bluuebunny/crossref_metadata_2025_split huggingface dataset:
Monte Carlo model of UV‐radiation interaction with TiO2‐coated spheres
Authors: Imoberdorf Gustavo E. , Alfano Orlando M. , Cassano Alberto E. , Irazoqui Horacio A. 
Published: August 2007

AbstractPhotocatalysis is one of the advanced oxidation techniques that are being studied for the treatment of polluted air and water from different sources. From a kinetic point of view, photocatalytic reaction rates are strongly dependent not only on the reactant and product concentrations, but also on the rate of photon absorption. Unfortunately, the local rate of photon absorption is usually difficult to evaluate because of (i) the inherent complexity of the system and (ii) the lack of data concerning the photocatalyst optical properties. The final objective of this project is focused on the development of a complete model of the radiation field; the bed structure, and the flow pattern to describe the operation of a fixed bed photocatalytic reactor. In this article, the interaction between radiative energy and TiO2‐coated fused‐silica sphere beds was studied. The proposed model was built applying the Monte Carlo method, taking into account the complex reflection/refraction/absorption interactions between radiation and the packed bed. To obtain experimental measurements, an ad hoc device was designed and built. This device allows us to validate the proposed radiation model, and to obtain the optical parameters of the composite photocatalyst, i.e., the refractive index and the surface rough index of the fused‐silica spheres, as well as the refractive index and the optical thickness of the TiO2 films. © 2007 American Institute of Chemical Engineers AIChE J, 2007
Mechanical strength of solid catalysts: Recent developments and future prospects
Authors: Wu Dongfang , Zhou Jiancheng , Li Yongdan 
Published: August 2007

AbstractMechanical strength of solid catalysts is one of the most important factors for the reliable and efficient performance of a reactor. Some recent developments on the basic mechanics of solid catalysts are reviewed in this article. The main concepts discussed are the brittle fracture which leads to the mechanical failure of the catalyst pellets, the measurement and statistical properties of the catalyst strength data, the mechanical reliability of the catalyst pellets, the mechanical properties of the catalyst packed beds, etc. For the purpose of an integrated research on catalyst mechanical properties, a multi‐scale framework for the mechanics of the fixed bed catalysts is also proposed. The scientific basis for the issues on the catalyst mechanical properties calls yet for further elucidation and advancement. © 2007 American Institute of Chemical Engineers AIChE J, 2007
Weight for age charts for children with achondroplasia
Authors: Hoover‐Fong J.E. , McGready J. , Schulze K.J. , Barnes H. , Scott C.I. 
Published: August 2007

AbstractTo develop accurate weight for age charts for individuals with achondroplasia. These novel weight for age, gender‐specific growth curves for achondroplasia patients from birth through 16 years were constructed from a longitudinal, retrospective, single observer cohort study of 334 individuals with achondroplasia. Weight for age data from 301 subjects in this achondroplasia cohort, constituting 1,964 total weight measurements, are presented in these weight for age curves. Percentiles (5, 25, 50, 75, 95th) were estimated across the age continuum by gender, using a 1 month window (±0.5 months) around each time point of interest. Percentiles were smoothed using a quadratic, penalized smoother by a semi‐parametric model approach. Raw weight data from the achondroplasia cohort are compared to that of average stature children presented in the current CDC growth curves, divided into 0–36 months and 2–16 years. There was overlap of birth weight between achondroplasia and average stature infants. This statistical modeling method can be applied to other anthropometric parameters collected from this achondroplasia cohort (e.g., length, BMI), other skeletal dysplasia diagnoses, and to syndromic, non‐skeletal dysplasia diagnoses which may benefit from standardization of weight for age. © 2007 Wiley‐Liss, Inc.
A novel multiple congenital anomaly–mental retardation syndrome with Pierre Robin sequence and cerebellar hypoplasia in two sisters
Authors: Stevenson David A. , Carey John C. 
Published: August 2007

