Department of Bioscience & Bioengineering

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The features of solitary waves observed in horizontal monodisperse chain of barely touching beads not only depend on geometrical and material properties of the beads but also on the initial perturbation provided at the edge of the chain. An impact of a large striker on a monodisperse chain, and similarly a sharp decrease of bead radius in a stepped chain, generates a solitary wave train containing many single solitary waves ordered by decreasing amplitudes. We find, by simple analytical arguments, that the unloading of compression force at the chain edge has a nearly exponential decrease. The characteristic time is mainly a function involving the grains' masses and the striker mass. Numerical calculations and experiments corroborate these findings. © 2007 Springer-Verlag.

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Granular Matter

Solitary wave trains in granular chains: Experiments, theory and simulations

Background & objectives: Spinocerebellar ataxias (SCAs) are often caused by expansions of GTG/CAG trinucleotide repeat in the genome. Expansions at the SCA1, 2 and 3 loci are the most frequent, but differences in their relative proportion in regions occur across the world. We carried out this study to assess the occurrence of SCA1, 2 and 3, at a tertiary neuro-psychiatric center in Bangalore, Karnataka. Methods: Probands (N=318) who were diagnosed to have an ataxia syndrome (progressive degenerative ataxia of unknown cause) attending the clinical services of the National Institute of Mental Health and Neuro Sciences (NIMHANS), Bangalore, were evaluated over a period of three years. Standard protocols were used for both clinical and molecular diagnosis. Results: Genotyping established that SCA1, 2 and 3 accounted for more than one third of the ataxia cases seen in the clinic. In the cases with established family history and autosomal dominant inheritance SCA1 was most prevalent followed by SCA2 and SCA3. Interpretation & conclutions: Our findings suggested SCA1 rather than SCA2 to be the more common mutation in southern India. Large numbers of SCA3 probands were also identified. Differences in prevalence of these syndromes within India need to be explored further for founder effects, correlations with phenotype, and patterns of outcome. Family history was not apparent in almost a fifth of those tested positive, highlighting the value of testing even in the absence of family history. Molecular testing should be extended to cover the other forms of ataxia, of which a large number are now known. Combined efforts to confirm the presence of these less common forms, as well as family studies to detect novel mutations, are necessary in this context in India.

Indian Journal of Medical Research

SCA 1, SCA 2 &amp; SCA 3/MJD mutations in ataxia syndromes in southern India

Connections of representations of the teeth and tongue in primary somatosensory cortex (area 3b) and adjoining cortex were revealed in owl, squirrel, and marmoset monkeys with injections of fluorescent tracers. Injection sites were identified by microelectrode recordings from neurons responsive to touch on the teeth or tongue. Patterns of cortical label were related to myeloarchitecture in sections cut parallel to the surface of flattened cortex, and to coronal sections of the thalamus processed for cytochrome oxidase (CO). Cortical sections revealed a caudorostral series of myelin dense ovals (O1-O4) in area 3b that represent the periodontal receptors of the contralateral teeth, the contralateral tongue, the ipsilateral teeth, and the ipsilateral tongue. The ventroposterior medial subnucleus, VPM, and the ventroposterior medial parvicellular nucleus for taste, VPMpc, were identified in the thalamic sections. Injections placed in the O1 oval representing teeth labeled neurons in VPM, while injections in O2 representing the tongue labeled neurons in both VPMpc and VPM. These injections also labeled adjacent part of areas 3a and 1, and locations in the lateral sulcus and frontal lobe. Callosally, connections of the ovals were most dense with corresponding ovals. Injections in the area 1 representation of the tongue labeled neurons in VPMpc and VPM, and ipsilateral area 3b ovals, area 3a, opercular cortex, and cortex in the lateral sulcus. Contralaterally, labeled neurons were mostly in area 1. The results implicate portions of areas 3b, 3a, and 1 in the processing of tactile information from the teeth and tongue, and possibly taste information from the tongue. © 2007 Wiley-Liss, Inc.

