bluuebunny/crossref_metadata_2025_split huggingface dataset:
Kinetics of Base‐Catalyzed Dehydrochlorination of Hexachlorocyclohexanes: I. Homogeneous Systems
Authors: Ren Mingzhong , Peng Ping'an , Huang Weilin , Liu Xiangmei 
Published: April 2006

ABSTRACTBase‐catalyzed dehydrochlorination of α‐, β‐, and γ‐hexachlorocyclohexane (HCH) was examined at different pH and temperature conditions. No reaction was observed for β‐HCH under all tested conditions likely due to the fact that all chlorines are at the equatorial positions. Highly pH‐ and temperature‐dependent reaction rates were observed for α‐ and γ‐HCH, and pentachlorocyclohexenes (PCCHs) and 1,2,4‐ and 1,2,3‐trichlorobenzene (TCB) were detected as the intermediates and final products of the transformation of both α‐ and γ‐HCH. The pseudo‐first‐order rate constants of each step of the reactions were calculated at different T and pH conditions. For the first step, the rate constants were at approximately 0.0005 d−1 in solutions below pH 7.0, and increased by about an order of magnitude per pH unit from pH 7.01 to pH 12.02. The second‐order reaction rate constants (kb) of this step were 3.57 ± 0.03 and 3.19 ± 0.19 M−1 d−1, respectively, and the associated activation energies (Ea) at pH 9.26 were 60.4 ± 7.8 and 67.7 ± 8.7 kJ mol−1, respectively, for α‐ and γ‐HCH. The rate constants for the formation of 1,2,3‐TCB (k21) and 1,2,4‐TCB (k22) were 0.0032 ± 0.0001 d−1 and 0.051 ± 0.003 d−1 from α‐HCH, and 0.0017 ± 0.0001 d−1 and 0.0041 ± 0.0002 d−1 from γ‐HCH at pH 8.28 and 25°C. Both k21 and k22 also showed an increase by about one order of magnitude per pH unit from pH 8.28 to pH 12.02. The Ea values were 64.4 ± 6.8 and 88.8 ± 5.2 kJ mol−1, respectively, for the formation of 1,2,4‐TCB and 1,2,3‐TCB from α‐HCH, and 70.6 ± 8.7 and 92.0 ± 4.9 kJ mol−1, respectively, for the formation of 1,2,4‐ and 1,2,3‐TCB from γ‐HCH at pH 9.26. Data provided by this study may be used for calculation of the percentages of the TCBs formed at different environmental conditions.
Multivalent‐Ion‐Mediated Stabilization of Hydrogen‐Bonded Multilayers
Authors: Quinn J. F. , Caruso F. 
Published: April 2006

AbstractHydrogen‐bonding interactions are an important alternative to electrostatic interactions for assembling multilayer thin films of uncharged components. Herein, a new method is reported for rendering such films stable at pH values close to physiological conditions. Multilayer films based on hydrogen bonding are assembled by the alternate deposition of poly[(styrene sulfonic acid)‐co‐(maleic acid)] (PSSMA) and poly(N‐isopropylacrylamide) (PNiPAAm) at pH 2.5. The use of PSSMA results in multilayers that contain free styrene sulfonate groups, as these moieties do not interact with the PNiPAAm functional groups. Subsequent infiltration of a multivalent ion (Ce4+ or Fe3+) leads to an increase in the total film mass, with little impact on the film morphology, as determined by using atomic force microscopy. To examine the film stability, the resulting films have been exposed to elevated pH (7.1). While there is substantial swelling of the multilayers (25 % and 55 % for Ce4+‐ and Fe3+‐stabilized films, respectively), film loss is negligible. This provides a stark contrast with non‐stabilized films, which disassemble almost immediately upon exposure to pH 7.1. This method represents a simple and effective strategy for stabilizing hydrogen‐bonded structures non‐covalently. Further, the multivalent ions also render the films responsive to changes in the local redox environment, as demonstrated by film disassembly after exposure of Fe3+‐treated films to iodide solutions.
Pervasive developmental disorders in Prader–Willi syndrome: The Leuven experience in 59 subjects and controls
Authors: Descheemaeker Mie‐Jef , Govers Veerle , Vermeulen Peter , Fryns Jean‐Pierre 
Published: April 2006

