bluuebunny/crossref_metadata_2025_split huggingface dataset:
Structure and expression of the mouse myelin proteolipid protein gene
Authors: Macklin W. B. , Campagnoni C. W. , Gardinier M. V. , Deininger P. L. 
Published: January 2005

AbstractThe gene for the mouse myelin proteolipid protein has been isolated and the seven exons have been sequenced. Since the sequence of a rat proteolipid protein cDNA and partial sequence of the human proteolipid protein gene have been determined, it was possible to demonstrate a very high degree of conservation for the protelipid protein gene exons among species. While there are some nucleotide changes, the protein coding region of the mouse gene encodes protein that is totally conserved relative to both rat and human prteolipid proteins. The regulatory and noncoding regions of the proteolipid protein gene are also highly conserved. The upstream regulatory and 5′‐noncoding region of the gene is 92% homologous to the comparable region of the human proteolipid protein gene, and the 3′‐noncoding region of the mouse gene is approximately 90% homologous to a rat proteolipid protein cDNA through 2,200 nucleotides of 3′‐noncoding DNA.S1 nuclease protection experiments indicated that the major 5′‐end for proteolipid protein mRNAs from mouse, rat human, ro baboon is approximately 147–160 nucleotides upstream from the initial methionine codon of the protein coding region. Other S1 nuclease protection experiments indicated the possible existence of an alernative splice site within exon 3, which may produce mRNA for DM20. This mRNA is approximately 100 nucleotides shorter than that for the protelipid protein, and it is missing the latter half of exon 3, that is, amino acids 116–150 of the proteolipid protein sequence.
Expression of myelin proteins in the developing human spinal cord: Cloning and sequencing of human proteolipid protein cDNA
Authors: Kronquist K. E. , Crandall B. F. , Macklin W. B. , Campagnoni A. T. 
Published: January 2005

AbstractA full‐length clone for the human proteolipid protein (PLP) was isolated from a cDNA library constructed from poly (A)+ RNA isolated from fetal spinal cords obtained at 15–24 weeks of conceptional age. The sequence of the human PLP cDNa was determined, and the deduced amino acid sequence was found to be identical with that of rat PLP. Comparison of human and rat PLP cDNA clones indicated that the coding regions retaind 97% homology and that there were also other areas of conserved sequence. The human 5′‐untranslated region was 93% homologous to that of the rat. The 3′‐untranslated region was, overall, 73% homologous to that of the rat with areas containing >84% homology in the first 400 and last 200 nucleotides. The most variability within the 3′‐untranslated region occurred between nucleotides 2,000–2,500, where homology with the rat cDNA dropped to 55%. Expression of PLP in the human spinal cord between 11 and 23 weeks after conception was examined and compared with the expression of the myelin basic protein (MBP). RNA was isolated from pooled human spinal cords obtained at three periods of development: 11–14 weeks, 17–19 weeks, and 21–23 weeks. Northern blot analysis revealed a 3.2‐kilobase (kb) PLP mRNA that was present at higher abundance in the 21–23‐week samples. The 17–19‐week RNA than in the 17–19‐week or the 11‐14‐week samples. The 17‐19–week RNA sample also contained a PLP‐hybridizing band at 2.2 kb which may possibly have arisen by utilization of alternative polysdenylation signals. Messenger RNA for MBP was detectable at 11–14 weeks but was readily evident in both the 17–19‐ and 21–23‐week age groups. Immunoblot analysis of whole spinal cord homogenates indicated that polypeptides for MBP preceded the appearance polypeptides for PLP by 3–4 weeks.
Antisera against taurin: Quantitative characterization of the antibody specificity and its applcation to immunohistochemical study in the rat brain
Authors: Ida S. , Kuriyama K. , Tomida Y. , Kimura H. 
Published: January 2005

AbstractAn antiserum against taurine was generated in rabbits by immunization with taurine that was conjugated to carrier protein via glutaraldehyde. When the antiserum was applied to immunohistochemistry, structures withtaurine‐like immunoreactivity were observed in both neuronal and glial components of rat brain. The specificity of the serum was quantitatively examined using an enzyme‐linked immunoassay method, which has been newly developed for detecting such small molecules as amino acids. The best serum obtained had a high titer against taurine. It showed low cross‐reactivity with taurine metabolites and with other amino acids (less than 0.5%), while considerably higher reactivities were noted in the case of taurinecontaining peptides susch as γ‐glutamyl‐taurine and glycyl‐taurine. The results indicate that much care should be taken with taurine peptides in the evaluation of immunohistochemical results using taurine antiserum.
Methods to study changing free amino acid pools during embryonic chick development
Authors: van Gelder N. M. , Bélanger F. 
Published: January 2005

