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At least 865 records · Page 48Linked to original sources
PubMed1999

beta1-4Galactosyltransferase activity of mouse brain as revealed by analysis of brain-specific complex-type N-linked sugar chains.

We previously reported two brain-specific agalactobiantennary N-linked sugar chains with bisecting GlcNAc and alpha1-6Fuc residues, (GlcNAcbeta1-2)(0)(or)(1)Manalpha1-3(GlcNAcbeta1-2M analpha1-6)(GlcNA cbeta1-4)Manbeta1-4GlcNAcbeta1-4(Fucalpha1-6)Glc NAc [Shimizu, H., Ochiai, K., Ikenaka, K., Mikoshiba, K., and Hase, S. (1993) J. Biochem. 114, 334-338]. Here, the reason for the absence of Gal on the sugar chains was analyzed through the detection of other complex type sugar chains. Analysis of N-linked sugar chains revealed the absence of Sia-Gal and Gal on the GlcNAc residues of brain-specific agalactobiantennary N-linked sugar chains. We therefore investigated the substrate specificity of galactosyltransferase activities in brain using pyridylamino derivatives of agalactobiantennary sugar chains with structural variations in the bisecting GlcNAc and alpha1-6Fuc residues as acceptor substrates. While the beta1-4galactosyltransferases in liver and kidney could utilize all four oligosaccharides as substrates, the beta1-4galactosyltransferase(s) in brain could not utilize the agalactobiantennary sugar chain with both bisecting GlcNAc and Fuc residues, but could utilize the other three acceptors. Similar results were obtained using glycopeptides with agalactobiantennary sugar chains and bisecting GlcNAc and alpha1-6Fuc residues as substrates. The beta1-4galactosyltransferase activity of adult mouse brain thus appears to be responsible for producing the brain-specific sugar chains and to be different from beta1-4galactosyltransferase-I. The agalactobiantennary sugar chain with bisecting GlcNAc and alpha1-6Fuc residues acts as an inhibitor against "brain type" beta1-4galactosyltransferase with a K(i) value of 0.29 mM.

Animals↗
PubMed1988

Protein tyrosine kinase in rat brain: neonatal rat brain expresses two types of pp60c-src and a novel protein tyrosine kinase.

Using angiotensin I as a substrate, the activity of protein tyrosine kinase was determined in various rat tissues, and its developmental change in rat brain was investigated. The specific activity was shown to be the highest in the brain among the tissues examined in neonatal rats, while it was the highest in the spleen in adult rats. In the brain, the activity varied during development and was the highest in the first postnatal week. To identify the protein tyrosine kinase and examine its relationship with pp60c-src, which is known to be highly expressed in neuronal cells, we attempted to characterize the enzyme from neonatal and adult rat brain, using poly(Glu,Tyr) as a substrate. Neonatal brain was found to express two types of pp60c-src and a novel protein tyrosine kinase to almost the same level, while adult brain expressed pp60c-src predominantly. The neonatal type of pp60c-src and the novel enzyme were designated as pp60nc-src and N-PTK in the present study, respectively. pp60c-src, pp60nc-src, and N-PTK were purified about 660-. 370-, and 260-fold from crude homogenate of neonatal brain, respectively, by procedures including sequential column chromatography on DEAE cellulose, hydroxylapatite, Ultrogel AcA44, and poly(Glu,Tyr) Sepharose. N-PTK behaved as a molecule with apparent Mr = 50,000 on Ultrogel AcA44 gel filtration chromatography. It was not immunoprecipitated by anti-pp60c-src antiserum and did not phosphorylate IgG heavy chain of anti-pp60c-src antibody. It required mainly Mn2+ for activity and phosphorylated tyrosine-containing polyamino acids and synthetic peptides such as angiotensin II and RR-SRC peptide.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1989

Physical, enzymatic, and contractile properties of brain myosin with anti-brain myosin Fab fragment bound on its tail.