Journal of Comparative Neurology

Cortical and thalamic connections of the representations of the teeth and tongue in somatosensory cortex of new world monkeys

Exploring near-surface mechanical wave propagation through cohesive and noncohesive soils is important for detecting buried objects (i.e., landmines and unexploded ordnance). Here, we determine that certain preferred frequencies travel through specific soils more efficiently. A controlled-frequency acoustic seismic source was developed to modulate the applied frequency and amplitude. Surface response due to continuous waves traveling through soils was recorded both instantaneously and after a finite load time. Preferred frequencies for sand, clay loam, and silt loam were measured to be 300-330, 100-140, and 140-260 Hz, respectively. Observed frequency shifts were dependent upon applied amplitude and load time. © 2007 American Institute of Physics.

Applied Physics Letters

Preferred frequencies for three unconsolidated earth materials

Curcumin, a natural polyphenolic compound, has long been known as an anti-tumour and anti-inflammatory compound; although, the common mechanism through which it exhibits such properties are remains unclear. Recently, we reported that the curcumin-induced apoptosis is mediated through the impairment of ubiquitin proteasome system (UPS). Here, we show that curcumin disrupts UPS function by directly inhibiting the enzyme activity of the proteasome's 20S core catalytic component. Like other proteasome inhibitors, curcumin exposure induces neurite outgrowth and the stress response, as evident from the induction of various cytosolic and endoplasmic reticulum chaperones as well as induction of transcription factor CHOP/GADD153. The direct inhibition of proteasome activity also causes an increase in half-life of IκB-α that ultimately leads to the down-regulation of NF-κB activation. These results suggest that curcumin-induced proteasomal malfunction might be linked with both anti-proliferative and anti-inflammatory activities. © Springer 2006.

Neurotoxicity Research

Curcumin induces stress response, neurite outgrowth and prevent NF-κB activation by inhibiting the proteasome function

The role of nonlinear DNA in replication, recombination, and transcription has become evident in recent years. Although several studies have predicted and characterized regulatory elements at the sequence level, very few have investigated DNA structure as regulatory motifs. Here, using G-quadruplex or G4 DNA motifs as a model, we have researched the role of DNA structure in transcription on a genome-wide scale. Analyses of &gt;61,000 open reading frames (ORFs) across 18 prokaryotes show enrichment of G4 motifs in regulatory regions and indicate its predominance within promoters of genes pertaining to transcription, secondary metabolite biosynthesis, and signal transduction. Based on this, we predict that G4 DNA may present regulatory signals. This is supported by conserved G4 motifs in promoters of orthologous genes across phylogenetically distant organisms. We hypothesized a regulatory role of G4 DNA during supercoiling stress, when duplex destabilization may result in G4 formation. This is in line with our observations from target site analysis for 55 DNA-binding proteins in Escherichia coli, which reveals significant (P &lt; 0.001) association of G4 motifs with target sites of global regulators FIS and Lrp and the sigma factor RpoD (σ70). These factors together control &gt;1000 genes in the early growth phase and are believed to be induced by supercoiled DNA. We also predict G4 motif-induced supercoiling sensitivity for &gt;30 operons in E. coli, and our findings implicate G4 DNA in DNA-topology-mediated global gene regulation in E. coli. ©2006 by Cold Spring Harbor Laboratory Press.

Genome Research

Genome-wide prediction of G4 DNA as regulatory motifs: Role in Escherichia coli global regulation

There are very few formalisms available to solve the Liouville equation for energy-conserved systems. The continued fraction formalism, introduced through the works of Zwanzig, Mori, Kubo, Lee, Grigolini and others is described here. A detailed discussion is presented on ways to apply the continued fraction formalism to solve for relaxation functions and for the dynamical variable itself for a simple and exactly solvable quantum spin system. © 2005 Elsevier B.V. All rights reserved.

