Nonlinear optical properties of mono-functional 1,2-dihydro-1,2-methanofullerene[60]-61-carboxylic acid /polymer composites

By using nanosecond laser pulses at 532-nm wavelength, we have studied the nonlinear optical properties of composites which consist of mono-functional 1,2-dihydro-1,2-methanofullerene[60]-61-carboxylic acid (FCA) and poly(styrene-co-4-vinylpyridine). The optical limiting performance of FCA itself is poorer than that of its parent C60, while FCA incorporated with polystyrene shows better optical limiting responses, with the limiting threshold reduced by about 35%. In addition, the FCA gives slightly stronger photoluminescence emission than that of both C60 and FCA/polymer composites. The possible sources for the improvement in the optical limiting are discussed.Comment: 14 pages, 4 figures, To appear in Chem. Phys. Let

Cadherin-mediated adhesion regulates posterior body formation

<p>Abstract</p> <p>Background</p> <p>The anterior-posterior axis of the vertebrate embryo undergoes a dramatic elongation during early development. Convergence and extension of the mesoderm, occurring during gastrulation, initiates the narrowing and lengthening of the embryo. However the lengthening of the axis continues during post-gastrula stages in the tailbud region, and is thought to involve convergent extension movements as well as other cell behaviors specific to posterior regions.</p> <p>Results</p> <p>We demonstrate here, using a semi-dominant <it>N-cadherin </it>allele, that members of the classical cadherin subfamily of cell-cell adhesion molecules are required for tailbud elongation in the zebrafish. <it>In vivo </it>imaging of cell behaviors suggests that the extension of posterior axial mesodermal cells is impaired in embryos that carry the semi-dominant <it>N-cadherin </it>allele. This defect most likely results from a general loss of cell-cell adhesion in the tailbud region. Consistent with these observations, <it>N-cadherin </it>is expressed throughout the tailbud during post-gastrulation stages. In addition, we show that <it>N-cadherin </it>interacts synergistically with <it>vang-like 2</it>, a member of the non-canonical Wnt signaling/planar cell polarity pathway, to mediate tail morphogenesis.</p> <p>Conclusion</p> <p>We provide the first evidence here that <it>N-cadherin </it>and other members of the classical cadherin subfamily function in parallel with the planar cell polarity pathway to shape the posterior axis during post-gastrulation stages. These findings further highlight the central role that adhesion molecules play in the cellular rearrangements that drive morphogenesis in vertebrates and identify classical cadherins as major contributors to tail development.</p

Congenital anomalies from a physics perspective. The key role of "manufacturing" volatility

Genetic and environmental factors are traditionally seen as the sole causes of congenital anomalies. In this paper we introduce a third possible cause, namely random "manufacturing" discrepancies with respect to ``design'' values. A clear way to demonstrate the existence of this component is to ``shut'' the two others and to see whether or not there is remaining variability. Perfect clones raised under well controlled laboratory conditions fulfill the conditions for such a test. Carried out for four different species, the test reveals a variability remainder of the order of 10%-20% in terms of coefficient of variation. As an example, the CV of the volume of E.coli bacteria immediately after binary fission is of the order of 10%. In short, ``manufacturing'' discrepancies occur randomly, even when no harmful mutation or environmental factors are involved. Not surprisingly, there is a strong connection between congenital defects and infant mortality. In the wake of birth there is a gradual elimination of defective units and this screening accounts for the post-natal fall of infant mortality. Apart from this trend, post-natal death rates also have humps and peaks associated with various inabilities and defects.\qL In short, infant mortality rates convert the case-by-case and mostly qualitative problem of congenital malformations into a global quantitative effect which, so to say, summarizes and registers what goes wrong in the embryonic phase. Based on the natural assumption that for simple organisms (e.g. rotifers) the manufacturing processes are shorter than for more complex organisms (e.g. mammals), fewer congenital anomalies are expected. Somehow, this feature should be visible on the infant mortality rate. How this conjecture can be tested is outlined in our conclusion.Comment: 43 pages, 9 figure

Nonlinear optics and optical limiting properties of multifunctional fullerenol/polymer composite

