bluuebunny/crossref_metadata_2025_split huggingface dataset:
Efficacy and safety of micafungin for treating febrile neutropenia in hematological malignancies
Authors: Goto Naoe , Hara Takeshi , Tsurumi Hisashi , Ogawa Kengo , Kitagawa Junichi , Kanemura Nobuhiro , Kasahara Senji , Yamada Toshiki , Shimizu Masahito , Nakamura Mitsuhiro , Matsuura Katsuhiko , Moriwaki Hisataka 
Published: August 2010

AbstractLess toxic antifungal drugs are required for empirical antifungal therapy. Micafungin is an echinocandin drug that is effective against both Candida and Aspergillus, and preliminary clinical studies have shown good antifungal activity. We prospectively examined the effect and safety of micafungin against febrile neutropenia with suspected fungal infection in 53 patients (median age, 56 years) who had undergone chemotherapy. The administered dose of micafungin was 150 mg/day, and its effect was evaluated as fever resolution as well as the results of chest imaging and serum fungal tests. Micafungin levels were measured on day 4 after the first administration using high‐performance liquid chromatography. We also measured trough levels of micafungin. Underlying diseases comprised acute lymphoblastic leukemia (n = 4), acute myeloid leukemia (n = 20), multiple myeloma (n = 3), and non‐Hodgkin's lymphoma (n = 26). The overall efficacy of micafungin was 70%. Breakthrough fungal infections were documented in two (3.8%) patients, both of whom died of invasive mycosis. None of the patients were switched to other antifungal drugs due to events unrelated to adverse effects. Plasma levels of micafungin and the degree of hepatic or renal dysfunction did not correlate. Micafungin is safe and effective for the empirical antifungal therapy of febrile neutropenia in patients with hematological malignancies. Am. J. Hematol., 2010. © 2010 Wiley‐Liss, Inc.
Hierarchical cluster analysis for exposure assessment of workers in the semiconductor health study
Authors: Hines Cynthia J. , Selvin Steve , Samuels Steven J. , Hammond S. Katharine , Woskie Susan R. , Hallock Marilyn F. , Schenker Marc B. 
Published: August 2010

AbstractThe fabrication of integrated circuits in the semiconductor industry involves worker exposures to multiple chemical and physical agents. The potential for a high degree of correlation among exposure variables was of concern in the Semiconductor Health Study. Hierarchical cluster analysis was used to identify groups or “clusters” of correlated variables. Several variations of hierarchical cluster analysis were performed on 14 chemical and physical agents, using exposure data on 882 subjects from the historical cohort of the epidemiological studies. Similarity between agent pairs was determined by calculating two metrics of dissimilarity, and hierarchical trees were constructed using three clustering methods. Among subjects exposed to ethylene‐based glycol ethers (EGE), xylene, or n‐butyl acetate (nBA), 83% were exposed to EGE and xylene, 86% to EGE and nBA, and 94% to xylene and nBA, suggesting that exposures to EGE, xylene, and nBA were highly correlated. A high correlation was also found for subjects exposed to boron and phosphorus (80%). The trees also revealed cluster groups containing agents associated with work‐group exposure categories developed for the epidemiologic analyses.
Communication issues in a multicomponent study of semiconductor employees
Authors: Saiki Cathy L. , Green Rochelle S. , Gold Ellen B. , Schenker Marc B. 
Published: August 2010

AbstractA variety of methods were used to address communication problems in the Semiconductor Health Study (SHS). The diverse employee population required investigators to consider language, ethnic, and cultural differences in planning and implementing the study design. Studies of reproductive health in the workplace raise special concerns, including the critical need to preserve confidentiality and privacy of subjects. Notification of results of epidemiological studies reporting workplace hazards requires sensitivity to needs of workers. SHS investigators directly communicated overall results of this multicomponent study to participating employees at all sites and notified subjects of results of individual industrial hygiene monitoring and endocrine hormone assays.
Older paternal age strongly increases the morbidity for schizophrenia in sisters of affected females
Authors: Perrin Mary , Harlap Susan , Kleinhaus Karine , Lichtenberg Pesach , Manor Orly , Draiman Benjamin , Fennig Shmuel , Malaspina Dolores 
Published: August 2010

