bluuebunny/crossref_metadata_2025_split huggingface dataset:
Experimental investigation of the hydrodynamics in a liquid–solid riser
Authors: Roy Shantanu , Kemoun Abdenour , Al‐Dahhan M. H. , Dudukovic M. P. 
Published: February 2005

AbstractLiquid–solid fluid dynamics has been investigated in a 6‐in. (0.15 m) “cold‐flow” circulating fluidized bed riser using non‐invasive flow monitoring methods. Gamma‐ray computed tomography (CT) was used to measure the time‐averaged cross‐sectional solids volume fraction distributions at several elevations. The time‐averaged mean and “fluctuating” solids velocity fields were quantified using the computer‐automated radioactive particle tracking (CARPT) technique. The experimental equipment, protocol of implementation, and data analysis have been discussed briefly, with particular emphasis on the specific features in the use of these techniques for studying high‐density turbulent flows as in a liquid–solid riser. The experimental study examines nine operating conditions, that is, three liquid superficial velocities and three solids flow rates. The solids holdup profile is found to be relatively uniform across the cross section of the riser, with marginal segregation near the walls. The time‐averaged solids velocity profiles are found to have a negative component at the walls, indicating significant solids backmixing. Detailed characterization of the solids velocity fields in terms of RMS velocities, kinetic energies, Hurst exponents, residence time distributions, trajectory length distributions, dispersion coefficients, and so forth are presented. Comparative and symbiotic analyses of the results were used to develop a coherent picture of the solids flow field. In addition, the work also serves to demonstrate the power and versatility of these flow‐imaging techniques in studying highly turbulent and opaque multiphase systems. © 2005 American Institute of Chemical Engineers AIChE J, 51: 802–835, 2005
Hearing in Drosophila: Development of Johnston's organ and emerging parallels to vertebrate ear development
Authors: Boekhoff‐Falk Grace 
Published: February 2005

AbstractIn this review, I describe recent progress toward understanding the developmental genetics governing formation of the Drosophila auditory apparatus. The Drosophila auditory organ, Johnston's organ, is housed in the antenna. Intriguingly, key genes needed for specification or function of auditory cell types in the Drosophila antenna also are required for normal development or function of the vertebrate ear. These genes include distal‐less, spalt and spalt‐related, atonal, crinkled, nanchung and inactive, and prestin, and their vertebrate counterparts Dlx, spalt‐like (sall), atonal homolog (ath), myosin VIIA, TRPV, and prestin, respectively. In addition, Drosophila auditory neurons recently were shown to serve actuating as well as transducing roles, much like their hair cell counterparts of the vertebrate cochlea. The emerging genetic and physiologic parallels have come as something of a surprise, because conventional wisdom holds that vertebrate and invertebrate hearing organs have separate evolutionary origins. The new findings raise the possibility that auditory organs are more ancient than previously thought and indicate that Drosophila is likely to be a powerful model system in which to gain insights regarding the etiologies of human deafness disorders. Developmental Dynamics 232:550–558, 2005. © 2005 Wiley‐Liss, Inc.
Dissecting JNK signaling, one KKKinase at a time
Authors: Stronach Beth 
Published: February 2005

AbstractSpecificity in signal transduction is essential to ensure distinct and appropriate cellular responses to extracellular cues. Determining the mechanisms that mediate specificity is key to understanding complex cell behaviors in development, when multiple pathways fire simultaneously and individual pathways are used recurrently. Jun kinase (JNK) signal transduction exemplifies a pathway that is used multiple times in animal development and homeostasis. Indeed, molecular genetic analysis of JNK signaling in Drosophila has shown that a core signaling module consisting of Hep (JNKK), Bsk (JNK), and Jun regulates various processes, including tissue morphogenesis, wound repair, stress response, innate immune response, and others. Six putative JNKK kinase (JNKKK) family members are present in the fly genome, which could activate the core module in response to distinct stimuli. The diversity of kinases at this level of the signaling hierarchy could substantially increase the number of possible signals that feed into activation of the core module. Recent studies have described the distinct phenotypic consequences of mutations in three of the genes, Slpr (dMLK), Tak1, and Mekk1. These data, together with Drosophila cell culture and genomic array analyses support the contention that the choice of JNKKK may contribute to signaling specificity in vivo. Whether this is achieved by individual JNKKKs or by means of a combinatorial mechanism will require a systematic characterization of compound mutants and a toolbox of transcriptional reporters specific for distinct JNK‐dependent processes. Developmental Dynamics 232:575–584, 2005. © 2005 Wiley‐Liss, Inc.
Setting the stage for development: mRNA translation and stability during oocyte maturation and egg activation in Drosophila
Authors: Tadros Wael , Lipshitz Howard D. 
Published: February 2005