AbstractWe report on the similar phenotypes and clinical course of two sisters. Both patients had an enlarged cisterna magna suggestive of cerebellar hypoplasia, agenesis/hypoplasia of the corpus callosum, Pierre Robin sequence requiring tracheostomy, camptodactyly, microphthalmia, colobomas, seizures, a distinctive facial appearance, global developmental delay, and mental retardation. We propose that the distinct pattern in these sisters constitutes a previously undescribed syndrome of likely autosomal recessive inheritance. © 2007 Wiley‐Liss, Inc.
Keratin as a filler for carboxylated acrylonitrile‐butadiene rubber XNBR
Authors: Prochoń M. , Przepiórkowska A. , Zaborski M. 
Published: August 2007

AbstractThe presented investigations concern the distribution and characterization of keratin waste, derived from the processes of cattle skins, and its use as a filler for carboxylated acrylonitrile‐butadiene rubber XNBR. The recovered keratin improves mechanical proprieties such as tensile strength, hardness, resistance to fuel and oil. The addition of keratin in a quantity of five parts per hundred rubber (XNBR) increases the crosslinking density of composites, as testified by the formed ion nodes and the existing mono and disulphide bonds. Electric conductance and water absorption increased with time for elastomers filled with protein. Therefore these composites are biodegradable after their period of use. As a result hydrophilic–hydrophobic protein–elastomeric composites will have usable properties. © 2007 Wiley Periodicals, Inc. J Appl Polym Sci, 2007
Effect of the fiber content and plasticizer type on the rheological and mechanical properties of poly(vinyl chloride)/green coconut fiber composites
Authors: Leblanc Jean L. , Furtado Cristina R. G. , Leite Marcia C. A. M. , Visconte Leila L. Y. , de Souza Ana M. F. 
Published: August 2007

AbstractA series of poly(vinyl chloride) (PVC)/green coconut fiber (GCF) composites, with dioctyl phthalate (DOP) or thermoplastic polyurethane (TPU) as a plasticizer, were prepared by melt mixing. Their properties were studied in the molten state with an advanced nonlinear harmonic testing technique; in the solid state, the hardness and impact resistance were evaluated, and scanning electron microscopy was used for fractured surfaces. The effect of the fiber loading was investigated, as well as the role of the plasticizer. PVC–GCF composites are heterogeneous materials that, in the molten state, exhibit essentially a nonlinear viscoelastic character, in contrast to pure PVC, which has a linear viscoelastic region up to 50–60% strain. The complex modulus increases with the GCF content but in such a manner that the observed reinforcement is at best of hydrodynamic origin, without any specific chemical (i.e., permanent) interaction occurring between the polymer matrix and the fibers. As expected, PVC offers good wetting of GCFs, as reflected by the easy mixing and the rheological and mechanical properties. Fibers can be incorporated into PVC up to a 30% concentration without any problem, with the PVC/plasticizer ratio kept constant. Higher GCF levels could therefore be considered. Replacing DOP in part with TPU gives some benefit in terms of impact resistance, likely because of the viscoelastic nature of the latter and the associated energy absorption effects. © 2007 Wiley Periodicals, Inc. J Appl Polym Sci, 2007
Synthesis of polystyrene microgel with a hyperbranched polyglycerol scaffold as core: Effect of shell congestion
Authors: Wan Decheng , Pu Hongting 
Published: August 2007