AbstractThe effect of a family history of schizophrenia on the risk for this disorder in the offspring has rarely been examined in a prospective population cohort accounting for the sex of the proband and the first‐degree relatives, and certainly not with respect to later paternal age. The influence of affected relatives on offspring risk of schizophrenia was estimated using Cox proportional hazards regression in models that accounted for sex, relation of affected first degree relatives and paternal age in the prospective population‐based cohort of the Jerusalem Perinatal Schizophrenia Study. Of all first‐degree relatives, an affected mother conferred the highest risk to male and female offspring among the cases with paternal age <35 years, however, female offspring of fathers ≥35 years with an affected sister had the highest risk (RR = 8.8; 95% CI = 3.9–19.8). The risk seen between sisters of older fathers was fourfold greater than the risk to sisters of affected females of younger fathers (RR = 2.2, 95% CI 0.7–6.7). The test for interaction was significant (P = 0.03). By contrast, the risk of schizophrenia to brothers of affected males was only doubled between older (RR = 3.3, 95% 1.6–6.6) and younger fathers (RR = 1.6, 95% CI 0.7–3.5). The most striking finding from this study was the very large increase in risk of schizophrenia to sisters of affected females born to older fathers. The authors speculate that the hypothesized paternally expressed genes on the X chromosome might play some role in these observations. © 2010 Wiley‐Liss, Inc.
Characterization of degraded hydrogels based on poly(vinyl alcohol) grafted with poly(lactide‐co‐glycolide)
Authors: Vidović Elvira , Klee Doris , Höcker Hartwig 
Published: August 2010

AbstractPoly(vinyl alcohol) (PVA) grafted with poly(lactide‐co‐glycolide) and cross‐linked as a material of increased hydrophobicity relative to PVA was produced. The properties were examined with respect to the mass loss, water uptake, hydrophilicity, and mechanical characteristics upon hydrolytical degradation. The hydrogels investigated display water uptake increasing with degradation time because of increasing hydrophilicity. The mass loss amounts up to 15% after eight weeks of degradation. The mechanical properties of the hydrogels are within the range of those of natural tissue, theEmodulus is 18 MPa, or even 100–200 MPa, depending on the structure of material. The mechanical characteristic and their dependence degradation show the most recognizable correlation with the chemical structure. Studies of the topography of degraded samples (scanning electron microscopy) and IR measurements demonstrate the degradation to occur at slow rate due to the high degree of grafting. The mass loss is rather low and a bulk degradation mechanism takes place. © 2010 Wiley Periodicals, Inc. J Appl Polym Sci, 2011
Mechanical characterization of untreated waste office paper/woven jute fabric hybrid reinforced epoxy composites
Authors: De Rosa Igor Maria , Santulli Carlo , Sarasini Fabrizio 
Published: August 2010

AbstractThe aim of this work is to assess the opportunity to use untreated waste office paper, alone and in combination with jute fabric, as a reinforcement in epoxy composites. Five different stacking sequences were manufactured and tested. Adding untreated waste office paper sheets has been revealed to increase both flexural and tensile strength of the neat resin and of the untreated jute fabric reinforced composites. The effect of the hybridization on tensile and flexural behavior has been evaluated through scanning electron microscopy observations and acoustic emission. The results confirm that waste office paper sheets can be used as a reinforcement for an epoxy resin, thus representing a viable alternative to paper recycling. © 2010 Wiley Periodicals, Inc. J Appl Polym Sci, 2011
A case of progressive multifocal leukoencephalopathy in a patient treated with infliximab
Authors: Kumar Deepak , Bouldin Thomas W. , Berger Robert G. 
Published: August 2010

AbstractWe describe a 72‐year‐old white man with erosive rheumatoid arthritis in whom subacute neurologic and psychiatric symptoms developed after 3 years of treatment with infliximab, prednisone, and methotrexate. White matter demyelination was seen on magnetic resonance imaging of the brain, and progressive multifocal leukoencephalopathy (PML) was ultimately confirmed by brain biopsy. The patient was treated with supportive therapy and discontinuation of disease‐modifying antirheumatic drugs, resulting in stabilization of the disease process. The patient survived, but neurologic and cognitive deficits persisted. The distribution and pathology of this patient's disease are unique from almost all reported incidents of oral methotrexate–associated leukoencephalopathy. The pathogenesis of disease may be linked to a T cell–mediated process that is potentially impacted by infliximab. This case provides the first reported evidence that PML can be seen in association with infliximab therapy.
Long‐term impact of delay in assessment of patients with early arthritis
Authors: van der Linden Michael P. M. , le Cessie Saskia , Raza Karim , van der Woude Diane , Knevel Rachel , Huizinga Tom W. J. , van der Helm‐van Mil Annette H. M. 
Published: August 2010