AbstractIn the present study we investigated the co‐morbidity of pervasive developmental disorder (PDD) in 59 Prader–Willi syndrome (PWS) individuals and in 59 non‐specific mentally retarded controls, matched for IQ, gender, and age. The ‘Pervasive Developmental Disorder Mentally Retardation Scale’ (PDD‐MRScale), a screening questionnaire based on the DSM‐III‐R criteria for PDD, has been applied in the PWS group and in the control group. Results of the present study revealed a striking autistic‐like behavioral phenotype in the majority of the PWS individuals, particularly deficits in the quality of language and communication and of imagination and interests. This intersection with autistic symptomatology is an important addition to the behavioral phenotype in PWS persons. A first approach to delineate subtypes of autistic symptomalogy among PWS persons was performed. Nineteen percent of the PWS group did meet the full diagnostic DSM‐III‐R criteria for PDD in comparison with 15% in the control group. Results revealed that a higher IQ in PWS does not protect to develop genuine PDD and that uniparental disomy/imprinting mutation as genetic origin seems to be an additional risk factor for developing genuine PDD. The results of the present study suggest the importance of reconsidering the commonly recognized obsessive‐compulsive like behavior in PWS persons within the broader spectrum of autism disorders. © 2006 Wiley‐Liss, Inc.
Brain derived neurotrophic factor (BDNF) gene variants and Alzheimer's disease, affective disorders, posttraumatic stress disorder, schizophrenia, and substance dependence
Authors: Zhang Huiping , Ozbay Fatih , Lappalainen Jaakko , Kranzler Henry R. , van Dyck Christopher H. , Charney Dennis S. , Price Lawrence H. , Southwick Steven , Yang Bao‐Zhu , Rasmussen Ann , Gelernter Joel 
Published: April 2006

AbstractGenetic variation at the locus encoding the brain derived neurotrophic factor (BDNF) has been implicated in some neuropsychiatric disorders such as Alzheimer's disease (AD), affective disorders (AFDs), schizophrenia, and substance dependence. We therefore performed a mutation scan of the BDNF gene to identify novel gene variants and examined the association between BDNF variants and several neuropsychiatric phenotypes in European American (EA) subjects and controls. Using denaturing high performance liquid chromatography (dHPLC), we identified a novel variant (G−712A) in the putative promoter region. This variant and two previously reported BDNF SNPs (C270T and Val66Met) were genotyped in 295 patients with AD, 108 with AFDs, 96 with posttraumatic stress disorder (PTSD), 84 with schizophrenia, 327 with alcohol and/or drug dependence, and 250 normal control subjects. No association was found between these three BDNF gene variants and AD, AFDs, PTSD, or schizophrenia. However, there was a nominally higher frequency of the G−712A G‐allele and the G/G genotype in subjects with substance dependence than in controls (Allele: χ2 = 4.080, df = 1, P = 0.043; Genotype: χ2 = 7.225, df = 2, P = 0.027). Although after correction for multiple testing, the findings are not considered significant (threshold P‐value was set at 0.020 by the program SNPSpD), logistic regression analyses confirmed the modest association between SNP G−712A and substance dependence, when the sex and age of subjects were taken into consideration. The negative results for AFDs, PTSD, and schizophrenia could be due to the low statistical power. Further study with larger samples is warranted. © 2006 Wiley‐Liss, Inc.
Increase in bone marrow lesions associated with cartilage loss: A longitudinal magnetic resonance imaging study of knee osteoarthritis
Authors: Hunter David J. , Zhang Yuqing , Niu Jingbo , Goggins Joyce , Amin Shreyasee , LaValley Michael P. , Guermazi Ali , Genant Harry , Gale Daniel , Felson David T. 
Published: April 2006

AbstractObjectiveAlthough bone marrow lesions (BMLs) are powerful predictors of joint space loss as visualized on radiographs, the natural history of these lesions, their relationship to cartilage loss, and the association between change in these lesions and cartilage loss are unknown. These questions were tested using longitudinal magnetic resonance imaging (MRI) data in a natural history study of symptomatic knee osteoarthritis (OA).MethodsMRI of the knee was performed at baseline, 15 months, and 30 months in 217 patients with primary knee OA (122 men, 95 women; mean ± SD age 66.4 ± 9.4 years). To assess mechanical alignment, long‐limb films were obtained at 15 months. Subchondral bone marrow abnormalities, graded in the medial and lateral tibiofemoral joints, were defined as poorly marginated areas of increased signal intensity in the marrow on fat‐suppressed, T2‐weighted images. Cartilage morphologic features in the medial and lateral tibiofemoral joints were scored at all time points using a semiquantitative scale. For each of the medial and lateral compartments, generalized estimating equations were used to evaluate the longitudinal relationship of tibiofemoral BMLs to the tibiofemoral cartilage score, with adjustment for malalignment.ResultsFifty‐seven percent of knees had BMLs at baseline, of which 99% remained the same or increased in size at followup. Knee compartments with a higher baseline BML score had greater cartilage loss. An increase in BMLs was strongly associated with further worsening of the cartilage score. Enlarging or new BMLs occurred mostly in malaligned limbs, on the side of the malalignment (e.g., new medial BMLs in varus‐aligned knees). The association of BML change with medial tibiofemoral cartilage loss was not significant after adjusting for alignment.ConclusionLesions of the bone marrow are unlikely to resolve and often get larger over time. Compared with BMLs that stay the same, enlarging BMLs are strongly associated with more cartilage loss. Furthermore, any change in BML is mediated by limb alignment.
Connective tissue growth factor/CCN2 overexpression in mouse synovial lining results in transient fibrosis and cartilage damage
Authors: Davidson E. N. Blaney , Vitters E. L. , Mooren F. M. , Oliver N. , Berg W. B. van den , Kraan P. M. van der 
Published: April 2006

