bluuebunny/crossref_metadata_2025_split huggingface dataset:
Predictors of prognosis in patients with olfactory disturbance
Authors: London Brian , Nabet Behnam , Fisher Andrew R. , White Brigitte , Sammel Mary D. , Doty Richard L. 
Published: November 2007

AbstractObjectiveAlthough olfaction is often compromised by such factors as head trauma, viruses, and toxic agents, the olfactory epithelium and sectors of the olfactory bulb have the potential for regeneration. This study assessed the degree to which olfactory function changes over time in patients presenting to a university‐based smell and taste center with complaints of olfactory dysfunction and the influences of etiology (eg, head trauma, upper respiratory infection), sex, age, smoking behavior, degree of initial dysfunction, and other factors on such change.MethodsWell‐validated odor identification tests were administered to 542 patients on 2 occasions separated from one another by 3 months to 24 years. Multivariable regression and χ2 analyses assessed the influences of the variables on the longitudinal changes in olfactory test scores.ResultsOn average, smell test scores improved modestly over time. Patient age, severity of initial olfactory loss, and the duration of dysfunction at first testing were significant predictors of the amount of the change. Etiology, sex, time between the two test administrations, and initial smoking behavior were not significant predictors. The percentage of anosmic and microsmic patients exhibiting statistically significant change in function was 56.72 and 42.86%, respectively. However, only 11.31% of anosmic and 23.31% of microsmic patients regained normal age‐related function over time.InterpretationSome recovery can be expected in a significant number of patients who experience smell loss. The amount of recovery depends on the degree of initial loss, age, and the duration of loss. Etiology, per se, is not a significant determinant of prognosis, in contrast with what is commonly believed. Ann Neurol 2007
Pharmacokinetics of selected chiral flavonoids: hesperetin, naringenin and eriodictyol in rats and their content in fruit juices
Authors: Yáñez Jaime A. , Remsberg Connie M. , Miranda Nicole D. , Vega‐Villa Karina R. , Andrews Preston K. , Davies Neal M. 
Published: November 2007

AbstractThe majority of pharmacokinetic studies of individual flavonoids or after ingestion of foodstuffs have overlooked the chirality of some of these xenobiotics. In order to characterize for the first time the stereoselective pharmacokinetics of three flavonoids, hesperetin, naringenin and eriodictyol were intravenously administered (20 mg/kg) to male Sprague‐Dawley rats, and their stereospecific content was assessed in various fruit juices. Concentrations in serum, urine and fruit juices were characterized via HPLC and verified by LC/MS. Short half‐lives (3–7 h) in serum were observed, while a better estimation of half‐life (12–48 h) and the other pharmacokinetic parameters was observed using urinary data. The three flavonoids are predominantly excreted via non‐renal routes (fe values of 3–7%), and undergo rapid and extensive phase II metabolism. The (2S)‐epimers of the flavonoid glycosides and the S(−)‐enantiomers of the aglycones were predominant and in some instances the organic fruit juices had higher concentrations than the conventional fruit juices. This study reports for the first time the stereospecific pharmacokinetics of three chiral flavonoids and their stereospecific content in fruit juices. It also reports for the first time the stereospecific pharmacokinetics of flavonoids employing urine as a more reliable biological matrix. Copyright © 2007 John Wiley & Sons, Ltd.
Structural basis for the binding of high affinity phosphopeptides to Stat3
Authors: McMurray John S. 
Published: November 2007

