bluuebunny/crossref_metadata_2025 huggingface dataset:
Characterization of cerebral microangiopathy using 3 Tesla MRI: Correlation with neurological impairment and vascular risk factors
Authors: Hund‐Georgiadis Margret , Ballaschke Olaf , Scheid Rainer , Norris David G. , von Cramon D. Yves
Published: August 2002

Purpose

To investigate whether clinical and neuropsychological impairment in cerebral small‐vessel disease (CSVD) can be evaluated by means of morphological magnetic resonance imaging (MRI).

Materials and Methods

MRI at 3 Tesla in T2‐ and T1‐weighted sequences was evaluated in 44 patients with cerebral microangiopathy, and 30 patients with combined cerebral micro‐ and macroangiopathy. The MR characteristics were correlated to clinical data, attentional impairment, and the patients' individual vascular risk factor profiles. Fifteen healthy age‐matched control subjects participated in the study to assess MR signal changes in nonhypertensive elderly subjects.

Results

Patients and normal controls differed significantly in the extent of MR signal changes. A close relation between age, obesity, hypertension, and MR signal abnormalities was evident in all patients. Patients with pure CSVD additionally showed an association between their MR‐defined severity of disease and their degree of neurological impairment, and their vascular risk score. In contrast, attentional impairment did not relate to the MR‐defined severity of CSVD.

Conclusion

MR signal changes in CSVD show a close relationship to some risk factors of individual patients. J. Magn. Reson. Imaging 2002;15:1–7. © 2002 Wiley‐Liss, Inc.
Investigation of mechanisms underlying transient T2 normalization in longitudinal studies of ischemic stroke
Authors: Lin Shao‐Pow , Schmidt Robert E. , McKinstry Robert C. , Ackerman Joseph J.H. , Neil Jeffrey J.
Published: August 2002

Purpose

To determine if the phenomenon of transient normalization of T2 relaxation in the subacute stage of ischemic stroke is associated with either magnetic susceptibility effects secondary to hemorrhage or changes in tissue water content.

Materials and Methods

We utilized a rat model of transient, focal, cerebral ischemia. The possibility of hemorrhage was evaluated with T2*‐weighted (T2*W) imaging and histology. Changes in water content were assessed by brain wet‐to‐dry weight.

Results

Susceptibility effects were not evident in T2*W images, and neither red blood cells nor unchelated Fe(III) was found in hematoxylin and eosin (H‐E)– or Prussian Blue–stained sections, respectively. However, between the peak of T2 contrast and the point of transient T2 normalization, water content consistently decreased by an average of 3%.

Conclusion

Transient T2 normalization is associated with normalization of water content and can occur without evidence of hemorrhage. J. Magn. Reson. Imaging 2002;15:130–136. © 2002 Wiley‐Liss, Inc.
Diffusion‐weighted MRI in the characterization of soft‐tissue tumors
Authors: van Rijswijk Catherina S.P. , Kunz Patrik , Hogendoorn Pancras C.W. , Taminiau Antonïe H.M. , Doornbos Joost , Bloem Johan L.
Published: August 2002

Purpose

To explore the potential of perfusion‐corrected diffusion‐weighted magnetic resonance imaging (MRI) in characterizing soft‐tissue tumors.

Materials and Methods

Diffusion‐weighted MRI was performed in 23 histologically proven soft‐tissue masses using a diffusion‐weighted spin‐echo sequence with diffusion gradient strengths yielding five b‐values (0–701 seconds/mm2). True diffusion coefficients and perfusion fractions were estimated and compared with apparent diffusion coefficients (ADCs).

Results

ADC values of all tumors, subcutaneous fat, and muscle were significantly higher than true diffusion coefficients, indicating a contribution of perfusion to the ADC. True diffusion coefficients of malignant tumors (1.08 × 10–3 mm2/second) were significantly lower than those of benign masses (1.71 × 10–3 mm2/second), whereas ADC values between these groups were not significantly different.

Conclusion

Perfusion‐corrected diffusion‐weighted MRI has potential in differentiating benign from malignant soft‐tissue masses. J. Magn. Reson. Imaging 2002;15:302–307. © 2002 Wiley‐Liss, Inc.
Correction of slab boundary artifact using histogram matching
Authors: Kholmovski Eugene G. , Alexander Andrew L. , Parker Dennis L.
Published: August 2002

Purpose

To improve the imaging efficiency of multi‐slab three‐dimensional acquisitions by decreasing slab overlap and the number of blanked slices.

Materials and Methods

Application of the histogram matching technique for correction of the slab boundary artifact (SBA) due to non‐ideal radiofrequency pulse profiles has been proposed. The technique was validated by studying its effectiveness in reducing the SBA in phantom images, as well as in proton density‐ and T2‐weighted brain images.

Results

The correction algorithm considerably decreases the disruption of image volume continuity due to the SBA, and improves slice‐to‐slice intensity continuity.

