bluuebunny/crossref_metadata_2025_split huggingface dataset:
Hypoxia upregulates Bcl‐2 expression and suppresses interferon‐γ induced antiangiogenic activity in human tumor derived endothelial cells
Authors: Wang Jiang Huai , Wu Qiong Di , Bouchier‐Hayes David , Redmond H. Paul 
Published: August 2002

AbstractBACKGROUNDHypoxia in solid tumors potentially stimulates angiogenesis by promoting vascular endothelial growth factor (VEGF) production and upregulating VEGF receptor expression. However, it is unknown whether hypoxia can modulate the effect of anti‐angiogenic treatment on tumor‐derived endothelium.METHODSHuman tumor‐derived endothelial cells (HTDEC) were freshly isolated from surgically removed human colorectal tumors by collagenase/DNase digestion and Percol gradient sedimentation. Cell proliferation was assessed by measuring BrdU incorporation, and capillary tube formation was measured using Matrigel. Cell apoptosis was assessed by flow cytometry and ELISA, and Bcl‐2 expression was detected by Western blot analysis.RESULTSUnder aerobic culture conditions (5% CO2 plus 21% O2) HTDEC expressed less Bcl‐2 and were more susceptible to IFN‐γ‐induced apoptosis with significant reductions in both cell proliferation and capillary tube formation, when compared with normal human macrovascular and microvascular EC. Following exposure of HTDEC to hypoxia (5% CO2 plus 2% O2), IFN‐γ ‐induced cell apoptosis, and antiangiogenic activity (i.e. an inhibition in cell proliferation and capillary tube formation) in HTDEC were markedly attenuated. This finding correlated with hypoxia‐induced upregulation of Bcl‐2 expression in HTDEC.CONCLUSIONSThese results indicate that hypoxia can protect HTDEC against IFN‐γ ‐mediated cell death and antiangiogenic activity, and suggest that improvement of tumor oxygenation may potentiate the efficacy of anti‐cancer therapies specifically targeting the inhibition of tumor angiogenesis. Cancer 2002;94:2745–55. © 2002 American Cancer Society.DOI 10.1002/cncr.10520
Neuroendocrine tumors of the sinonasal tract
Authors: Fitzek Markus M. , Thornton Allan F. , Varvares Marc , Ancukiewicz Marek , Mcintyre James , Adams Judy , Rosenthal Stanley , Joseph Michael , Amrein Philip 
Published: August 2002

AbstractBACKGROUNDThe authors report the results of a prospective study of patients with malignant neuroendocrine tumors of the sinonasal tract who received multimodality treatment incorporating high‐dose proton‐photon radiotherapy.METHODSNineteen patients with olfactory neuroblastoma (ONB) or neuroendocrine carcinoma (NEC) were treated between 1992 and 1998 on a prospective study. Four patients had Kadish Stage B disease, and 15 patients had Kadish Stage C disease. The median patient age was 44 years. Patients received chemotherapy with 2 courses of cisplatin and etoposide followed by high‐dose proton‐photon radiotherapy to 69.2 cobalt–Gray equivalents (CGE) using 1.6–1.8 CGE per fraction twice daily in a concomitant boost schedule. Two further courses of chemotherapy were given to responders.RESULTSOf 19 patients, 15 patients were alive at the time of this report with a median follow‐up of 45 months (range, 20–92 months). Four patients died from disseminated disease 8–47 months after their original diagnosis. The 5‐year survival rate was 74%. There were two local recurrences, and both patients underwent salvage surgery. The 5‐year local control rate of initial treatment was 88%. Acute toxicity of chemotherapy was tolerable, with no patient sustaining more than Grade 3 hematologic toxicity. Thirteen patients showed a partial or complete response to chemotherapy. One patient developed unilateral visual loss after the first course of chemotherapy; otherwise, visual preservation was achieved in all patients. Four patients who were clinically intact developed radiation‐induced damage to the frontal or temporal lobe by magnetic resonance imaging criteria. Two patients showed soft tissue and/or bone necrosis, and one of these patients required surgical repair of a cerebrospinal fluid leak.CONCLUSIONSNeoadjuvant chemotherapy and high‐dose proton‐photon radiotherapy is a successful treatment approach for patients with ONB and NEC. Radical surgery is reserved for nonresponders. Due to the precision of delivery of radiation with stereotactic setup and protons, no radiation‐induced visual loss was observed. Cancer 2002;94:2623–34. © 2002 American Cancer Society.DOI 10.1002/cncr.10537
Effects of oxygen and glucose deprivation on the expression and distribution of neuronal and inducible nitric oxide synthases and on protein nitration in rat cerebral cortex
Authors: Alonso David , Serrano Julia , Rodríguez Ignacio , Ruíz‐Cabello Jesús , Fernández Ana Patricia , Encinas Juan Manuel , Castro‐Blanco Susana , Bentura María Luisa , Santacana María , Richart Ana , Fernández‐Vizarra Paula , Uttenthal Lars Otto , Rodrigo José 
Published: August 2002