AbstractTwo hyperbranched polyglycerols (PG) (1a: Mn = 2000, 1b: Mn = 8000), both with 61% of the overall hydroxyl groups being transformed into trithiocarbonates (2a, 2b, with 16 and 65 OH groups being replaced by trithiocarbonates, respectively), can be used as a reversible addition‐fragmentation chain transfer (RAFT) agent. Polymerization of styrene mediated by 2a/2b was in a living manner, resulting in star‐like, amphiphilic, core‐shell structured polymers with 16 arms (3a) and 65 arms (3b), respectively. It was found that for system mediated by 2b, more serious side reaction (radical–radical coupling) occurred than that by 2a, most probably due to their difference in shell congestion. A shell‐crosslinked polymer could be prepared in the presence of divinylbenzene via a one‐pot route at solid content up to 20%, but analysis proved the crosslinking was incomplete. Furthermore, the 65‐arm‐star polymer (3b) more tended to undergo macroscopic rather than intramolecular crosslinking than the 16‐arm‐star polymer (3a) did. The phenomenon might again be attributed to their difference in shell congestion. © 2007 Wiley Periodicals, Inc. J Appl Polym Sci, 2007
Delayed memory B cell recovery in peripheral blood and lymphoid tissue in systemic lupus erythematosus after B cell depletion therapy
Authors: Anolik Jennifer H. , Barnard Jennifer , Owen Teresa , Zheng Bo , Kemshetti Sunil , Looney R. John , Sanz Iñaki 
Published: August 2007

AbstractObjectiveRecent data suggest that the reconstituting peripheral B cell compartment after B cell depletion therapy may be functionally immature, with a preponderance of transitional B cells and a paucity of memory B cells. This study was undertaken to determine the magnitude, duration, and cause of these defects in rituximab‐treated systemic lupus erythematosus (SLE) patients.MethodsFifteen patients with SLE previously treated with rituximab as part of a phase I/II dose‐escalation study were evaluated during a long‐term followup (mean followup period 41 months). B cells from peripheral blood and tonsils were assessed using multicolor flow cytometry, and their developmental pathway was classified based on the expression of defined surface markers.ResultsReconstitution of peripheral blood CD27+ memory B cells was delayed for several years after B cell depletion therapy in a subset of patients with prolonged clinical responses and autoantibody normalization. This delay correlated with the degree of expansion of B cells of a transitional phenotype during the B cell reconstitution phase (P = 0.005) and the absence of baseline autoantibodies directed against extractable nuclear antigens (RNP, Sm, Ro antigen, La antigen). Despite the paucity of peripheral blood memory cells and the prolonged expansion of functionally immature transitional B cells, tonsil biopsy tissues revealed active germinal center (GC) reactions, but with decreased Fc receptor homolog 4–positive memory B cells.ConclusionThese results suggest heterogeneity in the B cell depletion and reconstitution process that impacts clinical and immunologic outcomes in SLE. The presence of GC reactions, but with altered memory B cell subpopulations in tonsils, suggests that peripheral blood memory cell reconstitution lags behind a slow secondary lymphoid tissue recovery, with important implications for immunologic competence and tolerance.
Inverse relationship between matrix remodeling and lipid metabolism during osteoarthritis progression in the STR/ORT mouse
Authors: Watters James W. , Cheng Chun , Pickarski Maureen , Wesolowski Gregg A. , Zhuo Ya , Hayami Tadashi , Wang Wei , Szumiloski John , Phillips Robert L. , Duong Le T. 
Published: August 2007

