Demonstration of phase correlation in multiwavelength mode-locked semiconductor diode lasers.

Wideband spectral phase correlation is demonstrated from a multiwavelength mode-locked semiconductor laser. By use of frequency-resolved optical gating techniques, significant phase correlation was observed between multiple intracavity oscillating wavelengths, with wavelength separations of ~1 nm . The resultant temporal characteristics show a substantial modulation owing to the spectral coupling induced by intracavity-generated four-wave mixing.

Tunable-chirp pulse compression in quasi-phase-matched second-harmonic generation.

We demonstrate continuously tunable compensation of linear chirp on a first-harmonic pump pulse to produce a near-transform-limited second-harmonic output pulse through the use of a chirped, fanned, periodically poled lithium niobate quasi-phase-matching grating. Compensation of positive and negative chirps is possible through reversal of device orientation. The device is simple and monolithic and can be applied to compensation of a higher-order phase with minor modification.

Measurement of the nonlinear coefficient of orientation-patterned GaAs and demonstration of highly efficient second-harmonic generation.

Quasi-phase-matched (QPM) GaAs structures, 0.5 mm thick, 10 mm long, and with 61-mum grating periods, were grown by a combination of molecular-beam epitaxy and hydride vapor phase epitaxy. These were characterized by use of mid-IR second-harmonic generation (SHG) with a ZnGeP(2) (ZGP) optical parametric oscillator as a pump source.

Protective role of CXC receptor 4/CXC ligand 12 unveils the importance of neutrophils in atherosclerosis.

The CXC ligand (CXCL)12/CXC receptor (CXCR)4 chemokine-receptor axis controls hematopoiesis, organ development, and angiogenesis, but its role in the inflammatory pathogenesis of atherosclerosis is unknown. Here we show that interference with Cxcl12/Cxcr4 by a small-molecule antagonist, genetic Cxcr4 deficiency, or lentiviral transduction with Cxcr4 degrakine in bone marrow chimeras aggravated diet-induced atherosclerosis in apolipoprotein E-deficient (Apoe-/-) or LDL receptor-deficient (Ldlr-/-) mice. Chronic blockade of Cxcr4 caused leukocytosis and an expansion of neutrophils and increased neutrophil content in plaques, associated with apoptosis and a proinflammatory phenotype.

Expression of connexin30.2 in interneurons of the central nervous system in the mouse.

Electrical synapses, particularly gap junctions composed of connexin (Cx) 36, have been suggested to synchronize neuronal network oscillations. Recently, we generated Cx30.2-deficient mice which express beta-galactosidase under control of Cx30.

Expression of HIF-1alpha in injured arteries controls SDF-1alpha mediated neointima formation in apolipoprotein E deficient mice.

Objective: Hypoxia-inducible factor (HIF)-1alpha is the regulatory subunit of a transcriptional complex, which controls the recruitment of multipotent progenitor cells and tissue repair in ischemic tissue by inducing stromal cell-derived factor (SDF)-1alpha expression. Because HIF-1alpha can be activated under normoxic conditions in smooth muscle cells (SMCs) by platelet products, we investigated the role of HIF-1alpha in SDF-1alpha-mediated neointima formation after vascular injury.

Methods And Results: Wire-induced injury of the left carotid artery was performed in apolipoprotein E-deficient mice.

Chemokines in vascular remodeling.

The arterial vessel wall response to a variety of injuries consists in structural changes, which can result in luminal narrowing and aggravation of the underlying disease. This arterial remodeling is characterized by neointima formation and medial thickening, inflammatory cell recruitment and endothelial dysfunction. Chemokines and the corresponding receptors have been shown to participate at every step of the remodeling process.

MIF is a noncognate ligand of CXC chemokine receptors in inflammatory and atherogenic cell recruitment.