AbstractChanges in the nitric oxide (NO) system of the rat cerebral cortex were investigated by immunohistochemistry, immunoblotting, NO synthase (NOS) activity assay, and magnetic resonance imaging (MRI) in an experimental model of global cerebral ischemia and reperfusion. Brains were perfused transcardially with an oxygenated plasma substitute and subjected to 30 minutes of oxygen and glucose deprivation, followed by reperfusion for up to 12 hours with oxygenated medium containing glucose. A sham group was perfused without oxygen or glucose deprivation, and a further group was treated with the NOS inhibitor Nω‐nitro‐L‐arginine methyl ester (L‐NAME) before and during perfusion. Global ischemia led to cerebrocortical injury as shown by diffusion MRI. This was accompanied by increasing morphologic changes in the large type I interneurons expressing neuronal NOS (nNOS) and the appearance of nNOS immunoreactivity in small type II neurons. The nNOS‐immunoreactive band and calcium‐dependent NOS activity showed an initial increase, followed by a fall after 6 hours of reperfusion. Inducible NOS immunoreactivity appeared in neurons, especially pyramidal cells of layers IV–V, after 4 hours of reperfusion, with corresponding changes on immunoblotting and in calcium‐independent NOS activity. Immunoreactive protein nitrotyrosine, present in the nuclear area of neurons in nonperfused controls and sham‐perfused animals, showed changes in intensity and distribution, appearing in the neuronal processes during the reperfusion period. Prior and concurrent L‐NAME administration blocked the changes on diffusion MRI and attenuated the morphologic changes, suggesting that NO and consequent peroxynitrite formation during ischemia–reperfusion contributes to cerebral injury. J. Comp. Neurol. 443:183–200, 2002. © 2002 Wiley‐Liss, Inc.
Postnatal development of connectional specificity of corticospinal terminals in the cat
Authors: Li Qun , Martin John H. 
Published: August 2002

AbstractThe purpose of this study was to examine postnatal development of connectional specificity of corticospinal terminals. We labeled a small population of primary motor cortex neurons with the anterograde tracer biotinylated dextran amine. We reconstructed individual corticospinal segmental axon terminals in the spinal gray matter in cats of varying postnatal ages and adults. We found that at days 25 and 35 the segmental termination field of reconstructed axons was large, estimated to cover more than half of the contralateral gray matter. Branches and varicosities were sparse and had a relatively uniform distribution. When we examined the terminal fields of multiple axons, reconstructed over the same set of spinal sections (120–200 μm), we found that there was extensive overlap. By day 55, the morphology and termination fields had changed remarkably. There were many short branches, organized into discrete clusters, and varicosities were preferentially located within these clusters. The termination field of individual axons was substantially reduced compared with that of younger animals, and there was minimal overlap between the terminals of neighboring corticospinal neurons. In adults, a further reduction was seen in the spatial extent of terminals, branching, and varicosity density. Termination overlap was not substantially different from that in PD 55 animals. Development of spatially restricted clusters of short terminal branches and dense axonal varicosities occurred just prior to development of the motor map in primary motor cortex and may be necessary for ensuring that the corticospinal system can exert a dominant influence on skilled limb movement control in maturity. J. Comp. Neurol. 447:57–71, 2002. © 2002 Wiley‐Liss, Inc.
Motor neurons rapidly accumulate DNA single‐strand breaks after in vitro exposure to nitric oxide and peroxynitrite and in vivo axotomy
Authors: Liu Zhiping , Martin Lee J. 
Published: August 2002

