bluuebunny/crossref_metadata_2025_split huggingface dataset:
Surface behavior of axolemma monolayers: Physico‐chemical characterization and use as supported planar membranes for cultured Schwann cells
Authors: Calderon Reyna O. , Maggio B. , Neuberger T. J. , Devries G. H. 
Published: May 2005

AbstractThe axolemma membrane forms a stable and reproducible monomolecular layer at the air‐aqueous interface. The major lipids and proteins are present in this monolayer in molar ratios similar to the original membrane. Acetylcholinesterase and Na‐K‐ATPase activities are preserved in the monolayer to levels of 64% and 25%, respectively. The total lipid fraction forms a homogeneously mixed phase. The presence of proteins in the monolayer introduces surface inhomogeneties. Among other features, this is revealed by the presence of two values of lateral pressure at which the monolayer shows partial or total collapse: a broad partial collapse at surface pressures between 13 to 30 mN/m and a sharp collapse point at 46 mN/m. The average molecular areas, the broad collapse point, and the variation of the surface potential per molecule suggest the relocation of protein components at surface pressures between 13 to 30 mN/m. The behavior is consistent with the extrusion and exposure of proteins toward the aqueous medium that depends on the lateral pressure.Schwann cells grown on coverslips coated with axolemma monolayers at 13 mN/m (beginning of the broad collapse) and 34 mN/m (above the broad collapse) recognize the difference in the surface organization of axolemma caused by the lateral pressure which affects their proliferation, morphology, and spatial pattern of organization. Our results show for the first time that response of Schwann cells depends on the intermolecular organization of the axolemma surface with which they interact. These results suggest that the local expression of putative surface molecules of axolemma that may mediate membrane recognition and the signalling of morphological and proliferative changes can be modulated by long range supramolecular properties. © 1993 Wiley‐Liss, Inc.
Arachidonic acid lipoxygenation may mediate interleukin‐1 stimulation of nerve growth factor secretion in astroglial cultures
Authors: Čarman‐Krž M. , Wise Bradley C. 
Published: May 2005

AbstractInterleukin‐1β (IL‐1) stimulates by about fivefold NGF secretion from rat neonatal cortical astrocytes in primary culture. We investigated the possible intracellular second messenger mechanisms involved in the IL‐1 induced NGF secretion. Basal NGF secretion did not require extracellular Ca2+, whereas Ca2+ was necessary for the maximal NGF secretion stimulated by IL‐1 (10 units/ml). The protein kinase C activator TPA stimulated by sixfold NGF secretion, but in this case, TPA acted synergistically with IL‐1 to increase NGF secretion. Treatment of cells with the phospholipase A2 inhibitor mepacrine (30 μM) inhibited basal (by 50%) and IL‐1 stimulated (by 80%) NGF secretion. Indomethacin, a cyclooxygenase inhibitor, produced a slight increase in basal NGF secretion at low concentrations, while PGE2 (10 μM) inhibited basal and IL‐1 stimulated NGF secretion. In contrast, treatment of cells with nordihydroguaiaretic acid (NDGA), a lipoxygenase inhibitor, blocked in a concentration‐dependent manner (IC50 = 10 μM) IL‐1 stimulation of NGF secretion. The leukotriene LTB4 increased basal NGF secretion and this effect was not additive with IL‐1 when both agents were added at saturating concentrations, indicating a common mechanism of action for these two agents. Thus, one possible mechanism by which IL‐1 stimulates NGF secretion from astrocytes is by activation of the phospholipase A2‐lipoxygenase pathway. © 1993 Wiley‐Liss, Inc.
Recognition of the minimal epitope of monoclonal antibody Tau‐1 depends upon the presence of a phosphate group but not its location
Authors: Szendrei G. I. , Lee V. M.‐Y. , Otvos L. 
Published: May 2005