AbstractSignal transducer and activator of transcription 3 (Stat3) is constitutively active in a number of cancers where it participates in aberrant transcription of prosurvival, cell cycling, and angiogenesis genes. Since Stat3 initiates its signaling activity through binding of its SH2 domain to phosphotyrosine residues on cell surface receptors, inhibitors targeting this region of the protein are potential chemotherapeutic agents. To date, no NMR or X‐ray crystallographic structures of high‐affinity phosphopeptides complexed with the Stat3 SH2 domain are available to aid in the development of peptidomimetic antagonists. Examination of the crystal structures of several STAT proteins and the complex of Stat1 with Ac‐pTyr‐Asp‐Lys‐Pro‐His‐NH2 led to a hypothesis that the specificity determinant for Stat3, glutamine at position pY+3 in pTyr‐Xxx‐Xxx‐Gln sequences, resides in a unique pocket on the protein surface at the juncture of the third strand of the central β‐sheet and a unique, STAT specific α‐helix. Docking of Ac‐pTyr‐Leu‐Pro‐Gln‐NHBn to the SH2 domain of Stat3 using molecular modeling showed that the Gln binds tightly in this pocket and participates in a network of hydrogen bonds. Novel interactions between the peptide main chain and the protein were also discovered. Phosphopeptide structure‐affinity studies using unnatural amino acids and glutamine derivatives provide evidence for the peptide‐protein interactions revealed by the model and lend support to the binding hypothesis. © 2007 Wiley Periodicals, Inc. Biopolymers (Pept Sci) 90: 69–79, 2008.This article was originally published online as an accepted preprint. The “Published Online” date corresponds to the preprint version. You can request a copy of the preprint by emailing the Biopolymers editorial office at biopolymers@wiley.com
Catalytic Promiscuity in the α/β‐Hydrolase Superfamily: Hydroxamic Acid Formation, CC Bond Formation, Ester and Thioester Hydrolysis in the CC Hydrolase Family
Authors: Li Chen , Hassler Melanie , Bugg Timothy D. H. 
Published: November 2007

AbstractThe haloperoxidase family of α/β‐hydrolases contains enzymes of several different catalytic activities, including esterases, CC hydrolases and cofactor‐independent haloperoxidases (perhydrolases), but the molecular basis of this catalytic promiscuity is not fully understood. The CC hydrolase enzyme MhpC from E. coli is shown to possess esterase and thioesterase activity, and the ability to activate hydroxylamine as a nucleophile to form hydroxamic acid products. The ratio of these activities was examined for nine site‐directed mutant enzymes that contained mutations at nonessential residues in the enzyme active site. Higher levels of esterase and thioesterase activity were found in mutants Phe173Gly and Trp264Gly; this might be due to increased amounts of space in the active site. Higher levels of hydroxamic acid formation activity were found in mutant Asn109His—a mutation found in many haloperoxidase enzymes. Wild‐type and mutant MhpC enzymes were also capable of CC bond formation in organic solvents, and the highest activity was observed in nonpolar solvents. The results provide experimental support for the catalytic promiscuity shown in this family of enzymes, and indicate that differences in catalytic function can be introduced by point mutations.
“Click” Dendrimers: Synthesis, Redox Sensing of Pd(OAc)2, and Remarkable Catalytic Hydrogenation Activity of Precise Pd Nanoparticles Stabilized by 1,2,3‐Triazole‐Containing Dendrimers
Authors: Ornelas Cátia , Aranzaes Jaime Ruiz , Salmon Lionel , Astruc Didier 
Published: November 2007

Abstract“Click” dendrimers containing 1,2,3‐triazolyl ligands that coordinate to PdII(OAc)2 have been synthesized in view of catalytic applications. Five of these dendrimers contain ferrocenyl termini directly attached to the triazole ligand in order to monitor the number of PdII that are introduced into the dendrimers by cyclic voltammetry. Reduction of the PdII–triazole dendrimers by using NaBH4 or methanol yields Pd nanoparticles (PdNPs) that are stabilized either by several dendrimers (G0, DSN) or by encapsulation inside a dendrimer (G1 and G2: DEN), as confirmed by TEM. Relative to PAMAM–DENs (PAMAM=poly(amidoamine)), the “click” DSNs and DENs show a remarkable efficiency and stability for olefin hydrogenation under ambient conditions of various substrates. The influence of the reductant of PdII bound to the dendrimers is dramatic, reduction with methanol leading to much higher catalytic activity than reduction with NaBH4. The most active NPs are shown to be those derived from dendrimer G1, and variation of its termini groups (ferrocenyl, alkyl, phenyl) allowed us to clearly delineate, optimize, and rationalize the role of the dendrimer frameworks on the catalytic efficiencies. Finally, hydrogenation of various substrates catalyzed by these PdNPs shows remarkable selectivity features.
D‐SAP: A New, Noncytotoxic, and Fully Protease Resistant Cell‐Penetrating Peptide
Authors: Pujals Sílvia , Fernández‐Carneado Jimena , Ludevid M. Dolors , Giralt Ernest 
Published: November 2007

