bluuebunny/crossref_metadata_2025_split huggingface dataset:
Fibrin‐modifying serine proteases thrombin, tPA, and plasmin in ischemic stroke: A review
Authors: Sheehan John J. , Tsirka Stella E. 
Published: April 2005

AbstractIschemic stroke is a sudden loss of circulation to a portion of the brain that results in a loss of neurologic function. Many ischemic strokes are embolic. They result from a thrombus traveling into the central circulation and occluding a blood vessel. Treatment of ischemic stroke with recombinant tissue plasminogen activator (tPA) can improve patient outcomes. However, tPA must be used during a specific time window after the stroke onset to be effective and it risks converting an ischemic stroke into a hemorrhagic one. We explore the basic effects of fibrin‐modifying proteases on neurons, astrocytes, and microglia during ischemia. tPA, thrombin, and plasmin can initiate microglial activation and change both neuronal and astrocytic survival. As a result of these functions and of their role in blood homeostasis, all three of these proteases have profound effects on neurons and glial cells in the brain and are capable of altering the development and severity of ischemic stroke. © 2005 Wiley‐Liss, Inc.
Astrocytic contributions to bioenergetics of cerebral ischemia
Authors: Dienel Gerald A. , Hertz Leif 
Published: April 2005

AbstractAstrocytes are multifunctional cells that interact with neurons and other astrocytes in signaling and metabolic functions, and their resistance to pathophysiological conditions can help restrict loss of tissue after an ischemic event provided adequate nutrients are supplied to support their requirements. Astrocytes have substantial oxidative capacity and mechanisms to upregulate glycolytic capability when respiration is impaired. An astrocytic enzyme that synthesizes a powerful activator of glycolysis is not present in neurons, endowing astrocytes with the ability to sustain ATP production under restrictive conditions. The monocarboxylic acid transporter (MCT) isoforms predominating in astrocytes are optimized to facilitate very large increases in lactate flux as lactate concentration increases within (1–3 mM) and above (>3 mM) the normal range. In sharp contrast, the major neuronal MCT serves as a barrier to increased transmembrane transport as lactate rises above 1 mM, restricting both entry and efflux. Lactate can serve as fuel during recovery from ischemia but direct evidence that lactate is oxidized by neurons (vs. astrocytes) to maintain synaptic function is lacking. Astrocytes have critical roles in regulation of ionic homeostasis and control of extracellular glutamate levels, and spreading depression associated with ischemia places high demands on energy supplies in astrocytes and contributes to metabolic exhaustion and demise. Disruption of Ca2+homeostasis, generation of oxygen free radicals and nitric oxide, and mitochondrial depolarization contribute to astrocyte death during and after a metabolic insult. Novel pharmaceutical agents targeted to astrocytes and hyperoxic therapy that restores penumbral oxygen level during energy failure might improve postischemic outcome. © 2005 Wiley‐Liss, Inc.
Ischemia‐induced programmed cell death in astrocytes
Authors: Giffard Rona G. , Swanson Raymond A. 
Published: April 2005

AbstractAstrocytes are essential for neuronal survival and function, neurogenesis, and neural repair. Although astrocytes are more resistant than neurons to most stress conditions in vitro, certain astrocyte subtypes, such as the glial fibrillary acidic protein (GFAP)‐negative protoplasmic astrocytes that predominate in gray matter structures, may be equally or more sensitive than neurons to ischemia in vivo. Programmed cell death differs from passive, necrotic death in that cell constituents actively participate in cell demise. Like neurons, astrocytes undergo programmed cell death during normal development. Cell culture studies have shown that astrocytes can be induced to undergo apoptosis and other forms of programmed cell death by many factors relevant to ischemia, including acidosis, oxidative stress, substrate deprivation, and cytokines. Animal models of cerebral ischemia have confirmed nuclear condensation and upregulation of Bax and caspases in a subset of astrocytes exposed to ischemia, especially in immature brain. A causal role for these events in astrocyte death is supported by improved astrocyte survival after inhibition of caspase‐dependent cell death pathways. Astrocyte survival is also improved by blocking the poly(ADP‐ribose)‐1 cell death pathway. Markers of programmed cell death are generally less evident and less widespread in astrocytes than in neighboring neurons. However, most studies to date have relied only on markers of classical apoptosis. In addition, these studies have relied almost exclusively on GFAP to identify astrocytes. Since most protoplasmic astrocytes are poorly immunoreactive for GFAP, the extent of ischemia‐induced programmed cell death in this cell type remains uncertain. © 2005 Wiley‐Liss, Inc.
Astrocytic swelling in cerebral ischemia as a possible cause of injury and target for therapy
Authors: Kimelberg Harold K. 
Published: April 2005

