Biomedical subjects
Publications and source records attributed to A M Weiner.
What we believe to be the first use of a single-layer liquid-crystal modulator array for spectral phase pulse shaping that operates independently of input polarization is reported. Polarization insensitivity is essential to optical-fiber-based applications such as dispersion compensation.
We demonstrate the application of ultrafast pulse-shaping techniques for experimental wideband all-order polarization mode dispersion (PMD) compensation, for the first time to our knowledge. PMD is treated as arbitrary variations of state of polarization and phase versus wavelength, in an all-order sense. Consequently, two pulse shapers are implemented in a serial manner to compensate for the polarization and the phase spectra independently. We report compensation of subpicosecond pulses (14 nm bandwidth around 1550 nm) that are anomalously spread to more than 2 ps as a result of PMD. This PMD compensation scheme can potentially be a powerful and cost-effective solution for fiber optic telecommunication networks.
We demonstrate essentially distortionless 50 km fiber transmission for approximately 500 fs pulses, using dispersion-compensating fiber and a programmable pulse shaper as a spectral phase equalizer. This distance is approximately five times longer than previously achieved at similar pulse widths.
We experimentally demonstrate pulse-shaping experiments in which the individual spectral lines that are present in the output of a mode-locked laser (8.5 GHz mode spacing, centered at 1542 nm) are resolved. The shaped pulses overlap in time, and this leads to a new way to observe fluctuations of the comb-offset frequency in the time domain.
We experimentally demonstrate repetitive M-ary spectral phase pulse shaping by placing a programmable pulse shaper driven by a 10-GHz source in a closed loop. This permits generation of encoded and decoded signals in the same apparatus by forming a closed loop to circulate a part of the output back into the pulse shaper. As a result, a series of M - 1 distinct encoded waveforms is sequentially generated, followed by generation of a properly decoded pulse.
The zero-mean circular complex Gaussian field statistics of a random medium are experimentally demonstrated in the optical domain, thus verifying this key assumption of statistical optics. Using a frequency-tunable laser source in a fixed-path-length interferometer, we obtain optical field fluctuations in the time and frequency domains that clearly show that the ensemble-averaged temporal intensity converges to the photon transit time distribution, which for the samples used is in excellent agreement with a diffusion model.
We demonstrate femtosecond operation of an integrated-optic direct space-to-time pulse shaper for which there is a direct mapping (no Fourier transform) between the spatial position of the masking function and the temporal position in the output waveform. The apparatus is used to generate trains of more than 30 pulses as an ultrafast optical data packet over approximately an 80-ps temporal window.
We demonstrate a novel method of parallel, multiwavelength state-of-polarization (SOP) correction. Using a new liquid-crystal modulator array design, we are able to rotate the distorted input SOP spectrum to a fixed linear state on a wavelength-by-wavelength basis. We report experimental correction of up to 25.5-dB polarization-dependent loss over a 13-nm bandwidth around 1550 nm.
We describe a novel wavelength-parallel polarimeter operating in the light-wave band that measures the complete state of polarization of 256 wavelengths in parallel within 20 ms (software-limited), with the potential for submillisecond operation. By use of fast switching ferroelectric liquid crystals in conjunction with an InGaAs arrayed detector, selection and wavelength-parallel detection of individual polarization components can be achieved within approximately 150 microseconds. This instrument offers unprecedented sensing capability that is relevant to the compensation of polarization-related impairments in high-speed light-wave communications.
Phase-matched difference-frequency mixing in a thin GaSe crystal within the broad spectrum of 25-fs pulses from a Ti:sapphire oscillator multipass amplifier system permits the generation of few-cycle electric field transients, frequencies up to 30 THz, and amplitudes of more than 1 MV/cm. The field transients generated at a 1-kHz repetition rate are directly measured by electro-optic sampling by 12-f probe pulses from the 75-MHz repetition-rate Ti:sapphire oscillator in combination with a novel electronic gating technique.
