Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P50583 (asymmetrical)
 12,197 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To elucidate the role of aspartate as a signal molecule in the brain, its localization and those of related amino acids were examined by light and electron microscopic quantitative immunocytochemistry using antibodies specifically recognizing the aldehyde-fixed amino acids. Rat hippocampal slices were incubated at physiological and depolarizing [K+] before glutaraldehyde fixation. At normal [K+], aspartate-like and glutamate-like immunoreactivities were colocalized in nerve terminals forming asymmetrical synapses on spines in stratum radiatum of CA1 and the inner molecular layer of fascia dentata (i.e., excitatory afferents from CA3 and hilus, respectively). During K+ depolarization there was a loss of aspartate and glutamate from these terminals. Simultaneously the immunoreactivities strongly increased in glial cells. These changes were Ca2+-dependent and tetanus toxin-sensitive and did not comprise taurine-like immunoreactivity. Adding glutamine at CSF concentration prevented the loss of aspartate and glutamate and revealed an enhancement of aspartate in the terminals at moderate depolarization. In hippocampi from animals perfused with glutaraldehyde during insulin-induced hypoglycemia (to combine a strong aspartate signal with good ultrastructure) aspartate was colocalized with glutamate in excitatory terminals in stratum radiatum of CA1. The synaptic vesicle-to-cytoplasmic matrix ratios of immunogold particle density were similar for aspartate and glutamate, significantly higher than those observed for glutamine or taurine. Similar results were obtained in normoglycemic animals, although the nerve terminal contents of aspartate were lower. The results indicate that aspartate can be concentrated in synaptic vesicles and subject to sustained exocytotic release from the same nerve endings that contain and release glutamate.
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PMID:Synaptic vesicular localization and exocytosis of L-aspartate in excitatory nerve terminals: a quantitative immunogold analysis in rat hippocampus. 969 1

The deformation of the posterior part of the skull (occipito-vertebral region) induced directly, occurs in numerous pathological situations. Its significance is frequently overlooked. Lesions of the cranial content, alterations of the lambdoid suture or other premature synostosis, abnormal constraint related to posture or to muscular activity can modify the posterior curvature of the skull, generally flattening it. The authors propose a classification based on three points: intracranial pathology, bone pathology and extrinsic pathology. Concerning intracranial pathology, alterations of the brain or CSF fluid can induce either insufficient (microencephaly) or excessive (hydrocephalus, Dandy Walker or Arnold Chiari malformations) expansion. Concerning bone pathology, sagittal synostosis (scaphocephaly) induces a bulging and coronal synostosis a flatness of the posterior skull. Bilateral premature lambdoid synostosis (pachycephaly) produces total flatness of the back of the skull. Concerning extrinsic pathology, dysmorphism is often asymmetrical and results from extracranial mechanical application dysfunction such as inborn torticollis, cervical spine pathology (Klippel-Feil syndrome), or prolonged decubitus during the first year of life. The different surgical procedures are described and the authors describe a personal technique for correcting this dysmorphism: the turned biparietal flap transposition. The back of the skull is remodelled (either asymmetrical or bilateral flatness), and patients with no need for a helmet can lie on their backs immediately after the operation.
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PMID:[The posterior cranium and its dysmorphisms]. 976 16

In patients with malformations of cortical development (MCD), widespread structural abnormalities of the brain have been demonstrated using volumetric MRI, and associated with poor post-surgical outcome in patients with localization-related epilepsy. Proton magnetic resonance spectroscopic imaging (1H-MRSI) studies permit the non-invasive measurement of concentrations of a variety of cerebral metabolites implicated in cerebral structure and function. There is a dearth of quantitative 1H-MRSI studies of MCD. Ten controls and 10 patients with localization-related epilepsy who were found to have MCD on high resolution MRI underwent 1H-MRSI on a 1.5 T GE Signa scanner [TE (echo time) = 30 ms, TR (repetition time) = 3 s]. In all patients, the axial area studied contained lesional and perilesional tissue. In seven unilaterally affected patients, the area studied contained also apparently normal contralateral grey and white matter; in three patients with bilateral but asymmetrical MCD, it contained visually normal and abnormal tissue from both hemispheres. N-acetyl aspartate + N-acetyl aspartyl glutamate (NAA), creatine + phosphocreatine (Cr), choline-containing compounds (Cho), glutamate + glutamine (Glx) and myo-inositol (Ins) were automatically quantified in voxels covering these different regions. Metabolite concentrations were corrected for CSF content and correlated with the grey and white matter of the MRSI voxels. In control subjects, there were significant positive correlations between grey matter content and concentrations of NAA, Glx, Ins and Cr. Compared with a normal range that took grey matter content into account, defined as the control mean +/- 2 SD, all lesions but one showed metabolic abnormalities. The most common abnormality was a decrease in NAA, but findings were heterogeneous and there was increased NAA in one lesion. Perilesional tissue was abnormal in eight patients, with increased NAA in three. Tissue contralateral to the main MCD was abnormal in all three patients with bilateral but asymmetrical MCD, and in six of the seven apparently unilaterally affected patients. Spectroscopic grey and white matter abnormalities in patients with MCD exceeded the apparently focal abnormality shown by MRI, indicating widespread abnormalities of cerebral function.
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PMID:Quantitative short echo time proton magnetic resonance spectroscopic imaging study of malformations of cortical development causing epilepsy. 1115 69