AbstractDuring early embryogenesis of the chick, the yolk represents the only souce of free amino acids. Leucine and glutamic acid, together with valin, predominate in this nonrenewable nutrient supply; taurine and phosphoethanolamine are present in the lowest concentration. The tyrosine level is already twice as high as phenylalanine.At embryo day 2 (E2), the not‐yet fully functioning vitelline blood plexus demonstrates an amino acid profile that rather closely resembles that of the yolk, except for three amino acids. During the transfer process from yolk to plexus; a certain amount of glutamic acid appears to be metabolized to glutamine and aspartic acid. Taurine and phosphoetanolamine are highly concentrated in the circulation, with a tenfold increase of taurine and a 50‐fold rise in phosphoethanolamine. The tyrosine‐to‐phenylalanine ratio remains 2:1, but their levels relative to valine and other essential amino acids fall by roughly 50%.In the already contracting heart tube and the developing neural tissue on E2, taurine and phosphoethanolamine also accumulate preferentially; the levels in neural tissue are ten‐ and fivefold higher than in the circulation for the respective amino acids, whereas the heart has three time the plexus content of taurine and two times the amount of phosphoethanolamine. Tyrosine and phenylalanine, still in the same proportion, have risen to approximately twice the circulation values. The heart tube, unlike the primitive brain, concentrates leucine, whereas isoleucine accumulates in both organs.Injections of valine (50 μmol) and taurine (200 μmol) into the yolk on E1 demonstrate that a higher yolk content of an amino acid can result in a two‐ to threefold tissue increase. This implies that the comparative amino acid profiles of early embryonic organs are to a large extent determined by the relative abundance of amino acids acids in the yolk. However, within confines of this limited supply, the organs are already able to extract preferentially certain amino acids.
Human T‐cell response to myelin basic protein in multiple sclerosis patients and healthy subjects
Authors: Tournier‐Lasserve E. , Hashim G. A. , Bach M. A. 
Published: January 2005

AbstractIn order to explore the T‐cell repertoire to myelin basic protein (BP) of both multiple sclerosis (MS) patients and healthy subjects (HS), we raised BP reactive T‐cell lines from blood mononuclear cells of eight MS patients and five HS. Thes lines were trigered in vitro by human BP. When analyzing their patterns of recognition of human BP versus heterologous BP, we could observe differences between healthy subjects and MS patients. Whereas T‐cell lines from healthy subjects developed a response to heterologous BP, which was in most cases equal or higher than that elicited by human BP, T‐cell lines from most MS patients displayed a low response, or no response at all, to one or several of the heterologous BP tested. A low response to bovine BP was only observed in active cases, whereas decreased responses to rat and/or monkey BP were observed both during remission and during active disease. This may indicate that T‐cell repertoire to BP in MS patients differs from that of healthy subjects.BP‐reactive T‐cell clones were obtained by limiting dilution from two healthy subject lines. Their pattern of response to heterologous BP as compared to human BP suggest that T‐cell from the same individual can recognize different BP epitopes.
Comparative effects of morphine on leukwytic antigenic markers of monkeys and humans
Authors: Donahoe R. M. , Bueso‐Ramos C. , Falek A. , McClure H. , Nicholson J. K. A. 
Published: January 2005

AbstractKnowing the in vitro effects of morphine on monkey leukocytes would be helpful in extending the utility of vestigations. Morphine effects On T1l, Leu2a, Leu3a antigenic markers on leukocytes from rhesus monkeys and humans were assessed by using single‐and two‐colour cytofluorometric analysis. Kinetics of expression Of these markers was determined after modulation of the original complement of T11 markers from the surface of T11(+) cells. Percentages of leukocytes detectable by directly staining these markers before modulation were within the expected range for monkey and human cells. Also, as expected, T11 modulation reduced the percentages of cells expressing T11 in the single‐color analysis, with reductions being greater for monkeys than human cells. Furthermore, in the single‐color analyses, the effects of morphine on kinetics of T11 expression were quite similar for both human and monkey cells. In the two‐color analyses, the simultaneous expression of T11and Leu3a markers was uniform for both monkey and human cells. These effects of morphine on kinetics of these markers varied only slightly between species. On the other hand, the distribution of Leu2 on T11 cells was markedly different for monkey and human T‐cells. Whereas human Leu2a(+) expressed Of T1l receptors' monkey high‐density Leu2a expressed fewer T1l markers than On kinetics Of Leu2a and T1l expression were at Ob‐ those with vious variance between species. Morphine primarily affected monkey Leu2a at high density and T1l at low density. Only monkeys expressed Leu2a (+)/T11 (−) cells, and morphine enhanced Leu2a expression on these cells.
Substrate specificity of cerebral cathepsin D and high‐Mr aspartic endopeptidase
Authors: Azaryan A. V. , Galoyan A. A. 
Published: January 2005