AbstractProtease resistant cell‐penetrating peptides (CPPs) are promising carriers for drugs unable to cross the cell membrane. As these CPPs are stable in vivo for much longer periods of time compared to other classes of therapeutic peptides, noncytotoxicity is a property sine qua non for their pharmacological development. Described herein is a fully protease resistant CPP that is noncytotoxic at concentrations up to 1 mM. Proteolytic stability was obtained by chiral inversion of the residues of a known self‐assembling CPP—from all L‐amino acids to all D‐amino acids—and then assessed against trypsin and human serum. Circular dichroism studies confirmed the enantiomeric structure of the analogue, and transmission electron microscopy (TEM) studies indicated that the new inverso analogue retains the ability of the original peptide to self‐assemble. The results of uptake experiments indicate that the protease‐stable (that is, D‐amino acid) analogue of the peptide is internalised by cells to the same extent as the protease‐susceptible (that is, L‐amino acid) parent peptide. Also reported herein are the results of studies on the cellular internalisation mechanism of the all‐D analogue, which reveal the steps followed by the peptide upon its entry into the cell.
A prospective randomized trial of thalidomide with topotecan compared with topotecan alone in women with recurrent epithelial ovarian carcinoma
Authors: Downs Levi S. , Judson Patricia L. , Argenta Peter A. , Ghebre Rahel , Geller Melissa A. , Bliss Robin L. , Boente Matthew P. , Nahhas William A. , Abu‐Ghazaleh Samir Z. , Chen M. Dwight , Carson Linda F. 
Published: November 2007

AbstractBACKGROUND.Thalidomide is an antiangiogenic agent with immune modulating potential. The objective of this study was to determine response rates among women who were treated for recurrent ovarian cancer using topotecan with or without thalidomide.METHODS.Women were enrolled in this multicenter, prospective, randomized phase 2 trial between April 2001 and July 2005. Eligible patients had recurrent epithelial ovarian carcinoma with measurable disease or elevated CA 125 values. Patients had received prior platinum‐based chemotherapy. Treatment arms received topotecan at a dose of 1.25 mg/m2 on Days 1 through 5 of a 21‐day cycle with or without thalidomide starting at a dose of 200 mg per day and then increasing the dose as tolerated. Toxicity was graded according to the National Cancer Institute Common Toxicity Criteria. The chi‐square test was used to assess differences in response and toxicity, and the log‐rank test was used to compare Kaplan‐Meier survival curves.RESULTS.The analysis included 69 women (39 women in the control arm and 30 women in the thalidomide arm). Known prognostic factors, including platinum sensitivity, were represented equally in each arm. The median thalidomide dose was 200 mg per day. The overall response rate in the control arm was 21% (complete response [CR] rate, 18%; partial response [PR] rate, 3%) compared with 47% in the thalidomide arm (CR rate, 30%; PR rate, 17%) (P = .03). The median progression‐free survival for the control arm was 4 months compared with 6 months in the thalidomide arm (P = .02). The median overall survival was 15 months in the control arm and 19 months in the thalidomide arm (P = .67). Toxicities were similar between groups.CONCLUSIONS.The addition of thalidomide to topotecan for the treatment of recurrent ovarian cancer appears to improve response rates, and the authors believe that it warrants study through larger phase 3 trials. Cancer 2008. © 2007 American Cancer Society.
Polyoxomolybdate‐Stabilized Ru0 Nanoparticles Deposited on Mesoporous Silica as Catalysts for Aromatic Hydrogenation
Authors: Boujday Souhir , Blanchard Juliette , Villanneau Richard , Krafft Jean‐Marc , Geantet Christophe , Louis Catherine , Breysse Michèle , Proust Anna 
Published: November 2007