AbstractThe major constituent of the paired helical filaments (PHFs) of Alzheimer's disease is the abnormally phosphorylated form of the microtubule‐associated protein, τ. Monoclonal antibody (mAb) Tau‐1 is used extensively to stain normal human τ, and τ isolated from the brains of Alzheimer's disease patients after dephosphorylation. We used a panel of 6 synthetic peptides to localize the minimal epitope of Tau‐1 between amino acids 192–204. All 4 serine residues within this fragment were later phosphorylated individually by chemical methods, and it was shown that none of the peptides carrying a single phosphate group were recognized by the antibody. The serines included those that are probably not transformed in AD and consequently, conclusions drawn about malfunctioning kinase activity, based on Tau‐1 immunoreactivity, can be extremely misleading. The recognition was restored at a decreased level when one of the serines was replaced by an alanine residue. mAb AT8 was made by immunizing with the PHFs and was reported to recognize the same region of the protein in a phosphorylated form. AT8 did not, however, cross‐react with any of the singly phosphorylated peptides, indicating that the recognition site of the two antibodies are not entirely complementary or the binding to AT8 needs multiple phosphorylation of the antigen. The abolished recognition of the phosphorylated peptides cannot be attributed to a conformational change due to phosphorylation, since all peptides exhibited reverse‐turn secondary structures, as indicated by circular dichroism (CD) spectroscopy. Ant‐τ mAbs may distinguish between phosphorylated and non‐phosphorylated forms of epitopes regardless of the location of the phosphate group. © 1993 Wiley‐Liss, Inc.
Long‐term induction of c‐jun mRNA and jun protein in rabbit retinal ganglion cells following axotomy or colchicine treatment
Authors: Koistinaho J. , Hicks K. J. , Sagar S. M. 
Published: May 2005

AbstractThe expression of the c‐jun, c‐fos, and NGFI‐A genes was studied in the rabbit retina after optic nerve crush (ONC) or an intravitreal injection of colchicine. By Northern blotting, the basal expression of c‐fos and NGFI‐A mRNAs were undetectable, whereas c‐jun mRNA showed a low basal expression in shamoperated control retinas. Very few or no Jun‐ or Fosimmunoreactive nuclei were seen in control retinas. From 1 to 95 days after ONC a marked induction of JUN‐ but not FOS‐immunoreactive neurons was seen in the ganglion cell layer peaking at 3 and 7 days. Jun‐positive neurons also accumulated immunoreactive phosphorylated neurofilaments, indicating that they were ganglion cells. Northern blots demonstrated that retinal levels of c‐jun mRNA, but not of c‐fos or NGFI‐A mRNAs, were increased 3 and 7 days after ONC. An intravitreal injection of colchicine also induced Jun‐immunoreactivity within 24 hr in most of the neurons in the ganglion cell layer, but not in the inner nuclear and outer nuclear layers. The results indicate that axonal damage induces a specific pattern of IEG expression including a long‐term induction of the c‐jun gene in CNS neurons. © 1993 Wiley‐Liss, Inc.
Migrated fetal astrocytes modulate nerve growth factor expression in host nucleus gracilis of the medulla after grafting in third cervical hindlimb dorsal columns of the spinal cord
Authors: Bernstein J. J. , Willingham L. A. , Goldberg W. J. 
Published: May 2005

AbstractNerve growth factor (NGF) immunoreactivity in the nucleus gracilis of the medulla was quantitated for 90 days after aspiration of the C3 spinal hindlimb dorsal columns of 36 adult rats. Half the lesioned animals were a lesion‐only group. The remaining lesioned animals received an immediate graft of two 1.0‐mm pieces of 14 day gestation fetal rat cervical spinal cord (prelabeled with Phaseolus vulgaris leucoagglutinin) into the aspiration pocket (graft group). There were 3 normal controls. Groups of animals were analyzed at 7, 14, 21, 30, 60, and 90 days. At 90 days, NGF immunoreactivity was significantly elevated in the nucleus gracilis of lesion‐only animals. This increase in NGF immunoreactivity was augmented in glial end‐feet surrounding neurons and was also observed in the cytoplasm of astrocytes and some neurons. Previous experiments have shown that the cluster neurons of the nucleus gracilis undergo atrophy at this time with a concomitant decrease in hindlimb placement. NGF immunoreactivity (90 days) in grafted animals, however, was significantly less than in lesion‐only animals (P < 0.05) but remained significantly elevated above control animals (P < 0.05). Unlike in lesion‐only animals, there were no NGF positive neurons in the nucleus gracilis of grafted animals. Previous experiments have shown that astrocytes from fetal spinal cord grafts migrate to the nucleus gracilis, maintain cluster neuron cell size, and improve hindlimb placement at 90 days. The present data indicate that modulation of detrimental increases in NGF appeared to be a mechanism by which migrated fetal astrocytes can be used as a system for cell therapy. © 1993 Wiley‐Liss, Inc.
A developmentally regulated microsomal protein specific for the pigment epithelium of the vertebrate retina
Authors: Hamel C. P. , Tsilou E. , Harris E. , Pfeffer B. A. , Hooks J. J. , Detrick B. , Redmond T. Michael 
Published: May 2005

