bluuebunny/crossref_metadata_2025_split huggingface dataset:
Influence of Solution Composition on the Formation of Crystalline Scales
Authors: Glade H. , Ulrich J. 
Published: March 2003

AbstractScale formation is a difficulty encountered with water containing ions of sparingly soluble salts that can readily precipitate on heat transfer surfaces in evaporative concentration operations. Scale formation, hindering the heat transfer process, increases specific energy consumption and operating costs and causes frequent shut down of the evaporator for cleaning. The effects of changes in composition of the solution due to evaporation and CO2 release on the formation of crystalline scales in seawater evaporators are studied. A model that predicts the CO2 release is presented. The carbonate system in the salt solution on its whole flow path through the evaporator and the scaling (crystallization) tendency are described. Simulation results for different process configurations are shown and the differences are discussed, particularly with regard to the incrustation tendency.
Cluster Formation in Precrystalline Solutions
Authors: Sorensen T.J. , Sontum P.C. , Samseth J. , Thorsen G. , Malthe‐Sorenssen D. 
Published: March 2003

AbstractSmall Angle Neutron Scattering (SANS) gives evidence of colloidal structures or clusters in solutions of vanillin in aqueous alcohol. Interpretation of the data gives the same result as the Photon Correlation Spectroscopy technique: stable or metastable fractal clusters. The size of these clusters increases as a function of the parameters that control supersaturation, but is stable with respect to time. These structures, called metastable clusters, are closely related to the observed liquid‐liquid phase separation at high solute concentration. Another type of clusters is found to co‐exist with the metastable clusters at a lower solute concentration. The same type of structures is found in a two‐component system of vanillin in 2‐methyl‐2‐butanol. They slowly grow as a function of time, and are called labile clusters. These colloidal structures are assumed to be precrystalline clusters giving rise to nuclei in crystallization.
Formation of Monodispersed Nano‐ and Micro‐Particles Controlled in Size, Shape, and Internal Structure
Authors: Sugimoto T. 
Published: March 2003

AbstractSize control of monodispersed particles must normally be performed during the very short nucleation period, because the final particle number is determined by the end of the nucleation and it does not change until the end of the particle growth. On the other hand, the shape control is mainly performed by adsorption of shape controllers during the growth period, although in some cases the crystal structure of the nuclei may have essential influence on the morphology of the grown particles. The internal structure of each particle is often strongly affected by the action of shape controllers. This article deals with the fundamental mechanisms of the nucleation, growth, and structural formation of monodispersed nano‐ and micro‐particles, leading to the control of their size, shape, and internal structure.
Combining univariate calibration information through a mixed‐effects model
Authors: Liao Jason J. Z. 
Published: March 2003

AbstractIt is common practice to calibrate a common value by combining information from different sources such as days, people, instruments and laboratories. Under each individual source a univariate calibration can be used to calibrate the unknown. Then the common unknown can be estimated by combining the estimates from each source as a weighted mean (Johnson DJ, Krishnamoorthy K. J. Am. Statist. Assoc. 1996; 91: 1707–1715) or through a multivariate calibration setting by combining information first and then estimating the common value (Liao JJZ. J. Chemometrics 2001; 15: 789–794). In this paper a mixed‐effects model approach is proposed to combine good characteristics from both approaches. Simulations show that the mixed‐effects model has better bias and mean squared error (MSE) performance than the univariate and multivariate approaches. A real data set is used to demonstrate the good characteristics of the mixed‐effects model approach. Copyright © 2003 John Wiley & Sons, Ltd.
Differences in the pathologic and molecular features of intraductal breast carcinoma between younger and older women
Authors: Rodrigues Neesha A. , Dillon Deborah , Carter Darryl , Parisot Nicole , Haffty Bruce G. 
Published: March 2003