Conclusion

The proposed technique can greatly reduce the SBA when the SBA can be described as a global intensity variation along the slab. The technique may be used to improve imaging efficiency of the multi‐slab three‐dimensional fast spin‐echo sequences by decreasing the amount of required slab overlap. J. Magn. Reson. Imaging 2002;15:610–617. © 2002 Wiley‐Liss, Inc.
Accurate estimation of pharmacokinetic contrast‐enhanced dynamic MRI parameters of the prostate
Authors: Huisman Henkjan J. , Engelbrecht Marc R. , Barentsz Jelle O.
Published: August 2002

Quantitative analysis of contrast‐enhanced dynamic MR images has potential for diagnosing prostate cancer. Contemporary fast acquisition techniques can give sufficiently high temporal resolution to sample the fast dynamics observed in the prostate. Data reduction for parametric visualization requires automatic curve fitting to a pharmacokinetic model, which to date has been performed using least‐squares error minimization methods. We observed that these methods often produce unexpectedly noisy estimates, especially for the typically fast, intermediate parameters time‐to‐peak and start‐of‐enhancement, resulting in inaccurate pharmacokinetic parameter estimates. We developed a new curve fit method that focuses on the most probable slope. A set of 10 patients annotated using histopathology was used to compare the conventional and new methods. The results show that our new method is significantly more accurate, especially in the relatively less‐enhancing periferal zone. We conclude that estimation accuracy depends on the curve fit method, which is especially important when evaluating the periferal zone of the prostate. J. Magn. Reson. Imaging 2001;13:607–614. © 2001 Wiley‐Liss, Inc.
Comparison of gradient encoding schemes for diffusion‐tensor MRI
Authors: Hasan Khader M. , Parker Dennis L. , Alexander Andrew L.
Published: August 2002

The accuracy of single diffusion tensor MRI (DT‐MRI) measurements depends upon the encoding scheme used. In this study, the diffusion tensor accuracy of several strategies for DT‐MRI encoding are compared. The encoding strategies are based upon heuristic, numerically optimized, and regular polyhedra schemes. The criteria for numerical optimization include the minimum tensor variance (MV), minimum force (MF), minimum potential energy (ME), and minimum condition number. The regular polyhedra scheme includes variations of the icosahedron. Analytical comparisons and Monte Carlo simulations show that the icosahedron scheme is optimum for six encoding directions. The MV, MF, and ME solutions for six directions are functionally equivalent to the icosahedron scheme. Two commonly used heuristic DT‐MRI encoding schemes with six directions, which are based upon the geometric landmarks of a cube (vertices, edge centers, and face centers), are found to be suboptimal. For more than six encoding directions, many methods are able to generate a set of equivalent optimum encoding directions including the regular polyhedra, and the ME, MF and MV numerical optimization solutions. For seven directions, a previously described heuristic encoding scheme (tetrahedral plus x, y, z) was also found to be optimum. This study indicates that there is no significant advantage to using more than six encoding directions as long as an optimum encoding is used for six directions. Future DT‐MRI studies are necessary to validate these observations. J. Magn. Reson. Imaging 2001;13:769–780. © 2001 Wiley‐Liss, Inc.
Safety of metallic implants in magnetic resonance imaging
Authors: Ho Henry S.
Published: August 2002

Magnetic resonance (MR) imaging has become a commonly accepted medical procedure. Manufacturers of medical implant devices are submitting claims that their devices are safe and effective in a MR environment. This paper concentrates on the issue of heating of patients due to the interaction of metallic implants with the strong radiofrequency (RF) magnetic field produced by the MR scanner. The commercially available program XFDTD was used to calculate the specific absorption rate (SAR) distribution in a realistic model of the human body. The body contained a metallic implant and was exposed to RF magnetic fields at 64 MHz from a model of a MR birdcage body coil. The results of the calculation showed that the magnitude of the increased heating of tissues due to the presence of the metallic implant depended on the dimensions, orientation, shape, and location of the metallic implant in the patient. This increased heating of surrounding tissues primarily concentrates in a small volume near the tip of the metallic wire. When the whole‐body SAR was normalized to 1 W/kg, a calculated value of 41 W/kg was obtained at this location if the absorption was averaged over 1 g of tissue. However, a maximum value of 310 W/kg was calculated when the absorption was averaged over 1/8 g of tissue. J. Magn. Reson. Imaging 2001;14:472–477. Published 2001 Wiley‐Liss, Inc.
Organic ion imaging of biological tissue with secondary ion mass spectrometry and matrix‐assisted laser desorption/ionization
Authors: Todd Peter J. , Schaaff T. Gregory , Chaurand Pierre , Caprioli Richard M.
Published: August 2002

Organic secondary ion mass spectrometry (SIMS) and matrix‐assisted laser desorption/ionization (MALDI) mass spectrometry can be used to produce molecular images of samples. This is achieved through ionization from a clearly identified point on a flat sample, and performing a raster of the sample by moving the point of ionization over the sample surface. The unique analytical capabilities of mass spectrometry for mapping a variety of biological samples at the tissue level are discussed. SIMS provides information on the spatial distribution of the elements and low molecular mass compounds as well as molecular structures on these compounds, while MALDI yields spatial information about higher molecular mass compounds, including their distributions in tissues at very low levels, as well as information on the molecular structures of these compounds. Application of these methods to analytical problems requires appropriate instrumentation, sample preparation methodology, and a data presentation usually in a three‐coordinate plot where x and y are physical dimensions of the sample and z is the signal amplitude. The use of imaging mass spectrometry is illustrated with several biological systems. Copyright © 2001 John Wiley & Sons, Ltd.
A novel tandem quadrupole mass spectrometer allowing gaseous collisional activation and surface induced dissociation
Authors: Mohammed Shabaz , Chalmers Michael J. , Gielbert Janine , Ferro Myriam , Gora Les , Smith D. Charles , Gaskell Simon J.
Published: August 2002