AbstractObjectiveThe biologic changes associated with osteoarthritis (OA) are incompletely understood. The aim of this study was to elucidate the molecular mechanisms underlying OA progression in an STR/Ort murine model of spontaneous disease.MethodsGlobal patterns of gene expression were assessed using microarray analysis of articular cartilage/subchondral bone from the tibial plateaus of STR/Ort mice at 3, 9, and 12 months of age. The age‐dependent severity of osteophyte formation and extent of cartilage damage were determined in the corresponding femurs using microfocal computed tomography and the Mankin histologic scoring system. Pathway analysis was used to identify the functions of genes associated with OA progression, and changes in gene expression were confirmed using immunohistochemistry.ResultsSix hundred twenty‐one genes were associated with both osteophyte formation and cartilage damage in the STR/Ort joints. Genes involved in the development/function of connective tissue and in lipid metabolism were most significantly enriched and regulated during disease progression. Genes directly interacting with peroxisome proliferator–activated receptor α (PPARα)/PPARγ were down‐regulated, whereas those genes involved with connective tissue remodeling were up‐regulated during disease progression. Associations of down‐regulation of myotubularin‐related phosphatase 1 (a phosphoinositide 3‐phosphatase involved in lipid signaling) and up‐regulation of biglycan (a member of the small leucine‐rich protein family known to modulate osteoblast differentiation and matrix mineralization) with OA progression were confirmed by immunohistochemistry.ConclusionSince adipogenesis and osteogenesis are inversely related in the developing skeletal tissue, these results suggest that a shift in the differentiation of mesenchymal cells from adipogenesis toward osteogenesis is a component of the OA pathophysiologic processes occurring in the tibial plateau joints of STR/Ort mice.
Pattern of interleukin‐1β secretion in response to lipopolysaccharide and ATP before and after interleukin‐1 blockade in patients with CIAS1 mutations
Authors: Gattorno Marco , Tassi Sara , Carta Sonia , Delfino Laura , Ferlito Francesca , Pelagatti Maria Antonietta , D'Osualdo Andrea , Buoncompagni Antonella , Alpigiani Maria Giannina , Alessio Maria , Martini Alberto , Rubartelli Anna 
Published: August 2007

AbstractObjectiveTo examine the synthesis, processing, and secretion of interleukin‐1β (IL‐1β), as well as the clinical and biologic effects of IL‐1 blockade, in patients with chronic infantile neurologic, cutaneous, articular (CINCA) syndrome and Muckle‐Wells syndrome (MWS), in an effort to understand the molecular mechanisms linking mutations of the CIAS1 gene and IL‐1β hypersecretion, and the underlying response to IL‐1 receptor antagonist (IL‐1Ra).MethodsSix patients with CINCA syndrome or MWS were treated with IL‐1Ra and followed up longitudinally. Monocytes obtained from the patients and from 24 healthy donors were activated with lipopolysaccharide (LPS) for 3 hours, and intracellular and secreted IL‐1β levels were determined by Western blotting and enzyme‐linked immunosorbent assay before and after exposure to exogenous ATP.ResultsLPS‐induced IL‐1β secretion was markedly increased in monocytes from patients with CIAS1 mutations. However, unlike in healthy subjects, secretion of IL‐1β was not induced by exogenous ATP. Treatment with IL‐1Ra resulted in a dramatic clinical improvement, which was paralleled by an early and strong down‐regulation of LPS‐induced IL‐1β secretion by the patients' cells in vitro.ConclusionOur results showed that the requirements of ATP stimulation for IL‐1β release observed in healthy individuals are bypassed in patients bearing CIAS1 mutations. This indicates that cryopyrin is the direct target of ATP and that the mutations release the protein from the requirement of ATP for activation. In addition, the dramatic amelioration induced by IL‐1Ra treatment is at least partly due to the strong decrease in IL‐1β secretion that follows the first injections of the antagonist. These findings may have implications for other chronic inflammatory conditions characterized by increased IL‐1β.
Enhanced efficacy of regulatory T cell transfer against increasing resistance, by elevated Foxp3 expression induced in arthritic murine hosts
Authors: Ohata Junko , Miura Tomoko , Johnson Todd A. , Hori Shohei , Ziegler Steven F. , Kohsaka Hitoshi 
Published: August 2007