AbstractThe specificity of action of bovine brain cortex cathepsin D (EC 3.4.23.5) and high‐Mr aspartic endopeptidase (EC 3.4.23.‐) was studied with the vasoactive peptides renin substrate tetradecapeptide (RSTP), substance P (SP), and angiotensins I and II, and with model peptides‐Lys‐Pro‐Ala‐Glu‐Phe‐Phe (NO2)‐Ala‐Leu (I), Gly‐Gly‐His‐Phe (NO2)‐Phe‐Ala‐Leu‐NH2 (II), and Abz‐Ala‐Ala‐Phe‐Phe‐pNA (III). Cerebral aspartic peptidases show indentical substrate specificity, cleaving the Leu10‐Leu bond in RSTP and Phe‐Phe in SP and peptide I‐III, and not splitting angiotensins I and II. Because of the higher catalytic efficiency of cathepsin D (Kcat value), the specificity constants (Kcat/Km) for cathepsin D‐catalyzed hydrolysis of substrates 1–111 are much higher than those for the high‐Mr enzyme.High‐Mr aspartic peptidase shares a number of properties with cathepsin D (sensitivity to pepstatin, substrate specificity, pH activity profile) and shows partial immunological identity; however, high‐Mr aspartic peptidase has a specific activity 7–10 times lower than that of cathepsin D. The kinetic parameters of proteolysis of model peptides presented indicate that the high‐Mr enzyme may be a complex of a single‐chain cathepsin D with another polypeptide, although the possibility that it is an independent aspartic peptidase cannot be excluded.
Transplantation of male mouse submaxillary gland increase survival of axotomized basal forebrain neurons
Authors: Springer J. E. , Collier T. J. , Sladek J. R. , Loy R. 
Published: January 2005

AbstractTransaction of the fimbria‐fornix results in a loss of magnocellular neurons in the medial septum and vertical limb of the diagonal band (MS/VDB), possibly due to the deprivation of a retrogradely transported trophic substance, such as nerve growth factor (NGF), derived from the hippocampal formation. We have, utilized a transplantation model in which grafts of NGF‐rich male mouse submaxillary gland were placed in the lateral ventricle adjacent to the MS/VDB of rats with transactions of the fimbria‐fornix. At 2‐4 weeks following transection, animals with grafted submaxillary glands exhibited enhanced survival of MS/VDB neurons, which stained positive for acetycholinesterase and were immunoreactive for the NGF receptor. These experiments demonstrate that grafts of male mouse submaxillary gland can facilitate the survival of axotomized MS/VDB cholinergic neurons and may therefore prove beneficial in promoting regeneration of damaged neural systems.
Induction and quantitation of the RI cAMP‐binding protein in clonal mouse neuroblastastoma cell lines: Evidence that the increase in RI is not linked to neurite outgrowth
Authors: Liu A. Y.‐C. , Lin Z. , Kamalalannan V. , Chen K. Y. 
Published: January 2005

AbstractThis is a study of the regulation of expression of the RI cAMP‐binding in mouse neuroblastoma cells as it relates to neurotransmitter phenotype and neurite outgrowth. Dibutyryl cAMP was used to promote differentiation of the cholinergic NS‐20, the adrenergic N1E‐115, the neurotransmitter‐inactive N‐18, and the neurite‐minus N1A‐103 mouse neuroblastoma cells. The amount of the RI cAMP‐binding protein was quantitated by photoaffinity labeling of the 47,000‐dalton RI protein with 8‐N3‐[32P]cAMP and by Western blot, ELISA, and immunocytochemistry. Our results showed that dibutyryl cAMP inducted the RI cAMP‐binding protein by three to fivefold in each of the four neuroblastoma cell lines examined. The increased expression of the RI cAMP‐binding protein was not linked to neurite outgrowth, a parameter of morphological differentation in the neuroblastoma cells. Thus, the RI cAMP‐binding protein can be inducted in the neurite‐minus N1A‐103 neuroblastoma round cells; further, 8‐broma‐cAMP effected neurite outgrowth without inducing the RI cAMP‐binding protein in the neurite‐positive cell lines. Indirect immunocytochemistry of RI showed a cytoplasmic localization with little evidence of nuclear staining. The increase in RI cAMP‐binding protein coincided with an increase in the cAMP‐phosphodiesterase and a decrease in cAMP‐dependent phosphodiesterase activity in the mouse neuroblastoma cells. We propose that the induction of the RI cAMP‐binding protein may be a component of the homeostatic mechanism that regulates the action of cAMP in neuroblastoma calls and thet cAMP is capable of regulating its own activity through induction of cAMP‐ phosphodiesterase and RI cAMP‐binding protein and attenuation of the cAMP‐ phosphodiesterase activity.
The immunomodulatory effect of nerve growth factor
Authors: Abramchik G. V. , Yermakova S. S. , Kaliunov V. N. , Tanina R. M. , Tumilovich M. K. 
Published: January 2005

