bluuebunny/crossref_metadata_2025_split huggingface dataset:
The basis of intra‐blood‐brain‐barrier IgG synthesis
Authors: Tourtellotte Wallace W. , Staugaitis Susan M. , Walsh Michael J. , Shapshak Paul , Baumhefner Robert W. , Potvin Alfred R. , Syndulko Karl 
Published: January 2005

AbstractWe hold that the intra‐blood‐brain‐barrier (BBB) IgG synthesis (SYN) rate can be quantitated reliable and validly. Although several formulas distinguish patients with sclerosis from normal controls equally well, only the SYN rate formula has been validated in humans using isotopic tradcer techniques. Our formula for the IgG SYN rate is reducible to Reiber's formula; therefore, both can be used to quantify the IgG SYN rate in a manner not possible using the IgG index. Although our SYN rate formula has been validated for a modest range of BBB abnormalities (cerebrospinal fluid/serum albumin ratios), there is evidence to suggest that it may be used even in patients having severe BBB damage. We question the acceptance of unique cerebrospinal fluid IgG bands as indisputable evidence of intra‐BBB IgG SYN in the presence of a modest to severely damaged BBB. Finally, the utility of quantitation and detection of intra‐BBB IgG SYN by standardized methods in a group of asymptomatic, normal individuals compared with a group of patients with clinical definite multiple sclerosis is presented.
Clinical and experimental neurotoxicity of 2‐t‐butylazo‐2‐hydroxy‐5‐methylhexane
Authors: Spencer Peter S. , Beaubernard Christan M. , Bischoff‐Fenton Monica C. , Kurt Thomas L. 
Published: January 2005

AbstractSeven workers developed weight loss, sensorimotor neuropathy, visual dysfunction, impaired mentation, and emotional lability shortly after the introduction of a new synthetic catalyst in a plant manufacturing reinfoced bathtubs. The newly introduced catalyst, 2‐t‐butylazo‐2‐hydroxy‐5‐methylhexane, is shown to produce a similar syndrome in rats. Axonal degenration of optic nerves, ascending and descending spinal tracts, and peripheral nerves appears to underlie this syndrome.
High‐resolution computed tomography in multiple sclerosis
Authors: Barrett Lynn , Drayer Burton , Shin Chelsu 
Published: January 2005

AbstractEighty‐five patients were classified as having definite (n = 34), probable (n = 18), or possible (n = 33) multiple sclerosis using the criterial of Poser. Each Patient had an enhanced computed tomographic examination, and most had cerebrospinal fluid and evoked response studies at the same time. Abnormalities including focal decreased brain density, abnormal enhancement, and cerebrospinal fluid space enlargement were found in 62% of patients (85% of those with definite, 39% of those with probable, and 52% of those with possible multiple sclerosis), and abnormal enhancing areas were demonstrated in 29% (44% of those with definite, 17% of those with probable, and 21% of those with possible disease). In the subgroup of patients with definite multiple sclerosis and recent clinical exacerbation (within the prior 8 weeks), abnormal enhancement was present in 89%. There was a strong correlation between clinical exacerbation and abnormal contrast enchancement. Cerebrospinal fluid studies (IgG, white blood cell count, total protein) had no correlation with exacerbation or abnormal enhancement. Maps of low‐density and enhancing areas were similar to those previously described in postmortem studies. Computed tomography thus provides an in vivo, objective, and anatomically specific map of the brain parenchyma and the integrity of the blood‐brain barrier that is useful in research studies evaluating the treatment of multiple sclerosis. It is also useful in patients in whom the diagnosis of multiple sclerosis is suspected but not certain on the basis of clinical and laboratory evaluation.
The nucleus basalis of Meynert in neurological disease: A quantitative morphological study
Authors: Rogers John D. , Brogan Donna , Mirra Suzanne S. 
Published: January 2005