The cytokine macrophage migration inhibitory factor (MIF) plays a critical role in inflammatory diseases and atherogenesis. We identify the chemokine receptors CXCR2 and CXCR4 as functional receptors for MIF. MIF triggered G(alphai)- and integrin-dependent arrest and chemotaxis of monocytes and T cells, rapid integrin activation and calcium influx through CXCR2 or CXCR4.

GDNF applied to the MPTP-lesioned nigrostriatal system requires TGF-beta for its neuroprotective action.

GDNF is a potent neurotrophic factor for nigrostriatal dopaminergic neurons in vitro and in animal models of Parkinson's disease (PD), but has largely failed when tested in therapeutic applications in human PD. We report here that GDNF requires transforming growth factor-beta (TGF-beta) to elicit its neurotrophic activity. Lesioning the mouse nigrostriatal system with MPTP significantly upregulates striatal TGF-beta2 mRNA levels.

Indium-111 oxine labelling affects the cellular integrity of haematopoietic progenitor cells.

Purpose: Cell-based therapy by transplantation of progenitor cells has emerged as a promising development for organ repair, but non-invasive imaging approaches are required to monitor the fate of transplanted cells. Radioactive labelling with (111)In-oxine has been used in preclinical trials. This study aimed to validate (111)In-oxine labelling and subsequent in vivo and ex vivo detection of haematopoietic progenitor cells.

An active site tyrosine residue is essential for amidohydrolase but not for esterase activity of a class 2 histone deacetylase-like bacterial enzyme.

HDACs (histone deacetylases) are considered to be among the most important enzymes that regulate gene expression in eukaryotic cells acting through deacetylation of epsilon-acetyl-lysine residues within the N-terminal tail of core histones. In addition, both eukaryotic HDACs as well as their bacterial counterparts were reported to also act on non-histone targets. However, we are still far from a comprehensive understanding of the biological activities of this ancient class of enzymes.

Intracoronary infusion of autologous bone marrow cells and left ventricular function after acute myocardial infarction: a meta-analysis.

Recent clinical studies have demonstrated that intracoronary infusion of autologous bone marrow cells (BMC) in conjunction with standard treatment may improve left ventricular function after an acute myocardial infarction (AMI). However, the results of these studies remain controversial, as the studies were relatively small in size and partially differed in design. We reviewed primary controlled randomized clinical studies comparing intracoronary transfer of autologous non-mobilized BMC combined with standard therapy versus standard therapy alone in patients with AMI.

MPTP treatment impairs tyrosine hydroxylase immunopositive fibers not only in the striatum, but also in the amygdala.

Parkinson's disease (PD) is characterized by a triad of symptoms (tremor, rigidity, and bradykinesia). Aside from this, emotional deficits are known to be associated with PD. A key structure of emotional processing is the amygdala.

Possible sources and sites of action of the nitric oxide involved in synaptic plasticity at spinal lamina I projection neurons.

The synaptic long-term potentiation between primary afferent C-fibers and spinal lamina I projection neurons is a cellular model for hyperalgesia [Ikeda H, Heinke B, Ruscheweyh R, Sandkühler J (2003) Synaptic plasticity in spinal lamina I projection neurons that mediate hyperalgesia. Science 299:1237-1240]. In lamina I neurons with a projection to the periaqueductal gray, this long-term potentiation is dependent on nitric oxide.

SDF-1alpha-mediated tissue repair by stem cells: a promising tool in cardiovascular medicine?

Circulating smooth muscle progenitor cells have been identified as a source for neointimal smooth muscle cells after various types of injuries to the vessel wall contributing to neointimal hyperplasia, implying a fundamental role of these progenitor cells in the vascular response to injury. Recent studies have provided insight into the molecular mechanisms of mobilization and local recruitment of smooth muscle progenitor cells. The CXC chemokine SDF-1alpha and its receptor CXCR4 have been identified as the central signaling axis regulating the homing of smooth muscle progenitor cells into the injured vessel wall.

Substrate and inhibitor specificity of class 1 and class 2 histone deacetylases.