AbstractThe mechanisms of neuronal degeneration in motor neuron disease are not fully understood. We tested the hypothesis that oxidative stress in vitro and axotomy in vivo induce single‐strand breaks (SSB) in DNA, a form of early DNA damage, in adult motor neurons early during their degeneration. We developed and characterized a novel cell suspension system enriched in motor neurons from adult rat spinal cord ventral horn. This cell system is ∼84% neurons, with ∼86% of these neurons being motor neurons; ∼72% of these motor neurons are α‐motor neurons. Motor neuron viability in suspension is ∼100% immediately after isolation and ∼61% after 12 hours of incubation. During incubation, isolated motor neurons generate high levels of superoxide. We used single‐cell gel electrophoresis (comet assay) to detect DNA‐SSB in motor neurons. Exposure of motor neurons to nitric oxide (NO) donors (sodium nitroprusside or NONOate), H2O2, or NO donor plus H2O2 rapidly induces DNA‐SSB and causes motor neuron degeneration, the occurrence of which is dose and time related, as represented by comet formation and cell loss. Motor neuron toxicity is potentiated by cotreatment with NO donor and H2O2 (at nontoxic concentrations alone). Peroxynitrite causes DNA‐SSB in motor neurons. The DNA damage profiles (shown by the comet morphology and moment) of NO donors, NO donor plus H2O2, and peroxynitrite are similar. In an in vivo model of motor neuron apoptosis, DNA‐SSB accumulate slowly in avulsed motor neurons before apoptotic nuclear features emerge, and the comet fingerprint is similar to NO toxicity. We conclude that motor neurons challenged by oxidative stress and axotomy accumulate DNA‐SSB early in their degeneration and that the formation of peroxynitrite is involved in the mechanisms. J. Comp. Neurol. 432:35–60, 2001. © 2001 Wiley‐Liss, Inc.
Distribution and development of FMRFamide‐like immunoreactive neuronal systems in the brain of the brown trout, Salmo trutta fario
Authors: Castro Antonio , Becerra Manuela , Anadón Ramón , Manso María Jesús 
Published: August 2002

AbstractThe distribution of Phe‐Met‐Arg‐Phe‐amide (FMRFamide) peptide‐immunoreactive (FMRF‐ir) cells and fibers in the terminal nerve and central nervous system was investigated in developing stages and adults of the brown trout, Salmo trutta fario. The first FMRF‐ir neurons appeared in the terminal nerve system of 8‐mm embryos in and below the olfactory placode. In the brain, FMRF‐ir neurons were first observed in the rostral hypothalamus, primordial hypothalamic lobe, mesencephalic laminar nucleus, and locus coeruleus of 12‐ to 13 ‐m embryos. After hatching, FMRF‐ir cells appeared in the lateral part of the ventral telencephalic area and the anterior tuberal nucleus. In adult trout, FMRF‐ir cells were observed in all these areas. The number of FMRF‐ir neurons increased markedly in some of these populations during development. Dense innervation by FMRF‐ir fibers was observed in the dorsal and lateral parts of the dorsal telencephalic area, and in the ventral telencephalic area, the lateral preoptic area, the medial hypothalamic and posterior tubercle regions, midbrain tegmentum and rhombencephalic reticular areas, the central gray, the superior raphe nucleus, the secondary visceral nucleus, the vagal nuclei, and the area postrema. Fairly rich FMRF‐ir innervation was also observed in the optic tectum and some parts of the torus semicircularis. The saccus vasculosus and hypophysis received a moderate amount of FMRF‐ir fibers. Innervation of most of these regions appeared either in late alevins or fry, although FMRF‐ir fibers in the preoptic area, hypothalamus, and reticular areas appeared in embryos. Comparative analysis of the complex innervation pattern observed in the brain of trout suggests that FMRF is involved in a variety of functions, like the FMRF family of peptides in mammals. J. Comp. Neurol. 440:43–64, 2001. © 2001 Wiley‐Liss, Inc.
Neuroectodermal origin of brain pericytes and vascular smooth muscle cells
Authors: Korn Johannes , Christ Bodo , Kurz Haymo 
Published: August 2002

AbstractThe origin of vascular pericytes (PCs) and smooth muscle cells (vSMCs) in the brain has hitherto remained an open question. In the present study, we used the quail‐chick chimerization technique to elucidate the lineage of cranial PCs/vSMCs. We transplanted complete halves of brain anlagen, or dorsal (presumptive neural crest [NC]) or ventral cranial neural tube. Additional experiments included transplantations of neuroectoderm into limb mesenchyme, and of head mesoderm or limb mesenchyme into paraxial head mesoderm. After interspecific transplantation of quail brain rudiment, graft‐derived vSMCs were found in the vessel walls of the grafted brain. Notably, transplanted ventral neural tube also gave rise to vSMCs. After grafting of quail head mesoderm, quail endothelial cells were found in the host brain, but no vSMCs of donor origin. Grafting of quail whole or ventral neural tube into the limb bud led to endowment of graft and host vessels with graft‐derived vSMCs. Quail limb bud mesenchyme contributed to vSMCs in the ectopic neural graft, but, when transplanted into paraxial head mesenchyme, it did not form intraneural vSMCs. After orthotopic transplantation of cranial NC, graft‐derived vSMCs were not only found in meninges and brain of the operated side, but also on the contralateral side. Our results show that 1) avian cranial neuroectoderm is able to differentiate into vSMCs of the brain; 2) this potential is not restricted to the prospective NC; and 3) neither cranial mesoderm nor cranially transplanted limb bud mesoderm can give rise to brain vSMC. J. Comp. Neurol. 442:78–88, 2002. © 2002 Wiley‐Liss, Inc.
On the theory of a Cosserat point and shear locking in thin beams
Authors: Rubin M. B. 
Published: August 2002