AbstractThe recent finding of neuronal degeneration in the nucleus basalis of Meynert (nbM) in Alzheimer's disease suggests a possible role of this nucleus and the cholinergic system in dementing illness. We assessed neuronal population and density in two anatomical levels of the nbM in 38 coded brains from patients with a broad variety of neurological disorders. We found the most striking nbM degeneration in Alzheimer's and Parkinson's diseases. An intermediate loss of neurons was noted in the transmissible dementia Creutzfeldt‐Jakob disease and in progressive supranuclear palsy. The usually nondementing diseases amyotrophic lateral sclerosis and multiple sclerosis showed cell counts comparable to those in a control group of nondemented patients with cerebrovascular disease. Characteristic neuropathological changes of Alzheimer's, Parkinson's, and Creutzfeldt‐Jakob diseases, progressive supranuclear palsy, and subacute sclerosing panencephalitis were also found in the nbM. Most previous studies of the nbM have been based on small numbers of cases compared with controls. In our large series we used consistent methodology and a multiple‐comparison statstical procedure to avoid overreporting of statistical significance. Our comparison of the nbM not only confirms the marked degeneration of the nbM in Alzheimer's disease, but also places such degeneration into perspective in a spectrum of dementing and nondementing neurological diseases. Larger case studies, using appropriate statistical techniques for multiple group comparisons, are needed to establish the significance of nbM degeneration in neurological disease.
Positron emmission tomography in the asphyxiated term newborn: Parasagittal impairment of cerebral blood flow
Authors: Volpe Joseph J. , Herscovitch Peter , Perlman Jeffrey M. , Kreusser Katherine L. , Raichle Marcus E. 
Published: January 2005

AbstractHypoxic‐ischemic encephalopathy secondary to perinatal asphyxia in the term newborn is the most common recognized cause of the subsequent motor deficits often grouped under the rubric “cerebral palsy.” In order to provide insight into the basic nature and pathogenesis of the brain injury in such infants, we studied regional cerebral blood flow (CBF) by positron emission tomography (PET) in 17 asphyxiated term infants during the acute period of illness. A consistent and apparently unifying abnormality was observed, namely, a relative decrease in CBF to parasagittal regions, generally symmetrical and more marked posteriorly than anteriorly. Thus, parasagittal values for CBF were generally 25 to 50% lower than those for the sylvian cortex; in the normal or near normal infant, parasagittal values are only approxmately 10% lower than those for the sylvian cortex. (Additional normal findings for regional CBF were 50% higher flows to the cerebral cortex than to the cerebral white matter and flows to the basal ganglia and thalamus at least as high as those to the cerebral cortex.) That the relative deficit in CBF to parasagittal regions reflects tissue injury was indicated by the close topographic correlation on technetium brain scans in 3 patients of increased tissue uptake of radionuclide and the CBF abnormality. Moreover, the single patient studied at postmortem examination exhibited parasagittal ischemic cerebral injury that correlated well with the PET abnormaility of regional CBF.The topography of the PET abnormality, i.e., the cerebrovascular watershed regions, suggests that the brain injury is basically ischemic and that the pathogenesis relates to impaired cerebral perfusion, perhaps secondary to systemic hypotension occurring in association with the perinatal asphyxia. Experimental data support this formulation.
Atypical Alzheimer's disease with spastic paresis and ataxia
Authors: Aikawa Hisashi , Suzuki Kinuko , Iwasaki Yuzo , Iizuka Reiji 
Published: January 2005

AbstractAn unsusal case of Alzheimer's disease (AD) is reproted. The patient was a 33‐year old Japanese housewife who had progressive dementia, severe spasticity, and mild ataxial for six years. Postmortem emamination revealed severe changes of AD and degeneration of the corticspinal tracts, as well as neuritic plaques and plaquelike degeneration in the cerebellum. This appears to be the twelfth reported case of AD with spasticity and ataxia.
Electroencephalographic recording from the temporal lobes: A comparison of ear, anterior temporal, and nasopharyngeal electrodes
Authors: Sperling Michael R. , Engel Jerome 
Published: January 2005

AbstractA prospective study was performed to evaluate the usefulness of ear, anterior temporal, and nasopharyngeal electrodes for recognizing temporal lobe epileptic electroencephalographic (EFG) foci. One handred and three EFGs were performed on patients suspected of having epilepsy who had a previous normal record. Nasopharyngeal electrodes were simultaneously sompared with ear and anterior temporal electrodes to determine their relative abilities to detect pathological epileptiform transients from the temporal region. Epeliptic discharges were detected in 22% of the recordings. Pathological discharges seen in nasopharyngeal electrode derivations invariably were seen in ear and anterior temporal electrode derivations using carefully designed montages, and EEG diagnosis was not altered by use of nasopharyngeal electrode. We conclude that EEG recording with ear and anterior temporal electrodes is sufficient to detect pathological temporal epileptiform transients, and that the use of nasopharyngeal electrodes as a routine procedure offers no added benefit.
Ganglioside patterns in amyotrophic lateral sclerosis brain regions
Authors: Rapport Maurice M. , Donnenfeld Hyman , Brunner William , Hungund Basalingappa , Bartfeld Harry 
Published: January 2005