AbstractEarly animal development is controlled by maternally encoded RNAs and proteins, which are loaded into the egg during oogenesis. Oocyte maturation and egg activation trigger changes in the translational status and the stability of specific maternal mRNAs. Whereas both maturation and activation have been studied in depth in amphibians and echinoderms, only recently have these processes begun to be dissected using the powerful genetic and molecular tools available in Drosophila. This review focuses on the mechanisms and functions of regulated maternal mRNA translation and stability in Drosophila—and compares these mechanisms with those elucidated in other animal models, particularly Xenopus—beginning late in oogenesis and continuing to the mid‐blastula transition, when developmental control is transferred to zygotically synthesized transcripts. Developmental Dynamics 232:593–608, 2005. © 2005 Wiley‐Liss, Inc.
Amnioserosa is required for dorsal closure in Drosophila
Authors: Scuderi Anne , Letsou Anthea 
Published: February 2005

AbstractDorsal closure in the fruit fly Drosophila melanogaster is a complex morphogenetic process, driven by sequential signaling cascades and involving multiple forces, which contribute to cell movements and rearrangements as well as to changes in cell shape. During closure, lateral epidermal cells elongate along the dorsoventral axis and subsequently spread dorsally to cover the embryonic dorsal surface. Amnioserosal cells, which are the original occupants of the most dorsal position in the developing embryo, constrict during closure; thus, the increase in epidermal surface area is accommodated by a reduction in the amnioserosal surface area. Several of the epidermal requirements for closure have been established in functional assays. In contrast, amnioserosal requirements for closure have remained elusive, in part because laser ablation and clonal approaches are limited to only subsets of amnioserosal cells. Here, we report our use of the UAS‐GAL4 system to target expression of the cell autonomous toxin Ricin‐A to all cells of the amnioserosa. We show that ablation of the amnioserosa leads to clear defects in dorsal closure and, thus, directly demonstrate a role for the amnioserosa in dorsal closure. We also show that DJNK (Drosophila Jun N‐terminal kinase) signaling, an epidermal trigger of closure, is unaffected by amnioserosal ablation. These data, together with our demonstration that amnioserosal ablated and Dpp signaling mutant embryos exhibit shared loss‐of‐function phenotypes, point to a requirement for the amnioserosa in dorsal closure that is downstream of Dpp, perhaps as part of a paracrine response to this signaling cascade. Developmental Dynamics 232:791–800, 2005. © 2005 Wiley‐Liss, Inc.
Novel dominant‐negative mutation within the six domain of the conserved eye specification gene sine oculis inhibits eye development in Drosophila
Authors: Roederer Kristin , Cozy Loralyn , Anderson Jason , Kumar Justin P. 
Published: February 2005

AbstractThe development of the compound eye of Drosophila is controlled, in part, by the concerted actions of several nuclear proteins that form an intricate regulatory system. One member of this network is sine oculis (so), the founding member of the Six gene family. Mutations within so affect the entire visual system, including the compound eye. The vertebrate homologs Six3 and Six6 also appear to play crucial roles in retinal formation. Mutations in Six3 inhibit retinal formation in chickens and fish, whereas those in Six6 are the underlying cause of bilateral anophthalmia in humans. Together, these phenotypes suggest a conserved role for the Six genes in eye development. In this report, we describe the effects of a dominant‐negative mutation of sine oculis on the development of the compound eye of Drosophila. The mutation resides within the Six domain and may have implications for eye development and disease. Developmental Dynamics 232:753–766, 2005. © 2005 Wiley‐Liss, Inc.
Simulated annealing search through general structure floor plans using sequence‐pair
Authors: Kiyota Koji , Fujiyoshi Kunihiro 
Published: February 2005