AbstractIt is well known that with the assumption of constant strain elements, the Galerkin approach yields a numerical solution of the equilibrium equations of a beam with shear deformation which exhibits the unphysical feature of shear locking. Here, it is shown that the numerical solution that is based on the theory of a Cosserat point converges to the exact solution of the beam theory even when the kinematics are consistent with the constant strain assumption and the beam thickness approaches zero. The main difference between these two numerical approaches is the way they each determine the constitutive equations (or stiffnesses) of the elements. The Galerkin approach determines the stiffnesses of each element by integrating the constitutive equations for the beam assuming that the kinematic approximation is valid pointwise. In contrast, the constitutive equations of the Cosserat point are related to derivatives of a strain energy function and the constitutive constants are determined using a physical approach which matches the responses to simple shear and pure bending. The results indicate that the Cosserat approach takes full advantage of the reduced number of degrees of freedom used to describe the beam. Copyright © 2001 John Wiley & Sons, Ltd.
Visual perception of texture of textiles
Authors: Lee Wonjoung , Sato Masako 
Published: August 2002

AbstractThe mechanism of visual texture perception was investigated by measuring visual evaluation values. Textile samples of different surface structures were examined, along with corresponding image samples rendered on paper. The relation between physical properties of textiles and light reflected from the textiles, and the relation between the reflected light stimulating the eyes of the subject and the psychological perception of texture are discussed. © 2001 John Wiley & Sons, Inc. Col Res Appl, 26, 469–477, 2001
The Virtual Service Grid: an architecture for delivering high‐end network services
Authors: Weissman Jon B. , Lee Byoung‐Dai 
Published: August 2002

AbstractThis paper presents the design of a new system architecture, Virtual Service Grid (VSG), for delivering high‐performance network services. The VSG is based on the concept of the virtual service which provides location, replication, and fault transparency to clients accessing remotely deployed high‐end services. One of the novel features of the virtual service is the ability to self‐scale in response to client demand. The VSG exploits network and service information to make adaptive dynamic replica selection, creation, and deletion decisions. We describe the VSG architecture, middleware, and replica management policies. We have deployed the VSG on a wide‐area Internet testbed to evaluate its performance. The results indicate that the VSG can deliver efficient performance for a wide range of client workloads, both in terms of reduced response time and in the utilization of system resources. Copyright © 2002 John Wiley & Sons, Ltd.
Kinetics of HL‐60 cell entry to apoptosis during treatment with TNF‐α or camptothecin assayed by the stathmo‐apoptosis method
Authors: Smolewski Piotr , Grabarek Jerzy , Lee Brian W. , Johnson Gary L. , Darzynkiewicz Zbigniew 
Published: August 2002

AbstractBackgroundDuration of apoptosis, from onset to final disintegration of the cell, is often short and variable. The apoptotic index (AI), as a snapshot of a transient event of variable length, does not truly represent incidence of apoptosis in the studied cell population. We recently proposed to estimate the cumulative apoptotic index (CAI) by inducing stathmo‐apoptosis. A fluorescent inhibitor of caspases (FLICA) FAM‐VAD‐FMK is used to arrest the process of apoptosis and thereby prevent cell disintegration. Simultaneously, the arrested/apoptotic cells become FLICA‐labeled. In the present study, this approach was applied to measure kinetics of HL‐60 cell entrance into apoptosis induced via cell surface death receptor or a mitochondria‐initiated pathway.Materials and MethodsCultures of HL‐60 cells were treated with either TNF‐α or camptothecin (CPT) in the absence or constant presence of 10–50 μM FLICA. The CAI was measured at different time points for up to 48 h by flow cytometry. Bivariate analysis of DNA content and cell labeling with FLICA was used to correlate apoptosis with the cell‐cycle position.ResultsSelective loss of apoptotic cells seen in HL‐60 cell cultures exposed to either TNF‐α or CPT alone was prevented in cultures containing FLICA. Addition of FLICA alone had no effect on cell viability. The percentage of FLICA‐labeled cells was plotted as a function of time after addition of TNF‐α or CPT. The rate of cell entry to apop‐ tosis was subsequently estimated from the slopes of the stathmo‐apoptotic plot. The slopes revealed that the TNF‐α or CPT‐treated cells asynchronously underwent apoptosis with a stochastic‐like kinetics and at two different rates. About 50% of cells in the TNF‐α‐treated cultures underwent apoptosis during the initial 6 h at a rate of ∼8% of cells per hour; the remaining cells were undergoing apoptosis at a rate of ∼2.5% of cells per hour for up to 24 h. Also, about 50% of the CPT‐treated cells, predominantly those in S phase of the cell cycle, underwent apoptosis within the initial 8 h of CPT exposure, at a rate of ∼7% of cells per hour. Remaining cells were undergoing apoptosis at a rate of ∼1% of cells per hour during up to 48 h exposure to CPT. Spontaneous apoptosis in the untreated cultures occurred at a rate of 0.2% of cells per hour.ConclusionsThis approach provides a means for measuring the kinetics of cell entrance to apoptosis (caspase activation) in large populations of cells in relation to the cell‐cycle position. Cytometry 47:143–149, 2002. © 2002 Wiley‐Liss, Inc.
Fine‐needle aspiration cytology of umbilical nodules: “Sister Joseph's nodule”
Authors: Sahai Kavita , Kapila Kusum , Verma Kusum 
Published: August 2002

