bluuebunny/crossref_metadata_2025_split huggingface dataset:
Enhanced hydrogenation in a reverse flow chromatographic reactor
Authors: Viecco Guillermo A. , Carnish Brad J. , Caram Hugo S. 
Published: February 2006

AbstractAn experimental study of the reverse flow chromatographic reactor is carried with the equilibrium limited hydrogenation of 1,3,5‐trimethylbenzene (mesitylene, MES) to 1,3,5‐trimethylcyclohexane. The reaction is pseudo first‐order when carried out in excess hydrogen. A simple experimental setup is used to evaluate the effects of carrier flow, reactant feed concentration, and amount of catalyst on conversion. Conversions exceeding the thermodynamic equilibrium conversion are obtained for a wide variety of switching times, catalyst amounts, carrier flow rates, and reactant concentrations, showing the robustness of the system. While the qualitative features of the process can be predicted for a simple linear adsorption equilibrium model, the experimental results are best fitted by assuming a linear adsorption isotherm combined with an adjusted interfacial mass‐transfer resistance. The experimental results are very similar to those reported in previous research of the same reaction in a simulated moving‐bed chromatographic reactor. © 2006 American Institute of Chemical Engineers AIChE J, 2006
1,026 Experimental treatments in acute stroke
Authors: O'Collins Victoria E. , Macleod Malcolm R. , Donnan Geoffrey A. , Horky Laura L. , van der Worp Bart H. , Howells David W. 
Published: February 2006

AbstractObjectivePreclinical evaluation of neuroprotectants fostered high expectations of clinical efficacy. When not matched, the question arises whether experiments are poor indicators of clinical outcome or whether the best drugs were not taken forward to clinical trial. Therefore, we endeavored to contrast experimental efficacy and scope of testing of drugs used clinically and those tested only experimentally.MethodsWe identified neuroprotectants and reports of experimental efficacy via a systematic search. Controlled in vivo and in vitro experiments using functional or histological end points were selected for analysis. Relationships between outcome, drug mechanism, scope of testing, and clinical trial status were assessed statistically.ResultsThere was no evidence that drugs used clinically (114 drugs) were more effective experimentally than those tested only in animal models (912 drugs), for example, improvement in focal models averaged 31.3 ± 16.7% versus 24.4 ± 32.9%, p > 0.05, respectively. Scope of testing using Stroke Therapy Academic Industry Roundtable (STAIR) criteria was highly variable, and no relationship was found between mechanism and efficacy.InterpretationThe results question whether the most efficacious drugs are being selected for stroke clinical trials. This may partially explain the slow progress in developing treatments. Greater rigor in the conduct, reporting, and analysis of animal data will improve the transition of scientific advances from bench to bedside. Ann Neurol 2006
AHI1 gene mutations cause specific forms of Joubert syndrome–related disorders
Authors: Valente Enza Maria , Brancati Francesco , Silhavy Jennifer L. , Castori Marco , Marsh Sarah E. , Barrano Giuseppe , Bertini Enrico , Boltshauser Eugen , Zaki Maha S. , Abdel‐Aleem Alice , Abdel‐Salam Ghada M. H. , Bellacchio Emanuele , Battini Roberta , Cruse Robert P. , Dobyns William B. , Krishnamoorthy Kalpathy S. , Lagier‐Tourenne Clotilde , Magee Alex , Pascual‐Castroviejo Ignacio , Salpietro Carmelo D. , Sarco Dean ,   International JSRD Study Group, Dallapiccola Bruno , Gleeson Joseph G. 
Published: February 2006