A novel tandem quadrupole mass spectrometer is described that enables gaseous collision‐induced dissociation (CID) and surface‐induced dissociation (SID) experiments. The instrument consists of a commercially available triple quadrupole mass spectrometer connected to an SID region and an additional, orthogonal quadrupole mass analyser. The performance of the instrument was evaluated using leucine‐enkephalin, allowing a comparison between CID and SID, and with previous reports of other SID instruments. The reproducibility of SID data was assessed by replicate determinations of the collision energy required for 50% dissociation of leucine‐enkephalin; excellent precision was observed (standard deviation of 0.6 eV) though, unexpectedly, the reproducibility of the equivalent figure for CID was superior. Several peptides were analysed using SID in conjunction with liquid secondary‐ion mass spectrometry or electrospray; a comparison of the fragmentation of singly protonated peptide ions and the further dissociation of y‐type fragments was consistent with the equivalence of the latter fragments to protonated peptides. Few product ions attributable to high‐energy cleavages of amino acid side‐chains were observed. The SID properties were investigated of a series of peptides differing only in the derivatization of a cysteine residue; similar decomposition efficiencies were observed for all except the cysteic acid analogue, which demonstrated significantly more facile fragmentation. Copyright © 2001 John Wiley & Sons, Ltd.
Impaired cytotoxic T lymphocyte response to Epstein‐Barr virus‐infected NK cells in patients with severe chronic active EBV infection
Authors: Tsuge Ikuya , Morishima Tsuneo , Kimura Hiroshi , Kuzushima Kiyotaka , Matsuoka Hiroshi
Published: August 2002

Clinical evidence of a relationship between severe chronic active Epstein‐Barr virus (EBV) infection and clonal expansion of EBV‐infected T or NK cells has been accumulated. In order to clarify pathogenesis of EBV‐infected cell proliferation in patients with severe chronic active EBV infection, cytotoxic T lymphocyte (CTL) responses of two patients against B‐lymphoblastoid cell lines (B‐LCL) and EBV‐infected NK cells were examined in comparison with those of HLA‐identical healthy siblings. Unexpectedly, patients' CTL activities induced by mixed culture with autologous B‐LCLs were markedly reduced, although uncontrolled EBV‐related B‐cell proliferations have never been experienced. In contrast, limiting dilution analysis demonstrated that B‐LCL‐specific CTL precursor (CTLp) frequencies of patients were comparable to those of their healthy sisters. The existence of normal levels of B‐LCL‐specific T cell responses was confirmed by flow‐cytometric analysis of IFN‐γ‐producing T cells after stimulation with B‐LCLs. Infected NK‐cell‐specific CTLp frequencies of the patients were at undetectable levels despite their expression of latent membrane protein (LMP) 1, suggesting mechanisms to escape immunologic surveillance. In the patients' HLA‐identical healthy sisters, infected NK‐cell‐specific CTLps were detected, and infected NK‐cell‐specific CTL clones could be established. From these findings, two treatment options for severe chronic active EBV infection are offered for consideration: adoptive transfer of in vitro‐cultured CTL, and bone marrow transplantation from HLA‐identical donors. J. Med. Virol. 64:141–148, 2001. © 2001 Wiley‐Liss, Inc.
Multicentered study of viral acute lower respiratory infections in children from four cities of Argentina, 1993–1994*
Authors: Carballal Guadalupe , Videla Cristina M. , Espinosa M. Alejandra , Savy Vilma , Uez Osvaldo , Sequeira María D. , Knez Violeta , Requeijo Paula V. , Posse Clara Riva , Miceli Isabel
Published: August 2002

This study describes the first multicentered study of acute lower respiratory infection viral etiology in young children from four different geographical areas of Argentina. A total of 1,278 children under 5 years of age, hospitalized in primary care centers from Buenos Aires, Córdoba, Santa Fé and Mar del Plata cities during a 2‐year period were studied (1993–1994). Nasopharyngeal aspirates were investigated for respiratory syncytial virus (RSV), adenovirus, parainfluenza, and influenza A and B viruses by indirect immunofluorescence. Out of the patients studied, 946 (74%) were under 1 year of age. Viruses were detected in 399 patients (32%). RSV was observed in 25.3% of the samples, representing 78.2% of all viral positive cases. Adenoviruses were detected in 2.5% of the cases, parainfluenza in 2.2%, influenza A in 2.1%, and influenza B in 0.2%. Compared with other viruses, the higher RSV frequency was statistically significant (P < 0.000). Most RSV cases were detected between May and September with a significant peak in July (P < 0.000). Pneumonia was observed in 46% of the patients, bronchiolitis in 41% and other entities in 13%. The case fatality rate observed during the 2 year study was 0.73%. Most of the above respiratory viruses were detected in the four cities, however, the frequency of RSV and influenza were different in the southern city. J. Med. Virol. 64:167–174, 2001. © 2001 Wiley‐Liss, Inc.
Quantity of cytomegalovirus DNA in different leukocyte populations during active infection in vivo and the presence of gB and UL18 transcripts
Authors: Hassan‐Walker Aycan F. , Mattes Frank M. , Griffiths Paul D. , Emery Vincent C.
Published: August 2002

