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1. Helodermin, helospectin I and helospectin II, peptides recently isolated from the salivary gland venom of Heloderma suspectum, were compared to vasoactive intestinal peptide (VIP) with respect to effects on systemic blood pressure and on isolated femoral arteries in the rat. 2. They all reduced blood pressure in a dose-dependent manner; helodermin was less effective than VIP. However, at doses

The effects of neuropeptide Y (NPY) on systemic arterial blood pressure and heart rate were studied in anesthetized intact and pithed rats. I.v. doses of NPY (0.3-30 nmol/kg) raised the mean arterial blood pressure dose dependently. At doses of greater than or equal to 3.0 nmol/kg, the initial pressor response was followed by a dose-dependent fall in blood pressure in intact and pithed rats. The d

1. In the present study we have examined whether neuropeptide Y (NPY) interferes with non-adrenergic, non-cholinergic nerve-mediated contractions and relaxations in the guinea-pig airways. In these experiments we have used ring preparations of bronchi and trachea, incubated in the presence of atropine, propranolol and indomethacin (each 1 microM). 2. The contractile response to electrical stimulat

Heterogeneity among NPY (and PYY) receptors was first proposed on the basis of studies on sympathetic neuroeffector junctions, where NPY (and PYY) can exert three types of action: 1) a direct (e.g., vasoconstrictor) response; 2) a postjunctional potentiating effect on NE-evoked vasoconstriction; and 3) a prejunctional suppression of stimulated NE release; the two latter phenomena are probably reci

The effects of neuropeptide Y (NPY) on the contractile response to vagus nerve stimulation at different frequencies was studied in an isolated tracheal tube preparation from guinea pig. NPY had no effect on basal smooth muscle tension or on the contractile effect of carbachol, but inhibited vagally induced contractions in a concentration-dependent manner with a greater inhibition at low frequencie

The Advanced Light Source (ALS) at Berkeley Lab has seen many upgrades over the years, keeping it one of the brightest sources for soft x-rays worldwide. Recent developments in magnet technology and lattice design appear to open the door for very large further increases in brightness [1], particularly by reducing the horizontal emittance, even within the space constraints of the existing tunnel. I

Fast kicker systems are required for the proposed upgrade of ALS to a diffraction-limited light source (ALS-U). The main approach is to have multiple stripline kicker magnets driven by inductive adders. The design details of the kicker structures and the inductive adder options will be discussed.

The Advanced Light Source (ALS) at Berkeley Lab has seen many upgrades over the years, keeping it one of the brightest sources for soft x-rays worldwide. Recent developments in magnet and vacuum technology, as well as lattice design (multi bend achromat lattices) appear to open the door for very large further increases in brightness [1]. This could be achieved by reducing the horizontal emittance,

An overview of the design of compact elliptically polar-izing undulator with small round magnetic gap to provide full polarization control of synchrotron radiation in a more cost effective manner and consuming less built in space than the state of the art devices. This type of undulator is meant as source for the potential future Soft X-ray (SXL) FEL beamline using the linear accelerator at MAX IV

This article extends the common correlated effects pooled (CCEP) estimator to homogenous dynamic panels. In this setting, CCEP suffers from a large bias when the time span (T) of the dataset is fixed. We develop a bias-corrected CCEP estimator that is consistent as the number of cross-sectional units (N) tends to infinity, for T fixed or growing large, provided that the specification is augmented

Cell-based therapies represent a new therapeutic approach for stroke. In 2007, investigators from academia, industry leaders, and members of the National Institutes of Health crafted recommendations to facilitate the translational development of cellular therapies as a novel, emerging modality for stroke from animal studies to clinical trials. This meeting was called Stem Cell Therapies as an Emer

Old age is associated with an enhanced susceptibility to stroke and poor recovery from brain injury, but the cellular processes underlying these phenomena are not well understood. Potential mechanism underlying functional recovery after brain ischemia in aged subjects include neuroinflammation, changes in brain plasticity-promoting factors, unregulated expression of neurotoxic factors, or differen

This unit describes two methods of in situ hybridization: one uses an 35S-labeled oligonucleotide probe and the other uses a digoxigenin-labeled oligonucleotide probe on frozen, cryostat-sectioned samples. These methods allow detection of the physical distribution and expression levels of target mRNA. Protocols are also included for labeling the probes and preparing the sample material.

Seizure activity regulates gene expression for glial cell line-derived neurotrophic factor (GDNF) and neurturin (NRTN), and their receptor components, the transmembrane c-Ret tyrosine kinase and the glycosylphosphatidylinositol-anchored GDNF family receptor (GFR) α1 and α2 in limbic structures. We demonstrate here that epileptogenesis, as assessed in the hippocampal kindling model, is markedly sup

Loss of function mutations in the gene encoding the cysteine protease inhibitor, cystatin B (CSTB), are responsible for the primary defect in human progressive myoclonus epilepsy (EPM1). CSTB inhibits the cathepsins B, H, L and S by tight reversible binding, but little is known regarding its localization and physiological function in the brain and the relation between the depletion of the CSTB pro

The levels of brain-derived neurotrophic factor (BDNF) vary between different forebrain areas and show region-specific changes after cerebral ischemia. The present study explores the possibility that the levels of endogenous BDNF determine the susceptibility to ischemic neuronal death. To block BDNF activity the authors used the TrkB-Fc fusion protein, which was infused intraventriculary in rats d