same high degree of interface conservation as other homodimers, but their homologs may be heterodimers as well as homodimers. Their interfaces may be good models in terms of their size, composition and evolutionary conservation for the labile subunit contacts that allow protein assemblies to share and exchange components, allosteric proteins to undergo quaternary structure transitions and molecular machines to operate in the cell. {\textcopyright} 2010 Elsevier Ltd.

Journal of Molecular Biology

The subunit interfaces of weakly associated homodimeric proteins

Inflammation is increasingly recognized as an important contributor to a host of CNS disorders; however, its regulation in the brain is not well delineated. Nucleotide-binding domain, leucine-rich repeat, pyrin domain containing 3 (NLRP3) is a key component of the inflammasome complex, which also includes ASC (apoptotic speck-containing protein with a card) and procaspase-1. Inflammasome formation can be triggered by membrane P2X7R engagement leading to cleavage-induced maturation of caspase-1 and interleukin-1β (IL-1β)/IL-18. This work shows that expression of the Nlrp3 gene was increased &gt; 100-fold in a cuprizone-induced demyelination and neuroinflammation model. Mice lacking the Nlrp3 gene (Nlrp3-/-) exhibited delayed neuroinflammation, demyelination, and oligodendrocyte loss in this model. These mice also showed reduced demyelination in the experimental autoimmune encephalomyelitis model of neuroinflammation. This outcome is also observed for casp1-/- and IL-18-/- mice, whereas IL-1β-/- mice were indistinguishable from wild-type controls, indicating that Nlrp3-mediated function is through caspase-1 and IL-18. Additional analyses revealed that, unlike the IL-1β-/- mice, which have been previously shown to show delayed remyelination, Nlrp3 -/- mice did not exhibit delayed remyelination. Interestingly, IL-18-/- mice showed enhanced remyelination, thus providing a possible compensatory mechanism for the lack of a remyelination defect in Nlrp3-/- mice. These results suggest that NLRP3 plays an important role in a model of multiple sclerosis by exacerbating CNS inflammation, and this is partly mediated by caspase-1 and IL-18. Additionally, the therapeutic inhibition of IL-18 might decrease demyelination but enhance remyelination, which has broad implications for demyelinating diseases. Copyright © 2010 the authors.

Journal of Neuroscience

The inflammasome sensor, NLRP3, regulates CNS inflammation and demyelination via caspase-1 and interleukin-18

In our previous studies, Abrus agglutinin showed non-specific immunostimulatory activity both native (NA) and heat-denatured (HDA) condition in mouse model. The present study was investigated to decipher the specific immune response towards B and T cell by NA and HDA. It was observed that the proliferation index for NA and HDA of stimulated B cells are 1.35 and 1.41 respectively and on the other hand, T cell proliferation index for NA and HDA are 1.67 and 1.54 respectively. At the same time, expression of surface and activation marker for B and T cells was significantly different compared to control as quantified by flow cytometry. But the expression of co-stimulatory markers (CD 80 and CD 86) was not significantly different and NA and HDA in immunized splenocytes with Dalton's lymphoma antigen induced antibodies titer 4.37 and 4.2 times more than control. This study indicates Abrus agglutinin (NA and HDA) acts as a B cell and T cell stimulator. © 2008 Elsevier GmbH. All rights reserved.