bluuebunny/crossref_metadata_2025_split huggingface dataset:
Dexamethasone prophylaxis for paclitaxel hypersensitivity
Authors: Gilbar Peter , Ridge Alison 
Published: May 2003

Objective. To evaluate single-dose intravenous (IV) dexamethasone as a viable alternative to the standard two-dose oral protocol and as a method for the administration of corticosteroid prophylaxis in the prevention of paclitaxel-induced hypersensitivity reactions (HSR). Method. A retrospective analysis of pharmacy dispensing and medical records was undertaken to ascertain those patients who had received IV corticosteroid prophylaxis, details of therapy and incidence of HSR. A comprehensive literature review was also undertaken to determine the incidence of HSR to paclitaxel in patients receiving a similar IV dexamethasone premedication protocol. Results. Thirty-five patients received prophylactic dexamethasone 20 mg IV, given 30 minutes before paclitaxel infusion. Patients also received promethazine 25 mg IV and ranitidine 50 mg IV. No HSR were reported. A number of studies were identified in which IV corticosteroid prophylaxis was used, including retrospective analyses, a prospective report, clinical studies involving paclitaxel employing IV corticosteroids as part of the premedication regimen, and comparative retrospective studies. Only one study described IV corticosteroid therapy adversely. Conclusions. For the safe administration of paclitaxel, premedication with corticosteroids, and H1 and H2 receptor antagonists, is essential. The administration of IV dexamethasone 20 mg, given 30 minutes before paclitaxel infusion, is an appealing and practical alternative to the standard oral prophylactic regimen and offers benefits to patients in terms of compliance, convenience, ease of administration and flexibility.
Ca2+-Induced Ca2+ Release in the Pancreatic β-Cell: Direct Evidence of Endoplasmic Reticulum Ca2+ Release
Authors: Graves Thomas K. , Hinkle Patricia M. 
Published: May 2003

Abstract
The role of the Ca2+-induced Ca2+ release channel (ryanodine receptor) in MIN6 pancreatic β-cells was investigated. An endoplasmic reticulum (ER)-targeted “cameleon” was used to report lumenal free Ca2+. Depolarization of MIN6 cells with KCl led to release of Ca2+ from the ER. This ER Ca2+ release was mimicked by treatment with the ryanodine receptor agonists caffeine and 4-chloro-m-cresol, reversed by voltage-gated Ca2+ channel antagonists and blocked by treatment with antagonistic concentrations of ryanodine. The depolarization-induced rise in cytoplasmic Ca2+ was also inhibited by ryanodine, which did not alter voltage-gated Ca2+ channel activation. Both ER and cytoplasmic Ca2+ changes induced by depolarization occurred in a dose-dependent manner. Glucose caused a delayed rise in cytoplasmic Ca2+ but no detectable change in ER Ca2+. Carbamyl choline caused ER Ca2+ release, a response that was not altered by ryanodine. Taken together, these results provide strong evidence that Ca2+-induced Ca2+ release augments cytoplasmic Ca2+ signals in pancreatic β-cells.
Dehydroepiandrosterone Modulates Endothelial Nitric Oxide Synthesis Via Direct Genomic and Nongenomic Mechanisms
Authors: Simoncini Tommaso , Mannella Paolo , Fornari Letizia , Varone Gaetano , Caruso Antonella , Genazzani Andrea R. 
Published: May 2003