An antibody obtained by immunizing a rabbit with purified bovine brain myosin was found to react with the tail portion of the myosin heavy chain. An Fab fragment obtained by limited papain digestion of the antibody was allowed to bind to brain myosin, and the complex of the Fab fragment and brain myosin (Fab-myosin) was isolated. On examination of the rotary-shadowed Fab-myosin by electron microscopy, most of the Fab fragment was located on the middle to C-terminal regions of the tails of the myosin molecules. The solubility of Fab-myosin in low salt solutions was higher than that of control brain myosin. Fab-myosin was found to form small irregular aggregates in low salt solutions instead of regular bipolar filaments, and the relative population of the monomeric form of myosin molecules observed for the Fab-myosin was much larger than that observed for the control myosin. The actin-activated Mg2+-ATPase activity of Fab-myosin was stimulated two- to threefold by phosphorylation of the light chains with myosin light chain kinase, as observed for the control brain myosin. Furthermore, the levels of the ATPase activity of the phosphorylated and dephosphorylated Fab-myosins were similar to those of the phosphorylated and dephosphorylated control myosins, respectively. The superprecipitation activity of Fab-myosin was also highly dependent on phosphorylation of the light chains. Although control brain myosin formed a large superprecipitate network which contracted to a dense particle, Fab-myosin generated only numerous tiny superprecipitates under the same conditions. From these results it was deduced that a regular filamentous state of brain myosin was not prerequisite for its actin-activated Mg2+-ATPase and superprecipitation activities but was indispensable for the formation of a large and well contractible superprecipitate.

Animals↗
PubMed1999

Evaluation of reperfusion and recovery of brain function before and after intracarotid arterial urokinase therapy in acute cerebral infarction with brain SPECT.

PURPOSE: Perfusion defects can be demonstrated reliably at an early stage with regional cerebral blood flow studies using SPECT. The administration of thrombolytic therapy in ischemic stroke is targeted at restoring cerebral perfusion immediately, leading to salvage of ischemic penumbra, smaller infarct size, and improved clinical outcome. This study considered the role of brain perfusion SPECT in the evaluation of reperfusion and brain function recovery of the infarcted area after early recanalization (less than 6 hours) of the occluded artery using intracarotid arterial urokinase therapy (ICAU). METHODS: Intracranial artery occlusion was confirmed in seven patients using emergency carotid angiography performed within the initial 6-hour period. Intracarotid arterial urokinase (500,000 to 800,000 units) was administered into the occluded arterial system (the left middle cerebral artery in four and the right middle cerebral artery in three patients). CT scanning was performed when the patients arrived in the emergency department and was repeated 24 to 48 hours after ICAU and at 7 days or earlier if clinically indicated. All patients had two SPECT studies, the first before urokinase administration and the second 24 or 48 hours later. RESULTS: Complete recanalization of the occluded vessels was seen in one patient after ICAU, effective partial recanalization was achieved in four patients, and minimal recanalization occurred in the other two. Before ICAU, Tc-99m HMPAO brain SPECT showed decreased uptake of the infarcted area in all patients, whereas the follow-up brain SPECT performed 24 or 48 hours after ICAU revealed improvement in the uptake of the recanalized area on qualitative and semiquantitative assessments using an asymmetry index, suggestive of brain function recovery and clinical improvement. Hemorrhagic transformation adjacent to the reperfused regions occurred in two patients with partial recanalization of the left middle cerebral artery. CONCLUSIONS: Reperfusion of the recanalized area and brain function recovery could be achieved if the occluded artery is recanalized within the initial 6-hour period using ICAU, and this was documented using brain perfusion SPECT without a delay in the therapeutic time window. Because the number of patients we studied was limited, further study is necessary to evaluate the effect of ICAU and to determine its prognostic significance.

Acute Disease↗
PubMedDate not supplied

Accuracy of surface fit registration for PET and MR brain images using full and incomplete brain surfaces.

OBJECTIVE: The accuracy of a surface-fitting image registration technique has been investigated for matching [18F]fluorodeoxyglucose (FDG) and [15O]H2O PET brain images with MR images. Use of partial-brain surfaces (a single hemisphere or a limited number of slices) was investigated to simulate cases in which severe brain defects or limited axial field of view would preclude using the entire brain surface. MATERIALS AND METHODS: Three FDG and three H2O scans were performed on five volunteers, in addition to volume MR studies. Fiducial markers were placed on the subjects' scalps to provide references for registration accuracy. The registration procedure was applied to each PET-MR set, using the surfaces defined by locating the brain edge in multiple slices for each set. RESULTS: The surfaces fit well, with only 1% scaling necessary for the best fit. Errors in fiducial marker positions between MRI and transformed PET were < 2 mm in the transverse directions and < 4.5 mm in the axial direction. Fits based on the partial surfaces worked well and gave results very similar to the full-brain fits. CONCLUSION: The surface-fitting technique is accurate for FDG and H2O PET studies, even when part of the brain surface cannot be used.