AbstractBACKGROUNDPatients diagnosed with ductal carcinoma in situ (DCIS) at a young age appear to have a different natural history and biology, including a higher local relapse rate, than patients diagnosed later in life. The current study compared various pathologic and molecular features of DCIS arising in a cohort of young women with those of DCIS arising in a cohort of older women to identify potential biologic differences between these two populations of patients.METHODSThe study population consisted of 20 patients age < 42 years and 34 patients age > 60 years who were treated at Yale University School of Medicine with breast‐conserving therapy (BCT) and whose archival paraffin blocks were available and had sufficient tumor for staining. The original slides from each case were reviewed and the most representative specimen block from each case was processed for immunohistochemical staining. Pathologic characteristics evaluated for each case included histology, grade, and presence of necrosis. Paraffin‐embedded sections were immunohistochemically evaluated for expression of HER‐2/neu, estrogen receptor (ER), progesterone receptor (PR), bcl‐2, cyclin D1, Ki‐67, and p53.RESULTSAlthough there was no difference in pathologic features of the tumors between the two groups, HER‐2/neu was found to be overexpressed in a greater percentage of the younger population (P = 0.06). There was no apparent difference in expression of the other markers. Of note, HER‐2/neu expression was correlated with high nuclear grade (P = 0.004), necrosis (P = 0.06), and ER and PR negativity (P = 0.01 and P = 0.03, respectively) in the combined population.CONCLUSIONSThe current study data suggested that HER‐2/neu overexpression in younger patients may characterize a biologic difference in their tumor and may partially contribute to their higher risk of recurrence. Further studies are needed to assess whether this difference holds independent of grade and to evaluate the prognostic significance of HER‐2/neu overexpression in DCIS. Cancer 2003;97:1393–1403. © 2003 American Cancer Society.DOI 10.1002/cncr.11204
Flow cytometry and quantitative immunohistochemical study of cell cycle regulation proteins in invasive breast carcinoma
Authors: Michels Jean‐Jacques , Duigou Françoise , Marnay Jacques , Henry‐Amar Michel , Delozier Thierry , Denoux Yves , Chasle Jacques 
Published: March 2003

AbstractBACKGROUNDBetween January 11, 1991 and January 8, 1992, 104 patients with previously untreated, invasive, primitive breast carcinoma were admitted to the authors' hospital.METHODSFor each patient, flow cytometry DNA analyses on frozen samples and on immunohistochemical staining were performed, including Ki‐67, cyclin A, p53, and p21waf1 (p21), with assessment of the percentages of positive nuclei were assessed. Correlations with classic clinicopathologic data and survival (overall, metastasis free, or recurrence free) and a multivariate analysis were performed.RESULTSAfter a multivariate analysis according to a Cox model that was stratified by age, tumor size, tumor grade, lymph node status, and receptor status, among the factors studied, the presence of p21 was the unique remaining prognostic factor for patients with invasive breast carcinoma. Because of the lack of a correlation between p21 and proliferative factors (Ki‐67, S‐phase, and cyclin A), the authors combined p21 with those markers and found that, for the different combinations, after statistical analysis, only p21 combined with S‐phase or with cyclin A and lymph node status were salient survival prognostic factors.CONCLUSIONSImmunohistochemical study of proteins involved in the cell cycle and assessment of proliferative activity using flow cytometric DNA analysis aided the authors in singling out correlations of cyclin A and S‐phase, along with p21, with metastasis free survival and overall survival in patients with invasive breast carcinoma. These promising results will require confirmation in a larger series of patients. Cancer 2003;97:1376–86. © 2003 American Cancer Society.DOI 10.1002/cncr.11209
Impact of very old age on hypothalamic dopaminergic neurons in the female rat: A morphometric study
Authors: Sánchez Hilda Liliana , Silva Liliana Beatriz , Portiansky Enrique Leo , Goya Rodolfo Gustavo , Zuccolilli Gustavo Oscar 
Published: March 2003