AbstractObjectiveTo investigate the efficacy of type II collagen–reactive Foxp3‐expressing T cell transfer in suppressing collagen‐induced arthritis (CIA) in relation to disease progression.MethodsCD3‐activated CD4 T cells were retrovirally transduced with the Foxp3 gene, and their in vitro suppressive activity on T cell proliferation was assessed for correlation with Foxp3 levels. To suppress CIA, Foxp3‐transduced T cells generated with type II collagen– or ovalbumin (OVA)–pulsed dendritic cells (DCs), which were fractionated by Foxp3 levels, were adoptively transferred to mice at various time points.ResultsThe in vitro suppressive activity of Foxp3‐transduced cells correlated positively with Foxp3 levels. Type II collagen–reactive, but not OVA‐reactive, Foxp3‐transduced cells significantly suppressed CIA when they were transferred before immunization, and this suppression was accompanied by decreased anti–type II collagen antibody production. Larger cell numbers were required to suppress CIA when transfer occurred 20 days after immunization, indicating that hosts became resistant to suppression. Transfer of 1 × 105 Foxp3low cells had only a marginal effect on CIA suppression in immunized hosts, while transfer of Foxp3high cells at smaller doses significantly suppressed CIA. Transfer of 1 × 105 Foxp3high cells after establishment of arthritis attenuated disease progression but did not reverse joint swelling.ConclusionResistance to Foxp3‐transduced T cells proceeded as CIA progressed, suggesting that late‐stage aggressive arthritis is more resistant to regulatory T cell transfer. An elevated expression level of Foxp3 in type II collagen–specific T cells improved their suppressive function in CIA. Thus, transfer of T cells expressing high levels of Foxp3 could be a strategy to overcome the induced resistance to regulatory T cell therapy.
Regulation of apoptosis in fibroblast‐like synoviocytes by the hypoxia‐induced Bcl‐2 family member Bcl‐2/adenovirus E1B 19‐kd protein–interacting protein 3
Authors: Kammouni Wafa , Wong Keng , Ma Guoping , Firestein Gary S. , Gibson Spencer B. , El‐Gabalawy Hani S. 
Published: August 2007

AbstractObjectiveRheumatoid arthritis (RA) synovial hyperplasia is related in part to a resistance to apoptosis exhibited by fibroblast‐like synoviocytes (FLS). Since hypoxia is a regulator of apoptosis, and since RA synovium is hypoxic, we conducted this study to examine the effects of hypoxia on the Bcl‐2 pathway and the role this may play in regulating apoptosis in FLS.MethodsSynovium samples from RA patients, osteoarthritis (OA) patients, and normal subjects were used for immunohistologic assessments and for generating FLS lines in vitro. FLS were stimulated under conditions of hypoxia (1% O2) and using 100 μM CoCl2 to simulate the effects of severe hypoxia. Changes in the gene expression profile of FLS were evaluated using microarrays and were confirmed by quantitative polymerase chain reaction (PCR). Changes in protein expression were detected by Western blotting. The effect of transient transfection with a BNIP3 plasmid on the apoptosis of FLS was evaluated in the presence and absence of cytokines.ResultsGene expression profiling demonstrated that BNIP3 was unique among the BCL2 family, in that it was induced by hypoxia in FLS. Quantitative PCR indicated a 2–3‐fold induction of BNIP3 messenger RNA, and Western blotting showed a 3–5‐fold increase in the 30‐kd Bcl‐2/adenovirus E1B 19‐kd protein–interacting protein 3 (BNIP‐3) monomer. BNIP‐3 was widely expressed in RA synovium and was prominent in FLS from the lining layer. Overexpression of BNIP3 increased FLS apoptosis under hypoxic conditions, an effect that was inhibited by tumor necrosis factor α and interleukin‐1β.ConclusionThe proapoptotic protein BNIP‐3 is induced in FLS by hypoxia and is widely expressed in RA synovium, but its proapoptotic effects may be inhibited in vivo by proinflammatory cytokines. Since overexpression of BNIP3 in FLS increases apoptosis, this may provide a novel approach for controlling synovial hyperplasia in RA.
Targeting of Gr‐1+,CCR2+ monocytes in collagen‐induced arthritis
Authors: Brühl Hilke , Cihak Josef , Plachý Jiří , Kunz‐Schughart Leoni , Niedermeier Marianne , Denzel Andrea , Rodriguez Gomez Manuel , Talke Yvonne , Luckow Bruno , Stangassinger Manfred , Mack Matthias 
Published: August 2007