AbstractWe use polyoxometalates as precursors for the preparation of heterogeneous catalysts. In the starting molecular precursor [{Ru(C6Me6)}2Mo5O18{Ru(C6Me6)(H2O)}], three ruthenium arene fragments are supported on a formally lacunary Lindqvist‐type polyoxomolybdate. This species was introduced by incipient wetness impregnation into the porosity of a SBA‐15‐type mesoporous silica. The evolution of the system under reducing atmosphere is followed by several methods, such as temperature‐programmed reduction (TPR), Raman, and X‐ray absorption spectroscopy (XAS). The results indicate that the polyoxometalate structure is retained after grafting on silica and allows the stabilization of Ru0 nanoparticles after reduction. The resulting system exhibits interesting catalytic activity in benzene hydrogenation.
Chemical Transformations of Mono‐ and Bis(buta‐1,3‐dien‐1‐yl)porphyrins: A New Synthetic Approach to Mono‐ and Dibenzoporphyrins
Authors: Silva Ana M. G. , de Oliveira Kleber T. , Faustino Maria A. F. , Neves Maria G. P. M. S. , Tomé Augusto C. , Silva Artur M. S. , Cavaleiro José A. S. , Brandão Paula , Felix Vítor 
Published: November 2007

Abstractβ‐Butadienyl‐ and β,β′‐dibutadienylporphyrins were prepared by the Wittig reaction of β‐formyl‐ and β,β′‐diformyl‐meso‐tetraphenylporphyrins with allylic phosphorus ylide. Subsequent treatment of β‐butadienylporphyrin with dienophiles afforded the corresponding Diels–Alder adducts. In the absence of dienophiles, β‐butadienylporphyrin underwent electrocyclization, followed by oxidation, to give monobenzoporphyrin in good yield. Similarly, adjacent and opposite dibenzoporphyrins were successfully synthesized from adjacent and opposite β,β′‐dibutadienylporphyrins, respectively. This is the first report of electrocyclization of β‐butadienylporphyrins. The structures of mono‐ and dibenzoporphyrin nickel complexes, as well as of a Diels–Alder adduct, were determined by single‐crystal X‐ray diffraction; a strong distortion from the planarity of the porphyrin core was observed. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2008)
The effects of a COX‐2 inhibitor meloxicam on squamous cell carcinoma of the esophagus in vivo
Authors: Liu Jun‐Feng , Zhang Shao‐Wei , Jamieson Glyn G. , Zhu Gui‐Jun , Wu Tie‐Cheng , Zhu Tie‐Nian , Shan Bao‐En , Drew Paul A. 
Published: November 2007

AbstractOur previous study showed that aspirin induced apoptosis of esophageal cancer cells in vitro by inhibiting the pathway of NF‐kappaB downstream regulation of cyclooxygenase‐2. The purpose of this study was to determine if similar changes occurred in vivo in the tumors of patients with SCC of the esophagus who were given a preferential COX‐2 inhibitor, meloxicam. Fifty‐three patients who had an esophagectomy for SCC were allocated randomly to either a Treatment group (n = 25) or a control group (n = 28). Patients in the Treatment group were given 7.5 mg/day of meloxicam, for between 10 and 14 days before surgery. Patients in the control group did not take any type of NSAID during this time interval. Samples of the tumor taken from the resected specimens were collected. Proliferation and apoptosis were measured by flow cytometry. The concentration of 6‐keto‐prostaglandin F1α in cancer tissue was determined by radio‐immuno‐assay. Expression of COX‐2 mRNA was measured with RT‐PCR and COX‐2 protein levels with Western blot analysis. Nuclear NF‐kappaB and cytoplasmic IkappaB protein levels were determined by electrophoretic mobility shift assay and Western blot, respectively. There were significantly more apoptotic cells in the tumors of patients who were using meloxicam. It also decreased the levels of COX‐2 mRNA, COX‐2 protein and nuclear NF‐kappaB protein and increased the cytoplasmic IkappaB protein in the cancer. We conclude that meloxicam induces apoptosis in SCC of the esophagus in vivo by inhibiting the pathway of NF‐kappaB downstream regulation of COX‐2. © 2007 Wiley‐Liss, Inc.
15‐hydroxyprostaglandin dehydrogenase suppresses K‐RasV12‐dependent tumor formation in Nu/Nu mice
Authors: Pham Hung , Eibl Guido , Vincenti Romina , Chong Benny , Tai Hsin‐Hsiung , Slice Lee W. 
Published: November 2007