Abstract
Dehydroepiandrosterone (DHEA) and its sulfate ester (DHEAS) are the major circulating steroid hormones in humans, and their levels progressively decline with age. Epidemiological studies suggest that DHEA/DHEAS concentrations may be inversely related to cardiovascular risk, but disagreement exists on this issue. Preliminary studies show that DHEA regulates vascular function, but few data have been published on the mechanisms. We show that DHEA administration to human endothelial cells triggers nitric oxide synthesis, due to enhanced expression and stabilization of endothelial nitric oxide synthase (eNOS). Additionally, DHEA rapidly activates eNOS, through a nontranscriptional mechanism that depends on ERK1/2 MAPK, but not on phosphatidylinositol 3-kinase/Akt. DHEA is not converted to estrogens or androgens by endothelial cells, and its genomic and nongenomic effects are not blocked by antagonists of the estrogen, progesterone, glucocorticoid, or androgen receptors, suggesting that DHEA acts through a specific receptor. Oral DHEA administration to ovariectomized Wistar rats dose-dependently restores aortic eNOS levels and eNOS activity, confirming the effects of DHEA in vivo. Our present data suggest that DHEA may have direct genomic and nongenomic effects on the vascular wall that are not mediated by other steroid hormone receptors, leading to eNOS activation and induction.
Diazoxide Attenuates Glucose-Induced Defects in First-Phase Insulin Release and Pulsatile Insulin Secretion in Human Islets
Authors: Song Soon H. , Rhodes Christopher J. , Veldhuis Johannes D. , Butler Peter C. 
Published: May 2003

Abstract
Humans with type-2 diabetes mellitus (TTDM) have hyperglycemia (∼11 mm) and impaired glucose-mediated insulin secretion characterized by impaired first-phase insulin release (FPIR) and pulsatile insulin release. Culture of islets from nondiabetic humans in very high glucose concentrations (∼20–30 mm) for 96 h causes impaired FPIR. We sought to determine 1) whether human islets cultured at a glucose concentration of approximately 11 mm (comparable to TTDM) recapitulates impaired insulin secretion in TTDM, specifically impaired FPIR and insulin pulse mass with an increased proinsulin/insulin (PI/I) secretion ratio; and 2) whether these changes can be attenuated by addition of diazoxide to islets cultured with 11 mm glucose. Islets cultured with 11 mm glucose for 96 h had 75% depleted insulin stores (P &lt; 0.05), decreased FPIR and insulin pulse mass (P &lt; 0.05), and an approximately 3-fold increase in the ratio of PI/I islet content and in secretion ratio (P &lt; 0.05). Addition of diazoxide to islets cultured with 11 mm glucose decreased insulin secretion during static incubation, leading to relative preservation of insulin stores and enhanced insulin secretion during subsequent perifusion; FPIR increased by 162% (P &lt; 0.05) and insulin pulse mass by 150% (P &lt; 0.05) vs. no diazoxide. The mean islet PI/I content and islet PI/I secretion ratio were also decreased by approximately 70% (P &lt; 0.05) by prior addition of diazoxide to islets during culture with 11 mm glucose. FPIR and insulin pulse mass were related to islet insulin stores (P &lt; 0.001 for FPIR and P &lt; 0.001 for pulse amplitude). In conclusion, the pattern of defects of insulin secretion present in TTDM (impaired FPIR and pulsatile insulin secretion, increased PI/I ratio) can be recapitulated in human islets cultured with 11 mm glucose for 96 h. These defects can be at least partially offset by concurrent inhibition of insulin secretion by diazoxide, which also preserves insulin stores. Defective insulin secretion in TTDM may be, at least in part, due to depletion of available insulin stores secondary to chronic increased demand (insulin resistance and hyperglycemia) in the setting of a decreased β-cell mass.
Characterization of the Androgen-Regulated Prostate-Specific T Cell Receptor γ-Chain Alternate Reading Frame Protein (TARP) Promoter
Authors: Cheng Wing-Shing , Giandomenico Valeria , Pastan Ira , Essand Magnus 
Published: May 2003

AbstractTARP (T cell receptor γ-chain alternate reading frame protein) is uniquely expressed in males in prostate epithelial cells and prostate cancer cells. Here we demonstrate that TARP expression is regulated by testosterone at the transcriptional level through specific binding of androgen receptor to an androgen response element in the proximal TARP promoter. We further demonstrate that the promoter specifically initiates reporter gene expression in TARP-positive prostate cancer cell lines. To develop a regulatory sequence for prostate-specific gene expression, we constructed a chimeric sequence consisting of the TARP promoter and the prostate-specific antigen (PSA) enhancer. We found that in the prostatic adenocarcinoma cell line LNCaP, the transcriptional activity of the regulatory sequence consisting of a TARP promoter and PSA enhancer is 20 times higher than the activity of a regulatory sequence consisting of the PSA promoter and PSA enhancer. Thus, our studies define a regulatory sequence that may be used to restrict expression of therapeutic genes to prostate cancer cells and may therefore play a role in prostate cancer gene therapy.
Identification of a Putative Autocrine Bone Morphogenetic Protein-Signaling Pathway in Human Ovarian Surface Epithelium and Ovarian Cancer Cells
Authors: Shepherd Trevor G. , Nachtigal Mark W. 
Published: May 2003