AbstractObjectiveThe chemokine receptor CCR2 is highly expressed on monocytes and considered a promising target for treatment of rheumatoid arthritis. However, blockade of CCR2 with a monoclonal antibody (mAb) during progression of collagen‐induced arthritis results in a massive aggravation of the disease. In this study we investigated why CCR2 antibodies have proinflammatory effects, how these effects can be avoided, and whether CCR2+ monocytes are useful targets in the treatment of arthritis.MethodsArthritis was induced in DBA/1 mice by immunization with type II collagen. Mice were treated with mAb against CCR2 (MC‐21), IgE, or isotype control antibodies at various time points. Activation of basophils and depletion of monocyte subsets were determined by fluorescence‐activated cell sorter analysis and enzyme‐linked immunosorbent assay.ResultsCrosslinkage of CCR2 activated basophils to release interleukin‐6 (IL‐6) and IL‐4. In vivo, IL‐6 release occurred only after exposure to high doses of MC‐21, whereas application of low doses of the mAb circumvented the release of IL‐6. Regardless of the dose level used, the antibody MC‐21 efficiently depleted Gr‐1+,CCR2+ monocytes from the synovial tissue, peripheral blood, and spleen of DBA/1 mice. Activation of basophils with high doses of MC‐21 or with antibodies against IgE resulted in a marked aggravation of collagen‐induced arthritis and an increased release of IL‐6. In contrast, low‐dose treatment with MC‐21 in this therapeutic setting had no effect on IL‐6 and led to marked improvement of arthritis.ConclusionThese results show that depletion of CCR2+ monocytes may prove to be a therapeutic option in inflammatory arthritis, as long as the dose‐dependent proinflammatory effects of CCR2 mAb are taken into account.
Menopause hormonal therapy in women with systemic lupus erythematosus
Authors: Sánchez‐Guerrero Jorge , González‐Pérez Marisol , Durand‐Carbajal Marta , Lara‐Reyes Pilar , Jiménez‐Santana Luisa , Romero‐Díaz Juanita , Cravioto María‐del‐Carmen 
Published: August 2007

AbstractObjectiveTo evaluate the effects of menopause hormonal therapy on disease activity in women with systemic lupus erythematosus (SLE).MethodsWe conducted a double‐blind, randomized clinical trial involving 106 women with SLE who were in the menopausal transition or in early or late postmenopause. Patients received a continuous‐sequential estrogen‐progestogen regimen (n = 52) or placebo (n = 54). Disease activity was assessed at baseline and at 1, 2, 3, 6, 9, 12, 15, 18, 21, and 24 months, according to the SLE Disease Activity Index (SLEDAI). The primary outcome measure was global disease activity, estimated by measuring the area under the SLEDAI curve. Secondary outcome measures included maximum SLEDAI score, change in SLEDAI score, incidence of lupus flares, median time to flare, medication use, and adverse events. Results were studied using intent‐to‐treat analysis.ResultsAt baseline, demographic and disease characteristics were similar in both groups. Mean ± SD SLEDAI scores were 3.5 ± 3.3 and 3.1 ± 3.4 in the menopause hormonal therapy and placebo groups, respectively (P= 0.57). Disease activity remained mild and stable in both groups throughout the trial. There were no significant differences between the groups in global or maximum disease activity, incidence or probability of flares, or medication use. Median time to flare was 3 months in both groups. Thromboses occurred in 3 patients who received menopause hormonal therapy and in 1 patient who received placebo. One patient in each group died during the trial due to sepsis.ConclusionMenopause hormonal therapy did not alter disease activity during 2 years of treatment. However, an apparently increased risk of thrombosis seems to be a real threat in women with SLE who receive menopausal hormone therapy.