AbstractIn this viewpoint article, I summarize data showing that the astrocytic swelling that occurs early after the acute CNS pathologies ischemia and traumatic brain injury is damaging. We have proposed that one reason may be the release of excitatory amino acids (EAA) via volume‐activated anion channels (VRACs) that are activated by such swelling. This release could be a target for therapy, which could involve blocking the astrocytic swelling or the release mechanisms. The transport mechanisms likely causing the early astrocytic swelling are therefore summarized. In terms of targeting the release mechanisms, we have found a potent inhibitor of VRACs, tamoxifen, to be strongly neuroprotective in focal ischemia with a therapeutic window of 3 h after initiation of the ischemia. The question, however, of whether neuroprotection by tamoxifen can be solely attributed to VRAC inhibition in astrocytes has yet to be resolved. ©2005 Wiley‐Liss, Inc.
CD163‐positive perivascular macrophages in the human CNS express molecules for antigen recognition and presentation
Authors: Fabriek Babs O. , Van Haastert Elise S. , Galea Ian , Polfliet Machteld M.J. , Döpp Ed D. , Van Den Heuvel Michel M. , Van Den Berg Timo K. , De Groot Corline J.A. , Van Der Valk Paul , Dijkstra Christine D. 
Published: April 2005

AbstractPerivascular macrophages (PVM) constitute a subpopulation of resident macrophages in the central nervous system (CNS) that by virtue of their strategic location at the blood‐brain barrier potentially lend themselves to a variety of important functions in both health and disease. Functional evidence suggests that PVM play a supportive role during experimental autoimmune encephalomyelitis in rodents. However, the function of PVM in the human CNS remains poorly characterized. We first set out to investigate the validity of the antibody EDhu1, which recognizes human CD163, to specifically identify human PVM. Second, we wanted to gain insight into the function of PVM in antigen recognition and presentation and therefore we studied the expression of DC‐SIGN, mannose receptor, MHC class II, and several costimulatory molecules by PVM in the normal and inflamed human CNS (multiple sclerosis (MS) brain lesions). Conventional immunohistochemistry and double‐labeled immunofluorescence techniques were used. We show that CD163 specifically reveals PVM in the normal human CNS. In MS lesions, CD163 staining reveals expression on foamy macrophages and microglia, besides an upregulation of the amount of PVM stained. In contrast, mannose receptor expression is restricted to PVM in both normal and inflamed brain tissue. Furthermore, we show that a subpopulation of PVM in the human brain express several molecules involved in antigen recognition, presentation, and costimulation. Therefore PVM, which occupy a strategic location at the BBB, are equipped to recognize antigen and present it to T cells, supporting a role in the regulation of perivascular inflammation in the human CNS. © 2005 Wiley‐Liss, Inc.
Meta‐analysis of functional imaging data using replicator dynamics
Authors: Neumann Jane , Lohmann Gabriele , Derrfuss Jan , von Cramon D. Yves 
Published: April 2005

AbstractDespite the rapidly growing number of meta‐analyses in functional neuroimaging, the field lacks formal mathematical tools for the quantitative and qualitative evaluation of meta‐analytic data. We propose to use replicator dynamics in the meta‐analysis of functional imaging data to address an important aspect of neuroimaging research, the search for functional networks of cortical areas that underlie a specific cognitive task. The replicator process requires as input only a list of activation locations, and it results in a network of locations that jointly show significant activation in most studies included in the meta‐analysis. These locations are likely to play a critical role in solving the investigated cognitive task. Our method was applied to a meta‐analysis of the Stroop interference task using data provided by the publicly accessible database BrainMap DBJ. Hum Brain Mapp 25:165–173, 2005. © 2005 Wiley‐Liss, Inc.
Beyond hypofrontality: A quantitative meta‐analysis of functional neuroimaging studies of working memory in schizophrenia
Authors: Glahn David C. , Ragland J. Daniel , Abramoff Adir , Barrett Jennifer , Laird Angela R. , Bearden Carrie E. , Velligan Dawn I. 
Published: April 2005