AbstractBone morphogenetic proteins (BMPs) are members of the TGFβ superfamily of cytokines that are involved in development, differentiation, and disease. In an analysis of normal ovarian surface epithelium (OSE) and ovarian cancer (OC) cells, we observed BMP4 mRNA expression and found that primary OC cells produce mature BMP4. In addition, each member of the downstream signaling pathway was expressed in primary OSE and OC cells. Smad1 was phosphorylated and underwent nuclear translocation in normal OSE and OC cells upon treatment with BMP4. Interestingly, the BMP target genes ID1 and ID3 were up-regulated 10- to 15-fold in primary OC cells, compared with a 2- to 3-fold increase in normal OSE. The growth of several primary OC cells was relatively unaltered by BMP4 treatment; however, long-term BMP4 treatment of primary OC cells resulted in decreased cell density as well as increased cell spreading and adherence. These data demonstrate the existence and putative function of BMP signaling in normal OSE and OC cells, and thus the continued examination of BMP4 signaling in the regulation of these two processes will be critical to further our current understanding of the role of BMP biology in OC pathogenesis.
Effect of severe protein-calorie malnutrition on the penetration kinetics of trimethoprim and sulfamethoxazole to the deep tissues of Wistar rats
Authors: Lares-Asseff Ismael , Pérez Maria Gabriela , Camacho Guadalupe A , Toledo Aleiandra R , Guillé Maria del Carmen López Adrián J , Sosa Martha G 
Published: May 2003

Abstract
This study shows the effect that severe malnourishment has on the kinetics of antibiotic penetration in tissues. A total of 104 male Wistar rats, 21 days old, were randomly divided into eight groups. Five groups of experimental rats were severely malnourished (SM) and three further groups were considered well-nourished control groups (WN). A single dose of trimethoprim–sulfamethoxazole (TMP-SMX) was administered intraperitoneally. Blood samples were taken by heart puncture and five organs were extracted 0–24 h after the administration of the drug. HPLC was used to assess the amount of trimethoprim and sulfamethoxazole in fluids. The elimination half-life for trimethoprim from plasma was longer in SM rats with a median of 3.15 h; in WN rats, it was 0.390 h. Clearance was slower in SM rats: 646.72 mL μg−1 h−1 vs 3036.38 mL μg−1 h−1 in WN rats (P &lt; 0.05). Tissue penetration was much higher for trimethoprim, with penetration indexes of 0.80–5.66 in WN rats, compared with 0.35–2.14 in SM rats. In the case of sulfamethoxazole, penetration indexes were 0.029–1.13 for WN and 0.075–0.657 for SM rats. Similarly, the penetration ratio to muscle and heart tissue was lower in SM rats. However, penetration to kidney, lung, liver and spleen was greater in SM rats. It is evident that severe SM decreases the capacity of trimethoprim more importantly than sulfamethoxazole biotransformation.
Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit vascular smooth muscle cell proliferation via differential effects on the cell cycle
Authors: Brooks Gavin , Yu Xue-Mei , Wang Yuequn , Crabbe M James C , Shattock Michael J , Harper Jane V 
Published: May 2003

