bluuebunny/crossref_metadata_2025_split huggingface dataset:
Transradial renal angioplasty: Initial experience
Authors: Shuck John , Khan Amid , Cavros Nick , Galanakis Stylianos , Patel Vishal 
Published: August 2002

AbstractWe report our early experience of a new technique of renal angioplasty utilizing the radial approach. Certain anatomic considerations continue to make access from above via the arm the preferable approach in selected patients in renal artery stenosis. We have utilized the transradial technique for renal artery angioplasty and stenting successfully in four patients. The development of coronary guidewire (0.014″)‐based peripheral balloons and stent delivery systems has miniaturized equipment sufficiently to make the transradial approach attractive. Present equipment allows for stenting of renal arteries of up to 7 mm with the use of 6 Fr guiding catheters. Present equipment length remains a limitation in taller patients. The transradial approach should be considered in those patients with renal artery or aortoiliac anatomy favoring an approach from the arm. Cathet Cardiovasc Intervent 2001;54:346–349. © 2001 Wiley‐Liss, Inc.
Stereochemical terminology and its discontents
Authors: Mislow Kurt 
Published: August 2002

AbstractScrutiny of the purported misuse of some current stereochemical terms shows that obsolescence and faulty syntax may be less of a problem than previously assumed. Furthermore, changes in stereochemical terminology over time are not always due to obsolescence or to novel developments in chemical technology; for example, technical developments played no role whatsoever in the semantic transmutations over time of the terms “diastereomer” and “pseudoasymmetry.” Finally, definitions of many stereochemical terms acquire meaning only within a given context and therefore cannot always be easily formulated. A prime example is the definition of “chirality,” the concept at the heart of stereochemistry and, not coincidentally, the name of the journal in which this essay appears in print. Chirality 14:126–134, 2002. © 2002 Wiley‐Liss, Inc.
Cyclic AMP‐dependent protein kinase A plays a role in the directed migration of human keratinocytes in a DC electric field
Authors: Pullar Christine E. , Isseroff R. Rivkah , Nuccitelli Richard 
Published: August 2002

AbstractSkin wound healing requires epithelial cell migration for re‐epithelialization, wound closure, and re‐establishment of normal function. We believe that one of the earliest signals to initiate wound healing is the lateral electric field generated by the wound current. Normal human epidermal keratinocytes migrate towards the negative pole, representing the center of the wound, in direct currents of a physiological strength, 100 mV/mm. Virtually nothing is known about the signal transduction mechanisms used by these cells to sense the endogenous electric field. To elucidate possible protein kinase (PK) involvement in the process, PK inhibitors were utilized. Two important findings have been described. Firstly, addition of 50 nM KT5720, an inhibitor of PKA, resulted in a 53% percent reduction in the directional response of keratinocytes in the electric field, while not significantly affecting general cell motility. The reduction was dose‐dependent, there was a gradual decrease in the directional response from 5 to 50 nM. Secondly, addition of 1 μM ML‐7, a myosin light chain kinase inhibitor, resulted in an approximate 31% decrease in the distance the cells migrated without affecting directional migration. The PKC inhibitors GF109203X at 4 μM and H‐7 at 20 μM and W‐7, a CaM kinase inhibitor, did not significantly alter either directed migration or cell migration, although they all resulted in a slight reduction in directional migration. D‐erythro‐sphingosine at 15 μM, a PKC inhibitor, had virtually no effect on either migration distance or directed migration. These findings demonstrate that divergent kinase signaling pathways regulate general cell motility and sustained directional migration and highlight the complexity of the signal transduction mechanisms involved. The inhibitor studies described in this paper implicate a role for PKA in the regulation of the directional migratory response to applied electric fields, galvanotaxis. Cell Motil. Cytoskeleton 50:207–217, 2001. © 2001 Wiley‐Liss, Inc.
Initiation of cell locomotility is a morphogenetic checkpoint in thyroid epithelial cells regulated by ERK and PI3‐kinase signals
Authors: Yap Alpha S. 
Published: August 2002