AbstractIn a search for evidence of biochemical disorders in regions of postmortem brain other than the motor cortex in amyotrophic lateral sclerosis (ALS), ganglioside patterns were also examined in the frontal, temporal, and parahippocampal gyrus cortex. In 21 ALS brains studied (20 sporadic, 1 familial), abnormal patterns were found in the frontal cortex (81%), temporal cortex (75%), motor cortex (70%), and parahippocampal gyrus cortex (71%). Patterns were established by measuring the percentage distribution of 12 ganglioside species. Two abnormal patterns were detected. One was based on low proportions of GD1b, GT1b, and GQ1b associated with high proportions of GM2 and GD3 (GM1, GD1a, GD2, and GT1a values were normal). The second abnormality was the appearance of Gx. Neither abnormality was seen in the 13 non‐ALS control brains. The first, and predominant, abnormality was found in the frontal cortex in 14 brains, and the second was observed in 13 brains; 10 brains showed both abnormalities. These findings thus constitute evidence that the disease process in ALS extends beyond the motor cortex and involves neurons in several brain areas.
Localization of lead in rat peripheral nerve by electron microscopy
Authors: Windebank Anthony J. , Dyck Peter James 
Published: January 2005

AbstractLead intoxication in rats reliably produces segmental demyelination. Following a single intravenous injection of radioactive lead, localization of tracer was observed sequentially by quantitative electron microscopical autoradiog‐raphy. The animals injected had been on a lead‐containing diet for 70 days; as a result, the blood‐nerve barrier was broken down and demyelination was proceeding. Six hours after a single dose, the lead was localized to the endoneurial space of the peroneal nerve, and 72 hours later, to the myelin membrane. Lead may exert a direct effect on the membrane and alter its stability both by altering the lipid content of the membrane and by directly interfering with the lamellar structure.
Heterogeneity of human skeletal muscle tropomyosin
Authors: Giometti Carol S. , Danon Moris J. 
Published: January 2005

AbstractSix polypeptides resolved by two‐dimensional electrophoresis of homogenates from human skeletal muscle have been identified as tropomyosin by electrophoretic and immunochemical methods. The 6 proteins are consistently present in approximately the same abundance in normal biceps, deltoid, gastrocnemius, and quadriceps muscle. Analysis of samples from individuals with Becker's dystrophy, Duchenne dystrophy, limb girdle dystrophy, polymyositis, myopathy related to vitamin E deficiency, type II fiber deficiency, and from an infant with indistinct fiber type differentiation, however, showed quantitative variations in the tropomyosin pattern. Muscle with histochemically demonstrated type II fiber deficiency lacked two of the normal tropomyosin proteins and the type II myosin light chains. Muscles lacking type I myosin light chains were deficient in a different pair of tropomyosin proteins. The results suggest that normal human skeletal muscle contains one major type of tropomyosin protein (β‐tropomyosin) common to both fast and slow fibers, together with two other major proteins (α‐tropomyosin and α′‐tropomyosin), one of which is specific to fast fibers and the other to slow fibers. Preliminary data from the reaction of muscle homogenates with alkaline phosphatase indicate that 3 of the 6 tropomyosin polypeptides resolved by two‐dimensional electrophoresis are phosphorylated forms of the α‐, α′‐, and β‐tropomyosins.
Cardiac dysfunction during status epilepticus in the neonatal pig
Authors: Young Richard S. K. , Fripp Raymond R. , Yagel Susan K. , Werner John C. , McGrath Glenn , Schuler H. Gregg 
Published: January 2005