AbstractObjectiveDuring the last decade, rheumatologists have learned to initiate disease‐modifying antirheumatic drugs (DMARDs) early to improve the outcome of rheumatoid arthritis (RA). However, the effect of delay in assessment by a rheumatologist on the outcome of RA has scarcely been explored. The purpose of this study was to examine the association between delay in assessment by a rheumatologist, rates of joint destruction, and probability of achieving DMARD‐free remission in patients with RA. Patient characteristics associated with components of delay (by the patient, by the general practitioner [GP], and overall) were assessed.MethodsA total of 1,674 early arthritis patients from the Leiden Early Arthritis Clinic cohort were evaluated for patient delay, GP delay, and total delay in assessment by a rheumatologist. Among 598 RA patients, associations between total delay, achievement of sustained DMARD‐free remission, and the rate of joint destruction over 6 years followup were determined.ResultsThe median patient, GP, and total delays in seeing a rheumatologist among patients with early arthritis were 2.4 weeks, 8.0 weeks, and 13.7 weeks, respectively. Among all diagnoses, those diagnosed as having RA or spondylarthritis had the longest total delay (18 weeks). Among the RA patients, 69% were assessed in ≥12 weeks; this was associated with a hazard ratio of 1.87 for not achieving DMARD‐free remission and a 1.3 times higher rate of joint destruction over 6 years, as compared with assessment in <12 weeks. Older age, female sex, gradual symptom onset, involvement of the small joints, lower levels of C‐reactive protein, and the presence of autoantibodies were associated with longer total delay.ConclusionOnly 31% of the RA patients were assessed in <12 weeks of symptom onset. Assessment in <12 weeks is associated with less joint destruction and a higher chance of achieving DMARD‐free remission as compared with a longer delay in assessment. These results imply that attempts to diminish the delay in seeing a rheumatologist will improve disease outcome in patients with RA.
Relationship between the type I interferon signature and the response to rituximab in rheumatoid arthritis patients
Authors: Thurlings Rogier M. , Boumans Marie , Tekstra Janneke , van Roon Joel A. , Vos Koen , van Westing Daisy Marie , van Baarsen Lisa G. , Bos Carina , Kirou Kyriakos A. , Gerlag Danielle M. , Crow Mary K. , Bijlsma Johannes W. , Verweij Cornelis L. , Tak Paul P. 
Published: August 2010

AbstractObjectiveTo analyze the relationship between the type I interferon (IFN) signature and clinical response to rituximab in rheumatoid arthritis (RA) patients.MethodsTwenty RA patients were treated with rituximab (cohort 1). Clinical response was defined as a decrease in the Disease Activity Score evaluated in 28 joints (DAS28) and as a response according to the European League Against Rheumatism (EULAR) criteria at week 12 and week 24. The presence of an IFN signature was analyzed in peripheral blood mononuclear cells by measuring the expression levels of 3 IFN response genes by quantitative polymerase chain reaction analysis. After comparison with the findings in healthy controls, patients were classified as having an IFN high or an IFN low signature. The data were confirmed in a second independent cohort (n = 31). Serum IFNα bioactivity was analyzed using a reporter assay.ResultsIn cohort 1, there was a better clinical response to rituximab in the IFN low signature group. Consistent with these findings, patients with an IFN low signature had a significantly greater reduction in the DAS28 and more often achieved a EULAR response at weeks 12 and 24 as compared with the patients with an IFN high signature in cohort 2 versus cohort 1. The pooled data showed a significantly stronger decrease in the DAS28 in IFN low signature patients at weeks 12 and 24 as compared with the IFN high signature group and a more frequent EULAR response at week 12. Accordingly, serum IFNα bioactivity at baseline was inversely associated with the clinical response, although this result did not reach statistical significance.ConclusionThe type I IFN signature negatively predicts the clinical response to rituximab treatment in patients with RA. This finding supports the notion that IFN signaling plays a role in the immunopathology of RA.
Fasciitis as a common lesion of dermatomyositis, demonstrated early after disease onset by en bloc biopsy combined with magnetic resonance imaging
Authors: Yoshida Ken , Kurosaka Daitaro , Joh Kensuke , Matsushima Satoshi , Takahashi Eigo , Hirai Kenichiro , Noda Kentaro , Ukichi Taro , Furuya Kazuhiro , Yanagimachi Maimi , Kingetsu Isamu , Fukuda Kunihiko , Yamada Akio 
Published: August 2010