AbstractA prolonged application of nerve growth factor (NGF) to neonatal prepunberal rats induced selective hypertrophy and hyperfunc tion of ganglionic sympathetic neurons. This was accompained by higher density and fluorescence intensity of varicosw adrenergic fibers and terminals in the immunocompetent organs, total increase of catecholamines in them, catecholamine diffusion into the intercellular space, and their accumulation by macrophages and mast cells. The Plaqueforming and lymphocyte blast transformation responses were activated, signs of increased lymphocyte migration to peripheral lymphoid tissues appeared, and histamine concentration in the thymus and spleen increased. All of the foregoing indicate the immkunomodulatory effect of NGF and the dependence of immune responsiveness of the organism on the functional state of the adrenergic moiety. The net effect of the increase is attributed to knon‐specific protein sensitization, changes in the sympathetic (and, probably somatic) nervous system, and direct action on immunocompetent cells.
Estrogen concentration by substance p‐immunoreactive neurons in the medial basal hypothalamus of the female rat
Authors: Akesson T. R. , Micevych P. E. 
Published: January 2005

AbstractWe used the combined techinque of steroid autoradiography an dimmunohistochemistry to simultaneoulsy visulaize estrogen‐concentrating and substance P‐immunoreactive (sP‐IR) cells. A substantial proportion (26.1%) of sP‐IR celss that bound estrogen was found in the anterior two thirds of the arcuate nucleus with a rapidly diminishing number of cases (8.7%) in the posterior extent of this nucleus. Highest proportions (42.9%) of sP‐Ir cells retaining estrogen were found in the ventrolateral part of the ventromedial hypothalamic nucleus. The ventral premammillary nuleus was observed to have both populations but coexistence was comparatively infrequent (2.4%). Occasional cases of coesistence were also found in the leteral hypothalamic area. These results provide anatomicat evidence that a subset of SP‐IR neurons are directly reulated by estrogen and support the hypothesis that sP‐containing cells participate in the transduction of hormonal information into a CNS cirucitry taht regulates gonadotropin secretion and sexual bhaviour.
Fetal antigen retained by mature neurons and ependyma studied with a monoclonal antibody (6B9)
Authors: Malhotra S. K. , Predy R. , Singh R. , Gupta B. L. , Bhatnagar R. , Leeuw K. 
Published: January 2005

AbstractA mouse monoclonal antibody (MAb 6B9, isotype IgM) was raised against autopsy tissue sample from the central nervous system (CNS) of multiple sclerosis (MS) patients. By immunofluorescence microscopy, MAb 6B9 intensely stain most or all cell in fetal rats. However, MAb 6B9 differentially stains various cell types in adult rats. Neurons, ependymal cells, and adrenal chromaffin cells are stained intensely, whereas astrocytes and oligodendrocytes are not stained. The 6B9‐reactive antigen (6B9 antigen) is senstive to peodic acid, but insentive to treatment with protease, RNase, or hyaluronidase. Result form immunfluo‐‐microscopyon something section and cultured neuroblastoma cells indicated that 6B9 antigen is intracellular. This is supported by immunoelectron microscopy, where lableing for 6B9 antigen appear in the cytoplasm distinct from any identifiable organelle. Further studies on 6B9 antigen should reveal its chemical nature as well as the significance of developmental changes in its distribution.
Destruction by anti‐NGF of autonomic, sudomotor neurones and subsequent hyperinnervation of the foot pad by sensory fibres
Authors: Hill C. E. , Jelinek H. , Hendry I. A. , McLennan I. S. , Rush R. A. 
Published: January 2005