AbstractCardiovascular complications frequently occur during status epilepticus. To determine the changes in systemic and pulmonary arterial pressure, cardiops output, and left ventricular contractility during seizures, 1‐week‐old pigs were intubated, paralyzed, mechanicall
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entilated, and catheterized with a Swan‐Ganz catheter. Seizures were induced with intravenous bicuculline. Eariy changes consisted of significant systemic and pulmonary arterial hypertension. After 2 hours of seizures, the animals developed progressive systemic hypotension and decreased cardiac output. M‐mode echocardiography disclosed a decrease in left ventricular contractility. Cardiac tissue frozen in situ showed a significant increase in lactate and reductions in glucose, triglyceride, and adenosine triphosphate levels. Prolonged seizures in the neonatal pig result in cardiac dysfunction, which may play a role in the development of epileptic brain damage.
Azathioprine and steroids are not more effective in decreasing multiple sclerosis intra–blood‐brain‐barrier IgG synthesis than steroids alone
Authors: Staugaitis Susan M. , Shapshak Paul , Myers Lawrence W. , Ellison George W. , Tourtellotte Wallace W. , Lee Mike 
Published: January 2005

AbstractIntra–blood‐brain‐barrier IgG synthesis rates and oligoclonal IgG banding patterns were examined in 9 patients with multiple sclerosis who were treated with azathioprine and steroids for 2 to 4.5 years. The IgG synthesis rates of 5 patients were significantly decreased from the pretreatment mean values 1 month after treatment, and their synthesis rates remained at the decreased levels throughout treatment. However, among the remaining 4 patients, the rates exceeded the pretreatment means. This continuous suppressive effect of the combined azathioprine and steroids upon the IgG synthesis rate was similar to that of steroids, suggesting that azathioprine and steroids in combination were not more effective in reducing intra–blood‐brain‐barrier IgG synthesis than steroids alone. Oligoclonal IgG patterns in all cerebrospinal fluid samples were not significantly altered during the study.
Serial immunological studies in multiple sclerosis patients treated systemically with human alpha interferon
Authors: Panitch Hillel S. , Francis Gordon S. , Hooper Carol J. , Merigan Thomas C. , Johnson Kenneth P. 
Published: January 2005

AbstractA battery of immunological functions was studied over a 2‐year period in conjunction with a placebo‐controlled trial of natural human alpha interferon in patients with multiple sclerosis. IgG synthesis was increased both systemically and intrathecally by administration of interferon; however, there were only minor changes in cerebrospinal fluid oligoclonal bands. Levels of helper and suppressor T lymphocytes fluctuated independently of clinical exacerbations, although mean helper/suppressor ratios were higher in multiple sclerosis patients than in controls and increased further during interferon treatment. Cerebrospinal fluid myelin basic protein and antibodies to basic protein were not affected by exacerbations or by interferon administration. Circulating IgG antibodies induced by interferon treatment appeared to be directed at a non‐interferon contaminant of the preparation. None of the assays was a consistent indicator of disease activity or of clinical response to interferon.
Immunological complications in multiple sclerosis patients receiving interferon
Authors: Rice G. P. A. , Woelfel E. L. , Talbot P. J. , Braheny S. L. , Sipe J. C. , Knobler R. L. , Merigan T. C. , Oldstone M. B. A. 
Published: January 2005

AbstractIn a prospective, placebo‐controlled study designed to test the efficacy of human alpha interferon (1FN) in the treatment of multiple sclerosis, we monitored several immunological functions. Interferon was shown to have many effects on the immune system, including activation of natural killer cells in vivo and elevation of serum immunoglobulin and cerebrospinal fluid IgG ratios. Furthermore, all patients who received IFN developed antibody titers to a protein contaminant (molecular weight, 27 kilodaltons) in the IFN preparation. This antibody was associated with an elevation in serum concentrations of Clq‐ and Raji‐binding immune complexes in 6 of 12 patients. Some of these 12 patients developed symptoms suggestive of immune complex disease. IFN had pronounced effects on the immune system of these patients.
A derivative of myelin‐associated glycoprotein in cerebrospinal fluid of normal subjects and patients with neurological disease
Authors: Yanagisawa Katsuhiko , Quarles Richard H. , Johnson David , Brady Roscoe O. , Whitaker John N. 
Published: January 2005