AbstractAlthough there is considerable evidence that patients with schizophrenia fail to activate the dorsolateral prefrontal cortex (DLPFC) to the degree seen in normal comparison subjects when performing working memory or executive tasks, hypofrontality may be coupled with relatively increased activity in other brain regions. However, most imaging studies of working memory in schizophrenia have focused on DLPFC activity. The goal of this work is to review functional neuroimaging studies that contrasted patients with schizophrenia and healthy comparison subjects during a prototypical working memory task, the n‐back paradigm, to highlight areas of hyper‐ and hypoactivation in schizophrenia. We utilize a quantitative meta‐analysis method to review 12 imaging studies where patients with schizophrenia were contrasted with healthy comparison subjects while performing the n‐back paradigm. Although we find clear support for hypofrontality, we also document consistently increased activation in anterior cingulate and left frontal pole regions in patients with schizophrenia compared to that in controls. These data suggest that whereas reduced DLPFC activation is reported consistently in patients with schizophrenia relative to healthy subjects, abnormal activation patterns are not restricted to this region, raising questions as to whether the pathophysiological dysfunction in schizophrenia is specific to the DLPFC and about the relationship between impaired performance and aberrant activation patterns. The complex pattern of hyper‐ and hypoactivation consistently found across studies implies that rather than focusing on DLPFC dysregulation, researchers should consider the entire network of regions involved in a given task when making inferences about the biological mechanisms of schizophrenia. Hum Brain Mapp 25:60–69, 2005. © 2005 Wiley‐Liss, Inc.
A review of pervaporation for product recovery from biomass fermentation processes
Authors: Vane Leland M 
Published: April 2005

AbstractAlthough several separation technologies are technically capable of removing volatile products from fermentation broths, distillation remains the dominant technology. This is especially true for the recovery of biofuels such as ethanol. In this paper, the status of an emerging membrane‐based technology, called pervaporation, for this application is reviewed. Several issues and research priorities which will impact the ability of pervaporation to be competitive for biofuel recovery from fermentation systems are identified and discussed. They include: increased energy efficiency; reduction of capital cost for pervaporation systems; longer term trials with actual fermentation broths; optimized integration of pervaporation with fermentor; synergy of performing both alcohol recovery and solvent dehydration by pervaporation with dephlegmation fractional condensation technology; and updated economic analyses of pervaporation at various biofuel production scales. Pervaporation is currently viable for biofuel recovery in a number of situations, but more widespread application will be possible when progress has been made on these issues. Published in 2005 for SCI by John Wiley & Sons, Ltd.
Involvement of Ca2+/calmodulin‐dependent protein kinase II in the modulation of indolamines in diabetic and hyperglycemic rats
Authors: Ramakrishnan R. , Prabhakaran K. , Jayakumar A.R. , Gunasekaran P. , Sheeladevi R. , Suthanthirarajan N. 
Published: April 2005