AbstractOncogenic Ras mutations are early genetic events in colorectal cancer that induce cyclooxygenase (COX)‐2 expression and prostaglandin E2 (PGE2) biosynthesis. PGE2, a downstream product of COX‐2, promotes cancer progression by modulating proliferation, apoptosis and angiogenesis. 15‐hydroxyprostaglandin dehydrogenase (PGDH) degrades PGE2 and is down‐regulated in colorectal cancer, suggesting that PGDH plays a role in regulating PGE2 levels and that PGDH over‐expression could attenuate Ras‐mediated tumorigenesis. Lentiviral transduction was used to express GFP (18.GFP), K‐RasV12 (18.K‐RasV12), PGDH (18.PGDH) or both K‐RasV12 and PGDH (18.K‐RasV12.PGDH) in nontumorigenic rat intestinal epithelial (IEC‐18) cells. 18.K‐RasV12 cells exhibited increased phosphorylation of MAP kinases and CREB, proliferation rates, COX‐2 and microsomal prostaglandin E synthase (mPGES)‐1 expression and PGE2 and PGI2 levels. 18.PGDH and 18.K‐RasV12.PGDH cells had 104‐fold increases in PGDH activity with decreased PGE2 and PGI2 levels, COX‐2 and mPGES‐1 expression and proliferation rates. 18.GFP, 18.PGDH, and 18.K‐RasV12.PGDH cells were unable to grow in soft agar media whereas 18.K‐RasV12 cells exhibited anchorage‐independent cell growth. Xenografts of implanted 18.K‐RasV12 cells in nu/nu mice produced rapid (2 wk) tumors with uniform antibody staining for COX‐2 and mPGES‐1 throughout the tumor and elevated PGE2 levels. Xenografts of 18.K‐RasV12.PGDH cells exhibited delayed (8 wk) tumor formation with negligible COX‐2 and mPGES‐1 expression and significantly decreased PGE2 levels. 18.K‐RasV12.PGDH tumors had decreased staining of the proliferative marker, Ki‐67, and a significant increase in apoptosis in the central region of the tumor. Based on these data, we conclude that PGDH expression suppresses K‐RasV12‐mediated tumorigenesis in intestinal epithelial cells. © 2007 Wiley‐Liss, Inc.
Potentially inappropriate prescribing to hospitalised patients
Authors: Radošević Nives , Gantumur Monja , Vlahović‐Palčevski Vera 
Published: November 2007

AbstractPurposeThe objective of this study was to evaluate the prevalence of potential drug–drug interactions (DDIs) in hospitalised patients in correlation with patient's age and number of drugs prescribed and to determine the prevalence of inappropriate drugs prescribed to elderly patients.MethodsDrugs prescribed during 1 day to all hospitalised patients at seven wards of Department of Medicine in University Hospital Rijeka were recorded by reviewing patient medical charts. Potential DDIs were evaluated using a list of potentially harmful drug combinations compiled from the literature. Beers criteria were used to identify potentially inappropriate medications in patients aged 65 years or older.ResultsThe study included 225 patients that received a total of 1301 drugs. Twenty‐two percent of the patients receiving drug therapy were prescribed drug combinations that are potentially harmful. The most common potentially harmful drug combination was an ACE inhibitor with a potassium supplement (33.9% of all combinations). In the multivariate analysis, age and number of drugs are significantly associated with potential DDIs (r = 0.8629). One quarter of elderly patients received a drug potentially inappropriate considering their age. The most commonly prescribed potentially inappropriate drug was amiodarone, followed by diazepam.ConclusionPolypharmacy and older age have been proven to be important risk factors for potential drug interactions. We identified a high rate of prescribing potentially inappropriate medications among elders. Results of this study indicate that particular caution should be given when prescribing drugs to patients already receiving drugs and to elderly patients, considering the risk of drug‐related problems. Copyright © 2007 John Wiley & Sons, Ltd.
Alkane oxidation by the system ‘tert‐butyl hydroperoxide–[Mn2L2O3][PF6]2 (L = 1,4,7‐trimethyl‐1,4,7‐triazacyclononane)–carboxylic acid’
Authors: Kozlov Yuriy N. , Nizova Galina V. , Shul'pin Georgiy B. 
Published: November 2007