AbstractIn the vertebrate retina, the retinal pigment epithelium (RPE) performs specific functions critical to the normal process of vision. Although some of these functions are well documented, molecular data are still scarce. Using the RPE‐specific monoclonal antibody RPE9, raised against human RPE cells, we have identified a novel 65 kD protein, conserved in mammals, birds, and frogs. This RPE‐specific protein was found to be nonglycosylated. It was most effectively solubilized in the presence of detergent suggesting that it is associated with the RPE cell membranes. Its partitioning in the detergent phase of Triton X‐114 and its solubilization in 0.75 M and 1.0 M KCl suggest that it interacts with the membrane either through a polypeptide anchor or charged amino acids. Cell fractionation by differential solubilization and differential centrifugation demonstrated that the protein was preferentially associated with the microsomal membrane fraction, where it is the major protein. Developmental expression of this 65 kD protein was examined in neonatal rats. Morphologically well‐differentiated RPE cells did not express the 65 kD protein at birth. However, expression was detectable at postnatal day 4, that is, one to two days before the photoreceptors develop their outer segments, suggesting that the expression of the 65 kD protein may be coordinated with other developmental events in the intact retina. This is further supported by the fact that RPE cells in confluent culture lose the expression of this protein within two weeks, while they maintain their characteristic epithelial morphology. Because of its specificity, its evolutionary conservation, and its timing of expression, it is possible that this protein may be involved in one of the key roles of RPE and as such is an important molecular marker for RPE differentiation. © 1993 Wiley‐Liss, Inc.
Perinatal morphine treatment inhibits pruning effect and regeneration of serotoninergic pathways following neonatal 5,7‐HT lesions
Authors: Gorio Alfred , Di Giulio A. M. , Germani E. , Bendotti C. , Bertelli A. , Mantegazza P. 
Published: May 2005

AbstractLesion of the serotoninergic system in neonate rats is an ideal model for assessing the activity of chemical substances capable of affecting neuronal plasticity and regeneration (Jonsson et al., Dev Brain Res 16:171–180, 1984). Treatment of newborn rats within 6 hr from birth with the selective neurotoxin 5,7‐dihydroxytriptamine causes degeneration of the most distal serotoninergic axons. In our experimental conditions we have observed that after such neurotoxic treatment there is spinal cord denervation, which is particularly remarkable in the lumbar segment. This degenerative event is followed by gradual regeneration of the lesioned axons, with good reinnervation of the entire cord within 8 weeks. The degeneration‐regeneration process is correlated with a transient hyperinnervation of the pons‐medulla and hypothalamus by the short collaterals (pruning effect), as evidenced by increased serotonin content. Perinatal morphine exposure markedly impairs serotonin regeneration in the spinal cord. In addition, opiate treated rats are more susceptible to lesions, as shown by the neurotoxin induced denervation of the cortex, pons‐medulla, and hypothalamus, which does not occur in lesioned controls. Therefore, our observations suggest that perinatal exposure to morphine affects the plasticity and regeneration of the developing serotoninergic system by increasing its susceptibility to neurotoxic lessions and reducing its regenerative capacity. © 1993 Wiley‐Liss, Inc.
Interferon‐γ inhibits DNA synthesis and insulin‐like growth factor‐II expression in human neuroblastoma cells
Authors: Martin D. M. , Carlson R. O. , Feldman E. L. 
Published: May 2005

AbstractInterferon‐γ (IFN‐γ) is known to be an antiproliferative, differentiation agent in many cell types, including neuroblastoma. In this study, we determined the effects of IFN‐γ on cellular growth and expression of insulin‐like growth factor II (IGF‐II) and IGF receptors in the human neuroblastoma cell line SH‐SY5Y. Incubation of SH‐SY5Y cells in IFN‐γ (20–100 U/ml) induced the formation of long neuritic processes. IFN‐γ treatment also induced decreases in [3H]TdR incorporation, as well as serum‐dependent changes in cell number. Treatment with IFN‐γ reduced cell number 33% in the presence of serum but had no effect on cell number in the absence of serum. IGF‐II mRNA content was 60% inhibited by IFN‐γ, and was not serum dependent. The concentration of immunoreactive IGF‐II in SH‐SY5Y conditioned medium was also reduced in the presence of IFN‐γ, to less than half of control levels. In contrast, type I IGF receptor mRNA content was increased more than three‐fold after treatment with IFN‐γ and serum. Co‐incubation in IFN‐γ (20–100 U/ml) and IGF‐II on (3–10 nM) prevented the inhibitory effects of IFN‐γ on [3H]TdR ncorporation in serum‐free media. Our results suggest that IFN‐γ may inhibit DNA synthesis and cell growth by interfering with an IGF‐II/type I IGF receptor autocrine growth or survival mechanism.
Neuropeptide Y‐producing neurons of the arcuate nucleus regenerate axons after surgical deafferentation of the mediobasal hypothalamus
Authors: Alonso G. , Privat A. 
Published: May 2005