AbstractDopaminergic neurons of the A12 (tuberoinfundibular dopaminergic system) and A14 (periventricular dopaminergic system) hypothalamic areas exert a tonic inhibitory control of prolactin secretion. Tuberoinfundibular dopaminergic system neuron function is known to decline during aging in rats, but little is known about the impact of extreme age on neuron number and morphology in the two systems. We morphometrically assessed the neurons of the tuberoinfundibular dopaminergic system and the periventricular dopaminergic system in female rats 6 (young, Y), 24 (old, O), and 30–32 (senescent, S) months old. Serial coronal sections of fixed hypothalami were immunohistochemically labeled for tyrosine hydroxylase, and immunoreactive perikarya from the A12 and A14 areas were quantitatively characterized and compared among the three age groups. Radioimmunoassay was used to measure serum prolactin. The number of A12 tyrosine hydroxylase–immunoreactive perikarya showed a steady decline with age, whereas the number of A14 tyrosine hydroxylase–immunoreactive perikarya remained stable from young to old age but showed a sharp drop in the senescent rats. In the old rats, tyrosine hydroxylase–immunoreactive neuronal area (A12 = 135.37 and A14 = 158.79 μm2) was significantly higher than that of young (A12 = 72.56 and A14 = 99.7 μm2) and senescent animals (A12 = 95.5 and A14 = 106.5 μm2). Densitometric assessment of median eminence tyrosine hydroxylase immunoreactivity revealed a steady age‐related reduction of tyrosine hydroxylase content in the median eminence. Serum prolactin levels increased steadily with age. We conclude that, in the female rat, aging brings about a progressive loss of both tuberoinfundibular dopaminergic system and periventricular dopaminergic system neurons, which becomes more conspicuous at extreme ages. J. Comp. Neurol. 458:319–325, 2003. © 2003 Wiley‐Liss, Inc.
Ultrastructural analysis of a putative magnetoreceptor in the beak of homing pigeons
Authors: Fleissner Gerta , Holtkamp‐Rötzler Elke , Hanzlik Marianne , Winklhofer Michael , Fleissner Günther , Petersen Nikolai , Wiltschko Wolfgang 
Published: March 2003

AbstractWith the use of different light and electron microscopic methods, we investigated the subcellular organization of afferent trigeminal terminals in the upper beak of the homing pigeon, Columba livia, which are about 5 μm in diameter and contain superparamagnetic magnetite (SPM) crystals. The SPM nanocrystals are assembled in clusters (diameter, ∼1–2 μm). About 10 to 15 of these clusters occur inside one nerve terminal, arranged along the cell membrane. Each SPM cluster is embedded in a solid fibrous cup, open towards the cell surface, to which the cluster adheres by delicate fiber strands. In addition to the SPM clusters, a second inorganic iron compound has been identified: noncrystalline platelets of iron phosphate (about 500 nm wide and long and maximally 100 nm thick) that occur along a fibrous core of the terminal. The anatomic features suggested that these nerve endings could detect small intensity changes of the geomagnetic field. Such stimuli can induce deformations of the SPM clusters, which could be transduced into primary receptor potentials by mechanosensitive membrane receptor channels. The subepidermal fat cells surrounding the nerve endings prevent the inside from external mechanical stimuli. These structural findings corresponded to conclusions inferred from rock magnetic measurements, theoretical calculations, model experiments, and behavioral data, which also matched previous electrophysiologic recordings from migratory birds. J. Comp. Neurol. 458:350–360, 2003. © 2003 Wiley‐Liss, Inc.
False resurrections: Distinguishing regenerated from spared axons in the injured central nervous system
Authors: Steward Oswald , Zheng Binhai , Tessier‐Lavigne Marc 
Published: March 2003

AbstractSeveral recent studies report that axon regeneration can be induced in the mature mammalian nervous system by novel treatments or genetic manipulations. In assessing these reports, it is important to be mindful of the history of regeneration research, which is littered with the corpses of studies that reported regeneration that later proved incorrect. One important reason is the “spared axon conundrum,” in which axons that survive a lesion are mistakenly identified as having regenerated. Here, we illustrate the problem and propose criteria that may be used to identify regenerated vs. spared axons, focusing on the injured spinal cord. J. Comp. Neurol. 459:1–8, 2003. © 2003 Wiley‐Liss, Inc.
“Dormant basket cell” hypothesis revisited: Relative vulnerabilities of dentate gyrus mossy cells and inhibitory interneurons after hippocampal status epilepticus in the rat
Authors: Sloviter Robert S. , Zappone Colin A. , Harvey Brian D. , Bumanglag Argyle V. , Bender Roland A. , Frotscher Michael 
Published: March 2003