AbstractIn VLSI layout design, a “floor plan” is often derived prior to solving the placement problem. The floor plan is obtained by dividing the square representing the chip into several rectangular rooms, to which modules are assigned, and then the locations of the module and interconnects are approximately determined. In floor plan study, the use of slice structures is common. Recently, however, a method of converting the sequence‐pair, as a representation of the rectangular packing, to the floor plan has been proposed. Hence, it is now possible to list all floor plans with general configurations including the nonslice structure. However, in such a method there is the deficiency that an “empty room” without an assigned module may be generated. In the present paper, an adjacent solution is proposed for effective search of only the general configuration floor plan without empty rooms by using the simulated annealing method. An ingenious technique for effectively deriving this adjacent solution is described. The diameter of this solution space is proven to be of polynomial size. Also, the proposed solution space is experimentally compared with the solution space of slice structures. © 2005 Wiley Periodicals, Inc. Electron Comm Jpn Pt 3, 88(6): 28–38, 2005; Published online in Wiley InterScience (www.interscience. wiley.com). DOI 10.1002/ecjc.10003
Anti‐HER‐3 MAbs inhibit HER‐3‐mediated signaling in breast cancer cell lines resistant to anti‐HER‐2 antibodies
Authors: van der Horst Edward Htun , Murgia Marta , Treder Martin , Ullrich Axel 
Published: February 2005

AbstractTwo members of the EGF receptor family, HER2 and HER3, act as key oncogenes in breast cancer cells. A MAb against HER2, trastuzumab, interferes with HER2 signaling and istherapeutically effective in humans. Here, we explored the biologic effects of an antibody against HER3 (α‐HER3ECD) in the invasive breast cancer cell lines MCF‐7ADR and MDA‐MB‐468. Pretreating the breast cancer cells with α‐HER3ECD prior to Heregulin stimulation caused significant reduction of the migratory and proliferative properties. This reduction is due to a substantial decrease in the tyrosine phosphorylation content of HER2 and to a modification of the HER2/HER3 association, which ultimately inhibits the activity of the downstream effectors phosphatidyinositol‐3‐OH‐kinase and c‐jun‐terminal kinase. Furthermore, HER3 is internalized and not activated by HRG after pretreatment with α‐HER3ECD. Our data reinforce the notion that HER3 could be a key target in cancer drug design and show the great potential of anti‐HER3 antibodies for the therapy of breast cancer and other malignancies characterized by overexpression of HER3. © 2005 Wiley‐Liss, Inc.
Tumor‐specific CD4+ T cells from a patient with renal cell carcinoma recognize diverse shared antigens
Authors: Mautner Josef , Jaffee Elizabeth M. , Pardoll Drew M. 
Published: February 2005

AbstractMurine models for immune‐mediated tumor regression have defined an essential role for CD4+ T helper (Th) cells, but the contribution of these cells to antitumoral immune responses in humans remains poorly defined. Here, we investigated the Th cell response against the autologous tumor in a patient with metastasized renal cell carcinoma (RCC) exhibiting objective clinical response to immunotherapy. Peripheral blood T cells of the patient were repeatedly stimulated in vitro using either autologous IFNγ‐treated whole tumor cells or Epstein‐Barr virus‐immortalized B cells (EBV‐B) pulsed with tumor cell lysate. CD4+ T‐cell clones recognizing autologous tumor cells but not EBV‐B cells were efficiently reactivated and expanded with both types of stimulator cells, establishing the latter as potentially useful for isolating CD4+ T cells reactive against MHC class II‐negative tumors. Two T‐cell clones from both stimulation protocol were further characterized. The restricting MHC class II molecules were defined by using allogeneic EBV‐B cells pulsed with tumor lysate, and the expression pattern of the antigens was examined by analyzing lysates from normal kidney cells, allogeneic RCCs as well as tumors of different histologic origin. Furthermore, the subcellular localization of the antigens recognized by the T‐cell clones was examined by fractionating the tumor lysate, and the Th phenotype was determined by assessing the cytokines released after T cell activation. These experiments show that a dual Th1/Th2, MHC class II‐restricted T‐helper‐cell response against diverse shared tumor antigens has been elicited in this patient. © 2005 Wiley‐Liss, Inc.
CpG island methylation in aberrant crypt foci and cancers from the same patients
Authors: Luo Liping , Chen Wei‐dong , Pretlow Theresa P. 
Published: February 2005