AbstractObjectiveJoubert syndrome (JS) is a recessively inherited developmental brain disorder with several identified causative chromosomal loci. It is characterized by hypoplasia of the cerebellar vermis and a particular midbrain‐hindbrain “molar tooth” sign, a finding shared by a group of Joubert syndrome–related disorders (JSRDs), with wide phenotypic variability. The frequency of mutations in the first positionally cloned gene, AHI1, is unknown.MethodsWe searched for mutations in the AHI1 gene among a cohort of 137 families with JSRD and radiographically proven molar tooth sign.ResultsWe identified 15 deleterious mutations in 10 families with pure JS or JS plus retinal and/or additional central nervous system abnormalities. Mutations among families with JSRD including kidney or liver involvement were not detected. Transheterozygous mutations were identified in the majority of those without history of consanguinity. Most mutations were truncating or splicing errors, with only one missense mutation in the highly conserved WD40 repeat domain that led to disease of similar severity. InterpretationAHI1 mutations are a frequent cause of disease in patients with specific forms of JSRD. Ann Neurol 2006
Rapamycin causes regression of astrocytomas in tuberous sclerosis complex
Authors: Franz David Neal , Leonard Jennifer , Tudor Cynthia , Chuck Gail , Care Marguerite , Sethuraman Gopalan , Dinopoulos Argirios , Thomas George , Crone Kerry R. 
Published: February 2006

AbstractObjectiveTuberous sclerosis complex (TSC) is a genetic disorder characterized by the formation of hamartomas in multiple organs. Five to 15% of affected individuals display subependymal giant cell astrocytomas, which can lead to substantial neurological and postoperative morbidity due to the production of hydrocephalus, mass effect, and their typical location adjacent to the foramen of Monro. We sought to see whether therapy with oral rapamycin could affect growth or induce regression in astrocytomas associated with TSC.MethodsFive subjects with clinically definite TSC and either subependymal giant cell astrocytomas (n = 4) or a pilocytic astrocytoma (n = 1) were treated with oral rapamycin at standard immunosuppressive doses (serum levels 5–15ng/ml) from 2.5 to 20 months. All lesions demonstrated growth on serial neuroimaging studies. Magnetic resonance imaging scans were performed before and at regular intervals following initiation of therapy.ResultsAll lesions exhibited regression and, in one case, necrosis. Interruption of therapy resulted in regrowth of subependymal giant cell astrocytomas in one patient. Resumption of therapy resulted in further regression. Treatment was well tolerated.InterpretationOral rapamycin therapy can induce regression of astrocytomas associated with TSC and may offer an alternative to operative therapy of these lesions. Ann Neurol 2006
Synthesis of cyclopentadienyltricarbonylrhenium substituted benzhydryl species and oestrogen receptor binding properties
Authors: Plażuk D. , Le Bideau F. , Pérez‐Luna A. , Stéphan E. , Vessières A. , Zakrzewski J. , Jaouen G. 
Published: February 2006

Abstract6‐(4‐Methoxyphenyl)fulvene has been efficiently engaged in a process implying nucleophilic attack of methyllithium followed by a transmetallation reaction in the presence of different organorhenium sources {XRe(CO)5: X = Cl, Br, OTf; BrRe(CH3CN)2(CO)3, [BrRe(CO)3THF]2} to afford the corresponding cyclopentadienyltricarbonylrhenium‐substituted compound. This study allowed us to determine the best complex for that transformation, and similar reaction conditions were used with success to provide new potential radiopharmaceuticals in the cold series. One of these compounds [the (4,4′‐dihydroxybenzhydryl)cyclopentadienyltricarbonylrhenium] displays a good recognition for the α form of the oestrogen receptor. Copyright © 2006 John Wiley & Sons, Ltd.
A murine model of mixed connective tissue disease induced with U1 small nuclear RNP autoantigen
Authors: Greidinger Eric L. , Zang Yunjuan , Jaimes Kimberly , Hogenmiller Scott , Nassiri Mehdi , Bejarano Pablo , Barber Glen N. , Hoffman Robert W. 
Published: February 2006