The quantity of human cytomegalovirus (HCMV) DNA in the blood of immunocompromised individuals correlates with the development of HCMV disease. We wished to determine which leukocytes harboured DNA and whether this represented active viral replication. Magnetic bead separation techniques were used to obtain pure polymorphonuclear leukocyte (PMNL), monocyte, B and T cell fractions, and RT‐PCR and quantitative‐competitive PCR (QC‐PCR) to detect HCMV glycoprotein B (gB; UL55) transcripts and quantify HCMV DNA levels, respectively, in each cell fraction. QC‐PCR revealed that PMNLs contribute the greatest to the overall viral load in blood (median viral load: PMNLs, 105.37 genomes/ml of blood; monocytes, 104.40 genomes/ml; B cells, 103.70 genomes/ml; and T cells, 104.08 genomes/ml). However, monocytes have a viral burden of 0.65 genomes/monocyte which is greater than that within the other leukocyte populations (0.11 genomes/PMNL, 0.23 genomes/B cell, and 0.20 genomes/T cell). Glycoprotein B transcripts were detected in all four cell populations: 3/10 PMNL fractions, 6/13 monocyte fractions, 5/13 B cell fractions, and 4/13 T cell fractions. The data show that productive infection of these leukocyte subpopulations, including PMNLs, can occur in vivo. Furthermore, transcripts of gpUL18, the putative natural killer (NK) cell decoy, were detected in 2/6 monocyte fractions with active replication, and 1/4 T cell fractions but not in the other leukocyte fractions. The transient nature of UL18 gene expression, and the low abundance of the transcript relative to gB were confirmed. J. Med. Virol. 64:283–289, 2001. © 2001 Wiley‐Liss, Inc.
Influenza vaccination of HIV‐1‐positive and hiv‐1‐negative former intravenous drug users
Authors: Amendola Antonella , Boschini Antonio , Colzani Daniela , Anselmi Giovanni , Oltolina Arianna , Zucconi Roberta , Begnini Marco , Besana Silvia , Tanzi Elisabetta , Zanetti Alessandro Remo
Published: August 2002

The immunogenicity of an anti‐influenza vaccine was assessed in 409 former intravenous drug user volunteers and its effect on the levels of HIV‐1 RNA, proviral DNA and on CD4+ lymphocyte counts in a subset HIV‐1‐positive subjects was measured. HIV‐1‐positive individuals (n = 72) were divided into three groups on the basis of their CD4+ lymphocyte counts, while the 337 HIV‐1‐negative participants were allocated into group four. Haemagglutination inhibiting (HI) responses varied from 45.8 to 70% in the HIV‐1‐positive subjects and were significantly higher in group four (80.7% responses to the H1N1 strain, 81.6% to the H3N2 strain, and 83% to the B strain). The percentage of subjects with HI protective antibody titres (≥ 1:40) increased significantly after vaccination, especially in HIV‐1 uninfected subjects. Immunization caused no significant changes in CD4+ counts and in neither plasma HIV‐1 RNA nor proviral DNA levels. Therefore, vaccination against influenza may benefit persons infected by HIV‐1. J. Med. Virol. 65:644–648, 2001. © 2001 Wiley‐Liss, Inc.
Primary human herpesvirus‐6 associated with an afebrile seizure in a 3‐week‐old infant
Authors: Zerr Danielle M. , Yeung Laurence C. , Obrigewitch Rose Mary , Huang Meei‐Li , Frenkel Lisa M. , Corey Lawrence
Published: August 2002

We describe a 3‐week‐old male infant with an afebrile seizure in whom serologic and polymerase chain reaction (PCR) findings support concomitant primary human herpesvirus 6 (HHV‐6) infection. Although HHV‐6 infection has been associated with first‐time febrile seizures and encephalitis in both immunocompetent and immunocompromised hosts, it has not been associated previously with afebrile seizures in healthy infants. This report provides additional evidence of the neuropathogenic potential of HHV‐6. J. Med. Virol. 66:384‐387, 2002. © 2002 Wiley‐Liss, Inc.
Inhalation anesthetic‐induced neuroinvasion by an attenuated strain of West Nile virus in mice
Authors: Katz Yeshayahu , Lustig Shlomo , Ben‐Shlomo Izhar , Kobiler David , Ben‐Nathan David
Published: August 2002

There are contradictory reports regarding the effects of inhalation anesthetics on the immune system. Measurable immune responses have been studied in vitro, but little is known about the in vivo effects in the intact organism. We used an attenuated, non‐neuroinvasive, nonlethal strain of the encephalitic West Nile virus, termed WN‐25, which can become lethal in combination with environmental stressors, to study possible modulatory immune effects of inhalation anesthetics in mice. Both single short‐term exposure and repeated exposure to halothane and nitrous oxide were studied. Exposure to 30% CO2 served as a positive control. Mortality, brain invasion, spleen weight, and antiviral antibodies served as the experimental endpoints. Halothane and nitrous oxide led to viral brain invasion, increased mortality, and suppressed immune response in a concentration‐ and time‐dependent manner. Repeated exposures had a cumulative effect. Assessment of the stability of the viral attenuation did not demonstrate any alteration in the character of the virus, suggesting an increased access to the brain by inhalation anesthetics that led to the fatal encephalitis. These findings may be of special concern to populations at risk, such as operating room staff and patients undergoing general anesthesia in endemic areas of encephalitic virus species, in which subclinical infection may develop into an overt disease. J. Med. Virol. 66:576–580, 2002. © 2002 Wiley‐Liss, Inc.
Kinetics and localization of brain phosphate activated glutaminase
Authors: Kvamme Elling , Torgner Ingeborg Aa. , Roberg Bjørg
Published: August 2002