We demonstrate for the first time that the temporal response of a random medium can be obtained from optical intensity fluctuations. Our method uses third-order intensity correlations of measured speckle patterns from a multiple scattering random medium as a function of optical frequency. In particular, our experimental results for the temporal response extracted from third-order intensity correlations are in good agreement with the predictions of a diffusion model. Our results are valid for waves in random media where the scattered field is described by circular complex Gaussian statistics.
The universal 3'-terminal CCA sequence of all transfer RNAs (tRNAs) is repaired, and sometimes constructed de novo, by the CCA-adding enzyme [ATP(CTP):tRNA nucleotidyltransferase]. This RNA polymerase has no nucleic acid template, yet faithfully builds the CCA sequence one nucleotide at a time using cytidine triphosphate (CTP) and adenosine triphosphate (ATP) as substrates. All previously characterized CCA-adding enzymes from all three kingdoms are single polypeptides with CCA-adding activity. Here, we demonstrate through biochemical and genetic approaches that CCA addition in Aquifex aeolicus requires collaboration between two related polypeptides, one that adds CC and another that adds A.
Three different base paired stems form between U2 and U6 snRNA over the course of the mRNA splicing reaction (helices I, II and III). One possible function of U2/U6 helix II is to facilitate subsequent U2/U6 helix I and III interactions, which participate directly in catalysis. Using an in vitro trans-splicing assay, we investigated the function of sequences located just upstream from the branch site (BS). We find that these upstream sequences are essential for stable binding of U2 to the branch region, and for U2/U6 helix II formation, but not for initial U2/BS pairing. We also show that non-functional upstream sequences cause U2 snRNA stem-loop IIa to be exposed to dimethylsulfate modification, perhaps reflecting a U2 snRNA conformational change and/or loss of SF3b proteins. Our data suggest that initial binding of U2 snRNP to the BS region must be stabilized by an interaction with upstream sequences before U2/U6 helix II can form or U2 stem-loop IIa can participate in spliceosome assembly.
Infection by adenovirus 12, transfection with the Ad12 E1B 55 kDa gene, or activation of p53 cause metaphase fragility of four loci (RNU1, PSU1, RNU2, and RN5S) each containing tandemly repeated genes for an abundant small RNA (U1, U2, and 5S RNA). We now show that loss of the Cockayne syndrome group B protein (CSB) or overexpression of the p53 carboxy-terminal domain induces fragility of the same loci; moreover, p53 interacts with CSB in vivo and in vitro. We propose that CSB functions as an elongation factor for transcription of structured RNAs, including some mRNAs. Activation of p53 would inhibit CSB, stalling transcription complexes and locally blocking chromatin condensation. Impaired transcription elongation may also explain the diverse clinical features of Cockayne syndrome.
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Modified versions - paralogs - of the catalytic domain of at least three different aminoacyl-tRNA synthetases have been found to serve catalytic or regulatory roles in other reactions. These findings suggest that the first modern tRNA-synthetases could have been derived from amino-acid biosynthetic enzymes.
The genes encoding primate U2 snRNA are organized as a nearly perfect tandem array (the RNU2 locus) that has been evolving concertedly for >35 Myr since the divergence of baboons and humans. Thus the repeat units of the tandem array are essentially identical within each species, but differ between species. Homogeneity is maintained because any change in one repeat unit is purged from the array or fixed in all other repeats. Intriguingly, the cytological location of RNU2 has remained unchanged despite concerted evolution of the tandem array. We had found previously that junction sequences between the U2 tandem array and flanking DNA were subject to remodeling over a region of 200-300 bp during the past 5 Myr in the hominid lineage. Here we show that the junctions between the U2 tandem array and flanking DNA have undergone dramatic rearrangements over a region of 1 to >10 kbp in the 35 Myr since divergence of the Old World Monkey and hominid lineages. We argue that these rearrangements reflect the high level of genetic activity required to sustain concerted evolution, and propose a model to explain why maintenance of homogeneity within a tandemly repeated multigene family would lead to junctional diversity.