Homoclinic puzzles and chaos in a nonlinear laser model

We present a case study elaborating on the multiplicity and self-similarity of homoclinic and heteroclinic bifurcation structures in the 2D and 3D parameter spaces of a nonlinear laser model with a Lorenz-like chaotic attractor. In a symbiotic approach combining the traditional parameter continuation methods using MatCont and a newly developed technique called the Deterministic Chaos Prospector (DCP) utilizing symbolic dynamics on fast parallel computing hardware with graphics processing units (GPUs), we exhibit how specific codimension-two bifurcations originate and pattern regions of chaotic and simple dynamics in this classical model. We show detailed computational reconstructions of key bifurcation structures such as Bykov T-point spirals and inclination flips in 2D parameter space, as well as the spatial organization and 3D embedding of bifurcation surfaces, parametric saddles, and isolated closed curves (isolas).Comment: 28 pages, 23 figure

THE FOLD-FLIP BIFURCATION

International audienceThe fold-flip bifurcation occurs if a map has a fixed point with multipliers +1 and −1 simultaneously. In this paper the normal form of this singularity is calculated explicitly. Both local and global bifurcations of the unfolding are analyzed by exploring a close relationship between the derived normal form and the truncated amplitude system for the fold-Hopf bifurcation of ODEs. Two examples are presented, the generalized Hénon map and an extension of the Lorenz-84 model. In the latter example the first-, second- and third-order derivatives of the Poincaré map are computed using variational equations to find the normal form coefficients

Slowing heavy, ground-state molecules using an alternating gradient decelerator

Cold supersonic beams of molecules can be slowed down using a switched sequence of electrostatic field gradients. The energy to be removed is proportional to the mass of the molecules. Here we report deceleration of YbF, which is 7 times heavier than any molecule previously decelerated. We use an alternating gradient structure to decelerate and focus the molecules in their ground state. We show that the decelerator exhibits the axial and transverse stability required to bring these molecules to rest. Our work significantly extends the range of molecules amenable to this powerful method of cooling and trapping.Comment: 4 pages, 5 figure

Volumetric rheology of polymers

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Carboplatin- and cisplatin-induced potentiation of moderate-dose radiation cytotoxicity in human lung cancer cell lines.

The interaction between moderate-dose radiation and cisplatin or carboplatin was studied in a cisplatin-sensitive (GLC4) and -resistant (GLC4-CDDP) human small-cell lung cancer cell line. Cellular toxicity was analysed under oxic conditions with the microculture tetrazolium assay. For the platinum and radiation toxicity with the clinically relevant dose ranges applied, this assay was used to obtain information on cell survival after the treatments. Apart from effects on cell survival effects on DNA were also investigated. Configurational DNA changes could be induced by platinum drugs and thereby these drugs might change the frequency of DNA double-strand breaks (dsbs). DNA fragmentation assayed with the clamped homogeneous electric field (CHEF) technique was used as a measure for dsbs in DNA. The radiosensitising effect of the platinum drugs was expressed as enhancement ratio (ER) calculated directly from survival levels of the initial slope of the curve. The highest ER for cisplatin in GLC4 was 1.39 and in GLC4-CDDP 1.38. These were all at 75% cell survival. Carboplatin showed increased enhancement with prolonged incubation up to 1.21 in GLC4 and was equally effective as cisplatin in GLC4-CDDP. According to isobologram analysis, prolonged incubation with both platinum drugs showed at least additivity with radiation for both cell lines at clinically achievable doses. GLC4-CDDP showed cross-resistance to radiation. The radiosensitising capacity of both lung cancer cell lines was not dependent on their platinum sensitivity. The formation of dsbs in DNA directly after radiation was not influenced by pretreatment of either drug in the sensitive or in the resistant cell line. Drug treatment resulted in decreased DNA extractability in control as well as in irradiated cells. Modest enhancement ratio for radiosensitisation by platinum drugs cannot be explained on the level of dsb formation in DNA in both cell lines. Interaction of radiation with the clinically less toxic carboplatin can be improved by prolonged low-dose carboplatin exposure before irradiation and is as potent as cisplatin in the resistant lung cancer cell line. This suggests an advantage in combining radiation and carboplatin in lung cancer patients

Immunocytochemical analysis of cisplatin-induced platinum-DNA adducts with double-fluorescence video microscopy.

To detect low-level DNA platination, a sensitive immunocyto- and histochemical technique was developed using a polyclonal antibody. The antibody GPt, derived after immunization of rabbits with highly platinated DNA and purified with affinity chromatography, detected the main platinum (Pt)-containing intrastrand and interstrand adducts. Double-fluorescence microscopy image analysis was used to quantify Pt-DNA adducts with Hoechst 33258 fluorescence to locate the nuclei and with fluorescein isothiocyanate fluorescence to measure the immunosignal. A two- to five-fold dose-dependent difference in the level of cisplatin (CDDP)-induced Pt-DNA adducts between a CDDP-sensitive and -resistant human tumour cell line was detected. Large differences in Pt-DNA adduct levels after in vitro CDDP incubation between human buccal cells, lymphocytes and biopsies of different tumour types were observed. Pt-DNA adduct levels were fivefold higher in human testicular tumours than in colon tumours, representing CDDP-sensitive and -resistant tumours, respectively, in the clinic. These data suggest the possibility of predictive testing by measuring Pt-DNA adduct levels. Pt-DNA adducts in patients after treatment with CDDP were shown in normal buccal cells and in imprints of fresh tumour biopsies as well as in paraffin-embedded tumour cells. The analysis of Pt-DNA adducts at a single-cell level in small samples of normal and tumour cells during and/or after treatment is feasible with GPt and will hopefully enable more selective treatment of patients