Abstract
Abnormal vascular smooth muscle cell (VSMC) proliferation plays an important role in the pathogenesis of both atherosclerosis and restenosis. Recent studies suggest that high-dose salicylates, in addition to inhibiting cyclooxygenase activity, exert an antiproliferative effect on VSMC growth both in-vitro and in-vivo. However, whether all non-steroidal anti-inflammatory drugs (NSAIDs) exert similar antiproliferative effects on VSMCs, and do so via a common mechanism of action, remains to be shown. In this study, we demonstrate that the NSAIDs aspirin, sodium salicylate, diclofenac, ibuprofen, indometacin and sulindac induce a dose-dependent inhibition of proliferation in rat A10 VSMCs in the absence of significant cytotoxicity. Flow cytometric analyses showed that exposure of A10 cells to diclofenac, indometacin, ibuprofen and sulindac, in the presence of the mitotic inhibitor, nocodazole, led to a significant G0/G1 arrest. In contrast, the salicylates failed to induce a significant G1 arrest since flow cytometry profiles were not significantly different from control cells. Cyclin A levels were elevated, and hyperphosphorylated p107 was present at significant levels, in salicylate-treated A10 cells, consistent with a post-G1/S block, whereas cyclin A levels were low, and hypophosphorylated p107 was the dominant form, in cells treated with other NSAIDs consistent with a G1 arrest. The ubiquitously expressed cyclin-dependent kinase (CDK) inhibitors, p21 and p27, were increased in all NSAID-treated cells. Our results suggest that diclofenac, indometacin, ibuprofen and sulindac inhibit VSMC proliferation by arresting the cell cycle in the G1 phase, whereas the growth inhibitory effect of salicylates probably affects the late S and/or G2/M phases. Irrespective of mechanism, our results suggest that NSAIDs might be of benefit in the treatment of certain vasculoproliferative disorders.
Direct, differential-equation-based in-vitro–in-vivo correlation (IVIVC) method
Authors: Buchwald Peter 
Published: May 2003

Abstract
A new, differential equation-based in-vitro–in-vivo correlation (IVIVC) method is proposed that directly relates the time-profiles of in-vitro dissolution rates and in-vivo plasma concentrations by using one-or multi-compartment pharmacokinetic models and a corresponding system of differential equations. The rate of in-vivo input is connected to the rate of in-vitro dissolution through a general functional dependency that allows for time scaling and time shifting. A multiplying factor that accounts for the variability of absorption conditions as the drug moves along is also incorporated. Two data sets incorporating slow-, medium-, and fast-release formulations were used to test the applicability of the method, and predictive powers were assessed with a leave-one-formulation-out approach. All fitted parameters had realistic values, and good or acceptable fits and predictions were obtained as measured by plasma concentration mean squared errors and percent AUC errors. Introduction of step-down functions that account for the transit of the dosage form past the intestinal sites of absorption proved useful. By avoiding the integral transforms used in the existing deconvolution- or convolution-based IVIVC models, the present method can provide increased transparency, improved performance, and greater modelling flexibility.
Can the USP paddle method be used to represent in-vivo hydrodynamics?
Authors: Scholz Annette , Kostewicz Edmund , Abrahamsson Bertil , Dressman Jennifer B 
Published: May 2003

Abstract
Experiments in-vitro and in dogs were conducted to find in-vitro hydrodynamic conditions that can be used to represent gastrointestinal motility patterns. Specifically, the dissolution performance of micronised and coarse-grade felodipine (a poorly soluble, neutral, lipophilic drug) was studied in a biorelevant medium in the USP paddle apparatus at various paddle speeds. Ratios of percentage dissolved (slower:faster rev min−1) were calculated pairwise. These ratios were then compared with AUC ratios obtained in a corresponding pharmacokinetic study in Labradors, in which the absorption of both the micronised and coarse-grade felodipine had been compared under two gastrointestinal hydrodynamic conditions. Using a paddle speed combination of 75 and 125 rev min−1 to represent the motility patterns in response to administration of normal saline and 5% glucose, respectively, the in-vitro ratios (75:125 rev min−1 dissolution ratio was 91% for the micronised and 46% for the coarse-grade powder) showed good agreement with the pharmacokinetic data (saline-to-glucose absorption ratio was 98% for the micronised and 46% for the coarse-grade powder). It was concluded that, provided an appropriate composition is chosen for the dissolution test, the USP paddle apparatus can be used to reflect variations in hydrodynamic conditions in the upper gastrointestinal tract.
Quantitative structure–activity relationship (QSAR) analysis of cationic complexes of heart perfusion imaging agents and subsequent proposition of two different uptake mechanisms
Authors: Zhang Huabei , Li Bo , Dai Mei 
Published: May 2003