AbstractObjectiveTo test whether immunizing mice with autoantigens closely linked to mixed connective tissue disease (MCTD) could induce an MCTD‐like clinical syndrome distinguishable from systemic lupus erythematosus (SLE).MethodsTransgenic and knockout C57BL/6‐derived mice were immunized subcutaneously at age 8–12 weeks with U1–70‐kd small nuclear RNP (70K) fusion protein along with either Freund's complete adjuvant (CFA) or U1 RNA. After 2 months, mice were killed and analyzed histologically and serologically.ResultsImmunization of C57BL/6‐derived mice transgenic for human HLA–DR4 with 70K and either CFA or U1 RNA led to anti‐70K antibodies in 62% of mice (21 of 34), and diversified anti‐RNP immune responses. MCTD‐like lung disease also developed in 50% of immunized mice (17 of 34), and anti‐70K antibodies were strongly correlated with lung disease. CFA and U1 RNA were comparably able to induce this syndrome. Mice deficient in Toll‐like receptor 3 (TLR‐3) also developed this same syndrome when immunized with 70K and CFA. However, TLR‐3−/− mice failed to develop MCTD‐like lung disease when treated with 70K and U1 RNA. Rather, TLR‐3−/− mice immunized with 70K and U1 RNA developed an autoimmune syndrome characterized by glomerulonephritis typical of SLE.ConclusionExposure to 70K in an appropriate context is sufficient to induce autoimmunity and target organ injury consistent with MCTD. This system represents a new model of autoimmune interstitial lung disease, and establishes a closer link between anti‐70K immunity and MCTD‐like lung disease. Of note, changes in innate immune signaling can cause the same trigger to lead to the development of SLE‐like nephritis rather than MCTD‐like lung disease.
Reproducible genetic associations between candidate genes and clinical knee osteoarthritis in men and women
Authors: Valdes Ana M. , Van Oene Mark , Hart Deborah J. , Surdulescu Gabriela L. , Loughlin John , Doherty Michael , Spector Tim D. 
Published: February 2006

AbstractObjectiveOsteoarthritis (OA) is recognized to have a genetic component, and in this study, we aimed to replicate in a case–control study of men and women with clinical knee OA genetic associations in 12 candidate genes previously reported to be associated with OA.MethodsTwenty‐five single‐nucleotide polymorphisms were genotyped in 298 men and 305 women ages 50–86 who were diagnosed as having knee OA, as assessed both clinically and radiographically, and in 297 men and 299 women matched for age and ethnicity (controls). Standardized anteroposterior radiographs of the knee in extension were performed on each of the cases, and all cases met the American College of Rheumatology criteria for OA of the knee. Genotype and haplotype frequencies in cases and controls were compared separately in men and women. The 12 genes tested were AACT, ADAM12, BMP2, CD36, CILP, COX2, ESR1, NCOR2, OPG, TNA, TNFAIP6, and VDR.ResultsEight of the candidate genes were associated in women and 5 in men, and only 3 genes (TNFAIP6, NCOR2, and CD36) were not significantly associated in either sex. The strongest associations in terms of odds ratios (ORs) were a haplotype in ADAM12 (OR 7.1 [95% confidence interval (95% CI) 3.3–33.8]) and a haplotype in ESR1 (OR 3.6 [95% CI 1.18–10.98]) in women. The same ADAM12 haplotype (OR 2.54 [95% CI 1.2–5.4]) and a haplotype in the CILP gene (OR 0.38 [95% CI 0.23–0.62]) were the strongest associations in men.ConclusionWe found that genes previously identified by their association with subclinical features of knee OA or progression were also associated with clinical knee OA. These genetic associations may identify individuals at a particularly high risk of developing knee OA.
CD28‐dependent differentiation into the effector/memory phenotype is essential for induction of arthritis in interleukin‐1 receptor antagonist–deficient mice
Authors: Kotani Motoko , Hirata Kazuya , Ogawa Shuhei , Habiro Katsuyoshi , Ishida Yasuo , Tanuma Seiichi , Horai Reiko , Iwakura Yoichiro , Kishimoto Hidehiro , Abe Ryo 
Published: February 2006

AbstractObjectiveInterleukin‐1 receptor antagonist (IL‐1Ra)–deficient mice on a BALB/c background spontaneously develop a chronic inflammatory polyarthropathy closely resembling that of rheumatoid arthritis in humans. To elucidate the role of CD28 costimulatory signals in the development of this disease, we studied IL‐1Ra/CD28–double‐deficient mice.MethodsWe crossed IL‐1Ra–deficient mice with CD28–deficient mice and observed the incidence and severity of arthritis. To investigate functions of IL‐1Ra/CD28–double‐deficient T cells, cells were stimulated with CD3 monoclonal antibody or allogeneic antigen‐presenting cells (APCs) and their proliferative responses and levels of cytokine production were measured.ResultsDisease severity was lower in IL‐1Ra/CD28–double‐deficient mice than in mice that were deficient only in IL‐1Ra, although incidence of arthritis was not affected by the presence or absence of CD28. When pathogenic IL‐1Ra–KO T cells were transferred into nude mice, severe arthritis developed. Even though T cells from double‐deficient mice showed the same diminished proliferative capacity as was seen in T cells from CD28–single‐deficient animals, nude mice into which double‐deficient T cells were transferred never developed arthritis.ConclusionThese findings indicate that IL‐1Ra/CD28–double‐deficient T cells can be activated by IL‐1Ra–deficient activated APCs, resulting in induction of arthritis; however, these T cells did not induce the disease under normal conditions, because they did not differentiate into effector/memory phenotype.
Which user interaction for cross‐language information retrieval? Design issues and reflections
Authors: Petrelli Daniela , Levin Stephen , Beaulieu Micheline , Sanderson Mark 
Published: February 2006