Algorithms↗
PubMed1998

Comparison of SPET brain perfusion and 18F-FDG brain metabolism in patients with chronic fatigue syndrome.

Chronic fatigue syndrome is a clinically defined condition of uncertain aetiology. We compared 99Tcm-HMPAO single photon emission tomography (SPET) brain perfusion with dual-head 18F-FDG brain metabolism in patients with chronic fatigue syndrome. Eighteen patients (14 females, 4 males), who fulfilled the diagnostic criteria of the Centers for Disease Control for chronic fatigue syndrome, were investigated. Thirteen patients had abnormal SPET brain perfusion scans and five had normal scans. Fifteen patients had normal glucose brain metabolism scans and three had abnormal scans. We conclude that, in chronic fatigue syndrome patients, there is discordance between SPET brain perfusion and 18F-FDG brain uptake. It is possible to have brain perfusion abnormalities without corresponding changes in glucose uptake.

Brain↗
PubMed2003

Rat organic anion transporter 3 (rOAT3) is responsible for brain-to-blood efflux of homovanillic acid at the abluminal membrane of brain capillary endothelial cells.

The mechanism that removes homovanillic acid (HVA), an end metabolite of dopamine, from the brain is still poorly understood. The purpose of this study is to identify and characterize the brain-to-blood HVA efflux transporter at the rat blood-brain barrier (BBB). Using the Brain Efflux Index method, the apparent in vivo efflux rate constant of [3H]HVA from the brain, k(eff), was determined to be 1.69 x 10(-2) minute(-1). This elimination was significantly inhibited by para-aminohippuric acid (PAH), benzylpenicillin, indoxyl sulfate, and cimetidine, suggesting the involvement of rat organic anion transporter 3 (rOAT3). rOAT3-expressing oocytes exhibited [3H]HVA uptake (K(m) = 274 micromol/L), which was inhibited by several organic anions, such as PAH, indoxyl sulfate, octanoic acid, and metabolites of monoamine neurotransmitters. Neurotransmitters themselves did not affect the uptake. Furthermore, immunohistochemical analysis suggested that rOAT3 is localized at the abluminal membrane of brain capillary endothelial cells. These results provide the first evidence that rOAT3 is expressed at the abluminal membrane of the rat BBB and is involved in the brain-to-blood transport of HVA. This HVA efflux transport system is likely to play an important role in controlling the level of HVA in the CNS.

Animals↗
PubMed2005

Covariation between brain size and immunity in birds: implications for brain size evolution.

Parasitism can negatively affect learning and cognition, setting the scene for coevolution between brain and immunity. Greater susceptibility to parasitism by males may impair their cognitive ability, and relatively greater male investment in immunity could compensate for greater susceptibility to parasites, in particular when males have a relatively large brain. We analysed covariation between relative size of immune defence organs and brain in juvenile and adult birds. The relative size of the bursa of Fabricius and the spleen in adults covaried positively with relative brain size across bird species. The relative size of these two immune defence organs covaried with sex differences in relative size of the brain, indicating that the relationship between immune defence and brain size was stronger for males. In contrast, liver and heart size or sexual size dimorphism in size did not covary with immune defence. Thus, species in which males have relatively large brains also have relatively large immune defence organs.

Adaptation, Physiological↗
PubMed1982

Relationship between regional brain angiotensinogen and local blood flow and volume in the adrenalectomized rat: application of approach to quantification of brain corticosterone receptors.