AbstractEpithelial locomotility is a fundamental determinant of tissue patterning that is subject to strict physiological regulation. The current study sought to identify cellular signals that initiate cell migration in cultured thyroid epithelial cells. Porcine thyroid cells cultured as 3‐dimensional follicles convert to 2‐dimensional monolayers when deprived of agents that stimulate cAMP/PKA signaling. This morphogenetic event is driven by the activation of cell‐on‐substrate locomotility, providing a convenient assay for events that regulate the initiation of locomotion. In this system, the extracellular signal regulated kinase (ERK) pathway became activated as follicles converted to monolayer, as demonstrated by immunoblotting for activation‐specific phosphorylation and nuclear accumulation of ERK. Inhibition of ERK activation using the drug PD98059 effectively prevented cells from beginning to migrate. PD98059 inhibited cell spreading, actin filament reorganization and the assembly of focal adhesions, cellular events that mediate the initiation of thyroid cell locomotility. Akt (PKB) signaling was also activated during follicle‐to‐monolayer conversion and the phosphoinositide 3‐kinase (PI3‐kinase) inhibitor, wortmannin, also blocked the initiation of cell movement. Wortmannin did not, however, block activation of ERK signaling. These findings, therefore, identify the ERK and PI3‐kinase signaling pathways as important stimulators of thyroid cell locomotility. These findings are incorporated into a model where the initiation of thyroid cell motility constitutes a morphogenetic checkpoint regulated by coordinated changes in stimulatory (ERK, PI3‐kinase) and tonic inhibitory (cAMP/PKA) signaling pathways. Cell Motil. Cytoskeleton 49:93–103, 2001. © 2001 Wiley‐Liss, Inc.
Vascular endothelial growth factor overexpression is correlated with von Hippel‐Lindau tumor suppressor gene inactivation in patients with sporadic renal cell carcinoma
Authors: Igarashi Hiroshi , Esumi Mariko , Ishida Hajime , Okada Kiyoki 
Published: August 2002

AbstractBACKGROUNDA high frequency of genetic alterations of the von Hippel‐Lindau (VHL) gene and overexpression of the vascular endothelial growth factor (VEGF) gene have been observed independently in human sporadic renal cell carcinoma (RCCs), but to the authors' knowledge the association between the two has not been characterized in primary sporadic RCC. In the current study the authors report the simultaneous comparison of the biallelic inactivation status of the VHL gene and VEGF expression levels in patients with sporadic RCC.METHODSDNA and RNA were extracted from 27 sporadic RCC samples. Mutation was analyzed by direct sequencing of the amplified VHL DNA and cDNA. Loss of heterozygosity (LOH) of the gene was analyzed at three polymorphic markers. The VEGF mRNA was measured using Northern blot analysis.RESULTSMutations of the VHL gene were found in 14 of 27 RCC samples (51.9%). LOH analysis by a VHL‐intragenic polymorphic marker and 2 extragenic microsatellite markers, D3S1560 and D3S1317, showed that LOH occurred in 10 of 15 RCC samples (66.7%). Overexpression of VEGF mRNA was observed in 17 of 27 RCC cases (63.0%): 15 of the 18 RCC samples estimated to have at least 1 hit, but only 2 of the 6 RCC samples with 0‐1 hit, and none of the 3 RCC samples in which the VHL gene was not inactivated.CONCLUSIONSVEGF overexpression was found to be correlated with both monoallelic and biallelic VHL inactivation. Alteration of the VHL gene is believed to cause angiogenesis in RCC cases through the overexpression of VEGF. Cancer 2002;95:47–53. © 2002 American Cancer Society.DOI 10.1002/cncr.10635
Connection from cortical area V2 to MT in macaque monkey
Authors: Anderson John C. , Martin Kevan A.C. 
Published: August 2002

AbstractThe extrastriate visual area of the macaque monkey called MT or V5, receives its input from multiple sources. We have previously examined the synaptic connections made by V1 cells that project to MT (Anderson et al., 1998). Here, we provide a similar analysis of the projection from V2 to MT. The major target of the V2 projection in MT is layer 4, where it forms clusters of asymmetric (excitatory) synapses. Unlike the V1 projection, it also forms synapses in layers 1 and 2 and does not form synapses in layer 6. The most frequently encountered targets of boutons labeled from V2 were spines (67% in layer 4; 82% in layer 2/3). Unusually, only 5/12 boutons examined in layer 1 actually formed synapses. Unlike the V1 projection, multisynaptic boutons were rare (mean, 1.1 synapses per bouton vs. 1.7 for the V1 projection). Like the V1 projection, the input to MT from any point in V2 is sparse (contributing approximately 4–6% of the asymmetric synapses in the densest clusters in layer 4). The synapses of the V2 projection were similar in size to those of the V1 projection (0.1 μm2 vs. 0.09 μm2) and both formed more complex postsynaptic densities on spines than on dendritic shafts. The clear differences between the V1 and V2 projection to MT indicate that their functions are complementary rather than completely overlapping. J. Comp. Neurol. 443:56–70, 2002. © 2002 Wiley‐Liss, Inc.
Immunohistochemical localization of three different prepro‐GnRHs in the brain and pituitary of the European sea bass (Dicentrarchus labrax) using antibodies to the corresponding GnRH‐associated peptides
Authors: González‐Martínez David , Zmora Nilli , Mañanos Evaristo , Saligaut Dany , Zanuy Silvia , Zohar Yonathan , Elizur Abigail , Kah Olivier , Muñoz‐Cueto José Antonio 
Published: August 2002