AbstractA novel and complex form of information access is cross‐language information retrieval: searching for texts written in foreign languages based on native language queries. Although the underlying technology for achieving such a search is relatively well understood, the appropriate interface design is not. The authors present three user evaluations undertaken during the iterative design of Clarity, a cross‐language retrieval system for low‐density languages, and shows how the user‐interaction design evolved depending on the results of usability tests. The first test was instrumental to identify weaknesses in both functionalities and interface; the second was run to determine if query translation should be shown or not; the final was a global assessment and focused on user satisfaction criteria. Lessons were learned at every stage of the process leading to a much more informed view of what a cross‐language retrieval system should offer to users.
In vivo localization and identification of the antiplasmodial alkaloid dioncophylline A in the tropical liana Triphyophyllum peltatum by a combination of fluorescence, near infrared Fourier transform Raman microscopy, and density functional theory calculations
Authors: Frosch Torsten , Schmitt Michael , Schenzel Karla , Faber Johan H. , Bringmann Gerhard , Kiefer Wolfgang , Popp Jürgen 
Published: February 2006

AbstractNear infrared Fourier transform (NIR FT) micro Raman spectroscopy in combination with density functional theory (DFT) calculations has been applied for an in vivo localization of the antiplasmodial naphthylisoquinoline alkaloid dioncophylline A (1) in the tropical liana Triphyophyllum peltatum. Fluorescence microscopy images suggest finding this active agent in 10 μm big inclusions located in the cortex of the stem or the beginning of the leaves. By means of spatially resolved FT Raman micro spectroscopy, we could detect dioncophylline A (1) in these inclusions. FT Raman spectroscopy is an extremely selective tool capable of differentiating between various structurally similar naphthylisoquinoline alkaloids. With the help of DFT calculations, we succeeded in assigning the differences found in the FT Raman spectra of the various naphthylisoquinolines to νCC vibrations of the naphthyl ring. The presented results are of relevance for the investigation and extraction of new antimalarial active agents. © 2006 Wiley Periodicals, Inc. Biopolymers 82: 295–300, 2006This 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
The xyloglucan–cellulose assembly at the atomic scale
Authors: Hanus Jaroslav , Mazeau Karim 
Published: February 2006

AbstractThe assembly of cell wall components, cellulose and xyloglucan (XG), was investigated at the atomistic scale using molecular dynamics simulations. A molecular model of a cellulose crystal corresponding to the allomorph Iβ and exhibiting a flexible complex external morphology was employed to mimic the cellulose microfibril. The xyloglucan molecules considered were the three typical basic repeat units, differing only in the size of one of the lateral chain. All the investigated XG fragments adsorb nonspecifically onto cellulose fiber; multiple arrangements are equally probable, and every cellulose surface was capable of binding the short XG molecules. The following structural effects emerged: XG molecules that do not have any long side chains tended to adapt themselves nicely to the topology of the microfibril, forming a flat, outstretched conformation with all the sugar residues interacting with the surface. In contrast, the XG molecules, which have long side chains, were not able to adopt a flat conformation that would enable the interaction of all the XG residues with the surface. In addition to revealing the fundamental atomistic details of the XG adsorption on cellulose, the present calculations give a comprehensive understanding of the way the XG molecules can unsorb from cellulose to create a network that forms the cell wall. Our revisited view of the adsorption features of XG on cellulose microfibrils is consistent with experimental data, and a model of the network is proposed. © 2006 Wiley Periodicals, Inc. Biopolymers 82: 59–73, 2006This 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
Average assignment method for predicting the stability of protein mutants
Authors: Saraboji K. , Gromiha M. Michael , Ponnuswamy M. N. 
Published: February 2006