AbstractAberrant methylation of CpG islands is a common alteration in human colon cancer. Methylation of only a limited number of loci has been studied in aberrant crypt foci (ACF), the earliest identified premalignant lesions in the colon, and in only a limited number of lesions from the same patients. Methylation‐specific PCR was used to analyze 35 ACF, samples of normal crypts with the same number of crypts as were in each ACF and 22 cancers from the same patients. Aberrant methylation in cellular retinol‐binding protein 1 (CRBP1), MINT31 or H‐cadherin (CDH13) was identified in 19 of 35 (54%) ACF. Hypermethylation of CRBP1, MINT31 or CDH13 was more frequent (15 of 22, 68%) in cancers. DNA methylation of CRBP1, MINT31 or CDH13 was not correlated between cancers and ACF from the same patients. Aberrant methylation was not correlated with patient age, number of crypts in the ACF or cancer stage. These results suggest that hypermethylation in the promoter region of some genes is an independent event, occurs early in human colon tumorigenesis and may play an important role during the transformation and progression of some lesions to colon cancers. © 2005 Wiley‐Liss, Inc.
Allele loss and epigenetic inactivation of 3p21.3 in malignant liver tumors
Authors: Tischoff Iris , Markwarth Annett , Witzigmann Helmut , Uhlmann Dirk , Hauss Johann , Mirmohammadsadegh Alireza , Wittekind Christian , Hengge Ulrich R. , Tannapfel Andrea 
Published: February 2005

AbstractPreviously, the RASSF1A, BLU and SEMAPHORIN 3B (SEMA3B) candidate tumor suppressor genes on chromosome 3p21.3 were found to be inactivated and downregulated by genetic and epigenetic changes in lung cancer. We analyzed the methylation status of RASSF1A, BLU and SEMA3B in 35 hepatocellular carcinomas (HCCs) and 15 cholangiocarcinomas (CCs) by methylation‐specific PCR and loss of heterozygosity (LOH) at 3p21.3 after microdissection. The presence of mRNA transcripts was confirmed by semiquantitative PCR. SEMA3B hypermethylation was found in 29/35 HCCs (83%) and in all (15/15) patients with CC. BLU promoter hypermethylation was detected in 7/35 (20%) HCCs and 3/15 (20%) CCs. In 2 corresponding specimens of hepatitis B virus‐related liver cirrhosis, BLU methylation was also observed, but not in uninvolved normal liver tissue. RASSF1A was methylated in 21/35 HCCs (60%) and in 10/15 CCs (67%). LOH at 3p21.3 occurred in 8/35 (23%) HCCs and 3/15 (20%) CCs. The presence of hypermethylation was statistically associated with LOH of SEMA3B and correlated with downregulation of mRNA transcripts. SEMA3B transcripts increased upon treatment of HCC cell lines with the demethylation compound 5‐aza‐2‐deoxycytidine. In conclusion, our data indicate that 2‐hit gene silencing of SEMA3B through epigenetic changes and allele loss is a common and important event in the carcinogenesis of malignant liver tumors. © 2005 Wiley‐Liss, Inc.
In vitro interaction of human fibroblasts and platelets with a shape‐memory polyurethane
Authors: Farè Silvia , Valtulina Viviana , Petrini Paola , Alessandrini Edoardo , Pietrocola Giampiero , Tanzi M. Cristina , Speziale Pietro , Visai Livia 
Published: February 2005

AbstractPhysicochemical and mechanical properties, in vitro cytotoxicity, cytocompatibility, and platelet adhesion were investigated on a shape‐memory polyether‐based polyurethane (MM‐5520 SMPu) using the polyether‐based Pellethane 2363‐80AE (Pell‐2363 SPU) as reference. MM‐5520 SMPu and Pell‐2363 SPU showed similar average molecular weights and different surface properties, with a higher hydrophilicity and roughness for the SMPu. By tensile tests and dynamic mechanical analysis, the peculiar characteristics of the MM‐5520 SMPu were evidenced: strong temperature‐dependent behavior for SMPu compared with SPU, and a high shape recovery. MM‐5520 SMPu did not show any cytotoxic effect on the adhesion and proliferation of human skin fibroblasts and gingival fibroblasts, and a good cytocompatibility was observed with both cell types, as demonstrated by cell counting and scanning electron microscopy observations. SMPu compared with SPU showed higher adsorption of extracellular matrix proteins such as fibronectin, fibrinogen, and collagens. Proteins adsorbed onto SMPu significantly enhanced the adhesion and proliferation of human fibroblasts. The interaction of SMPu with platelets was studied with platelet rich plasma. Fewer platelets adhered to the SMPu, with minor morphological variations than onto the SPU. The cytocompatibility and hemocompatibility of MM‐5520 SMPu combined with its unique properties such as change in shape or in stiffness, depending on practical requirements, make this shape‐memory material potentially advantageous for biomedical applications. © 2005 Wiley Periodicals, Inc. J Biomed Mater Res 73A: 1–11, 2005
Osteoblast response to thermally oxidized Ti6Al4V alloy
Authors: Saldaña L. , Vilaboa N. , Vallés G. , González‐Cabrero J. , Munuera L. 
Published: February 2005