AbstractTreatment of newborn rats with antiserum to nerve growth factor (NGF) for the first 6 postnatal days produced a loss of the sympathetic neurones that nor‐ mally project to the sweat glands of the hind paws of the rat, indicating that cholinergic sympathetic neu‐ rones require NGF postnatally for their survival. Fol‐ lowing this immunosympathectomy, there was an increase in the proportion of glands containing sen‐ sory fibres having substance‐P‐like immunoreactivity (SP‐LO. This sensory sprouting was not as extensive as that after sympathectomy using 6‐hydroxydopa‐ mine (6‐OHDA)). During normal development, fibres showing SP‐LI are associated with the glands, partic‐ ularly during the first and second postnatal weeks. Prolongation of the antibody treatment until the third postnatal week reduced the sensory fibre ingrowth from the region of the glands, suggesting that the basis of this growth is the increased availability of NGF following sympathetic denervation. Retrograde cell labelling using the fluorescent dye, fast blue, indicated that the anti‐NGF treatment did not significantly decrease the number of sensory neurones projecting to an individual foot pad. These results support the hy‐ pothesis that sympathetic and sensory neurones com‐ pete for NGF produced by target tissues.
Inhibition of the electrogenic Na,K pump and Na,K‐ATPase activity by tetraethylammonium, tetrabutylammonium, and apamin
Authors: Zemková H. , Tesinger J. , Vyskočil F. 
Published: January 2005

AbstractThe K+‐induced hyperploarization of of Na‐loaded mouse diaphragm muscle, enzymatic activity of Na,K‐ATpase and3H‐ouabain binding to rat brian mocro‐somes was measured in the presence of K+ channel blockers teterathylammonium (TEA), tetrabutylammomium (TBA) and apamin. TBA, and to a lesser extent TEA in millimolar conceptrations, inhibited the electrogenic of the Na,K pump, Na,K‐ATPase activity, and3H‐ouabain binging. The inhibition of3H‐ouabain binging by TEA or TBA was more evident in the presence of ATP and Na+ ions.Apamin in nonomolar concentrations inhibited the electrogeic effect of Na,K pump and Na,K‐ATPase but not the3H‐ouabain binding. The hyperpolarizing effects of insulin and NADH, but not that of nor‐adrenaline, were also prevented by apamin.The inhibition of Na,K pump of TEA and TBA is apparently due to both competition with K+ for a binding site on the Na,K‐ATPase is different from that of tetra‐alkylammonium compounds; it apparently decrease the turnover rate of the enzyme.
Expression of myelin protein genes in quaking mouse brain
Authors: Konat G. , Trojanowska M. , Gantt G. , Hogan E. L. 
Published: January 2005

AbstractThe expression of myelin proteins in actively myelinating quaking and control brains was studied. RNA was extracted from the brains of 18‐ and 27‐day‐old mice and analyzed by northern blot using cDNA probes for proteolipid protein (PLP), basic protein (BP), and myelin‐associated glycoprotein (MAG). Two PLP transcripts of 3.2 and 2.4 kb (kilobase) were found, whereas PB and MAG probes hybridized to single regions of 2.2 and 2.5 kb, respectively. No abnormality in the transcript pattern was detectable in the quaking brain at either 18 or 27 days of age. Over this 9‐day period the level of PLP and BP message in the control brain decreased by approximately 10%, whereas the level of MAG message decreased by approximately 50%. In the 18‐day‐old quaking brain the expression of PLP and BP was severely reduced amounting to one‐third and one‐half of the control values, respectively. The reduction at the age of 27 days was less. On the other hand, the quaking brain produced more MAG mRNA amounting to 1.6‐ and 3.2‐fold control on the 18th and 27th day. The results indicate a reduced expression of the PLP and BP genes and a developmental delay in the mutant, whereas the genetic expression of MAG is enhanced and appears to be progressively dysregulated.
Fetal cortical astrocytes migrate from cortical homografts throughout the host brain and over the glia limitans
Authors: Goldberg W. J. , Bernstein J. J. 
Published: January 2005

AbstractThe cerebral cortices from 14‐day gestation rat embryos were prelabeled with Phaseolus vulgaris leucoagglutin (PHAL) and then homografted into freshly made implantation pockets in the host cerebral cortex. Animals were sacrificed at 30 and 60 days postimplantation (DPI). Paraffin sections were double labeled for the presence of glial fibrillary acidic protein (GFAP), a specific marker for astrocytes, and PHAL, utilized as a marker for transplant‐derived cells. Transplant‐derived astrocytes were found on the glia limitans along the entire circumference of the brain, in the hippocampal commissure, corpus callosum, internal capsule, entopeduncular nucleus, habenular commissure, brachium of the superior colliculus, optic tract, optic chiasm, and sensory root of the trigeminal nerve. Transplanted astrocytes entered the spaces of Virchow‐Robin, and migrated along parenchymal blood vessels and between the ependymal and subependymal layers of the third and lateral ventricles. The presence of basal lamina or parallel nerve fiber bundles was a common factor for these migration routes.