AbstractDorsolateral and ventomedial surgical deafferentation of the hypothalamus were used to study the capacity of different types of neuropeptide Y‐containing axons afferent to the dorsal hypothalamus to regenerate through surgical lesions. The kinetics of the postlesional responses of transected neuropeptide Y‐axons was studied on 30–40 μm thick vibratome sections, either (i) by light or electron microscopy after peroxidase immunostaining for neuropeptide Y or (ii) by confocal microscopy after double fluorescence immunostaining for neuropeptide Y and for glial fibrillary acidic protein. The dorsolateral cut was found to sever 2 main pathways containing neuropeptide Y axons located, respectively, below the bed nucleus of the stria terminalis and in the perifornical region. In both regions transected fibers were found to abut onto the surgical lesion, but even 45 days after the lesion, they were very rarely observed to penetrate into the astroglial scar formed along the lesion. The ventromedial cut was found to sever numerous neuropeptide axons that originate in the underlying arcuate nucleus. Seven to 15 days after the lesion neuropeptide Y fibers located below this type of cut presented a dramatic increase in both their numerical density and their immunostaining intensity. With increasing post‐surgery times, an increased number of neuropeptide Y fibers was observed to penetrate and to cross the lesional scar formed by densely packed astrocytic processes. Electron microscope observations further demonstrated that 45 days after the lesion, numerous neuropeptide Y‐immunoreactive axonal profiles were included in the scar matrix, which appeared to be mainly composed of closely interdigitating astrocytic processes containing dense bundles of filaments. These data indicate that, in contrast to other neuropeptide Y neurons innervating the dorsal hypothalamus, neuropeptide Y neurons of the arcuate nucleus regenerate axons through the astroglial scar produced by a surgical lesion placed in the ventromedial hypothalamus. © 1993 Wiley‐Liss, Inc.
Time‐dependent effects of insulin on Schwann cell proliferation in the in vitro regenerating adult frog sciatic nerve
Authors: Ekström P. A. R. , Edbladh M. , Edström A. 
Published: May 2005

AbstractThe present study showed that insulin (0.01 μg/ml, ≈︂ 2 nM) inhibited [3H]‐thymidine incorporation in support cells, most likely Schwann cells, of the cultured frog sciatic nerve. A 25–35% inhibition took place in regenerating nerve preparations as well as in preparations devoid of neuronal protein synthesis, i.e., in isolated 5 mm nerve segments and in gangliectomized nerves, suggesting that the effect was direct and not mediated via the neuronal cells. The inhibition by insulin was time‐dependent in that an effect was seen after 4 days but not at shorter or at longer periods of culturing. In separate experiments biotinylated insulin was shown to be taken up by Schwann cells in the regenerating nerve. Addition of serum increased the [3H]‐thymidine incorporation severalfold and abolished the inhibitory action of insulin. Our results suggest that insulin, at a certain stage of the regeneration programme, exerts a direct, inhibitory effect on the proliferation of the Schwann cells in the cultured frog sciatic nerve. © 1993 Wiley‐Liss, Inc.
Characterization of a transmissible growth‐promoting agent derived from CSF of schizophrenic patients which is active on human neuroblastoma cells
Authors: Shirabe Susumu , Stevens J. R. , Schwartz J. P. 
Published: May 2005

AbstractA growth‐promoting agent for the human neuroblastoma cell line SK‐N‐SH(EP) (SH‐EP) has been detected in human cerebrospinal fluid (CSF) derived from schizophrenic patients. Following treatment with the CSF, a number of properties of the SH‐EP cells changed permanently. These included an accelerated rate of growth, an increased cell density at confluence, a change of cell shape, and an increased ability to form colonies in soft agar. All of these changes are consistent with further cellular transformation of the SH‐EP cells. Once the cells' properties had changed following CSF treatment, the growth‐promoting activity was found to be present in freeze‐thawed cell extracts and in the culture medium, and could be passed to untreated SH‐EP cells. The activity could be detected in culture media diluted as high as 108. It was inactivated by proteinases, chloroform, or heat but passed through a 0.22‐μm filter. The growth‐promoting activity can be banded on a Percoll gradient, suggesting that it is particulate rather than a soluble growth factor. © 1993 Wiley‐Liss, Inc.
Expression of non‐adrenergic imidazoline sites in rat cerebral cortical astrocytes
Authors: Regunathan S. , Feinstein D. L. , Reis D. J. 
Published: May 2005