AbstractThe distribution of the cells expressing three prepro‐gonadotrophin‐releasing hormones (GnRH), corresponding to salmon GnRH (sGnRH), seabream GnRH (sbGnRH), and chicken GnRH‐II (cGnRH‐II) forms, was studied in the brain and pituitary of the sea bass (Dicentrarchus labrax) by using immunohistochemistry. To circumvent the cross‐reactivity problems of antibodies raised to GnRH decapeptides, we used specific antibodies generated against the different sea bass GnRH‐associated peptides (GAP): salmon GAP (sGAP), seabream GAP (sbGAP), and chicken‐II GAP (cIIGAP). The salmon GAP immunostaining was mostly detected in terminal nerve neurons but also in ventral telencephalic and preoptic perikarya. Salmon GAP‐immunoreactive (ir) fibers were observed mainly in the forebrain, although sGAP‐ir projections were also evident in the optic tectum, mesencephalic tegmentum, and ventral rhombencephalon. The pituitary only receives a few sGAP‐ir fibers. The seabream GAP‐ir cells were mainly detected in the preoptic area. Nevertheless, sbGAP‐ir neurons were also found in olfactory bulbs, ventral telencephalon, and ventrolateral hypothalamus. The sbGAP‐ir fibers were only observed in the ventral forebrain, innervating strongly the pituitary gland. Finally, chicken‐II GAP immunoreactivity was only detected in large synencephalic cells, which are the origin of a profuse innervation reaching the telencephalon, preoptic area, hypothalamus, thalamus, pretectum, posterior tuberculum, mesencephalic tectum and tegmentum, cerebellum, and rhombencephalon. However, no cIIGAP‐ir fibers were detected in the hypophysis. These results corroborate the overlapping of sGAP‐ and sbGAP‐expressing cells in the forebrain of the sea bass, and provide, for the first time, unambiguous information on the distribution of projections of the three different GnRH forms expressed in the brain of a single species. J. Comp. Neurol. 446:95–113, 2002. © 2002 Wiley‐Liss, Inc.
Neonatally elevated serotonin levels alter terminal arbors of individual retinal ganglion cells in superior colliculus of hamsters
Authors: Crnko‐Hoppenjans Tracy A. , Mooney Richard D. , Rhoades Robert W. 
Published: August 2002

AbstractPrevious studies from this laboratory showed that sprouting of serotoninergic (5‐HT) axons in the hamster's superior colliculus (SC), induced by a single subcutaneous injection of 5,7‐dihydroxytryptamine (5,7‐DHT) at birth (postnatal day 0 [P‐0]), resulted in an increased terminal distribution of the uncrossed retinocollicular projection that was not associated with any changes in the number or distribution of ipsilaterally projecting retinal ganglion cells. The present study was undertaken to determine what effect this manipulation had on the terminal arbors of such axons. Retinocollicular axons of normal and 5,7‐DHT‐treated animals were anterogradely labeled with small intraretinal injections of the lipophilic dye 1,1′‐dioctadecyl‐3,3,3′,3′‐tetramethylindocarbocyanine perchlorate (DiI) on P‐16. After tissue processing on P‐19, single retinocollicular axon arbors were reconstructed by using confocal microscopy. Quantitative analysis indicated that arbors from 5,7‐DHT‐treated hamsters had significantly greater total fiber lengths, areas, and volumes than those from normal animals. There were no differences between axons from the two groups in number of branch points, distribution of relative branch lengths, and numbers of bouton‐like swellings. These results support the hypothesis that increased SC concentrations of 5‐HT alter development of the uncrossed retinocollicular pathway such that a greater territory is covered by individual terminal arbors but that the number of synaptic contacts per arbor remains constant. This may explain, at least in part, the abnormally widespread distribution of the aggregate ipsilateral projection. J. Comp. Neurol. 432:528–536, 2001. © 2001 Wiley‐Liss, Inc.
Target‐derived BDNF (brain‐derived neurotrophic factor) is essential for the survival of developing neurons in the isthmo‐optic nucleus
Authors: Von Bartheld Christopher S. , Johnson James E. 
Published: August 2002

