Biomedical subjects

Ursula Keller

Publications and source records attributed to Ursula Keller.

9 recordsLinked to original sources

PubMed2007

Solid-state Er:Yb:glass laser mode-locked by using single-wall carbon nanotube thin film.

We design single-wall carbon nanotube (SWNT) thin-film saturable absorbers (SAs) integrated onto semiconductor distributed Bragg reflectors for mode-locking solid-state Er:Yb:glass lasers. We characterize the low nonsaturable loss, high-damage-threshold SWNT SAs and verify their operation up to a pulse fluence of 2 mJ/cm(2). We demonstrate passive fundamental continuous-wave mode locking with and without group-delay dispersion compensation. Without compensation the laser produces chirped 1.8 ps pulses with a spectral width of 3.8 nm. With compensation, we obtain 261 fs Fourier-transform-limited pulses with a spectral width of 9.6 nm.

Journal Article↗

PubMed2006

Pulse energy scaling to 5 microJ from a femtosecond thin disk laser.

We report an increase in pulse energy to 5.1 microJ obtained directly from a femtosecond diode-pumped Yb:YAG thin disk laser without external amplification. Stable passive mode locking was obtained with a semiconductor saturable absorber mirror (SESAM). The laser delivers 63 W of average output power in a nearly diffraction-limited beam (M2=1.1) at a center wavelength of 1030 nm. The pulse repetition rate is 12.3 MHz, and the pulses have a duration of 800 fs, which results in a peak power of 5.6 MW. The laser was operated in a box flooded with helium because the nonlinearity of air was found to be a limiting factor for the stability of the pulse formation at increasing pulse energies.

Journal Article↗

PubMed2005

Characterization of ultrashort optical pulse properties by amplitude-modulation-balanced heterodyne gating.

We present a general approach for the measurement of the properties of optical pulses by exploiting features of the optical carrier domain. We demonstrate the principle of a novel balanced detection scheme that avoids the difficulties associated with homodyne detection in the baseband used in linear optical sampling methods so far. The residual timing instability of the repetition rate synchronization between mode-locked lasers is measured with the new detection technique.

Journal Article↗

PubMed2005

The transcriptional repressor Nab1 is a specific regulator of pathological cardiac hypertrophy.

Hypertrophy represents the major physiological response of the heart to adapt to chronically enhanced workload, but is also crucial in the development of heart failure. Although we know of numerous inducers of cardiac hypertrophy, little is known about mechanisms that limit cardiac hypertrophy. Here, we describe the transcriptional repressor NAB1 as an endogenous regulator of cardiac growth. We identified NAB1 as being upregulated in both mouse and human heart failure. Nab1 is highly expressed in mammalian cardiac myocytes and it inhibited cardiomyocyte hypertrophy through repression of its targets, transcription factor Egr. Transgenic mice with cardiac-specific overexpression of Nab1 showed that Nab1 is a potent inhibitor of cardiac growth in response to pathological stimuli in vivo. Nab1 overexpression suppressed adrenergically induced and pressure overload-induced hypertrophy, whereas physiological growth during development and in response to exercise was not affected. These findings implicate the Nab1-Egr1 axis as a crucial regulator of pathological cardiac growth.

Analysis of Variance↗

PubMed2005

Optical parametric oscillator with a pulse repetition rate of 39 GHz and 2.1-W signal average output power in the spectral region near 1.5 microm.

We present a singly resonant, synchronously pumped optical parametric oscillator with a record-high repetition rate of 39 GHz. The transform-limited 2.2-ps pulses at 1570 nm have as much as 2.1-W average output power. The all-solid-state pump source is based on a diode-pumped passively mode-locked 39-GHz Nd:YVO4 laser and an efficient ytterbium-doped fiber amplifier.

Journal Article↗

PubMed2004

Powerful red-green-blue laser source pumped with a mode-locked thin disk laser.

We present a red-green-blue laser source with average powers of 8 W in the red, 23 W in the green, and 10.1 W in the blue. The entire pump power for the nonlinear conversion stages is provided by a single laser oscillator without any amplifier stages. Our system does not require any synchronized cavities, and all nonlinear crystals except one are critically phase matched at room temperature.

Journal Article↗

PubMed2004

Strong field quantum path control using attosecond pulse trains.

We show that attosecond pulse trains have a natural application in the control of strong field processes. In combination with an intense infrared laser field, the pulse train can be used to microscopically select a single quantum path contribution to a process that would otherwise consist of several interfering components. We present calculations that demonstrate this by manipulating the time-frequency properties of high order harmonics at the single atom level. This quantum path selection can also be used to define a high resolution attosecond clock.

Journal Article↗

PubMed2003

Recent developments in compact ultrafast lasers.

Ultrafast lasers, which generate optical pulses in the picosecond and femtosecond range, have progressed over the past decade from complicated and specialized laboratory systems to compact, reliable instruments. Semiconductor lasers for optical pumping and fast optical saturable absorbers, based on either semiconductor devices or the optical nonlinear Kerr effect, have dramatically improved these lasers and opened up new frontiers for applications with extremely short temporal resolution (much smaller than 10 fs), extremely high peak optical intensities (greater than 10 TW/cm2) and extremely fast pulse repetition rates (greater than 100 GHz).

Journal Article↗

PubMed2002

Inhibition of Na(+)-H(+) exchange prevents hypertrophy, fibrosis, and heart failure in beta(1)-adrenergic receptor transgenic mice.

Chronic stimulation of the beta(1)-adrenergic receptor leads to hypertrophy and heart failure in beta(1)-adrenergic receptor transgenic mice and contributes to disease progression in heart failure patients. The cellular mechanisms underlying these detrimental effects are largely unknown. In this study, we have identified the cardiac Na(+)-H(+) exchanger (NHE1) as a novel mediator of adrenergically induced heart failure. beta(1)-Adrenergic receptor transgenic mice showed upregulation of both NHE1 mRNA (+140+/-6%) and protein (+42+/-19%). In order to test whether increased NHE1 is causally related to beta(1)-adrenergic-induced hypertrophy, fibrosis, and heart failure, beta(1)-adrenergic receptor transgenic (TG) and wild-type (WT) littermates were treated with a diet containing 6000 ppm of the NHE1 inhibitor cariporide or control chow for 8 months. There was significant hypertrophy of cardiac myocytes in beta(1)-adrenergic receptor transgenic mice (2.3-fold increase in myocyte cross-sectional area), which was virtually absent in cariporide-fed animals. Interstitial fibrosis was prominent throughout the left ventricular wall in nontreated beta(1)-adrenergic receptor transgenic mice (4.8-fold increase in collagen volume fraction); cariporide treatment completely prevented this development of fibrosis. Left ventricular catheterization showed that cariporide also prevented the loss of contractile function in beta(1)-adrenergic receptor transgenic mice: whereas untreated transgenic mice showed a significant decrease in left ventricular contractility (5250+/-570 mm Hg/s TG versus 7360+/-540 mm Hg/s WT, dp/dt(max)), this decrease was completely prevented by cariporide (8150+/-520 mm Hg/s TG cariporide). Inhibition of NHE1 prevented the development of heart failure in beta(1)-receptor transgenic mice. We conclude that the cardiac Na(+)-H(+) exchanger 1 is essential for the detrimental cardiac effects of chronic beta(1)-receptor stimulation in the heart.

Administration, Oral↗