Physica A: Statistical Mechanics and its Applications

Solving the Liouville equation for conservative systems: Continued fraction formalism and a simple application

Formation of neuronal intranuclear inclusions of the disease proteins that are ubiquitinated and often associated with various proteasome components is the major hallmark of the polyglutamine diseases. Curcumin is a polyphenolic compound having anti-inflammatory, anti-tumor, and anti-oxidative properties. Recently, curcumin has been reported to suppress the amyloid-β accumulation, oxidative damage, and inflammation in the transgenic mice model of Alzheimer's disease. Here, we found that the treatment of curcumin increases the polyglutamine-expanded truncated N-terminal huntingtin (mutant huntingtin) aggregation and mutant huntingtin-dependent cell death. Curcumin also causes rapid proteasomal malfunction in the mutant huntingtin expressing cells in comparison with normal glutamine repeat expressing cells. Finally, we show that N-acetyl cysteine (NAC), a potent antioxidant, reverted the curcumin-induced mutant huntingtin aggregation and proteasomal malfunction in the mutant huntingtin expressing cells. NAC also protects curcumin-induced cell death. Our result suggests that curcumin promotes mutant huntingtin-induced cell death by mimicking proteasomal dysfunction. © 2006 Elsevier Inc. All rights reserved.

Biochemical and Biophysical Research Communications

Curcumin enhances the polyglutamine-expanded truncated N-terminal huntingtin-induced cell death by promoting proteasomal malfunction

Huntington's disease (HD) is a familial neurodegenerative disorder caused by an abnormal expansion of CAG repeats in the coding region of huntingtin gene. A major hallmark of HD is the proteolytic production of N-terminal fragments of huntingtin containing polyglutamine repeats that form ubiquitinated aggregates in the nucleus and cytoplasm of the affected neurons. However, the mechanism by which the mutant huntingtin causes neurodegeneration is not well understood. Here, we found that oxidative stimuli enhance the polyglutamine-expanded truncated N-terminal huntingtin (mutant huntingtin) aggregation and mutant huntingtin-induced cell death. Oxidative stimuli also lead to rapid proteasomal dysfunction in the mutant huntingtin expressing cells as compared to normal glutamine repeat expressing cells. Overexpression of Cu/Zn superoxide dismutase (SOD1), Hsp40 or Hsp70 reverses the oxidative stress-induced proteasomal malfunction, mutant huntingtin aggregation, and death of the mutant huntingtin expressing cells. Finally, we show the higher levels of expression of SOD1 and DJ-1 in the mutant huntingtin expressing cells. Our result suggests that oxidative stress-induced proteasomal malfunction might be linked with mutant huntingtin-induced cell death. © 2006 Elsevier Inc. All rights reserved.

Oxidative stress promotes mutant huntingtin aggregation and mutant huntingtin-dependent cell death by mimicking proteasomal malfunction

A major pathological hallmark of the polyglutamine diseases is the formation of neuronal intranuclear inclusions of the disease proteins that are ubiquitinated and often associated with various transcription factors, chaperones, and proteasome components. However, how the expanded polyglutamine proteins or their aggregates elicit complex pathogenic responses in the neuronal cells is not fully understood. Here, we have demonstrated that the expression of expanded polyglutamine proteins downregulated the NFκB-dependent transcriptional activity. The expression of expanded polyglutamine proteins increased the stability and the levels of IκB-α and its phosphorylated derivatives. We have also found that various NFκB subunits and IκB-α aberrantly interacted with the expanded polyglutamine proteins and associated with their aggregates. Finally, we have shown that several NFκB-dependent genes are down-regulated in the expanded polyglutamine protein-expressing cells and down-regulation of NFκB activity enhances expanded polyglutamine protein-induced cell death. Because the NFκB pathway plays a very important role in cell survival, altered regulation of this pathway in expanded polyglutamine protein-expressing cells might be linked with the disease pathogenesis. © 2006 by The American Society for Biochemistry and Molecular Biology, Inc.