The cellular concentration of phosphate, the main activator of phosphate activated glutaminase (PAG) is rather constant in brain and kidney. The enzyme activity, however, is modulated by a variety of compounds affecting the binding of phosphate, such as glutamate, calcium, certain long chain fatty acids, fatty acyl CoA derivatives, members of the tricarboxylic acid cycle and protons (Kvamme et al. [2000] Neurochem. Res. 25:1407–1419). Therefore, the kinetic and allosteric properties of the enzyme are essential for regulating the enzyme activity in situ, especially because the enzymically active pool of PAG is assumed to have an external localization in the inner mitochondrial membrane, being exposed to cytosolic variation in the content of effectors. This has largely been overlooked. A hypothetical model for the allosteric interactions based on the sequential induced fit allosteric model by Koshland et al. ([1966] Biochemistry 5:365–385) is presented. Furthermore, it has been generally accepted that there exist only two isoforms of PAG, the kidney PAG that is similar to brain PAG, and the liver PAG. Therefore, the immunoreactivity of brain cells against kidney PAG antibodies has been considered a measure of PAG protein. Gomez‐Fabre et al. ([2000] Biochem. J. 345:365–375) recently found, however, that a PAG mRNA from human breast cancer ZR75 cells is present in human brain and liver, but not in the kidney. We observed only traces of PAG immunoreactivity in cultured astrocytes and cultured neuroblastoma cells, regardless whether antibodies against the C‐ and N‐termini of kidney PAG or antibodies against liver PAG were used, but considerable enzyme activity, demonstrating hitherto unknown isoforms of PAG (Torgner et al. [2001] FEBS Lett. 268(Suppl 1):PS2–031). © 2001 Wiley‐Liss, Inc.
Alterations in expression of genes coding for key astrocytic proteins in acute liver failure
Authors: Desjardins Paul , Bélanger Mireille , Butterworth Roger F.
Published: August 2002

Cerebral edema and hepatic encephalopathy are major complications of acute liver failure. Brain herniation caused by increased intracranial pressure as a result of cell swelling is the major cause of death in this condition. Evidence available currently suggests that the rapid accumulation of ammonia by the brain is the major cause of the central nervous system complications of acute liver failure. Increased brain ammonia may cause cell swelling via the osmotic effects of an increase in astrocytic glutamine concentrations or by inhibition of glutamate removal from brain extracellular space. Acute liver failure results in altered expression of several genes in brain, some of which code for important proteins involved in CNS function such as the glucose (GLUT‐1) and glutamate (GLT‐1) transporters, the astrocytic structural protein glial fibrillary acidic protein (GFAP) the “peripheral‐type” benzodiazepine receptor (PTBR) and the water channel protein, aquaporin IV. Loss of expression of GLT‐1 results in increased extracellular brain glutamate in acute liver failure. Experimental acute liver failure also results in post‐translational modifications of the serotonin and noradrenaline transporters resulting in increased extracellular concentrations of these monoamines. Therapeutic measures currently used to prevent and treat brain edema and encephalopathy in patients with acute liver failure include mild hypothermia and the ammonia‐lowering agent L‐ornithine‐L‐aspartate. © 2001 Wiley‐Liss, Inc.
Measurement of human tricarboxylic acid cycle rates during visual activation by 13C magnetic resonance spectroscopy
Authors: Chhina Navjeet , Kuestermann Ekkehard , Halliday Jane , Simpson Liz J. , Macdonald Ian A. , Bachelard Herman S. , Morris Peter G.
Published: August 2002

Measurement by 13C magnetic resonance spectroscopy (MRS) of the incorporation of label from [1‐13C] glucose, initially into C4 of glutamate, allows the regional tricarboxylic acid (TCA) cycle flux (FTCA) to be determined in the human brain. In this study, a direct 13C MRS approach was used at 3T, with NOE enhancement and 1H decoupling with WALTZ16, to determine basal FTCA in six volunteers. The values found in the visual cortex are similar to those reported in previous 13C MRS studies, and consistent with PET measurements of the cerebral metabolic rate for glucose, CMRglc. In two preliminary activation studies using light emitting diode (LED) goggles flashing at 8 Hz, compared to darkness as control, increases in FTCA were found from 0.60 ± 0.10 to 0.94 ± 0.03 μmol/min/g (56%) and from 0.34 ± 0.14 to 0.56 ± 0.07 μmol/min/g (65%). These are upper estimates, but they are similar to the increases in CMRglc reported in PET studies, and strongly suggest, in contrast to these PET studies, that cerebral glucose is metabolized oxidatively, even during intense visual stimulation. This is supported by the observation that very little 13C label is incorporated into C3 lactate, as would be expected if glucose were metabolized anaerobically. There is evidence for incorporation of glucose into cerebral glycogen, but this is a relatively minor component of cerebral glucose metabolism. © 2001 Wiley‐Liss, Inc.
Local uptake of 14C‐labeled acetate and butyrate in rat brain in vivo during spreading cortical depression
Authors: Dienel Gerald A. , Liu Kenian , Cruz Nancy F.
Published: August 2002

Spreading depression severely disrupts ion homeostasis, causes sensory neglect and motor impairment, and is associated with stroke and migraine. Glucose utilization (CMRglc) and lactate production rise during spreading depression, but the metabolic changes in different brain cell types are unknown. Uptake of 14C‐labeled compounds known to be preferentially metabolized by the glial tricarboxylic acid cycle was, therefore, examined during unilateral KCl‐induced spreading cortical depression in conscious, normoxic rats. [14C]Metabolites derived from [14C]butyrate in K+‐treated tissue rose 21% compared to that of untreated contralateral control cortex, whereas incorporation of H14CO3 into metabolites in K+‐treated tissue was reduced to 86% of control. Autoradiographic analysis showed that laminar labeling of cerebral cortex by both 14C‐labeled acetate and butyrate was elevated heterogeneously throughout cortex by an average of 23%; the increase was greatest (∼40%) in tissue adjacent to the K+ application site. Local uptake of acetate, butyrate, and deoxyglucose showed similar patterns, and monocarboxylic acid uptake was highest in the structures in which apparent loss of labeled metabolites of [6‐14C]glucose was greatest. Enhancement of net uptake of acetate and butyrate in cerebral cortex during spreading depression is tentatively ascribed to increased astrocyte metabolism. © 2001 Wiley‐Liss, Inc.
In vitro evidence that 5‐hydroxytryptamine increases efflux of glial glutamate via 5‐HT2A receptor activation
Authors: Meller R. , Harrison P.J. , Elliott J.M. , Sharp T.
Published: August 2002