AbstractHyperglycemia and acidosis are the key factors in diabetic complications. It has been shown that acute or chronic diabetes alters serotonin levels in brain. However, the mechanism of hyperglycemia‐ or acidosis‐induced changes in serotonin levels remains poorly understood. Because Ca2+‐dependent protein kinases play a major role in the regulation of serotonin synthesis and release, we investigated the effect of diabetes, hyperglycemia, and acidosis on the level of indolamines [5‐hydroxytryptamine (5‐HT) and/or 5‐hydroxyindoleacetic acid (5‐HIAA)] and Ca(2+)/calmodulin‐dependent protein kinase II (CaMKII) enzyme activity or protein expression in different brain regions. Alloxan‐induced (45 mg/kg bw) diabetic rats (30 days) showed increased level of 5‐HT in striatum (ST; 183%), midbrain (MB; 199%), pons medulla (PM; 151%), cerebellum (CB; 214%), and cerebral cortex (CCX; 162%) compared with control (P < 0.05), and these changes were reversed after insulin administration. Rats treated with glucose (500 mg/kg bw) for 30 days showed a 146%, 183%, 208%, and 177% (P < 0.05) increase in 5‐HT levels in ST, PM, CB, and CCX, respectively. 5‐HIAA level increased in hippocampus (HC; 172%) and in MB (145%; P < 0.05). In addition, rats treated with sodium acetoacetate (NaAcAc) for 30 days (60 mg/kg bw) showed significant increases (P < 0.05) of 5‐HT level in ST (152%) and MB (174%). However, the levels of 5‐HIAA increased only in MB (151%, P < 0.05). Rats treated with NH4Cl, which induced acidosis (150 mg/kg bw), showed an increased level of 5‐HT only in HC (165%, P < 0.05). The increased activity and protein expression of CaMKII in ST, MB, PM, CB, and CCX under diabetic conditions were correlated with the levels of indolamines changes during diabetic, hyperglycemic, or acidotic conditions. These results suggest that CaMKII may be involved in the regulation of indolamines in diabetic animals. © 2005 Wiley‐Liss, Inc.
Low‐Density Polyethylene (LDPE) Surface With a Wettability Gradient by Tuning its Microstructures
Authors: Lu Xiaoying , Zhang Jilin , Zhang Changchun , Han Yanchun 
Published: April 2005

AbstractSummary: We describe an interesting approach to the fabrication of wettability gradients from hydrophobicity to superhydrophobicity in low‐density polyethylene (LDPE) films by first forming high porosity surfaces and placing the specimens onto linear temperature gradients. While the polymer chosen for the study is non‐polar, its microporous layer provides sufficient superhydrophobicity. Lateral gradient heating of the layer results in partial melting of the polymer and correspondingly decreases porosity thus decreasing hydrophobicity.
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Hairy PEO‐Silica Nanoparticles through Surface‐Initiated Polymerization of Ethylene Oxide
Authors: Joubert Mathieu , Delaite Christelle , Bourgeat‐Lami Elodie , Dumas Philippe 
Published: April 2005

AbstractSummary: The grafting of poly(ethylene oxide) (PEO) onto silica nanoparticles was performed in situ by the ring‐opening polymerization of the oxirane monomer initiated from the mineral surface using aluminium isopropoxide as an initiator/heterogeneous catalyst. Alcohol groups were first introduced onto silica by reacting the surfacic silanols with prehydrolyzed 3‐glycidoxypropyl trimethoxysilane. The alcohol‐grafted silica played the role of a coinitiator/chain‐transfer agent in the polymerization reaction and enabled the formation of irreversibly bonded polymer chains. Silica nanoparticles containing up to 40 wt.‐% of a hairy layer of grafted PEO chains were successfully produced by this technique.The grafting of poly(ethylene oxide) (PEO) onto silica nanoparticles by in‐situ ring‐opening polymerization of the oxirane monomer.magnified imageThe grafting of poly(ethylene oxide) (PEO) onto silica nanoparticles by in‐situ ring‐opening polymerization of the oxirane monomer.
Polypeptide‐Shelled Poly(propylene imine) Dendrimers and Their Complexing Properties towards Copper(II) Ions
Authors: Appelhans Dietmar , Komber Hartmut , Kirchner Ralf , Seidel Jürgen , Huang Chih‐Feng , Voigt Dieter , Kuckling Dirk , Chang Feng‐Chih , Voit Brigitte 
Published: April 2005

AbstractSummary: Polypeptide‐shelled poly(propylene imine) dendrimers were realized by ring‐opening polymerization of α‐amino acid N‐carboxyanhydrides, initiated by dendrimers as core molecules. Polypeptides with 2nd generation core were used as model compounds to investigate interior complexes between metal ion and surface‐modified dendrimers. Micro‐calorimetric measurements outlined the formation of approximate 1:1 complexes between CuII and polypeptide‐shelled dendrimers and the influence of polypeptide chain compositions on differential molar heats of complexation.Composition of one of the polypeptides synthesized.magnified imageComposition of one of the polypeptides synthesized.
Determination of the Vapor Density of Triacetone Triperoxide (TATP) Using a Gas Chromatography Headspace Technique
Authors: Oxley Jimmie C. , Smith James L. , Shinde Kajal , Moran Jesse 
Published: April 2005