AbstractObjectiveTo investigate whether fasciitis is histopathologically demonstrable in patients with dermatomyositis (DM), and to analyze the process of inflammatory progression in myopathy accompanying DM.MethodsSTIR or fat‐suppressed T2‐weighted magnetic resonance imaging (MRI) and en bloc biopsy were performed in 14 patients with newly diagnosed adult‐onset DM. The severity of inflammatory cell infiltration around the fascial and intramuscular small blood vessels was evaluated using the total vascular inflammation score (TVIS).ResultsIn all patients, MRI revealed abnormal hyperintensity in the fascia and in marginal sites of the muscle, predominantly over central sites. En bloc biopsy revealed the presence of fasciitis in most of the patients, as shown by inflammatory infiltrates around the fascial small blood vessels. In those patients who underwent en bloc biopsy earlier than 2 months after the appearance of muscle symptoms, the TVIS of the fascia was significantly higher than the TVIS of the muscle. In contrast, in those patients who underwent en bloc biopsy ≥2 months after muscle symptom onset, the TVIS of the fascia did not differ significantly from the TVIS of the muscle.ConclusionFasciitis was histopathologically demonstrated in patients with newly diagnosed adult‐onset DM as early as 2 months after the onset of muscle symptoms. These results indicate that fasciitis is a common lesion of DM and suggest that the fascial microvasculature is the primary site of inflammatory cell infiltration in DM. Fasciitis may contribute to muscle symptoms in patients with DM without myositis.
Tumor necrosis factor causes persistent sensitization of joint nociceptors to mechanical stimuli in rats
Authors: Richter Frank , Natura Gabriel , Löser Stefan , Schmidt Katarina , Viisanen Hanna , Schaible Hans‐Georg 
Published: August 2010

AbstractObjectiveDuring inflammation in the joint, normal joint movements are usually painful. A neuronal mechanism for this form of mechanical hyperalgesia is the persistent sensitization of joint nociceptors to mechanical stimuli. Because tumor necrosis factor (TNF) is a major mediator of joint inflammation, we undertook the present study both to explore the potential of TNF to sensitize joint nociceptors to mechanical stimuli and to address the cellular mechanism involved.MethodsIn anesthetized rats, action potentials (APs) were recorded from sensory nociceptive Aδ fibers and C fibers supplying the knee joint. We monitored responses to rotation of the knee joint at innocuous and noxious intensities. TNF, etanercept, and a p38 inhibitor were injected into the knee joint, and the cyclooxygenase (COX) inhibitor diclofenac was administered intraperitoneally. APs were also recorded in isolated cultured dorsal root ganglion (DRG) neurons in order to test for changes in neuronal excitability induced by TNF.ResultsA single application of TNF into the normal knee joint caused a significant persistent sensitization of nociceptive sensory fibers to mechanical stimuli applied to the joint. This effect was dose dependent. It was prevented by coadministration of etanercept or by an inhibitor of p38, and it was attenuated by systemic application of a COX inhibitor. Patch clamp recordings from isolated DRG neurons showed a rapid increase in neuronal excitability induced by TNF.ConclusionTNF can induce a long‐lasting sensitization of joint nociceptors to mechanical stimuli and thus can induce long‐lasting mechanical hyperalgesia in joints. TNF can act directly on neurons, underscoring its role as a sensitizing pain mediator.
Associations of cigarette smoking with rheumatoid arthritis in African Americans
Authors: Mikuls Ted R. , Sayles Harlan , Yu Fang , LeVan Tricia , Gould Karen A. , Thiele Geoffrey M. , Conn Doyt L. , Jonas Beth L. , Callahan Leigh F. , Smith Edwin , Brasington Richard , Moreland Larry W. , Reynolds Richard J. , Bridges S. Louis 
Published: August 2010

AbstractObjectiveTo examine the associations of cigarette smoking with rheumatoid arthritis (RA) in African Americans, and to determine whether this association is impacted by the HLA–DRB1 shared epitope (SE).MethodsSmoking status, cumulative smoking exposure, and SE status were determined in African American patients with RA and African American healthy controls. Associations of smoking with RA were examined using age‐ and sex‐adjusted logistic regression analyses. Additive and multiplicative SE–smoking interactions were examined.ResultsAfter adjustment for age and sex, ever smoking (odds ratio [OR] 1.45, 95% confidence interval [95% CI] 1.07, 1.97) and current smoking (OR 1.56, 95% CI 1.07, 2.26), relative to never smoking, were more common in African American patients with RA (n = 605) than in controls (n = 255). The association of smoking with RA was limited to those with a cumulative exposure exceeding 10 pack‐years, associations that were evident both in autoantibody‐positive and in autoantibody‐negative disease. There was evidence of a significant additive interaction between SE status and heavy smoking (≥10 pack‐years) in relation to RA risk (attributable proportion [AP] due to interaction 0.58, P = 0.007), with similar results for the additive interaction between SE status and ever smoking (AP 0.47, P = 0.006). There was no evidence of multiplicative interactions.ConclusionAmong African Americans, cigarette smoking is associated not only with the risk of autoantibody‐positive RA but also with the risk of autoantibody‐negative disease. The risk of RA attributable to smoking is limited to African Americans with more than 10 pack‐years of exposure and is more pronounced among individuals positive for the HLA–DRB1 SE.
Progressive drawing: A novel “lid–opener” and “monotony–breaker”
Authors: Nayak Satheesha B. , Kodimajalu Soumya 
Published: August 2010