AbstractObjectiveCharacteristics of osteoarthritis (OA) include cartilage damage, fibrosis, and osteophyte formation. Connective tissue growth factor (CTGF; also known as CCN2), is found in high levels in OA chondrocytes and is frequently involved in fibrosis, bone formation, and cartilage repair. The present study was therefore undertaken to investigate the potential role of CTGF in OA pathophysiology.MethodsWe transfected the synovial lining of mouse knee joints with a recombinant adenovirus expressing human CTGF and measured synovial fibrosis and proteoglycan content in cartilage on days 1, 3, 7, 14, and 28. Messenger RNA (mRNA) expression in synovium and cartilage was measured on days 3, 7, and 21.ResultsCTGF induced synovial fibrosis, as indicated by accumulation of extracellular matrix and an increase in procollagen type I–positive cells. The fibrosis reached a maximum on day 7 and had reversed by day 28. Levels of mRNA for matrix metalloproteinase 3 (MMP‐3), MMP‐13, ADAMTS‐4, ADAMTS‐5, tissue inhibitor of metalloproteinases 1 (TIMP‐1), and transforming growth factor β were elevated in the fibrotic tissue. TIMP‐1 expression was elevated on day 3, while expression of other genes did not increase until day 7 or later. CTGF induced proteoglycan depletion in cartilage as early as day 1. Maximal depletion was observed on days 3–7. Cartilage damage was reduced by day 28. A high level of MMP‐3 mRNA expression was found in cartilage. CTGF overexpression did not induce osteophyte formation.ConclusionCTGF induces transient fibrosis that is reversible within 28 days. Overexpression of CTGF in knee joints results in reversible cartilage damage, induced either by the high CTGF levels or via factors produced by the CTGF‐induced fibrotic tissue.
Mouse monoclonal anti–human thrombomodulin antibodies bind to and activate endothelial cells through NF‐κB activation in vitro
Authors: Nara Hiroyuki , Okamoto Hiroshi , Minota Seiji , Yoshio Taku 
Published: April 2006

AbstractObjectiveTo clarify whether mouse monoclonal antibodies (mAb) against human thrombomodulin (TM), which react with human TM present on the endothelial cell (EC) surface, have anti–endothelial cell antibody (AECA) activity and influence antiinflammatory properties of human TM expressed on the EC surface in vitro.MethodsThree preparations of mouse mAb against human TM that react with different sites of the human TM epidermal growth factor–like domain were tested for their ability to 1) bind to ECs, 2) modulate cytokine secretion from ECs, EC adhesion molecule expression, and neutrophil adhesion to ECs, and 3) stimulate nuclear translocation of NF‐κB through the degradation of cytoplasmic IκB in ECs. Recombinant human interleukin‐1β (IL‐1β) was used as a positive control, and mouse IgG1 and mouse IgG2a were used as negative controls.ResultsThe 3 preparations of mouse mAb against human TM that bind to unfixed EC monolayers enhanced IL‐6 and IL‐8 secretion from ECs, up‐regulated expression of endothelial leukocyte adhesion molecule 1, vascular cell adhesion molecule 1, and intercellular adhesion molecule 1 on EC monolayers, and enhanced neutrophil adhesion to ECs to a degree similar to that observed with IL‐1β stimulation, but they did not induce the secretion of tumor necrosis factor α or IL‐1β from ECs throughout the incubation period. The 3 preparations stimulated nuclear translocation of NF‐κB through the degradation of cytoplasmic IκB. Mouse IgG1 and mouse IgG2a did not exhibit such effects.ConclusionThese results suggest the possibility that AECA can react with antigens such as TM that are present on the EC surface and activate ECs. Such events on ECs may lead to vascular inflammation and damage in patients with connective tissue diseases and vasculitis in which AECA are present.
Lupus‐like disease and high interferon levels corresponding to trisomy of the type I interferon cluster on chromosome 9p
Authors: Zhuang Haoyang , Kosboth Mona , Lee Pui , Rice Amanda , Driscoll Daniel J. , Zori Roberto , Narain Sonali , Lyons Robert , Satoh Minoru , Sobel Eric , Reeves Westley H. 
Published: April 2006