AbstractUsing a GC headspace measurement technique, the vapor pressure of TATP was determined over the temperature range 12 to 60 °C. As a check on the experimental method, TNT vapor pressure was likewise computed. Values for TNT are in excellent agreement with previous published ones. For TATP the vapor pressure was found to be ~ 7 Pa at ambient conditions. This value translates to a factor of 104 more molecules of TATP in air than TNT at room temperature. The dependence of TATP vapor pressure on temperature can be described by the equation log10P(Pa)=19.791−5708/T(K). Its heat of sublimation has been calculated as 109 kJ/mol.
Comprehensive evaluation of chip interleaving effect on turbo‐coded DS‐SS in a Rayleigh fading channel with antenna diversity reception
Authors: Garg Deepshikha , Adachi Fumiyuki 
Published: April 2005

AbstractIn this paper, we present a comprehensive performance evaluation of chip interleaving effect on turbo coded direct sequence spread spectrum (DS‐SS) system in a frequency non‐selective Rayleigh fading channel with antenna diversity reception. At the transmitter, chip interleaver scrambles the SF (spreading factor) chips associated with a data symbol and transforms the transmission channel into a highly time‐selective or highly memoryless channel at the chip level. The use of chip interleaving is equivalent to using SF‐antenna diversity reception with correlated fading among the branches and with reduced average received signal power per antenna by a factor of SF. We theoretically analyze how chip interleaving alters the received signal statistics. Then, the effect of the various parameters, viz. interleaver size, interleaving depth, information sequence length, spreading factor and the fading maximum Doppler frequency, are also evaluated. It is found that the bit error rate (BER) performance improves with increasing spreading factor and increasing frame length. Chip interleaving is found to be effective in the presence of receive antenna diversity as well. Copyright © 2005 John Wiley & Sons, Ltd.
Reoperation for hyperparathyroidism
Authors: Edis Anthony J. , Beahrs Oliver H. , Sheedy Patrick F. 
Published: April 2005

AbstractReoperation for persistent or recurrent hyperparathyroidism is more hazardous than is primary cervical exploration and is also much less likely to result in cure of the disease. Only 21 of 34 reoperations (62%) were successful during the period 1970 through 1972 at the Mayo Clinic, compared with success in 312 of 327 primary operations (95%). In 9 patients who had their initial exploration at this institution, the most common cause of failure at the first operation was inadequate treatment of multiglandular disease; in 25 patients who were first operated on elsewhere, missed adenomas were far more common.Parathyroid arteriography and selective venous sampling with parathyroid hormone assays should improve the results of reoperation by providing preoperative localization of hyperfunctioning parathyroid glands in difficult cases. These procedures, however, are expensive and technically difficult, and they are not always successful. They are also associated with a definite morbidity, which must be weighed against any anticipated benefits. The systematic evaluation and treatment of patients facing reoperation for hyperparathyroidism should be undertaken in special centers accustomed to dealing with these difficult problems.
Bile duct and liver pathology in biliary atresia
Authors: Haas Joel E. 
Published: April 2005

AbstractProgression to cirrhosis despite restoration of bile flow by successful portoenterostomy suggests that factors other than obstruction alone are operative in biliary atresia. This paper describes pathologic changes at all levels of the hepatobiliary secretory apparatus from hepatocyte to common duct, exhibited in liver biopsies, resected portions of liver adjacent to the porta hepatis, and extrahepatic duct remnants from 17 patients operated upon for relief of biliary atresia. In both intra‐ and extrahepatic bile ducts, there were epithelial changes interpreted as occurring in a sequence of vacuolar degeneration, necrosis, inflammatory infiltration, and proliferative epithelial repair that precede obliterative fibrosis. From their distribution, it is inferred that these cytopathologic changes may not be simply due to distal obstruction. These ductal epithelial changes are similar to those that occur in livers of some patients with severe viral hepatitis. The association of these changes with giant cell transformation in all cases suggests that they reflect a common etiology for ductal and hepatocellular damage in the neonatal hepatitis‐biliary atresia spectrum. The persistence of these changes in liver biopsies following portoenterostomy suggests that they may be of pathogenetic significance in the progressive liver disease seen in most patients with biliary atresia.