AbstractThe “dormant basket cell” hypothesis suggests that postinjury hippocampal network hyperexcitability results from the loss of vulnerable neurons that normally excite insult‐resistant inhibitory basket cells. We have reexamined the experimental basis of this hypothesis in light of reports that excitatory hilar mossy cells are not consistently vulnerable and inhibitory basket cells are not consistently seizure resistant. Prolonged afferent stimulation that reliably evoked granule cell discharges always produced extensive hilar neuron degeneration and immediate granule cell disinhibition. Conversely, kainic acid‐induced status epilepticus in chronically implanted animals produced similarly extensive hilar cell loss and immediate granule cell disinhibition, but only when granule cells discharged continuously during status epilepticus. In both preparations, electron microscopy revealed degeneration of presynaptic terminals forming asymmetrical synapses in the mossy cell target zone, including some terminating on γ‐aminobutyric acid‐immunoreactive elements, but no evidence of axosomatic or axoaxonic degeneration in the adjacent granule cell layer. Although parvalbumin immunocytochemistry and in situ hybridization revealed decreased staining, this apparently was due to altered parvalbumin expression rather than basket cell death, because substance P receptor‐positive interneurons, some of which contained residual parvalbumin immunoreactivity, survived. These results confirm the inherent vulnerability of dendritically projecting hilar mossy cells and interneurons and the relative resistance of dentate inhibitory basket and chandelier cells that target granule cell somata. The variability of hippocampal cell loss after status epilepticus suggests that altered hippocampal structure and function cannot be assumed to cause the spontaneous seizures that develop in these animals and highlights the importance of confirming hippocampal pathology and pathophysiology in vivo in each case. J. Comp. Neurol. 459:44–76, 2003. © 2003 Wiley‐Liss, Inc.
Circuit theory of power factor correction in switching converters
Authors: Tse C. K. 
Published: March 2003

AbstractThis paper discusses the circuit theory aspects of power factor correction in switching converter circuits. The discussion begins with an examination of the requirement of power factor correction in dc/dc converters. Using the concept of zero‐order converter circuits, sufficient conditions for a dc/dc converter circuit to provide power factor correction are derived. The duality principle is applied to generate new converter circuits that can achieve power factor correction. The practical application of power factor correction is considered in conjunction with the requirement of tight output voltage regulation. Detailed study of the circuit configuration that can simultaneously provide power factor correction and output regulation is given. Based on a general three‐port model, the voltage regulator with power factor correction capability is studied in terms of the power flow between the input port, output port and energy storage port. A detailed consideration of the power flow among the three ports leads to the derivation of all possible minimal configurations that can achieve power factor correction and voltage regulation. The efficiencies of these minimal configurations are studied theoretically, leading to the concept of ‘reduced redundant power processing’ which provides important clue to efficiency improvement. Another issue addressed in this paper is the synthesis of practical circuits that can provide power factor correction and output regulation. In particular, four practical minimal configurations that achieve reduced redundant power processing are considered. A systematic synthesis procedure is derived for creating converter circuits that achieve power factor correction and output voltage regulation. The control issue is also investigated in depth, pinpointing the basic requirement on the number of control parameters needed and its relationship with the operating mode. Copyright © 2003 John Wiley & Sons, Ltd.
1,4‐dihydropyridine calcium channel ligands: Selectivity of action. The roles of pharmacokinetics, state‐dependent interactions, channel isoforms, and other factors
Authors: Triggle David J. 
Published: March 2003