AbstractWe have recently reported that thermal oxidation treatments of Ti6Al4V at 500° and 700°C for 1 h result in the formation of an outer “ceramic” layer of rutile that do not decrease the high in vitro corrosion resistance of the alloy. In the present work, surface roughness was measured and found marginally increased as a consequence of oxidation of the alloy at 700°C, but not at 500°C. We have evaluated the biocompatibility of the oxidized surfaces, by assessing cell adhesion, proliferation, and differentiation of primary cultures of human osteoblastic cells. Compared with polished alloy, both thermal treatments increased osteoblast adhesion measured as cell attachment, β1 integrin and FAK‐Y397 expression, as well as cytoskeletal reorganization. Compared with treatment at 500°C, thermal oxidation at 700°C enhanced cell adhesion. Treatment at 700°C transiently impaired cell proliferation and viability, which were not altered in alloys oxidized at 500°C. Several markers of osteoblastic differentiation such as procollagen I peptide, alkaline phosphatase, osteocalcin, and mineralized nodule formation were found either unaffected or differentially increased by alloys treated either at 500° or 700°C. In addition, thermal oxidation at 700°C also increased osteoprotegerin secretion. Taken together, our results indicate that thermal oxidation treatments at 500° or 700°C for 1 h improve the in vitro biocompatibility of Ti6Al4V. © 2005 Wiley Periodicals, Inc. J Biomed Mater Res 73A: 97–107, 2005
Assessment of the cytocompatibility of different coated titanium surfaces to fibroblasts and osteoblasts
Authors: Harris Llinos G. , Patterson Louisa M. , Bacon Claire , Gwynn Iolo ap , Richards R. Geoff 
Published: February 2005

AbstractOver the years, many metal and polymer implants have been developed for internal fracture fixation. However, there are always some problems associated with their application, such as implant loosening or infection. This study describes how the morphology and adhesion of both fibroblasts and osteoblasts to two manufactured commercially pure, medical implant‐quality anodized titanium surfaces (TS and TSS), and five modified titanium surfaces (TLF, low friction gray anodized titanium; TIG, nitrogen ion implanted TSS; THY, TSS grafted with sodium hyaluronate; TAST, TSS coated with hydrophilic hydrogel; and TT, tiodized TS) were used to obtain an indication of their relative cytocompatibility and to assess which modified surface could potentially be used in vivo. Small variations were observed both qualitatively and quantitatively in the spreading and adhesion of fibroblasts and osteoblasts to the studied surfaces. Overall, fibroblast spreading and adhesion were greatest on the TIG and TLF surfaces. Osteoblast spreading and adhesion were greatest on TS, TIG, and TAST surfaces. No fibroblasts or osteoblasts were found attached to the THY‐coated surfaces. Coating medical implant‐quality anodized titanium surfaces (TS and TSS) with a TLF, TAST, or more specifically TIG could probably improve soft tissue adhesion and/or osseointegration of bone in vivo. However, it seemed that a hyaluronic acid coating (THY) has potential as a coating in areas where cell adhesion is undesirable, such as orbital fractures, where muscles should avoid adhesion to the implant, and distal radius fractures, where tendons should freely glide over the implant. © 2005 Wiley Periodicals, Inc. J Biomed Mater Res 73A: 12–20, 2005
XMVB: A program for ab initio nonorthogonal valence bond computations
Authors: Song Lingchun , Mo Yirong , Zhang Qianer , Wu Wei 
Published: February 2005

AbstractAn ab initio nonorthogonal valence bond program, called XMVB, is described in this article. The XMVB package uses Heitler–London–Slater–Pauling (HLSP) functions as state functions, and calculations can be performed with either all independent state functions for a molecule or preferably a few selected important state functions. Both our proposed paired‐permanent–determinant approach and conventional Slater determinant expansion algorithm are implemented for the evaluation of the Hamiltonian and overlap matrix elements among VB functions. XMVB contains the capabilities of valence bond self‐consistent field (VBSCF), breathing orbital valence bond (BOVB), and valence bond configuration interaction (VBCI) computations. The VB orbitals, used to construct VB functions, can be defined flexibly in the calculations depending on particular applications and focused problems, and they may be strictly localized, delocalized, or bonded‐distorted (semidelocalized). The parallel version of XMVB based on MPI (Message Passing Interface) is also available. © 2005 Wiley Periodicals, Inc. J Comput Chem 26: 514–521, 2005