Prior studies from this laboratory have established that angiotensinogen, the prohormone of angiotensin, is unevenly distributed in the rat brain and that adrenalectomy selectively perturbs levels of the prohormone in regions associated with cardiovascular neural pathways. However, plasma angiotensinogen levels are 10(2)--10(3) times higher in plasma than in brain, so that the observation of a unique distribution of brain angiotensinogen may reflect variable plasma contamination. Studies were therefore undertaken to establish whether adrenalectomy selectively alters regional blood flow, blood volume, or plasma contamination of brain tissue, thereby artifactitiously altering apparent angiotensinogen levels. Radioactive 2-deoxyglucose, iodoantipyrine, and inulin were employed in these analyses. We conclude that variations in blood flow do not explain the selective effects of adrenalectomy, but that a variable extent of residual plasma contamination (remaining after transcardiac perfusion) is partially reflected in our earlier data. However, after correcting for plasma contamination, we still find significant changes in selected areas of the rat brain following adrenalectomy. Finally, our results demonstrate the necessity for direct quantitation of plasma contamination od brain tissue segments. This is shown to have relevance in other situations, such as corticosterone binding globulin contamination of brain corticosterone receptor binding.

Adrenalectomy↗
PubMed1985

Brain gangliosides of quaking and shiverer mutants: qualitative and quantitative changes of monosialogangliosides in the quaking brain.

Ganglioside compositions in the brains of the mutant mice quaking and shiverer were compared with those of their littermate controls, C57BL/6 and C3HSWV. Neither ganglioside content nor composition of shiverer brains differed from those of the control brains. Change in the ganglioside composition of the mutant brain from that of the control was observed only in the quaking mutant brain, in which monosialoganglioside GM1 was significantly reduced and GM4 was completely absent. The structures of the gangliosides were determined by negative ion fast atom bombardment mass spectrometry, and the GM3 and GM4 gangliosides in the quaking brain were found to be altered in regard to their long-chain base and fatty acid compositions when compared to the normal C57BL/6 brain.

Animals↗
PubMed2004

Mammalian brain consumption by blood donors in the United States: brains today, deferred tomorrow?

BACKGROUND: Theoretical concerns of possible variant CJD (vCJD) transmission by transfusion have led to deferral of US donors potentially exposed to the bovine spongiform encephalopathy agent. Although the efficacy of these policies is unknown, impact on blood collections has been substantial. Under the precautionary principle, deferral of donors consuming bovine (or other mam-malian) brains, possibly contaminated with the vCJD agent, might be considered. Blood donors were surveyed to determine lifetime mammalian brain consumption. STUDY DESIGN AND METHODS: The Retrovirus Epidemiology Donor Study (REDS) conducted an anonymous mail survey of 92,581 donors from eight US blood centers. RESULTS: Responses were received from 52,650 donors (57%). Of these, 6.4 percent reported lifetime brain consumption; bovine (3.6%) and hog brains (1.7%) were the most common. Bovine brain consumption varied fourfold by center (1.7-7.0%) and was highest among male (4.5%), older (age 55+, 6.5%), foreign-born (9.2%), Asian (7.2%), and Hispanic (8.6%) donors. Among bovine brain consumers, 67 percent engaged in the practice 4 times or less, 79 percent were repeat donors, and 61 percent reported giving at least 11 donations in the past 10 years. CONCLUSION: Following the precautionary principle, further steps to reduce the theoretical vCJD risk could include deferring donors who eat bovine (or other mammalian) brains. The impact of such a policy would not be trivial, especially in areas with older, foreign-born, Asian, or Hispanic donors. Cautious implementation and periodic evaluation of deferral policies is warranted.

Adolescent↗
PubMed2004

Distinct transcriptional changes in donor kidneys upon brain death induction in rats: insights in the processes of brain death.

Brain death affects hormone regulation, inflammatory reactivity and hemodynamic stability. In transplant models, donor organs retrieved from brain dead (BD) rats suffer from increased rates of primary non-function and lower graft survival. To unravel the mechanisms behind brain death we have performed DNA microarray studies with kidney-derived RNA from normo- and hypotensive BD rats, corresponding with optimal and marginal BD donors, respectively. In kidneys from normotensive donors 63 genes were identified as either up- (55) or down-regulated (8), while 90 genes were differentially expressed (67 up-regulated) in hypotensive BD donor kidneys. Most genes were categorized in different functional groups: metabolism/transport (including the down-regulated water channel Aqp-2), inflammation/coagulation (containing the largest number (16) of up-regulated genes including selectins, Il-6, alpha- and beta-fibrinogen), cell division/fibrosis (including KIM-1 involved in tubular regeneration) and defense/repair (with the cytoprotective genes HO-1, Hsp70, MnSOD2). Also, genes encoding transcription factors (including immediate early genes as Atf-3, Egr-1) and proteins involved in signal transduction (Pik3r1) were identified. Summarizing, the use of DNA microarrays has clarified parts of the process of brain death: Brain-death-induced effects ultimately lead, via activation of transcription factors and signal transduction cascades, to differential expression of different "effector" genes. Not only deleterious processes such as inflammation and fibrosis occur in brain dead donor kidneys but genes involved in protection and early repair processes are activated as well. These findings can be used to introduce specific cytoprotective interventions in the brain dead donor to better maintain or even increase organ viability.