The Sylvian fissure region gathers lateral frontotemporal cortices and subcortical structures that are frequently disturbed in patients with mood disorders. We have investigated possible CSF space changes in this brain region in severe melancholic depression. Fifty-seven patients and 37 control subjects received three-dimensional MRI. CSF volumes were obtained for cerebral CSF, lateral ventricles, and both Sylvian fissure regions. As a group, patients showed a significant CSF space enlargement that was prominent around the Sylvian fissure, particularly in the left hemisphere. Likewise, evident leftward asymmetry was more frequent in the patient group (patients 31.6%, controls 2.7%). The combination of CSF space enlargement and the pattern of Sylvian CSF asymmetry predicted the patient condition with 62.2% specificity and 82.5% sensitivity. We conclude that, in the context of a broad severity spectrum of imaging alterations in severe melancholic depression, asymmetrical CSF space enlargement may be evident in the Sylvian fissure region.
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PMID:CSF spaces of the Sylvian fissure region in severe melancholic depression. 1177 78

Multifocal motor neuropathy with persistent conduction blocks was firstly reported in 1986 and outlined from the group of purely motor diseases of the peripheral nervous system. The main criterion is the presence of conduction blocks located only on the motor nerves; additionally 30 percent of patients have IgM subclass serum antibodies directed against GM1 ganglioside. The clinical picture is a multifocal, asymmetrical, neuropathy, starting and predominant in the upper limbs, occurring in males aged 50 years and more, and having a progressive course. There is no biological sign besides elevated anti-GM1 antibodies. CSF analysis discloses mild increased protein count. The course is unpredictable, the neuropathy may be strictly limited to one or two motor nerves, or spread to other motor nerves in the four limbs. There is no involvement of the sensory and the cranial nerves, no involvement of the autonomic and the central nervous system. The pathophysiology is unknown, animal models do not allow to confirm the role of humoral immunity, and the role of anti-GM1 antibodies is controversial. Randomized controlled trials have assessed the efficacy of intravenous immunoglobulins which dramatically improve strength in 70-80 percent of patients in the short term, but remain unable to prevent motor deterioration in most patients, together with the occurrence of new conduction blocks. Corticosteroids and plasma exchanges do not improve the patients and may be followed by transient worsening. Long-term efficacy of immunosuppressive agents is not known.
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PMID:[Multifocal motor neuropathy with persistent conduction blocks: 18 years on]. 1549 15

We report the first case of an autoimmune thyroid encephalopathy presenting with multifocal motor status epilepticus. A 37-year-old female patient was admitted with multifocal motor seizures intractable to intravenous status epilepticus treatments, asymmetrical quadriparesis, truncal ataxia and continuous semi-rhythmical jerks. Pathological signal alterations were detected in both precentral cortices in MRI examination. Autoimmune thyroiditis was diagnosed after radiological examinations of the thyroid gland and thyroid function tests. Seizures promptly ceased following intravenous steroid treatment. Immunohistochemistry studies showed mild to moderate neuronal staining with the plasma and CSF samples. Remarkably, autoimmune thyroiditis may present with migrating focal motor status epilepticus. We recommend anti-thyroid antibody screening for multifocal motor status epilepticus cases of unspecified cause.
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PMID:Autoimmune thyroid encephalopathy presenting with epilepsia partialis continua. 1692 5

The present cadaveric study, describes asymmetrical right cerebral hemisphere and anomalous posterior horn of the right lateral ventricle and discusses its clinical implications. The occipital lobe of right cerebral hemisphere extended more posteriorly as compared to the left and so did the posterior horn of the lateral ventricle, resulting in the thinning of the occipital cortex. Till now, the dimension and volumetric study of the lateral ventricles have been usually performed by MRI and CT scans. A gross anatomical study of such a case, is the rarest of its kind. The abnormal anatomy of the lateral ventricles may be of great academic interest regarding CSF circulation and also important for clinical, radiological and surgical interventions (Fig. 2, Ref 8). Full Text (Free, PDF) www.bmj.sk.
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PMID:Anatomical study of anomalous posterior horn of lateral ventricle of brain and its clinical significance. 1822 83