AbstractAn innovative strategy called “progressive drawing” was used at the beginning (lid‐opener) and later (monotony‐breaker) during gross anatomy lectures. Diagrams were drawn on the classroom blackboard with anatomic structures added one by one. Students identified and labeled the diagrams and predicted the next structures to be drawn. Students felt that the strategy helped to activate prior knowledge, created interest in the current lecture, and made lecture sessions more interactive. The strategy has appeal for visual, auditory, read/write, and kinesthetic learners. Anat Sci Educ, 2010. © 2010 American Association of Anatomists.
Circular proteins and mechanisms of cyclization
Authors: Conlan Brendon F. , Gillon Amanda D. , Craik David J. , Anderson Marilyn A. 
Published: August 2010

AbstractCyclization via head‐to‐tail linkage of the termini of a peptide chain occurs in only a small percentage of proteins, but engenders the resultant cyclic proteins with exceptional stability. The mechanisms involved are poorly understood and this review attempts to summarize what is known of the events that lead to cyclization. Cyclic proteins are found in both prokaryotic and eukaryotic species. The prokaryotic circular proteins include the bacteriocins and pilins. The eukaryotic circular proteins in mammals include the theta defensins, found in rhesus macaques, and the retrocyclins. Two types of cyclic proteins have been found in plants, the sunflower trypsin inhibitor and the larger, more prolific, group known as cyclotides. The cyclotides from Oldenlandia affinis, the plant in which these cyclotides were first discovered, are processed by an asparaginyl endopeptidase which is a cysteine protease. Cysteine proteases are commonly associated with transpeptidation reactions, which, for suitable substrates can lead to cyclization events. These proteases cleave an amide bond and form an acyl enzyme intermediate before nucleophilic attack by the amine group of the N‐terminal residue to form a peptide bond, resulting in a cyclic peptide. © 2010 Wiley Periodicals, Inc. Biopolymers (Pept Sci) 94: 573–583, 2010.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
Hedge Mustard (Sisymbrium officinale): Chemical Diversity of Volatiles and Their Antimicrobial Activity
Authors: Blažević Ivica , Radonić Ani , Mastelić Josip , Zekić Marina , Skočibušić Mirjana , Maravić Ana 
Published: August 2010

AbstractVolatile compounds of hedge mustard (Sysimbrium officinale) have been investigated for the first time. Forthy‐two compounds were identified after hydrodistillation (without or upon autolysis) after gas chromatography and gas chromatography/mass spectrometry analyses. In addition, after decoction and hydrolysis of O‐glycosides, 18 volatile O‐aglycones were identified. In general, the main volatiles found in hydrodistillates were: isopropyl isothiocyanate (27.6–48.9%), 2‐methylpropanenitrile (0.5–18.8%), (Z)‐hex‐3‐en‐1‐ol (0.5–18.0%), sec‐butyl isothiocyanate (4.9–9.4%), (E)‐hex‐2‐enal (3.5–8.6%), (Z)‐hex‐2‐en‐1‐ol (0.3–8.4%), octanoic (0.5–8.6%) and dodecanoic acid (0–5.0%), 2‐methylbutanenitrile (0–4.6%), dibutyl phthalate (0–4.5%), and ethyl linolenate (0–3.6%). The main volatile O‐aglycones were: 2‐phenylethyl alcohol (21.5%), 6,7‐dehydro‐7,8‐dihydro‐3‐oxo‐α‐ionol (9.3%), eugenol (8.3%), benzyl alcohol (7.0%), ethyl vanillate (5.2%), 6‐(tert‐butyl)‐5‐methylphenol (5.1%), vanillin acetone (4.7%), ethyl 4‐hydroxybenzoate (4.3%), and 2‐hydroxy‐β‐ionone (3.8%). All hydrodistillates exhibited great potential of antibacterial activity against five Gram‐positive bacteria, nine ampicillin‐resistant Gram‐negative bacteria, and four fungi at a concentration of 500 μg/ml using the disc diffusion method.