AbstractThe selectivity of action of the clinically available calcium channel antagonists depends on a number of factors: 1) Mode of calcium mobilization—intracellular and extracellular sources. 2) Class and subclass of calcium channel involved. 3) Pharmacokinetic considerations, including distribution and interactions with cell membranes. 4) State‐dependent interactions—voltage‐ and frequency‐dependent interactions. 5) Pathologic state of tissue and channel regulation. These factors will be illustrated with particular reference to the 1,4‐dihydropyridine series of ligands. The Ca2+ channel antagonists may be placed in several classes according to their rates of onset and offset of action, and the overall cardiovascular activity of an agent can profoundly alter its hemodynamic response. Additionally, third‐generation agents such as lacidipine and lercenadipine partition extensively into plasma membranes according to membrane composition. Calcium mobilization through the L‐type channel is the dominant target of the available antagonists: hence, systems that rely dominantly or exclusively on other mobilization processes are insensitive. Renal afferent and efferent arterioles that regulate glomerular flow and resistance are sensitive to the powerful vasoconstrictive effects of angiotensin II; however, only the processes in the afferent arteriole are sensitive to the Ca2+ channel antagonists. An important and subtle process for conferring tissue selectivity of action is derived from state‐dependent interactions between channel and drug, whereby, according to the modulated‐receptor hypothesis, drugs may exhibit preferential affinity for or access to different states of the channel—resting, open, or inactivated. Transitions between these states are determined by membrane potential and biochemical factors, including channel phosphorylation. The 1,4‐dihydropyridine series exhibit significant and structure‐dependent voltage‐dependent interactions, which reflect a preferential interaction with open and/or inactivated channel states. The differential pharmacology of the L‐type Ca2+ channel is a further determinant of tissue selectivity. The cardiovascular system expresses three different α1 subunits—CaV1.2A–C—and although a detailed pharmacological comparison is not yet available, there is sufficient evidence to indicate important differences. Thus, the 1,4‐dihydropyridine nisoldipine interacts differentially with recombinant channels derived from cardiac and vascular smooth muscle. A number of disease states, both clinical and experimental, have been associated with changes in Ca2+ channel expression and function, although the causal relationship is often not established. Thus, in cardiac hypertrophy and failure the majority of studies reveal a reduction in L‐type channel number or function. Drug Dev. Res. 58:5–17, 2003. © 2003 Wiley‐Liss, Inc.
Two patterns of ion channelopathies relating to arrhythmias and direct and indirect blockade of ion channels by antiarrhythmic agents
Authors: Dai De‐Zai , Zhang Guang‐Qin , Yang Ping , Ma Yu‐Ping 
Published: March 2003

AbstractCardiac arrhythmias remain a major cause of mortality in cardiovascular diseases. Abnormal repolarization of the myocardium which relates to the occurrence of arrhythmias is developed by cardiac ion channelopathies. LQTS is an inherited disorder of mutations in genes encoding K+ and Na+ channels. A novel mutation in the HERG gene was discovered in a patient from an LQTS family. The mutation was at 2184 position by A→C of the cDNA of the HERG gene where tyrosine (TAC) was replaced by an early appearance of STOP (TAA). A loss of 492 amino acids from the nucleotide binding domain to the carboxyl group resulted in channel dysfunction and a prolonged QTc of >460 mS. Another mutation of insertion of 9 bps at the minor site between S1 to the –NH2 terminal and a novel mutation of the HMINK gene to replace serine (AGT) by cysteine (GGT) at position 38 were discovered. These two changes exert no effect on the QT interval. An investigation of ion channelopathies was conducted in a previously developed animal model of cardiac remodeling which was developed by chronic treatment with L‐thyroxine for 10 days and shows significant arrhythmogenesis. The upregulation of IKS in the remodeled myocardium was uncovered as an increment of more than two times over control when depolarizing to +20 mV and +40 mV (P < 0.01). IKr was also upregulated by a marked increment of the current density at 0 mV and +20 mV against control (P <0.01). A suppression of IKS and INa by CPU 86017 was observed by direct drug application with an IC50 for IKS with CPU 86017 of 14.4 µM and a significant suppression of INa by 10 µM CPU 86017 (P <0.01). An indirect effect on IKS and IKr was measured by chronic treatment with propranolol and bepridil on days 8–10 of the L‐thyroxine treatment. A reversal of the enhanced IKS and IKr currents was significant in the propranolol group, but less so in the bepridil group. The effect was associated with a relief of the hypertrophied myocardium and production of MDA. In conclusion, there are two patterns of ion channelopathies for inducing arrhythmias. A mutation in genes produces a selective change in the primary sequence of amino acids of a single ion channel, and cardiac remodeling affects multiple channels rather than a selective influence on a single channel by a primary damage to the lipid membrane and transmembrane signaling system. CPU 86017 exerts its blockade directly on the ion channel itself and propranolol and bepridil by chronic treatment block ion channels by an indirect effect mediated by regression of the insult of the membrane and hyperphosphorylation of the ion channels with stimulation by β‐receptors. Drug Dev. Res. 58:42–50, 2003. © 2003 Wiley‐Liss, Inc.