175 research outputs found
Dynamics of stick-slip in peeling of an adhesive tape
We investigate the dynamics of peeling of an adhesive tape subjected to a
constant pull speed. We derive the equations of motion for the angular speed of
the roller tape, the peel angle and the pull force used in earlier
investigations using a Lagrangian. Due to the constraint between the pull
force, peel angle and the peel force, it falls into the category of
differential-algebraic equations requiring an appropriate algorithm for its
numerical solution. Using such a scheme, we show that stick-slip jumps emerge
in a purely dynamical manner. Our detailed numerical study shows that these set
of equations exhibit rich dynamics hitherto not reported. In particular, our
analysis shows that inertia has considerable influence on the nature of the
dynamics. Following studies in the Portevin-Le Chatelier effect, we suggest a
phenomenological peel force function which includes the influence of the pull
speed. This reproduces the decreasing nature of the rupture force with the pull
speed observed in experiments. This rich dynamics is made transparent by using
a set of approximations valid in different regimes of the parameter space. The
approximate solutions capture major features of the exact numerical solutions
and also produce reasonably accurate values for the various quantities of
interest.Comment: 12 pages, 9 figures. Minor modifications as suggested by refere
Multifractal burst in the spatio-temporal dynamics of jerky flow
The collective behavior of dislocations in jerky flow is studied in Al-Mg
polycrystalline samples subjected to constant strain rate tests. Complementary
dynamical, statistical and multifractal analyses are carried out on the
stress-time series recorded during jerky flow to characterize the distinct
spatio-temporal dynamical regimes. It is shown that the hopping type B and the
propagating type A bands correspond to chaotic and self-organized critical
states respectively. The crossover between these types of bands is identified
by a large spread in the multifractal spectrum. These results are interpreted
on the basis of competing scales and mechanisms.Comment: 4 pages, 6 figures To be published in Phys. Rev. Lett. (2001
Relaxation oscillations and negative strain rate sensitivity in the Portevin - Le Chatelier effect
A characteristic feature of the Portevin - Le Chatelier effect or the jerky
flow is the stick-slip nature of stress-strain curves which is believed to
result from the negative strain rate dependence of the flow stress. The latter
is assumed to result from the competition of a few relevant time scales
controlling the dynamics of jerky flow. We address the issue of time scales and
its connection to the negative strain rate sensitivity of the flow stress
within the framework of a model for the jerky flow which is known to reproduce
several experimentally observed features including the negative strain rate
sensitivity of the flow stress. We attempt to understand the above issues by
analyzing the geometry of the slow manifold underlying the relaxational
oscillations in the model. We show that the nature of the relaxational
oscillations is a result of the atypical bent geometry of the slow manifold.
The analysis of the slow manifold structure helps us to understand the time
scales operating in different regions of the slow manifold. Using this
information we are able to establish connection with the strain rate
sensitivity of the flow stress. The analysis also helps us to provide a proper
dynamical interpretation for the negative branch of the strain rate
sensitivity.Comment: 7 figures, To appear in Phys. Rev.
Critical Dynamics of Burst Instabilities in the Portevin-Le Chatelier Effect
We investigate the Portevin-Le Chatelier effect (PLC), by compressing Al-Mg
alloys in a very large deformation range, and interpret the results from the
viewpoint of phase transitions and critical phenomena. The system undergoes two
dynamical phase transitions between intermittent (or "jerky") and "laminar"
plastic dynamic phases. Near these two dynamic critical points, the order
parameter 1/\tau of the PLC effect exhibits large fluctuations, and "critical
slowing down" (i.e., the number of bursts, or plastic instabilities, per
unit time slows down considerably).Comment: the published 4-page version is in the PRL web sit
The role of acyl-coenzyme A carboxylase complex in lipstatin biosynthesis of Streptomyces toxytricini
Streptomyces toxytricini produces lipstatin, a specific inhibitor of pancreatic lipase, which is derived from two fatty acid moieties with eight and 14 carbon atoms. The pccB gene locus in 10.6 kb fragment of S. toxytricini chromosomal DNA contains three genes for acyl-coenzyme A carboxylase (ACCase) complex accA3, pccB, and pccE that are presumed to be involved in secondary metabolism. The pccB gene encoding a β subunit of ACCase [carboxyltransferase (CT)] was identified upstream of pccE gene for a small protein of ε subunit. The accA3 encoding the α subunit of ACCase [biotin carboxylase (BC)] was also identified downstream of pccB gene. When the pccB and pccE genes were inactivated by homologous recombination, the lipstatin production was reduced as much as 80%. In contrast, the accumulation of another compound, tetradeca-5.8-dienoic acid (the major lipstatin precursor), was 4.5-fold increased in disruptant compared with wild-type. It implies that PccB of S. toxytricini is involved in the activation of octanoic acid to hexylmalonic acid for lipstatin biosynthesis