We report a case of a perinatally HIV-infected patient aged 9 years, who presented with right-sided hemiplegia. His initial CD4 T-cell was of 0.21% (4 cells/muL) and plasma HIV RNA virus of 185 976 copies/mL (log 5.27). Plasma and CSF samples were subsequently positive for JCV. Twelve days after the initiation of highly active antiretroviral therapy (HAART), the MRI showed progressive white matter lesions with asymmetrical deep and subcortical white matter lesions over the left frontotemporoparietal region and the right frontal lobe. Immune Reconstitution Inflammatory Syndrome (IRIS) was suspected, and the patient was treated with methylprednisolone. His clinical symptoms worsened and despite therapy the patient deteriorated.
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PMID:Progressive Multifocal Leukoencephalopathy in HIV-Infected Children: A Case Report and Literature Review. 2004 Oct 4

Severe immunogenic and other debilitating human disorders potentially induced by protein aggregates have brought this phenomenon into the focus of biopharmaceutical science over the past decade. Depending on its driving forces, the process induced in the model protein rHuG-CSF may be either reversible or irreversible, resulting in the assembly of self-associated protein species or irreversible aggregates of various final morphologies. The aim of our work was to investigate the correlation between irreversible and reversible aggregation and the protective effect of non-specific formulation stabilisers, selected from the group of carbohydrates and polyols including trehalose, xylitol, cellobiitol, turanose, cellobiose, leucrose, lactitol, lyxose, and sorbitol, against both irreversible protein aggregation and reversible self-association processes of the rHuG-CSF. The formation of irreversible aggregates was thermally induced and evaluated using differential scanning calorimetry and size-exclusion chromatography. As opposed to the irreversible aggregation process, the process of self-association was induced by the agitation experiment by directly augmenting the protein solution contact surfaces. Absence of statistical connectivity between different stabilisers' ability to inhibit self-association or aggregation reactions indicates that these are two distinct physicochemical processes with different formulation stabilizing outcomes. Reaction mechanism of thermally induced aggregation observed in the study was in line with published literature data, while the reaction mechanism for self-association process was postulated. The postulate has been verified experimentally by isothermal calorimetry and agitation set of experiments conducted after size-exclusion chromatography and asymmetrical flow field-flow fractionation separation of monomeric, dimeric, trimeric, oligomeric, and large self-associated forms detected on multi-angle light scattering, fluorescence, UV, and refractive index detectors. Besides defining the mechanism and kinetic of self-association in stabilized rHuG-CSF formulations, special attention was also paid to the shifts and ranks of the free energy of the aggregation or self-association transition states.
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PMID:Differences between reversible (self-association) and irreversible aggregation of rHuG-CSF in carbohydrate and polyol formulations. 2085 8

Tuberculum sellae meningiomas frequently extend into the optic canals. Radical tumor resection including the involved dural attachment, underlying hyperostotic bone, and intracanalicular tumor in the optic canal offers the best chance of a Simpson Grade I resection to minimize recurrence. Decompression of the optic canal with removal of the intracanalicular tumor also improves visual outcome since this portion of the tumor is usually the cause of asymmetrical visual loss. The purely endoscopic endonasal extended transsphenoidal approach offers a direct midline trajectory and immediate access to tuberculum sellae meningiomas without brain retraction and manipulation of neurovascular structures. Although the endoscopic approach has been previously criticized for its inability to remove tumor within the optic canals, complete Simpson Grade I tumor removal including intracanalicular tumor, dural attachment, and involved hyperostotic bone can be achieved in properly selected patients. Excellent visualization of the suprasellar region and the inferomedial aspects of both optic canals allows for extracapsular, extraarachnoid dissection of the tumor from the critical structures using bimanual microsurgical dissection. In this report, the authors describe the operative nuances for removal of tuberculum sellae meningiomas with optic canal involvement using a purely endoscopic endonasal extended transsphenoidal (transplanum transtuberculum) approach. They specifically highlight the technique for endonasal bilateral optic nerve decompression and removal of intracanalicular tumor to improve postoperative visual function, as demonstrated in 2 illustrative cases. Special attention is also given to cranial base reconstruction to prevent CSF leakage using the vascularized pedicled nasoseptal flap.
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PMID:Surgical nuances for removal of tuberculum sellae meningiomas with optic canal involvement using the endoscopic endonasal extended transsphenoidal transplanum transtuberculum approach. 2152 73


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