Animals↗
PubMed1985

Brain "identifier sequence" is not restricted to brain: similar abundance in nuclear RNA of other organs.

A repeated 82 base pair sequence in genomic DNA of the rat was previously proposed as being a control element governing brain (neuron) specific genetic expression. This intronic sequence, termed the brain "identifier" (ID), is complementary to small RNA species localized in brain cytoplasm, and it was thought to be represented specifically in RNA produced by brain nuclei in vitro. The RNA blot analyses of total nuclear and polyadenylated heterogeneous nuclear RNA described in the present report show that this ID sequence is also present in the liver and kidney in abundances similar to those in the brain. This repeated sequence is not, therefore, restricted to transcripts produced in the brain as suggested from previous transcriptional "runoff" experiments. Measurements on rat and mouse nuclear RNA indicate that the abundance of ID sequence transcript is roughly proportional to the number of copies of this repeat in the respective genomes. This suggests a rather random genomic location and transcription of this sequence. From these results it seems improbable that the ID sequence functions as a transcriptional-level control element in genes expressed specifically in the brain.

Animals↗
PubMedDate not supplied

Confirmation of brain death using brain radionuclide perfusion imaging technique.

OBJECTIVE: To determine the reliability of radionuclide cerebral blood perfusion imaging in confirming brain death irrespective of continued heartbeat. SUBJECTS AND METHODS: Twenty-eight patients (19 male and 9 female, aged 17-63 years) with severe brain injury and fully supported until the final cardiac asystole were included in the study. Two sets of clinical tests aimed at ascertaining brain death in each subject were performed separately for each case within an interval of 24 h. Dynamic, planar and single photon emission computed tomographic (SPECT) brain scintigraphy were also performed after intravenous administration of 550 MBq (15 mCi) technetium-99m hexamethyl propyleneamine oxime. RESULTS: Following the clinical diagnosis of brain death, none of the patients was withdrawn from cardiopulmonary support or had any organ harvested. Dynamic, planar and SPECT imaging performed thereafter did not reveal any intracranial cerebral perfusion in any of the subjects, except in 1 patient where the initial scan showed posterior fossa activity that ceased, in a subsequent scan obtained after 24 h. All of the patients were declared dead only after the emergence of cardiac asystole. CONCLUSION: The findings indicate that radionuclide brain perfusion imaging is reliable, reproducible, noninvasive and simple to perform for the confirmation of brain death and as such we recommend it as an alternative to exhaustive neurophysiological tests and invasive catheter angiography.

Adolescent↗
PubMed2007

Diversity of brain morphology in teleosts: brain and ecological niche.

Modern teleosts have more copies of developmental regulatory genes than other vertebrates, probably due to a whole genome duplication that occurred specifically at the base of the lineage of ray-finned fishes. The genome duplication generates duplicated genes (including their regulatory regions), and one of the duplicates might become redundant and free from selective pressures. These redundant genes might be more easily mutated during evolution. Brain morphogenesis is a process that is dependent on a large genetic program in which a subprogram for the regionalization of the brain is coupled with that for cell-proliferation control. If beneficial mutations took place in key genes within the genetic program for brain morphogenesis, it might result in the enhancement of region-specific cell proliferation and cell survival in the corresponding brain subdivisions. This mechanism might account for the appearance of various forms of teleost brains, which have been preserved under selection pressure in diverse environments. It is conceivable that variously modified brains might evolve under the conditions of natural selection so that the brains help fit the teleost species for diverse ecological niches.

Animals↗
PubMed1993

Prolactin receptors in dove brain: autoradiographic analysis of binding characteristics in discrete brain regions and accessibility to blood-borne prolactin.