AbstractObjectiveSystemic lupus erythematosus (SLE) is associated with type I interferons (IFNs) and can be induced by IFNα treatment. This study looked for evidence of autoimmunity in a pedigree consisting of 4 family members with a balanced translocation 9;21 and 2 members with an unbalanced translocation resulting in trisomy of the short (p) arm and part of the long (q) arm of chromosome 9. These latter 2 subjects had 3 copies of the IFN gene cluster.MethodsSubjects were evaluated clinically and serologically for autoimmune disease. Expression levels of IFNα4, IFNβ, the type I IFN–inducible gene Mx1, the type I IFN receptor, interleukin‐6, and tumor necrosis factor α were determined by real‐time polymerase chain reaction. Circulating plasmacytoid dendritic cells, the main IFN‐producing cells, were quantified by flow cytometry.ResultsBoth subjects with trisomy of chromosome 9p had a lupus‐like syndrome with joint manifestations and antinuclear antibodies: one had anti‐RNP and antiphospholipid autoantibodies, and the other had anti–Ro 60. The 3 family members with a balanced translocation 9;21 had no clinical or serologic evidence of autoimmunity, similar to that in relatives who were unaffected by the chromosomal translocation. In the 2 subjects with trisomy of 9p, high levels of IFNα/β (comparable with those found in patients with SLE), increased signaling through the IFN receptor (as indicated by high Mx1 expression), and low levels of circulating plasmacytoid dendritic cells (as observed in patients with SLE) were evident. These abnormalities were not seen in individuals with a balanced translocation.ConclusionTrisomy of the type I IFN cluster of chromosome 9p was associated with lupus‐like autoimmunity and increased IFNα/β and IFN receptor signaling. The data support the idea that abnormal regulation of type I IFN production is involved in the pathogenesis of SLE.
Guillain‐Barré and Miller Fisher syndromes occurring with tumor necrosis factor α antagonist therapy
Authors: Shin In‐Sook J. , Baer Alan N. , Kwon Hyon J. , Papadopoulos Elektra J. , Siegel Jeffrey N. 
Published: April 2006

AbstractObjectiveDiverse neurologic syndromes have been described in association with tumor necrosis factor α (TNFα) antagonist therapy for inflammatory arthritides and Crohn's disease. The objective of this study was to review the occurrence and clinical features of Guillain‐Barré syndrome and its variant, the Miller Fisher syndrome, during TNFα antagonist therapy.MethodsThe postmarketing database of the US Food and Drug Administration (FDA) was searched, following our experience with a patient with rheumatoid arthritis in whom the Miller Fisher syndrome variant of the Guillain‐Barré syndrome developed while he was receiving infliximab therapy.ResultsOur index patient had a neurologic illness defined initially by ataxia and dysarthria, which fluctuated in relation to each subsequent infliximab infusion and, after 6 months, culminated in areflexic flaccid quadriplegia. In addition, 15 patients in whom Guillain‐Barré syndrome developed following TNFα antagonist therapy were identified from the FDA database. Guillain‐Barré syndrome developed following infliximab therapy in 9 patients, following etanercept therapy in 5 patients, and following adalimumab therapy in 1 patient. Among the 13 patients for whom followup data were available, 1 patient experienced no resolution, 9 patients had partial resolution, and 3 patients had complete resolution of Guillain‐Barré syndrome following therapy.ConclusionAn association of Guillain‐Barré syndrome with TNFα antagonist therapy is supported by the worsening of neurologic symptoms that occurred in our index patient following each infusion of infliximab, and by the temporal association of this syndrome with TNFα antagonist therapy in 15 other patients. An acute or subacute demyelinating polyneuropathy should be considered a potential adverse effect of TNFα antagonist therapy.
Brachio‐cervical inflammatory myopathies: Clinical, immune, and myopathologic features
Authors: Pestronk Alan , Kos Ksenija , Lopate Glenn , Al‐Lozi Muhammad T. 
Published: April 2006