AbstractThe kinetics of cyclohexane (CyH) oxygenation with tert‐butyl hydroperoxide (TBHP) in acetonitrile at 50 °C catalysed by a dinuclear manganese(IV) complex 1 containing 1,4,7‐trimethyl‐1,4,7‐triazacyclononane and co‐catalysed by oxalic acid have been studied. It has been shown that an active form of the catalyst (mixed‐valent dimeric species ‘MnIIIMnIV’) is generated only in the interaction between complex 1 and TBHP and oxalic acid in the presence of water. The formation of this active form is assumed to be due to the hydrolysis of the MnOMn bonds in starting compound 1 and reduction of one MnIV to MnIII. A species which induces the CyH oxidation is radical tert‐BuO. generated by the decomposition of a monoperoxo derivative of the active form. The constants of the equilibrium formation and the decomposition of the intermediate adduct between TBHP and 1 have been measured: K = 7.4 mol−1 dm3 and k = 8.4 × 10−2 s−1, respectively, at [H2O] = 1.5 mol dm−3 and [oxalic acid] = 10−2 mol dm−3. The constant ratio for reactions of the monomolecular decomposition of tert‐butoxy radical (tert‐BuO. → CH3COCH3 + CH) and its interaction with the CyH (tert‐BuO. + CyH → tert‐BuOH + Cy.) was calculated: 0.26 mol dm−3. One of the reasons why oxalic acid accelerates the oxidation is due to the formation of an adduct between oxalic acid and 1 (K ≈ 103 mol−1 dm3). Copyright © 2007 John Wiley & Sons, Ltd.
Synthesis and Characterization of 3,4,5‐Triamino‐1,2,4‐triazolium and 1‐Methyl‐3,4,5‐triamino‐1,2,4‐triazolium Iodides
Authors: Darwich Chaza , Karaghiosoff Konstantin , Klapötke Thomas M. , Miró Sabaté Carles 
Published: November 2007

Abstract3,4,5‐Triamino‐1,2,4‐triazolium iodide (1) was obtained in good yield and purity and characterized using vibrational (IR, Raman) and multinuclear NMR spectroscopy (1H, 13C, 15N), EA, MS, DSC, and X‐ray crystallography. The compound was synthesized by two different methods rendering two different polymorphs (α and β) as proved by X‐ray measurements, vibrational spectroscopy and DSC. 1‐Methyl‐3,4,5‐triamino‐1,2,4‐triazolium iodide (2) was synthesized by reaction of guanazine with methyliodide and fully characterized by the same techniques mentioned above. Both compounds showed to be suitable starting materials for the synthesis of guanazinium salts of energetic interest.
Zur Löslichkeit von Cobalt(IV) in Li8SiO6
Authors: Mühle Claus , Jansen Martin 
Published: November 2007

AbstractOn the Solubility of Cobalt(IV) in Li8SiO6Li8SiO6 dissolves up to 2 at.‐%, cobalt(IV). Crystals of such solid solutions are transparent and of deep ruby red colour. Cobalt concentrations as determined by ICP‐OES, EDX and magnetic susceptibility measurements are in good accordance. The X‐ray powder diffraction and the magnetic properties confirm integration of Co4+ into the lithiumoxosilicate. These new results are indicating that the ruby red phase, previously addressed as “Li8CoO6”, is in fact cobalt doped Li8SiO6.