Abstract
Some physicochemical and quantum-chemical discriptors of two series of cationic complexes of heart perfusion imaging agents ([99mTc1(NO)Cl(PL)2]+ and [99mTc-Mine]+ series) have been obtained using a semi-empirical quantum mechanics method — ZINDO/1. Quantitative structure–activity relationships (QSARs) between these descriptors and heart uptake were investigated by multiple linear regression analysis method, as the result of which, several equations were obtained. Fairly complete new heart uptake mechanisms, redox mechanism for [99mTc1(NO)Cl(PL)2]+ series and passively transport mechanism for [99mTc-Mine]+ series are proposed based on the results shown in the equations.
Thiomersal enhances the binding of histamine to the H1 receptor, but not histamine-stimulated inositol phosphate formation
Authors: Jain Vandana , McWilliams Emma , Young Michael 
Published: May 2003

Abstract
Thiomersal (thimerosal) was a weak inhibitor of the binding of [3H]mepyramine to histamine H1 receptors in guinea-pig cerebellar membranes (11 ± 1% inhibition at 10 μm, 32 ± 3% inhibition at 300 μm). However, in the concentration range 3–30 μm, thiomersal enhanced the binding of histamine to the H1 receptor, as reflected by the displacement of curves of histamine inhibition of [3H]mepyramine binding to lower concentrations, without any change in the Hill coefficient. The ratio of the IC50 values (the concentration giving 50% inhibition) in the absence and presence of thiomersal increased from 1.8 with 3 μm to 3.6 with 30 μm thiomersal. There was no consistent effect of thiomersal at concentrations of 30 μm and below on curves of mepyramine inhibition of [3H]mepyramine binding. In the presence of 10 μm thiomersal histamine-induced accumulation of inositol phosphates in U373 MG astrocytoma cells was partially inhibited (37 ± 8% inhibition of the maximum response), without any significant change in the EC50 (the concentration giving the half maximal response) for histamine. Thus although histamine binding was potentiated by thiomersal, there was no potentiation of an H1 receptor-mediated functional response.
A Novel Three-dimensional Rhombic Network Self-assembled by the First Reported cis-[Mn(4,4′-azpy)2(H2O)4]2+ Cations through Hydrogen Bonding Interactions
Authors: Li Baolong , Li Baozong , Lang Jianping , Zhang Yong 
Published: May 2003

Abstract
A novel complex [Mn(4,4′-azpy)2(H2O)4](ClO4)2·2(4,4′-azpy)·0.5(H2O) was synthesized and characterized. It is composed of the first example cis-[Mn(4,4′-azpy)2(H2O)4]2+ cations. Three-dimensional rhombic network is formed through hydrogen bonding interactions between coordinated water and mono-coordinated 4,4′-azpy and noncoordinated 4,4′-azpy.
(Salen)ruthenium-catalyzed Desymmetrization of meso-Diols (2). Apical Ligand Effect on Enantioselectivity
Authors: Shimizu Hideki , Katsuki Tsutomu 
Published: May 2003

Abstract
Enantiotopos-selectivity of aerobic oxidation of meso-diols using chiral (nitrosyl)Ru(salen) complexes as catalyst was found to be dependent on the nature of their apical ligand. The oxidation with complex 5 possessing an apical hydroxo ligand as the catalyst showed moderate to good enantioselectivity (up to 80% ee).
A Novel TTP Donor Containing a PROXYL Radical for Magnetic Molecular Conductors
Authors: Fujiwara Hideki , Lee Ha-Jin , Kobayashi Hayao , Fujiwara Emiko , Kobayashi Akiko 
Published: May 2003

Abstract
A TTP donor containing a stable PROXYL radical was synthesized to develop conducting-magnetic bifunctional materials and its structure and physical properties were investigated. Furthermore its cation radical salts were prepared and revealed their conducting and magnetic properties.
Non-aggregated Intercalation of Dicationic Tetraphenylporphyrinatoantimony(V) Complexes into Smectite Clay Layers
Authors: Shiragami Tsutomu , Nabeshima Keiko , Matsumoto Jin , Yasuda Masahide , Inoue Haruo 
Published: May 2003