Recent studies have established the presence of 5‐hydroxytryptamine (5‐HT)2A receptors on glial cells in culture and in the brain in situ. Here we used cultured C6 glioma cells to investigate the possibility that 5‐HT2A receptors on glia regulate glutamate release from the cell. The efflux of endogenous glutamate from cultured C6 glioma cells was increased by addition of 5‐HT in a concentration‐dependent manner (maximal effect +200%). The efflux of serine and aspartate was not altered. The effect of 5‐HT was mimicked by both the nonselective 5‐HT receptor agonist quipazine and the selective 5‐HT2 receptor agonist 4‐iodo‐2,5‐dimethoxyamphetamine (DOI; both 0.01–100 μM). The 5‐HT2A receptor antagonists ketanserin (1 μM) and spiperone (1 μM) inhibited the glutamate response to 5‐HT, quipazine, and DOI, whereas the effect of 5‐HT was not inhibited by the 5‐HT2B/C receptor antagonist SB200646 (1 μM). The effect of 5‐HT on glutamate was specific in that it was reduced in low‐calcium medium but was not prevented by furosemide (5 mM), which prevents cell swelling‐induced glutamate release. Finally, the glutamate uptake inhibitor 2,4,trans‐pyrollidine dicarboxylic acid (50 μM) did not block the 5‐HT‐induced efflux of glutamate, making involvement of glutamate transport unlikely. In conclusion, 5‐HT stimulates the efflux of glutamate from C6 glioma cells following 5‐HT2A receptor activation and involves a calcium‐dependent mechanism. © 2002 Wiley‐Liss, Inc.
Study of expression of myelin basic proteins (MBPs) in developing rat brain using a novel antibody reacting with four major isoforms of MBP
Authors: Akiyama Kyoichi , Ichinose Sachiyo , Omori Akira , Sakurai Yoko , Asou Hiroaki
Published: August 2002

Myelin basic proteins (MBPs) are the major protein components of myelin. MBP isoforms are known to have different expression patterns. In order to distinguish the different expression patterns on myelination, we have developed a novel antibody reacting with the four major isoforms of MBPs with molecular masses of 21.5 kDa, 18.5 kDa, 17.0 kDa, and 14.0 kDa. These MBPs were initially separated by acid urea gel and sodium dodecyl sulfate polyacrylamide gel electrophoreses and detected with the luminol reaction. Then the antibody developed was used to determine the relative amounts of MBP isoforms. The MBPs of oligodendrocytes were detected by the enhanced luminol reaction using Renaissance (Dupont NEN, Boston, MA). From the immunological aspect, the MBP monoclonal antibody (Sires et al. [1981] Science 214:87–89) was revealed to recognize MBPs with molecular masses of 21.5 kDa and 18.5 kDa. Furthermore, we found that Ile‐166 in the rat 18.5‐kDa MBP isomers was replaced by methionine. The 14.0‐kDa and 18.5‐kDa isoforms of MBP are the most abundant MBP species and comprise more than 70% of the total MBPs in 3.5‐and 24‐month‐old rats. MBPs are expressed during development and the compositions of MBPs in mature (3.5 months old) and aged (24 months old) rats were almost the same. The expression of the 14.0‐kDa and 18.5‐kDa MBPs occurred earlier in the cerebellum and the spinal cord than in the cerebrum by approximately 1 week. MBPs are also expressed upon oligodendrocyte maturation by interacting with astrocytes. The above results suggest that the regulation of MBP isoforms during development and oligodendrocyte differentiation may indicate the point of occurrence of both the unique patterns of isoform expression and the shift in intracellular localization of MBPs with the maturation of oligodendrocytes. © 2002 Wiley‐Liss, Inc.
Glial transporters for glutamate, glycine, and GABA: II. GABA transporters
Authors: Gadea Ana , López‐Colomé Ana María
Published: August 2002

The termination of chemical neurotransmission in the central nervous system (CNS) involves the rapid removal of neurotransmitter from synapses. This is fulfilled by specific transport systems in neurons and glia, including those for γ‐aminobutyric acid (GABA), the main inhibitory neurotransmitter in the brain. Glial cells express the cloned Na+/Cl−‐dependent, high‐affinity GABA transporters (GATs) GAT1, GAT2, and GAT3, as well as the low‐affinity transporter BGT1. In situ hybridization and immunocytochemistry have revealed that each transporter shows distinct regional distribution in the brain and the retina. The neuronal vs. glial localization of the different transporters is not clear‐cut, and variations according to species, neighboring excitatory synapses, and developmental stage have been reported. The localization, stoichiometry, and regulation of glial GATs are outlined, and the participation of these structures in development, osmoregulation, and neuroprotection are discussed. A decrease in GABAergic neurotransmission has been implicated in the pathophysiology of several CNS disorders, particularly in epilepsy. Since drugs which selectively inhibit glial but not neuronal GABA uptake exert anticonvulsant activity, clearly the establishment of the molecular mechanisms controlling GATs in glial cells will be an aid in the chemical treatment of several CNS‐related diseases. J. Neurosci. Res. 63:461–468, 2001. © 2001 Wiley‐Liss, Inc.
Domoic acid‐induced neuronal damage in the rat hippocampus: Changes in apoptosis related genes (Bcl‐2, Bax, caspase‐3) and microglial response
Authors: Ananth C. , Thameem Dheen S. , Gopalakrishnakone P. , Kaur C.
Published: August 2002