Mycobacterium tuberculosis Rv3802c Encodes a Phospholipase/Thioesterase and Is Inhibited by the Antimycobacterial Agent Tetrahydrolipstatin
The cell wall of M. tuberculosis is central to its success as a pathogen. Mycolic acids are key components of this cell wall. The genes involved in joining the α and mero mycolates are located in a cluster, beginning with Rv3799c and extending at least until Rv3804c. The role of each enzyme encoded by these five genes is fairly well understood, except for Rv3802c. Rv3802 is one of seven putative cutinases encoded by the genome of M. tuberculosis. In phytopathogens, cutinases hydrolyze the waxy layer of plants, cutin. In a strictly mammalian pathogen, such as M. tuberculosis, it is likely that these proteins perform a different function. Of the seven, we chose to focus on Rv3802c because of its location in a mycolic acid synthesis gene cluster, its putative essentiality, its ubiquitous presence in actinomycetes, and its conservation in the minimal genome of Mycobacterium leprae. We expressed Rv3802 in Escherichia coli and purified the enzymatically active form. We probed its activities and inhibitors characterizing those relevant to its possible role in mycolic acid biosynthesis. In addition to its reported phospholipase A activity, Rv3802 has significant thioesterase activity, and it is inhibited by tetrahydrolipstatin (THL). THL is a described anti-tuberculous compound with an unknown mechanism, but it reportedly targets cell wall synthesis. Taken together, these data circumstantially support a role for Rv3802 in mycolic acid synthesis and, as the cell wall is integral to M. tuberculosis pathogenesis, identification of a novel cell wall enzyme and its inhibition has therapeutic and diagnostic implications
HIV Infection Functionally Impairs Mycobacterium tuberculosis-Specific CD4 and CD8 T-Cell Responses.
Human immunodeficiency virus (HIV) infection is the major risk factor predisposing for Mycobacterium tuberculosis progression from latent tuberculosis infection (LTBI) to tuberculosis disease (TB). Since long-term-treated aviremic HIV-infected individuals remained at higher risk of developing TB than HIV-uninfected individuals, we hypothesized that progression from LTBI to pulmonary TB (PTB) might be due not only to CD4 T-cell depletion but also to M. tuberculosis-specific CD4 T-cell functional impairment. To test this hypothesis, M. tuberculosis-specific T-cell frequencies and cytokine profiles were investigated in untreated Tanzanian individuals suffering from LTBI (n = 20) or PTB (n = 67) and compared to those of untreated M. tuberculosis/HIV-coinfected individuals suffering from LTBI (n = 15) or PTB (n = 10). We showed that HIV infection significantly reduced the proportion of Th2 (interleukin 4 [IL-4]/IL-5/IL-13) producing M. tuberculosis-specific CD4 T cells and IL-2-producing M. tuberculosis-specific CD4 and CD8 T cells in individuals with LTBI or PTB (P < 0.05). Interestingly, the loss of IL-2 production was associated with a significant increase of PD-1 expression on M. tuberculosis-specific CD4 and CD8 T cells (P < 0.05), while the loss of Th2 cytokine production was associated with a significant reduction of Gata-3 expression in memory CD4 T cells (P < 0.05). Finally, we showed that the serum levels of IL-1α, IL-6, C-reactive protein (CRP), IL-23, and IP-10 were significantly reduced in M. tuberculosis/HIV-coinfected individuals with PTB compared to those in HIV-negative individuals with PTB (P < 0.05), suggesting that HIV infection significantly suppresses M. tuberculosis-induced systemic proinflammatory cytokine responses. Taken together, this study suggests that in addition to depleting M. tuberculosis-specific CD4 T cells, HIV infection significantly impairs functionally favorable M. tuberculosis-specific CD4 T-cell responses in Tanzanian individuals with LTBI or PTB.IMPORTANCEMycobacterium tuberculosis and human immunodeficiency virus (HIV) infections are coendemic in several regions of the world, and M. tuberculosis/HIV-coinfected individuals are more susceptible to progression to tuberculosis disease. We therefore hypothesized that HIV infection would potentially impair M. tuberculosis-specific protective immunity in individuals suffering from latent tuberculosis infection (LTBI) or active pulmonary tuberculosis (PTB). In this study, we demonstrated that M. tuberculosis/HIV-coinfected individuals have fewer circulating M. tuberculosis-specific CD4 T cells and that those that remained were functionally impaired in both LTBI and PTB settings. In addition, we showed that HIV infection significantly interferes with M. tuberculosis-induced systemic proinflammatory cytokine/chemokine responses. Taken together, these data suggest that HIV infection impairs functionally favorable M. tuberculosis-specific immunity
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