AbstractClonidine and related imidazoline agents, beside binding to α2‐adrenergic receptors, have been shown to bind to a non‐adrenergic site (imidazoline sites) in brain and peripheral tissues. However, which cell types in brain, namely neurons or glia, express this binding site and the cellular effects of activation of this site are not known. We investigated the cellular localization of imidazoline binding sites in cultured rat cortical astrocytes and neurons. Membranes prepared from cultured astrocytes showed specific, high affinity binding (KD: 4 nM) for 3H‐idazoxan with about tenfold higher number of binding sites than α2‐adrenergic sites (Bmax: 220 vs. 20 fmol/mg protein). Displacement studies exhibited the rank order of potency: cirazoline > idazoxan > amiloride > clonidine >>> epinephrine = ruawolscine defining this site as I‐2a subtype of imidazoline binding sites. Moreover, the binding was inhibited by K+ but not by Na+, another characteristic of imidazoline binding sites. In contrast, membranes prepared from cultured neurons showed fewer binding sites for 3H‐idazoxan that were completely displaced by adrenergic agents. Incubation of astrocytes with idazoxan, but not rauwolscine, resulted in a concentration‐dependent increase in the levels of mRNA for the astrocyte specific molecule glial fibrillary acidic protein. We conclude that (a) the non‐adrenergic imidazoline binding sites are expressed in astrocytes but not in neurons in rat cerebral cortex and (b) these “receptors” may influence astrocyte physiology by regulating the levels of GFAP. © 1993 Wiley‐Liss, Inc.
Widespread constitutive expression of HSP90 messenger RNA in rat brain
Authors: Izumoto S. , Herbert J. 
Published: May 2005

AbstractThe distribution of constitutively expressed mRNA encoding 2 isoforms of heat shock protein 90 (HSP90) was investigated in adult rat brain by in situ hybridization with 35S‐labeled cRNA probes. HSP90 mRNA density was estimated by semiquantitative autoradiography and by microscopic analysis. The distribution of HSP90 transcripts was similar for the 2 probes. HSP90 mRNA was widespread but not ubiquitous, and labeling intensity varied among different regions. In particular, HSP90 mRNA was abundant in limbic system‐related structures, such as the hippocampus, amygdala, mamillary body, piriform cortex, enthorhinal cortex, bed nucleus of the stria terminalis, medial habenular nucleus, and preoptic hypothalamic nuclei. The highest abundance of mRNA was detected in the Purkinje cell layer of the cerebellum. High abundance was also present in pineal body, choroid plexus, cerebellar granule cell layer, and cranial nerve nuclei. HSP90 mRNA was present in moderate abundance throughout the cortical gray mantle, in the caudate‐putamen, most other thalamic and hypothalamic nuclei, the pontine and spinal gray matter, and the anterior lobe of the hypophysis. Weak hybridization was observed in white matter fiber tracts, glial cells, and leptomeninges, and none was observed in endothelial cells and the smooth muscle of the cerebral microvasculature. Our findings suggest that HSP90 gene products may serve constitutive neuron‐specific functions in the unstressed brain. © 1993 Wiley‐Liss, Inc.
Localized vibrations in GaP doped with Mn or As
Authors: Haanstra J. H. , Vink A. T. 
Published: May 2005

AbstractRaman lines in GaP doped with Mn (0.1 at %) or As (up to 10 at %) are reported and discussed. In GaP‐Mn an impurity mode is found which also is observed in the low temperature luminescence. In GaP‐As five additional lines are seen. From the identification and relative intensities of these lines conclusions are drawn concerning the clustering of As ions around Ga ions.
Resonance Raman spectroscopic study on iodine in various organic solvents: Spectroscopic constants and halfband widths of the I2 vibration
Authors: Kiefer W. , Bernstein H. J. 
Published: May 2005

AbstractResonance Raman spectra have been obained from various iodine solutions. High intensity overtone progressions of the stretching vibration were observed, allowing the determination of the spectroscopy constants ωe and ωexe and estimation of ωeye for the stretching vibration for the ground state in various environments. The values are compared to those obtained for the gas phase. The overtone progression shows a large increase in half‐bandwidth with increasing vibrational quantum number.
Computer fitting of Voigt profiles to Raman lines
Authors: Sundius T. 
Published: May 2005

AbstractA FORTRAN program has been developed for the accurate computation of the convolution of a Lorentzian with a Gaussian line shape (the Voigt function). This program has been included in a larger program written by the author to resolve overlapping lines in complex Raman spectra. It has been found that the program is very useful to determine accurate line widths and peak positions from slit‐distorted spectra, which is important in high‐resolution Raman spectroscopy.