AbstractA procedure for quantitating the myelin‐associated glycoproiein (MAG) in cerebrospinal fluid (CSF) was developed. The procedure involved immunoprecipitation with rabbit polyclonal anti‐MAG antiserum followed by immune staining of electroblots with the monoclonal antibody HNK‐1. This method could detect as little as 2 ng of MAG per ml of CSF and could accurately measure levels of 5 ng/ml or greater. No intact MAG was detected in any of the CSF samples examined, but all samples contained the 90K dalton proteolytic derivative of MAG called dMAG. Samples from normal volunteers and patients with demyelinating diseases contained levels of dMAG ranging from 2 to 13 ng/ml. There was no correlation of dMAG levels with levels of myelin basic protein or with active demyelinating disease. The relatively high levels of dMAG, even in control CSF samples, probably resulted from normal physiological turnover of MAG and could possibly obscure any additional increments of MAG or dMAG release that might occur as a result of demyelination.
Neurogenic flare responses following topical application of capsaicin in humans
Authors: Helme R. D. , McKernan S. 
Published: January 2005

AbstractThe flare response to noxious stimulation of the skin is mediated by polymodal nociceptors of C fiber primary afferent nerves. Topical application of capsaicin initiates a flare response and burning pain. In this study, the variability of capsaicin‐induced flare and pain was assessed in 220 subjects. The major factors in flare response are body site and age; more severe reactions occur in more proximal sites and in younger subjects. Larger flares were shown to be associated with greater pain. Variability is probably due to differences in the structure and reactivity of the neurovascular unit as proposed in the Lewis model of the axon reflex. It may prove possible to assess polymodal nociceptor function using topical capsaicin in disease states that affect the peripheral terminals of primary afferent nerves.
The effect of carbidopa on the pharmacokinetics of intravenously administered levodopa: The mechanism of action in the treatment of parkinsonism
Authors: Nutt John G. , Woodward William R. , Anderson John L. 
Published: January 2005

AbstractThe pharmacokinetics of short and long intravenous infusions of levodopa with and without concurrent oral administration of carbidopa was studied in 9 parkinsonian patients. Carbidopa reduced by 50% both the infusion rate required to produce a clinical response and the time required for plasma clearance of levodopa. Using this value for clearance, it is estimated that carbidopa doubles the bioavailability of orally administered levodopa. Carbidopa did not alter the therapeutically effective plasma concentration of levodopa, suggesting that carbidopa does not modify the so‐called enzymatic blood‐brain barrier. The decline of the plasma levodopa concentration was biphasic; carbidopa modestly increased half‐lives of both phases. The apparent volume of distribution was not significantly altered. Carbidopa did not change the duration of the clinical response after the discontinuation of short infusions. From these observations we infer that the therapeutic effects of carbidopa can be attributed to doubling the bioavailability of orally administered levodopa and halving its plasma clearance.
Neuropathy associated with experimental Chagas' disease
Authors: Said Gérard , Joskowicz Mireille , Barreira Amilton Antunes , Eisen Harvey 
Published: January 2005

AbstractMice were acutely and chronically infected with Trypanosoma cruzi and then examined histologically for the presence of lesions in the peripheral nervous system. In acutely infected animals, small lymphocytic and macrophagic infiltrates were found in the nerves in association with intracellular parasites. Little or no nerve damage was present at this stage. In chronically infected animals, large perivascular granulomatous infiltrates were found in association with multifocal, predominantly demyelinative lesions of neighboring nerve fibers. Similar inflammatory infiltrates were present in muscles and were frequently associated with vasculitis and destruction of muscle fibers. Our pathological findings and the negative results produced by intraneural injections of sera from chronically infected animals and the positive results following injections of small numbers of live trypanosomes suggest that the demyelination is not due to circulating serum factors such as antibodies cross‐reacting with peripheral myelin. Delayed‐type hypersensitivity may be induced by the presence of the parasites, a notion supported by the development of granulomas in naive mice injected intravenously with helper T cells from chronically infected animals.
Thyrotropin‐releasing hormone enhances motor neuron–evoked contractions of cultured human muscle
Authors: Askanas Valerie , Engel W. King , Kobayashi Takayoshi 
Published: January 2005

AbstractThyrotropin‐releasing hormone (TRH), 1 to 2.7 mM, introduced to the medium of monolayer‐cultured human muscle innervated by cocultured fetal rat spinal cord with dorsal root ganglia, increased muscle fiber contractions 4.9 times (p < 0.005). Doses higher than 5 mM, after increasing contractions for a few seconds, caused complete inhibition of contraction (autorefractoriness). Neither aneurally cultured human muscle nor innervated cultured human muscle blocked by 1 mM d‐tubocurarine was excited by TRH. Thus, in this system TRH appeared to excite muscle contractions through direct or indirect action on motor neurons.