Film autoradiography and densitometry were employed to obtain a detailed map of prolactin (PRL) receptor distribution in ring dove brain and to characterize the affinity, capacity, specificity, and in vivo saturability of 125I-ovine PRL binding in individual brain regions. Significant specific binding was detected in choroid plexus and in a variety of forebrain and midbrain sites, with highest levels observed in the preoptic area, tuberoinfundibular region, lateral hypothalamic area, and the suprachiasmatic, paraventricular, and ventromedial hypothalamic nuclei. A comparison of PRL receptors in the choroid plexus, preoptic area, ventromedial nucleus, suprachiasmatic nucleus, and tuberal hypothalamus revealed significant regional differences in binding capacity, but not differences in binding affinity (Kd = 0.4-0.9 nM; Bmax = 6-14 fmol/mg protein). Unlabelled ovine PRL proved to be an effective competitor of labelled ovine PRL at concentrations of 43 pM, 0.43 nM, and 4.3 nM in the choroid plexus and in 5 diencephalic areas. In contrast, no significant competition was observed in any of these brain areas in tests with unlabelled turkey GH, ovine GH, or ovine LH at similar concentrations. Unlabelled ovine PRL (37 nmol) significantly reduced the uptake of 125I-ovine PRL (37 pmol) in the preoptic area, tuberal hypothalamus, and bed nucleus of the pallial commissure at 2 h after intravenous injection. In addition, specific binding of 125I-ovine PRL in vitro was reduced by over 67% in these brain areas and in several other brain regions following a 7 day period of systemic ovine PRL administration. These results indicate that PRL receptors in different regions of the dove brain exhibit similar binding characteristics. In addition, they suggest that at least some of these PRL-sensitive brain loci are accessible to blood-borne hormone.

Animals↗
PubMed2003

Localization of a brain sulfotransferase, SULT4A1, in the human and rat brain: an immunohistochemical study.

Cytosolic sulfotransferases are believed to play a role in the neuromodulation of certain neurotransmitters and drugs. To date, four cytosolic sulfotransferases have been shown to be expressed in human brain. Recently, a novel human brain sulfotransferase has been identified and characterized, although its role and localization in the brain are unknown. Here we present the first immunohistochemical (IHC) localization of SULT4A1 in human brain using an affinity-purified polyclonal antibody raised against recombinant human SULT4A1. These results are supported and supplemented by the IHC localization of SULT4A1 in rat brain. In both human and rat brains, strong reactivity was found in several brain regions, including cerebral cortex, cerebellum, pituitary, and brainstem. Specific signal was entirely absent on sections for which preimmune serum from the corresponding animal, processed in the same way as the postimmune serum, was used in the primary screen. The findings from this study may assist in determining the physiological role of this SULT isoform.

Animals↗
PubMed2006

Brain-derived proteins in the CSF: do they correlate with brain pathology in CJD?

BACKGROUND: Brain derived proteins such as 14-3-3, neuron-specific enolase (NSE), S 100b, tau, phosphorylated tau and Abeta1-42 were found to be altered in the cerebrospinal fluid (CSF) in Creutzfeldt-Jakob disease (CJD) patients. The pathogenic mechanisms leading to these abnormalities are not known, but a relation to rapid neuronal damage is assumed. No systematic analysis on brain-derived proteins in the CSF and neuropathological lesion profiles has been performed. METHODS: CSF protein levels of brain-derived proteins and the degree of spongiform changes, neuronal loss and gliosis in various brain areas were analyzed in 57 CJD patients. RESULTS: We observed three different patterns of CSF alteration associated with the degree of cortical and subcortical changes. NSE levels increased with lesion severity of subcortical areas. Tau and 14-3-3 levels increased with minor pathological changes, a negative correlation was observed with severity of cortical lesions. Levels of the physiological form of the prion protein (PrPc) and Abeta1-42 levels correlated negatively with cortical pathology, most clearly with temporal and occipital lesions. CONCLUSION: Our results indicate that the alteration of levels of brain-derived proteins in the CSF does not only reflect the degree of neuronal damage, but it is also modified by the localization on the brain pathology. Brain specific lesion patterns have to be considered when analyzing CSF neuronal proteins.

14-3-3 Proteins↗