AbstractObjectiveTo characterize patients with inflammatory myopathies who present with weakness in the proximal regions of the arms.MethodsClinical, laboratory, and myopathologic features were evaluated in 10 patients, identified consecutively over 12 years, with inflammatory myopathies and weakness that was most severe in the proximal regions of the arms. The features of these brachio‐cervical inflammatory myopathy (BCIM) syndromes were compared with those of other inflammatory and immune‐mediated myopathies evaluated during the same period.ResultsPatients with BCIM developed progressive weakness at ages 24–82 years (mean ± SD age 55 ± 9 years). Posterior neck weakness occurred in 60% of patients, while motor neuron disease was the referring diagnosis in 30%. All patients had other systemic autoimmune disorders, including myasthenia gravis (40%) and rheumatoid arthritis (20%). Antinuclear antibodies were present in all patients. Serum creatine kinase levels were usually moderately high (mean 910 IU/liter). Active myopathy was identified in muscle biopsy samples from the patients. Focal collections of mononuclear cells, some predominantly B cells, were present in perivascular and perimysial regions. MxA‐ and CD123‐positive dendritic cells were present in the endomysium. C5b–9 components of complement were present diffusely in endomysial connective tissue. Most patients improved in strength after receiving corticosteroids.ConclusionPatients with BCIM syndromes have progressive weakness in the proximal regions of the arms and neck. The predominant myopathologic findings are active myopathy, C5b–9 staining of endomysium, focal perivascular and perimysial inflammation, often with a prominent B cell component, and endomysial dendritic cells. Corticosteroid treatment of BCIM is often followed by improvement in strength.
Alefacept in combination with methotrexate for the treatment of psoriatic arthritis: Results of a randomized, double‐blind, placebo‐controlled study
Authors: Mease Philip J. , Gladman Dafna D. , Keystone Edward C. 
Published: April 2006

AbstractObjectiveTo evaluate the efficacy and safety of alefacept in combination with methotrexate (MTX) for the treatment of psoriatic arthritis (PsA).MethodsPatients were eligible for this randomized, double‐blind, placebo‐controlled trial if they were ages 18–70 years and had active PsA (≥3 swollen joints and ≥3 tender joints) despite treatment with MTX for ≥3 months (a stable dosage for ≥4 weeks prior to enrollment). Patients were stratified according to psoriasis body surface area (BSA) involvement (≥3% or <3%). Alefacept (15 mg) or placebo was administered intramuscularly once weekly for 12 weeks in combination with MTX, followed by 12 weeks of observation during which only MTX treatment was continued. The primary efficacy end point was the proportion of patients achieving a 20% improvement in disease activity according to the American College of Rheumatology criteria (an ACR20 response) at week 24.ResultsOne hundred eighty‐five patients were randomly assigned to receive alefacept plus MTX (n = 123) or placebo plus MTX (n = 62). At week 24, 54% of patients in the alefacept plus MTX group achieved an ACR20 response, compared with 23% of patients in the placebo plus MTX group (P < 0.001). Mean reductions in tender and swollen joint counts in patients receiving alefacept plus MTX were –8.0 and –6.3, respectively. In patients with psoriasis involving ≥3% BSA (n = 87), a 50% reduction from the baseline Psoriasis Area Severity Index at week 14 was achieved by 53% of patients receiving alefacept plus MTX compared with 17% of those receiving placebo plus MTX (P < 0.001). Most adverse events were mild to moderate in severity. In the alefacept plus MTX group, the incidence of serious adverse events was low (1.6%), and no opportunistic infections or malignancies were reported.ConclusionAlefacept in combination with MTX may be an effective and safe treatment for PsA.
The sensitive determination of nucleic acids using a fluorescence‐quenching method
Authors: Jia Zhen , Yang Jinghe , Wu Xia , Sun Changxia , Wang Fei , Liu Shufang , Wang Feng 
Published: April 2006

AbstractExperiments indicated that nucleic acids can quench the fluorescence of the Eu3+–2‐thenoyltrifluoroacetone (TTA)–1,10‐phenanthroline (Phen) system. Based on this, a sensitive method for the determination of nucleic acids was proposed. The experiments indicated that under the optimum conditions, the quenched fluorescence intensity was in proportion to the concentration of nucleic acids in the range 1.0 × 10−11–1.0 × 10−6 g/mL for yeast RNA (yRNA), 5.0 × 10−11–5.0 × 10−7 g/mL for fish sperm (fsDNA) and 1.0 × 10−10–1.5 × 10−6 g/mL for calf thymus DNA (ctDNA). Their detection limits were 3.0 × 10−12, 4.0 × 10−12 and 5.0 × 10−11 g/mL, respectively. Therefore, the proposed method is one of the most sensitive methods available. The interaction between nucleic acids and Eu3+‐TTA‐Phen is also discussed. Copyright © 2006 John Wiley & Sons, Ltd.