Histone deacetylases (HDACs) are key enzymes in the transcriptional regulation of gene expression in eukaryotic cells. In recent years HDACs have attracted considerable attention as promising new targets in anticancer therapy. Currently, different histone deacetylase subtypes are divided into four groups denoted as classes 1-4.

FGF-2 deficiency does not alter vulnerability of the dopaminergic nigrostriatal system towards MPTP intoxication in mice.

Fibroblast growth factor 2 (FGF-2) was the first growth factor discovered that exerted prominent protective and regenerative effects in an animal model of Parkinson's disease, the MPTP-lesioned dopaminergic nigrostriatal system. To address the putative physiological relevance of endogenous FGF-2 for midbrain dopaminergic neurons, we have analysed densities of tyrosine hydroxylase (TH)-positive cells in the substantia nigra (SN) and TH-positive fibers in the striatum and amygdala of adult FGF-2-deficient mice. We found that densities of TH-immunoreactive (ir) cells in the SN as well as densities of TH-ir fibers in the striatum and amygdala were unaltered as compared with wild-type littermates.

Loss of leukemia inhibitory factor receptor beta or cardiotrophin-1 causes similar deficits in preganglionic sympathetic neurons and adrenal medulla.

Leukemia inhibitory factor (LIF) receptor beta (LIFRbeta) is a receptor for a variety of neurotrophic cytokines, including LIF, ciliary neurotrophic factor (CNTF), and cardiotrophin-1 (CT-1). These cytokines play an essential role for the survival and maintenance of developing and postnatal somatic motoneurons. CNTF may also serve the maintenance of autonomic, preganglionic sympathetic neurons (PSNs) in the spinal cord, as suggested by its capacity to prevent their death after destruction of one of their major targets, the adrenal medulla.

Expression pattern and functional characterization of connexin29 in transgenic mice.

Using newly generated transgenic mice in which the coding region of the connexin29 (Cx29) gene was replaced by the lacZ reporter gene, we confirmed previous immunochemical results that Cx29 is expressed in Schwann cells, oligodendrocytes and Bergmann glia cells. In addition, we detected lacZ/Cx29 in Schwann cells of the sciatic nerve and in particular of the spiral ganglion in the inner ear, as well as at low abundance in the stria vascularis. Furthermore, we found lacZ/Cx29 expression in nonmyelinating Schwann cells of the adrenal gland, in chondrocytes of intervertebral discs and the epiphysis of developing bones.

Peripheral CD34+ cells and the risk of in-stent restenosis in patients with coronary heart disease.

In-stent restenosis represents the major limitation of percutaneous coronary revascularization. The underlying neointimal hyperplasia mainly consists of smooth muscle cells (SMCs), which can be derived from bone marrow cells. We hypothesized that changes in the peripheral progenitor cell counts after coronary stenting may predict the development of restenosis.

Mechanisms of monocyte recruitment in vascular repair after injury.

The inflammatory response to acute vessel wall injury has been increasingly recognized to play a decisive role in neointima formation. In particular, the exuberant infiltration with monocytes aggravates neointimal growth and can thereby promote restenosis. The adhesion of circulating monocytes to the site of mechanical injury represents the key event in monocyte recruitment, and this review highlights recent insights into the molecular mechanisms of monocyte adhesion throughout the course of neointimal growth.

Engineering of multicolor spatial solitons with chirped-period quasi-phase-matching gratings in optical parametric amplification.

We demonstrate the excitation of solitons in a parametric amplifier with enhanced signal content through the use of a chirped-period quasi-phase-matching grating. This technique affords a low soliton threshold at the input end of a parametric amplifier, and the subsequent transformation to a desired soliton that exists at nonzero wave-vector mismatch through the use of a linearly chirped quasi-phase-matching grating. This approach has an advantage over direct excitation of solitons at nonzero wave-vector mismatch in uniform nonlinear materials and holds potential for improving the efficiency and mode quality of high-gain parametric amplifiers.