Abstract
Adsorption and intercalation of +2 charged cationic [3-(trimethylammonio)propoxo(methoxo)(tetraphenylporphyrinato)antimony(V)]2+ (1a) into an artificially synthesized smectite clay were studied. The red shift of Soret band in UV-spectra for 1a in an aqueous colloidal clay solution and analyses of X-ray diffraction of the obtained complex between 1a and the clay indicate the intercalation of 1a into the clay interlayer. Ammonium cationic part on an axial ligand led to the effective non-aggregated intercalation of 1a into the clay.
Conversion of a Hydroperoxo Complex, (TpiPr2)(py)Pd-OOH, into a Cyclic Alkylperoxo Complex, [HB(pziPr2)2(pz-3-CMe2-5-i-Pr)](py)Pd-OO, Catalyzed by Cu(II) Species [TpiPr2: Hydrotris(3,5-diisopropylpyrazolyl)borato]
Authors: Kujime Masato , Hikichi Shiro , Akita Munetaka 
Published: May 2003

Abstract
Treatment of a hydroperoxopalladium complex, (TpiPr2)(py)Pd-OOH, with a catalytic amount of a Cu(II) species resulted in peroxidation of the methine moiety of an isopropyl group proximal to the metal center to give a cyclic alkylperoxopalladium complex.
Fast Removal of Basic Dyes by a Novel Magnetic Nano-adsorbent
Authors: Liao Min-Hung , Wu Kun-Yang , Chen Dong-Hwang 
Published: May 2003

Abstract
A novel magnetic nano-adsorbent, prepared by covalently binding polyacrylic acid onto Fe3O4 magnetic nanoparticles, possessed high ion-exchange capacity and was successfully used for the fast removal of crystal violet.
Double Strand DNA Cleavage by a Dinuclear Cu(II) Complex
Authors: Kim Jung Hee , Kim Soo Hyun 
Published: May 2003

Abstract
A dinuclear Cu(II) complex with 1,3-bis(1,4,7-triaza-1-cyclononyl)propane cleaved plasmid DNA to relaxed circular and linear forms at pH 7.3 and 30 °C. Under the same conditions, double strand cleavage by the corresponding mononuclear Cu(II)([9]aneN3) complex was negligible.
Structure and Luminescence Properties of the Tetradentate β-Diketonate–Europium(III) Complexes
Authors: Yuan Jingli , Sueda Shinji , Somazawa Ryosuke , Matsumoto Keiichiro , Matsumoto Kazuko 
Published: May 2003

Abstract
The luminescence properties of Eu3+ complexes with a series of tetradentate β-diketones were compared and it was found that the Eu3+ complexes of bis(β-diketonyl)-o-terphenyl type ligands have stronger luminescence. The crystal structure determination of the Eu3+ complex with 4,4″-bis(4,4,4-trifluoro-1,3-dioxobutyl)-o-terphenyl (H2btbt) showed that the complex is dinuclear having a unique cage structure.
Synthesis of Novel Liquid Crystals which Possess gem-Difluorocyclopropane Moieties
Authors: Itoh Toshiyuki , Ishida Nanae , Ohashi Masakazu , Asep Riswoko , Nohira Hiroyuki 
Published: May 2003

Abstract
Synthesis of two types of novel chiral liquid crystal molecules that possess a gem-difluorocyclopropane moiety has been accomplished and their properties of liquid crystal were examined.
Enhancement of Peroxygenase Activity of Horse Heart Myoglobin by Modification of Heme-propionate Side Chains
Authors: Hayashi Takashi , Matsuda Takaaki , Hisaeda Yoshio 
Published: May 2003

Abstract
A myoglobin reconstituted with an artificially created heme having two benzene moieties bound at the terminal of two heme-propionates shows a clear enhancement in peroxygenase activity toward thioether and styrene oxidations due to the expanding hydrophobic heme pocket.