AbstractNeurons in the peripheral nervous system depend on single neurotrophic factors, whereas those in the brain are thought to utilize many different trophic factors. This study examined whether some neurons in the brain critically depend on a single trophic factor during development. Neurons in the isthmo‐optic nucleus (ION) of chick embryos respond to exogenous brain‐derived neurotrophic factor (BDNF). Relatively high concentrations of endogenous BDNF were present in the ION of 14–18‐day‐old chick embryos. ION target cells in the retina were immunolabeled for BDNF but showed surprisingly low levels of BDNF mRNA. These data suggest that ION target cells derive some BDNF from other retinal sources. No BDNF mRNA was detected in the ION itself. ION neurons had a very efficient retrograde transport system for BDNF and exogenous BDNF arrived in the ION intact. When the ION was deprived of endogenous trkB ligands by injection of trkB fusion proteins in the eye, cell death of ION neurons was enhanced, and this effect was mimicked by BDNF‐specific blocking antibodies in the eye. TrkB fusion proteins in the retina induced cell death of ION neurons prior to visible effects on ION target cells in the retina. Immunolabel for endogenous BDNF was sparse in pyknotic ION neurons, suggesting that ION neurons with low BDNF content were eliminated by apoptosis. These data show that BDNF is an essential target‐derived trophic factor for developing ION neurons and thereby validate the neurotrophic hypothesis for at least one neuronal population in the brain. J. Comp. Neurol. 433:550–564, 2001. © 2001 Wiley‐Liss, Inc.
Complementary finite element methods applied to the numerical homogenization of 3D absolute permeability
Authors: Trykozko Anna , Zijl Wouter 
Published: August 2002

AbstractTo be able to use a limited number of relatively large grid cells in numerical oil reservoir simulators and groundwater models, upscaling of the absolute permeability is frequently applied. The spatial fine‐scale permeability distribution, which is generally obtained from geological and geostatistical models, is incorporated in the relatively large grid cells of the numerical model. If the porous medium may be approximated as a periodic medium, upscaling can be performed by the homogenization method. Numerical homogenization gives rise to an approximation error. The complementarity between the conformal–nodal finite element method and the mixed–hybrid finite element method has been used to quantify this error. The two methods yield, respectively, upper and lower bounds for the eigenvalues of the coarse‐scale permeability tensor. Results of numerical experiments obtained using tetrahedral meshes are shown both in the far field and in the near well region. Copyright © 2001 John Wiley & Sons, Ltd.
A Monte Carlo simulation of the determination of mean particle volume using the Cavalieri estimator
Authors: Hammel Ilan , Lagunoff David 
Published: August 2002

AbstractBackgroundA common morphometric problem is the determination of an estimate of the size of biological particles obtained from measurements made on a sample of profiles observed in sections. Results are reported typically in terms of mean caliper diameter or mean volume of the particle.MethodsWe have investigated the use of the Cavalieri estimator for obtaining estimates of mean particle volume using a Monte Carlo simulation. Samples of spherical and ellipsoidal particles were generated by computer and serially sectioned at a fixed mean thickness with a small, imposed random variation. The area of each profile was determined and the volume of the particle was calculated according to the Cavalieri estimator. The influence on the estimate of the mean particle volume and its 95% confidence interval was evaluated for several variables: the shape of the particles, the standard deviation of the particle volume in the population, the section thickness, and the standard deviation of the section thickness.ResultsThe results obtained with the Cavalieri estimator correspond favorably with those obtained with previously reported alternative methods. This leads to a recommendation for the strong consideration for the use of the Cavalieri estimator in cases in which it is technically feasible to obtain at least three sections through the individual particles. Graphs are provided, which relate the confidence interval for the mean volume to the number of particles measured. Cytometry 47:138–141, 2002. © 2002 Wiley‐Liss, Inc.
Therapeutic use of nucleotides in respiratory and ophthalmic diseases
Authors: Yerxa Benjamin R. 
Published: August 2002