AbstractPrediction of protein stability upon amino acid substitutions is an important problem in molecular biology and it will be helpful for designing stable mutants. In this work, we have analyzed the stability of protein mutants using three different data sets of 1791, 1396, and 2204 mutants, respectively, for thermal stability (ΔTm), free energy change due to thermal (ΔΔG), and denaturant denaturations (ΔΔG), obtained from the ProTherm database. We have classified the mutants into 380 possible substitutions and assigned the stability of each mutant using the information obtained with similar type of mutations. We observed that this assignment could distinguish the stabilizing and destabilizing mutants to an accuracy of 70–80% at different measures of stability. Further, we have classified the mutants based on secondary structure and solvent accessibility (ASA) and observed that the classification significantly improved the accuracy of prediction. The classification of mutants based on helix, strand, and coil distinguished the stabilizing/destabilizing mutants at an average accuracy of 82% and the correlation is 0.56; information about the location of residues at the interior, partially buried, and surface regions of a protein correctly identified the stabilizing/destabilizing residues at an average accuracy of 81% and the correlation is 0.59. The nine subclassifications based on three secondary structures and solvent accessibilities improved the accuracy of assigning stabilizing/destabilizing mutants to an accuracy of 84–89% for the three data sets. Further, the present method is able to predict the free energy change (ΔΔG) upon mutations within a deviation of 0.64 kcal/mol. We suggest that this method could be used for predicting the stability of protein mutants. © 2006 Wiley Periodicals, Inc. Biopolymers 82: 80–92, 2006This 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
Solvent polarity effect on excited‐state lifetime of carotenoids and some dyes
Authors: Pavlovich Vladimir S. 
Published: February 2006

AbstractThe theory demonstrating the role of medium at the fluorescence quenching of polar compounds in solutions is briefly presented. It has been shown, that the rate of S1 → Xn nonradiative conversion between the intramolecular charge transfer states depends on the permanent dipole moments in the ground (S0) and excited (S1, Xn) states as well as on solvent polarity. A relation for the rate of nonradiative excited‐state energy conversion has been obtained and employed to test the known literature data for solvent effect on the S1‐state lifetime of some biologically significant carotenoids and dyes (phthalimides). For phthalimides, the solvent isotope effect on the S1‐state energy conversion, when hydrogen is replaced by deuterium in the OH groups of alcohols and water, has been analyzed. Based on the data for fluorescence quenching in solvents of different polarity, the dipole moments in the intermolecular charge transfer S1 state have been obtained for carotenoids (peridinin, fucoxanthin, uriolide acetate) and for hydrogen‐bonding complexes, which are formed by 4‐amino‐, 4‐methylamino‐, and 4‐dimethylamino‐N‐methylphthalimides in alcohols and water. © 2006 Wiley Periodicals, Inc. Biopolymers 82: 435–441, 2006This 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
Surface‐enhanced resonance Raman scattering of porphyrins on gold nanoparticles attached to silanized glass plates
Authors: Procházka Marek , Hajduková Natália , S̆těpánek Josef 
Published: February 2006

AbstractSurface‐enhanced resonance Raman scattering (SERRS) spectra of cationic 5,10,15,20‐tetrakis(1‐methyl‐4‐pyridyl) porphyrin (TMPyP) and anionic 5,10,15,20‐tetrakis(4‐sulfonatophenyl) porphyrin (TSPP) were measured from gold surfaces prepared by attaching citrate‐reduced colloidal nanoparticles to glass slides silanized by 3‐aminopropyltrimethoxysilane. SERRS spectra of both porphyrins obtained in a large concentration range (1 × 10−4 to 1 × 10−7M) of primary solution do not show any sign of porphyrin metalation or perturbation of its native structure. Optimal adsorption time (15–20 min) and covering concentration limit (lower than 1 × 10−5M) of porphyrins have been estimated from the concentration and soaking time dependences of SERRS spectra. © 2006 Wiley Periodicals, Inc. Biopolymers 82: 390–393, 2006This 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