AbstractMetastatic tumor deposits in the umbilicus are not uncommon. Fine‐needle aspiration cytology is an important, simple, cost‐effective diagnostic tool for delineating the value of umbilical nodules. However, only a few reviews and case reports of diagnosis of umbilical metastases by fine‐needle aspiration cytology are available. A review of 52 cases of umbilical nodule aspirates over a 16‐yr period forms the basis of this brief report. Diagn. Cytopathol. 25:309–310, 2001. © 2001 Wiley‐Liss, Inc.
Permeability and single‐channel properties of mesenteric, basilar, and septal (coronary) artery smooth‐muscle P2X receptors
Authors: Lewis Carolyn J. , Davies Noel W. , Evans Richard J. 
Published: August 2002

AbstractP2X1 receptors for ATP are expressed in vascular smooth muscle and are thought to underlie the native artery smooth muscle rapidly desensitising α,β‐methylene ATP (α,β‐meATP) sensitive P2X receptor phenotype. We have characterised the ionic permeability and single‐channel conductance from rat mesenteric, basilar, and septal (coronary) arteries. The relative permeabilities (PX/PNa) to methylamine, dimethylamine, and Tris were essentially the same for all three arteries and give an estimate of the minimum diameter of the ionic pore as 0.8 nm. The P2X receptor channels in arteries had a high calcium permeability (PCa2+/PNa ∼3.5). In outside‐out patches, α,β‐meATP evoked transient currents with a single‐channel conductance of ∼12 pS (in physiological solution with 2.5 mM Ca2+ and 1 mM Mg2+). The single‐channel conductance was increased to ∼17 pS with a 0.1 mM Ca2+‐ and nominally Mg2+‐free physiological solution. These properties for artery P2X receptors are essentially the same as for recombinant P2X1 receptors and confirm that homomeric P2X1 receptors underlie the native P2X receptor current phenotype in these arteries. Drug Dev. Res. 52:164–169, 2001. © 2001 Wiley‐Liss, Inc.
Regulation of biliary secretion by extracellular nucleotides
Authors: Feranchak Andrew P. , Fitz J. Gregory 
Published: August 2002

AbstractBile formation is an essential function of the liver and depends upon complimentary actions of hepatocytes and intrahepatic bile duct cells, or cholangiocytes. Cholangiocytes contribute importantly to the volume and composition of bile secreted by the liver through absorption and secretion of fluid and electrolytes. Biophysical measurements suggest that increases in Cl– permeability at the apical membrane of cholangiocytes represent an important cellular site for regulation of secretion. Recent evidence suggests that extracellular ATP may serve as a signal modifying cholangiocyte secretion through the regulation of membrane Cl– permeability. Through activation of P2Y2 receptors in the apical (luminal) membrane of cholangiocytes, ATP functions as a local autocrine/paracrine regulatory factor that modulates biliary secretion. Consequently, the purpose of this review is to describe the cellular mechanisms thought to contribute to ATP release and review the evidence supporting a role for ATP in the regulation of cholangiocyte Cl– secretion and bile formation. Characterization of the factors that regulate local nucleotide concentrations and purinergic signaling may represent therapeutic targets for the pharmacologic modulation of bile composition and flow. Drug Dev. Res. 52:232–238, 2001. © 2001 Wiley‐Liss, Inc.