AbstractNucleotide agonists of P2Y2 receptors are potentially useful therapeutics for treating respiratory diseases such as chronic bronchitis and cystic fibrosis, and for treating ophthalmic indications such as dry eye and retinal detachment. INS365 is a chemically stable nucleotide P2Y2 agonist that, when inhaled, enhances mucociliary clearance of the airways and thus may be useful for treating chronic bronchitis in which retained mucus is a hallmark. On the ocular mucosa, P2Y2 agonists stimulate the secretion of salt, water, and mucus. This mechanism of basal tear secretion forms the scientific basis for the clinical investigation of INS365 as a tear film secretagogue for the treatment of dry eye disease. INS365 ophthalmic solution is currently in Phase II clinical trials in the US. INS37217, a next‐generation nucleotide P2Y2 agonist with enhanced metabolic stability and a potentially longer duration of action, is being developed for the treatment of cystic fibrosis and retinal detachment. In cystic fibrosis, P2Y2 agonists activate an alternative chloride channel, thereby restoring hydration of the airway surface and promoting mucociliary clearance. In experimental models of retinal detachment, INS37217 injected into the back of the eye activates P2Y2 receptors on the retinal pigmented epithelium, promoting fluid absorption in the subretinal space and thus facilitating retinal reattachment. Since receptors for nucleotides are found throughout the body, nucleotides and their analogs have great therapeutic promise when administered locally to the desired site of action. Drug Dev. Res. 52:196–201, 2001. © 2001 Wiley‐Liss, Inc.
Corpus cavernosum dysfunction in diabetic rats: effects of combined α‐lipoic acid and γ‐linolenic acid treatment
Authors: Keegan Alan , Cotter Mary A. , Cameron Norman E. 
Published: August 2002

AbstractBackgroundThe effects of streptozotocin‐induced diabetes on nitric oxide (NO)‐mediated relaxation of rat corpus cavernosum smooth muscle to neurogenic and endothelial stimulation was examined. The aim was to assess the effects of treatment with low doses of the antioxidant, α‐lipoic acid, and the ω‐6 essential fatty acid, γ‐linolenic acid, either separately or in combination.MethodsTreatment was preventive from diabetes induction or corrective over 4 weeks after 4 weeks of untreated diabetes. Corpus cavernosum responses were examined in vitro.ResultsNeither diabetes nor treatment affected contractile responses to transmural electrical field stimulation of noradrenergic nerves. Stimulation of phenylephrine precontracted cavernosa in the presence of guanethidine and atropine caused relaxation via the nitrergic innervation. Maximum relaxation responses were 40% and 46% decreased after 4 and 8 weeks of diabetes, respectively. α‐Lipoic acid, γ‐linolenic acid combination treatment fully prevented this deficit, and partially (52%) corrected the effect of 4 weeks of untreated diabetes. Neither α‐lipoic acid nor γ‐linolenic components alone had significant effects, which suggests that there were synergistic interactions between the drugs. Both 4 and 8 weeks of untreated diabetes reduced maximum endothelium‐dependent relaxation of phenylephrine precontracted cavernosa to acetylcholine by approximately 40%. While α‐lipoic acid or γ‐linolenic acid were ineffective, joint treatment fully prevented and corrected this diabetic endothelial deficit. Neither diabetes nor treatment affected endothelium‐independent relaxation to the NO donor, sodium nitroprusside.ConclusionThe data show that α‐lipoic acid and γ‐linolenic acid interact synergistically to improve NO‐mediated neurogenic and endothelium‐dependent relaxation of corpus cavernosum in experimental diabetes. Copyright © 2001 John Wiley & Sons, Ltd.
No role of calcium‐ and ATP‐dependent potassium channels in insulin‐induced vasodilation in humans in vivo
Authors: Abbink Evertine J. , Walker Annabel J. , van der Sluijs Henk A. , Tack Cees J. , Smits Paul 
Published: August 2002

AbstractThe mechanism of insulin‐induced vasodilation has not been completely clarified, but could be important in future treatment strategies of insulin resistance. Recently, a role for calcium‐dependent and ATP‐dependent potassium (KCa and KATP) channels in insulin‐induced vasodilation has been demonstrated in in vitro studies. A role for these channels has never been confirmed in humans in vivo. Therefore, we investigated the role of these channels in insulin‐induced vasodilation in humans in vivo. A hyperinsulinemic euglycemic clamp was combined with intra‐arterial infusion of placebo, tetraethylammonium (blocker of KCa channels) or glibenclamide (blocker of KATP channels) in three groups of 12 healthy volunteers. Bilateral forearm blood flow was measured with venous occlusion plethysmography. Systemic hyperinsulinemia induced a 20±9% vasodilation (p=0.001). Neither tetraethylammonium nor glibenclamide reduced this vasodilation as compared to placebo. According to the results of the present study, insulin‐induced vasodilation seems not to be mediated by the opening of KCa and KATP channels in humans in vivo. Copyright © 2002 John Wiley & Sons, Ltd.