Domoic acid (DA), a potent neurotoxin, administered intravenously (0.75 mg/kg body weight) in adult rats evoked seizures accompanied by nerve cell damage in the present study. Neuronal degeneration and microglial reaction in the hippocampus were investigated, and the temporal profile of bcl‐2, bax, and caspase‐3 genes in cell death or survival was assessed following the administration of DA. Nissl staining showed darkly stained degenerating neurons in the hippocampus following the administration of DA at 1–21 days, the degeneration being most severe at 5 days. Ultrastructural study in CA1 and CA3 regions of hippocampus revealed two types of neuronal degeneration, cells that exhibited swollen morphology and shrunken electron‐dense cells. Immunoreactivity of Bcl‐2 and Bax was increased considerably at 16 hr and 24 hr in the neurons of the hippocampus following DA administration. No significant change was observed in the immunoreactivity of caspase‐3 in the controls and DA‐treated rats at any time interval. Microglial cells in the hippocampus showed intense immunoreaction with the antibodies OX‐42 and OX‐6 at 1–21 days after DA administration, indicating the up‐regulation of complement type 3 receptors and major histocompatibility complex type II antigens for increased phagocytic activity and antigen presentation, respectively. Terminal deoxynucleotidyl‐transferase‐mediated dUTP nick end labeling (TUNEL) showed occasional positive neurons in the CA1 and CA3 regions at 5 days after DA administration, with no positive cells in the controls. RT‐PCR analysis revealed that bcl‐2 and bax mRNA transcripts in the hippocampus were significantly increased at 16 hr and gradually decreased at 24 hr following the administration of DA. Although bax and bcl‐2 mRNA expression is rapidly induced at early stages, in situ hybridization analysis revealed complete loss of bcl‐2, bax, and caspase‐3 mRNA at 24 hr after DA administration in the region of neuronal degeneration in the hippocampus. These results indicate that the pattern of neuronal degeneration observed during DA‐induced excitotoxic damage is mostly necrotic. J. Neurosci. Res. 66:177–190, 2001. © 2001 Wiley‐Liss, Inc.
Reduced expression of neuronal nicotinic acetylcholine receptors during the early stages of damage by oxidative stress in PC12 cells
Authors: Guan Zhi‐Zhong , Zhang Xiao , Mousavi Malahat , Tian Jian‐Ying , Unger Christina , Nordberg Agneta
Published: August 2002

The mechanism for a large loss of neuronal nicotinic acetylcholine receptors (nAChRs) in brains with neurodegenerative diseases remains unclear. Based on our previous results of [3H]epibatidine binding influenced by lipid peroxidation, we suggest that nAChR deficit in neurodegenerative diseases might be related to the neurons attacked by free radicals. To further understand how free radicals influence the expression of nAChRs, we detected [125I]α‐bungarotoxin binding, nAChR subunit protein and mRNA during the early stage of damage by oxidative stress in PC12 cells in the present study. The results showed that free radical insult (FeSO4) within the concentration range (1 –100 μM) used in the study induced dose‐dependent increases in lipid peroxidation and toxicity to PC12 cells, but did not result in apoptosis or necrosis. Significant reductions in [125I]α‐bungarotoxin binding site, protein level for the α3 and α7 subunits, and mRNA level for the α7 subunit were observed in PC12 cells treated by FeSO4 at the concentrations without inducing cell death compared to control. Pretreatment of cultural cells with antioxidant such as Vitamin E and reduced glutathione prevented the inhibiting effect of free radicals on [125I]α‐bungarotoxin and [3H]epibatidine bindings. The present results further demonstrate that oxidative stress might reduce the number of [125I]α‐bungarotoxin binding site and selectively suppress the expression of the nAChR subunits at protein and mRNA levels during the early stages of damage in PC12 cells. J. Neurosci. Res. 66:551–558, 2001. © 2001 Wiley‐Liss, Inc.
PKC and PKA, but not PKG mediate LPS‐induced CGRP release and [Ca2+]i elevation in DRG neurons of neonatal rats
Authors: Hou Lingfei , Wang Xian
Published: August 2002

Calcitonin gene‐related peptide (CGRP), is produced in dorsal root ganglia (DRG) neurons and released from primary afferent neurons to mediate hemodynamic effects and neurogenic inflammation. In this work, we determined whether lipopolysaccharide (LPS), an inflammatory stimulator, could trigger CGRP release from cultured DRG neurons and if so, which cellular signaling pathway was involved in this response. Cytoplasmic concentration of calcium ([Ca2+]i) plays a key role in neurotransmitter release, therefore [Ca2+]i was also determined in cultured DRG cells using fluo‐3/AM. The results showed that LPS (0.1–10 μg/ml) evoked CGRP release in a time‐ and concentration‐dependent manner from DRG neurons. LPS also increased [Ca2+]i in a concentration‐dependent manner. The protein kinase C (PKC) inhibitors, calphostin C 0.5 μM or RO‐31‐8220 0.1 μM, and the cAMP‐dependent protein kinase (PKA) specific inhibitor RP‐CAMPS 30 μM or nonspecific inhibitor H8 1 μM inhibited 1 μg/ml LPS‐evoked CGRP release and [Ca2+]i increase from DRG neurons. The cGMP‐dependent protein kinase (PKG) inhibitor Rp‐8‐pCPT‐cGMPS 30 μM did not block the LPS response. These data suggest that LPS may stimulate CGRP release and [Ca2+]i elevation through PKC and PKA, but not PKG signaling pathway in DRG neurons of neonatal rats. J. Neurosci. Res. 66:592–600, 2001. © 2001 Wiley‐Liss, Inc.
Social support, group consensus and stressor–strain relationships: social context matters*
Authors: Bliese Paul D. , Britt Thomas W.
Published: August 2002