The nonlinear optics and optical limiting properties of materials based on multifunctional fullerenol and poly(styrene-co-4-vinylpyridine) matrix were studied using 7 ns pulses of nanosecond laser operating at 532 nm wavelength. The observed imaginary and real parts of third order susceptibility of the fullerenol/polymer composite are found to be lower than that of its parent C60. The optical limiting performances of fullerenol and fullerenol incorporated with poly(styrene-co-4-vinylpyridine) have been proved to be poorer than that of C60 due to their higher limiting thresholds. Concentration dependence of poly(styrene-co-4-vinylpyridine) containing 32 mol% has been mainly contributed to the optical limiting performance of fullerenol.Comment: 23 pages, 9 figures, presented in ISMOA-2002, Bandung, Indonesia. Submitted to J. Nonlinear Opt. Phys. (December 2002

MECHANISTIC INSIGHTS INTO SECONDARY NEURULATION

The central nervous system is formed by a series of movements referred to as neurulation. There are two modes of neurulation, known as primary and secondary neurulation. Primary neurulation occurs in anterior regions and involves an epithelial folding process. During secondary neurulation, which takes place in posterior regions, mesenchymal cells coalesce into a rod-like structure and subsequently undergo a mesenchymal-to-epithelial transition (MET) to create a lumen and form the neural tube. Although extensive studies have furthered our understanding of primary neurulation, mechanisms underlying secondary neurulation are not clearly understood. Several pieces of evidence from this research dissertation and published by other laboratories suggest that the zebrafish embryo undergoes a mode of secondary neurulation. Moreover, the optical properties of zebrafish embryos have enabled a detailed and real-time analysis of the dynamic cell behaviors that drive neurulation. These observations establish the zebrafish as a prime model system to study the molecular underpinnings of secondary neurulation. Studies outlined in this dissertation have revealed several molecules implicated in different stages of neurulation. During neural convergence, cells migrate in a polarized manner towards the midline. Generation of cell traction and polarization are essential during migration. Evidence suggests that the cell adhesion molecule N-cadherin promotes cell movement by stabilizing cell-cell contacts, thereby enabling cell traction. Polarization of cell movement appears to be mediated by the microtubule network, as treatment with the microtubule-destabilizing drug nocodazole randomizes the orientation of membrane protrusions. A central role for microtubules is further supported by the analysis of linguini mutants in which microtubules appear unstable and cells behave in a similar manner as in nocodazole-treated embryos. During MET, the centrosome migrates from a central position close to the nucleus to the apical cortex, where it docks and becomes a nucleating center for cilia. In par3-deficient cells, the centrosome fails to migrate to the apical surface and as a consequence cilia form intracellularly. This study identifies a previously undescribed role for Par3 in centrosome migration. Overall, these studies establish the zebrafish as a model system to study secondary neurulation and have identified key players that are required for different phases of secondary neurulation.Additional files available: 7 .avi files, stored on CONTENTdm server with ETD .pdf

Left Habenular Activity Attenuates Fear Responses in Larval Zebrafish

Fear responses are defensive states that ensure survival of an organism in the presence of a threat. Perception of an aversive cue causes changes in behavior and physiology, such as freezing and elevated cortisol, followed by a return to the baseline state when the threat is evaded [1]. Neural systems that elicit fear behaviors include the amygdala, hippocampus, and medial prefrontal cortex. However, aside from a few examples, little is known about brain regions that promote recovery from an aversive event [2]. Previous studies had implicated the dorsal habenular nuclei in regulating fear responses and boldness in zebrafish [3-7]. We now show, through perturbation of its inherent left-right (L-R) asymmetry at larval stages, that the dorsal habenulo-interpeduncular (dHb-IPN) pathway expedites the return of locomotor activity following an unexpected negative stimulus, electric shock. Severing habenular efferents to the IPN, or only those from the left dHb, prolongs the freezing behavior that follows shock. Individuals with a symmetric, right-isomerized dHb also exhibit increased freezing. In contrast, larvae that have a symmetric, left-isomerized dHb, or in which just the left dHb-IPN projection is optogenetically activated, rapidly resume swimming post shock. In vivo calcium imaging reveals a neuronal subset, predominantly in the left dHb, whose activation is correlated with resumption of swimming. The results demonstrate functional specialization of the left dHb-IPN pathway in attenuating the response to fear