In this study, we examined the degree to which individuals' reactions to stressors were influenced by the quality of their shared social environments. Based on social support theory, we proposed that individuals in positive social environments would show lower levels of strain when exposed to stressors than would individuals in negative social environments. The quality of the shared social environment was assessed by measuring the degree of consensus among group members about an issue of importance to the group—namely about the group leadership. Social influence theory provides compelling reasons to believe that this measure of consensus should be a strong indicator of the quality of the social environment within the groups. In multilevel analyses using a sample of 1923 soldiers who were members of 52 Companies deployed to Haiti, we found that the quality of the social environment moderated relationships between (a) work stressors and morale and (b) work stressors and depression. Copyright © 2001 John Wiley & Sons, Ltd.
Sky‐view factor approximation using GPS receivers
Authors: Chapman Lee , Thornes John E. , Bradley Andrew V.
Published: August 2002

A technique is described which allows the real time measurement of sky‐view factors by proxy. A simple and inexpensive global positioning system (GPS) receiver is used to acquire satellite visibility data, which is then used to develop indices related to the sky‐view factor of a location. The number of visible satellites, dilution of precision and strength of satellite signal are used for analysis and demonstrate that up to 88% of the variation of the variation of the sky‐view factor in urban environments can be explained by a simple index. Explanation is reduced in rural (R2 = 72%) and suburban (R2 = 52%) environments as a consequence of increased image complexity caused by variations in tree cover type and canopy height in addition to just crown closure. The complicity and expensive nature of existing sky‐view factor calculation techniques should mean that utilization of the outlined methodology will improve the accessibility of sky‐view data for future climate studies. Copyright © 2002 Royal Meteorological Society.
Spatial variation in the duration of the rainy season in monsoonal Australia
Authors: Cook Garry D. , Heerdegen Richard G.
Published: August 2002

Climatological research in the tropics of northern Australia has focused particularly on the Australian summer monsoon. However, the timing of many ecologically important processes is determined not by the monsoon but by extra‐monsoonal rainfall events. These events produce a temporal pattern of wet and dry spells that is at least as important ecologically as the amount of rain. We defined the rainy season as that period when the probability of 10‐day dry spells was less than 0.5, and the wet season as that period within the rainy season when the probability of dry spells was less than 0.1. We applied these criteria to seven stations along a strong north–south rainfall gradient spanning more than 12° of latitude in tropical north Australia. The duration of the rainy and wet seasons in northern Australia decreases with increasing latitude. The timing and duration of these seasons were also affected by the El Niño–Southern Oscillation (ENSO). The relative contribution of temporally isolated rainfall events to both the duration of the rainy season and the amount of rainfall increases with latitude. The geographic variation in these seasons corresponds to many patterns occurring in natural ecosystems. We argue that understanding the extra‐monsoon rainfall events is critical to understanding how climate variation affects natural ecosystems. Copyright © 2001 Royal Meteorological Society
Raman spectroscopic and calculated vibrational wavenumbers of anion hydrates
Authors: Craig J. D. C.
Published: August 2002

Direct experimental evidence of anion hydrogen bonding was examined for fluoride and other anions. The centre wavenumber of the polarized Raman band assigned to the symmetric hydrogen bond stretching mode agreed very well with ab initio calculations for all anions but fluoride, whose theoretical wavenumber was significantly higher than the spectroscopic value. Calculations were repeated at a higher level of theory but the difference persisted. The heavy water isotope shifts and the potential energy surface for the hydrogen bond stretching motion were similar for fluoride and the other hydrates, suggesting that the difference could be due to interactions with other molecules. It was postulated that water cluster formation about the fluoride ion contributes to the difference in wavenumbers. Copyright © 2002 John Wiley & Sons, Ltd.
Fourier transform Raman spectroscopic study of pressure‐induced ligand bond activation in a molybdenum–sulfur cluster
Authors: Butler Ian S. , Hofstätter Michael , Müller Achim
Published: August 2002

Fourier transform Raman spectra of the prototype, triangular, transition metal–sulfur cluster anion [Mo3(S2)6S]2− were recorded at pressures up to 60 kbar with the aid of a diamond‐anvil cell (DAC). The pressure dependences (∂ν/∂p) of the Raman bands indicate a structural change at around 10–15 kbar. The SS stretching mode for the bridging disulfide ligands exhibits a slightly negative ∂ν/∂p value (−0.08), suggesting that SS bonds are weakened, i.e. activated, at high pressures. This pressure‐induced activity parallels the observed nucleophilic substitution reactivity of the S2 groups in this molybdenum cluster anion. In view of this, a preliminary investigation of the reaction between [Mo3(S2)6S]2− and CN− was undertaken in the solid state in the DAC under high pressure. Copyright © 2002 John Wiley & Sons, Ltd.