bluuebunny/crossref_metadata_2025_split huggingface dataset:
Induction of glutathione S‐transferases activities in Drosophila melanogaster exposed to phenol
Authors: Shen S. , Chien Y. , Chien C. 
Published: May 2003

AbstractStudying the toxic effects of long‐term exposing fruit flies to phenol is the object of this study. The induction of the glutathione S‐transferases enzymatic activities, the change in the amount of mRNA related to phenol exposure, the change in survival rate of adult fruit flies, and the chemical interaction between phenol and benzene were the problems to be investigated. Glutathione S‐transferases were separated by affinity chromatography and the mRNAs levels were quantified by reverse‐transcription polymerase chain reaction. Long‐term feeding phenol to wild type fruit flies had caused some toxic effects included increasing the resistance to phenol toxicity, lowering the benzene toxicity, and induction of glutathione S‐transferases enzymatic activities. But no significant change in the amount of glutathione S‐transferases GstD1 and GstD5 mRNAs had occurred. From these results, we concluded that fruit flies could develop resistance to phenol by decreasing its toxicity; phenol was a inducer of glutathione S‐transferases; phenol could increase the glutathione S‐transferases enzymatic activities by increasing the amount of proteins; phenol exposure could decrease the benzene toxicity; no new glutathione S‐transferase isozyme subunit was induced; and the level of GstD1 and GstD5 mRNAs did not significantly increase in phenol‐treated strain. Arch. Insect Biochem. Physiol. 53:80–91, 2003. © 2003 Wiley‐Liss, Inc.
EphA4 provides repulsive signals to developing cochlear ganglion neurites mediated through ephrin‐B2 and ‐B3
Authors: Brors Dominik , Bodmer Daniel , Pak Kwang , Aletsee Christoph , Schäfers Maria , Dazert Stefan , Ryan Allen F. 
Published: May 2003

AbstractThe ephrins and Eph receptors make up two large families of bi‐directional signaling molecules that are known to play a role in the development of the nervous system. Recently, expression of EphA4 in the developing cochlea was shown, with strong expression in cells lining the osseous spiral lamina (OSL) through which afferent dendrites must pass to reach the organ of Corti (OC). It was also demonstrated that ephrin‐B2 and ‐B3, both of which are known to interact with EphA4, are expressed by spiral ganglion (SG) neurons. To investigate the functional role of EphA4 in the development of inner ear neurons, neonatal rat SG explants were cultured for 72 hours on uniformly coated surfaces or near stripes of EphA4/IgG‐Fc‐chimera. Control explants were cultured on or near IgG‐Fc and EphA1/IgG‐Fc‐chimera. To assess the roles of ephrin‐B2 and ‐B3 in EphA4 signaling, SG explants were cultured with or without anti‐ephrin‐B2 and/or ‐B3 blocking antibodies. Growth patterns of SG neurites at the border of EphA4 receptor stripes showed repulsion, characterized by turning, stopping and/or reversal. In the case of IgG‐Fc and EphA1, the neurites grew straight onto the stripes. Treatment with either anti‐ephrin‐B2 or ‐B3 blocking antibodies significantly reduced the repulsive effect of an EphA4 stripe. Moreover, when both antibodies were used together, neurites crossed onto EphA4 stripes with no evidence of repulsion. The results suggest that EphA4 provides repulsive signals to SG neurites in the developing cochlea, and that ephrin‐B2 and ‐B3 together mediate this response. J. Comp. Neurol. 462:90–100, 2003. © 2003 Wiley‐Liss, Inc.
Differential expression of angiogenic and vasodilatory factors by invasive trophoblast giant cells depending on depth of invasion
Authors: Hemberger Myriam , Nozaki Tadashige , Masutani Mitsuko , Cross James C. 
Published: May 2003

AbstractThe uterine bed undergoes remarkable changes during pregnancy, including proliferation and decidualization of the uterine stroma and remodeling and angiogenesis of the maternal vasculature. Fetal‐derived trophoblast giant cells invade into the uterus where they gain access to the maternal blood circulation to ensure sufficient nutrient supply of the embryo. In serial sections through early‐ to mid‐gestation conceptuses, we have determined the exact distance of trophoblast invasion and the expression of angiogenic, vasodilatory, and anticoagulative factors that are likely to influence remodeling and redirection of the maternal circulatory system. Trophoblast derivatives were detected at a distance as far as ∼300 μm from the placental border, where they are allocated exclusively along the mid‐line of the decidua. The farthest invading cells characteristically expressed proliferin and proliferin‐related protein, hormones that affect endothelial cell migration and vascularization. Occasionally, these cells replaced the normal vascular endothelium and acquired a “pseudo‐endothelial” shape. Complete vascular disintegration was observed 50–80 μm outside of the placental border where maternal blood was entirely lined by a trophoblast giant cell‐derived network of blood sinuses. This transition in blood space lining correlated with trophoblast expression of various vasodilatory and anticoagulative factors that are likely to promote blood flow toward the placenta. Analysis of teratocarcinoma‐like tumors demonstrated that trophoblast giant cell‐induced promotion and redirection of blood flow is not restricted to the uterine environment. These results show that trophoblast giant cells have the intrinsic capacity to attract and increase blood flow and to gradually displace the vascular endothelium resulting in the formation of canals entirely lined by trophoblast cells. Developmental Dynamics 227:185–191, 2003. © 2003 Wiley‐Liss, Inc.
Differential expression of β3 integrin gene in chick and mouse cranial neural crest cells
Authors: Pietri Thomas , Thiery Jean Paul , Dufour Sylvie 
Published: May 2003

AbstractRNA in situ hybridization on early chicken embryos revealed that the β3 integrin gene started to be expressed after Hamburger and Hamilton (HH) stage 6 in the presumptive epidermis adjacent to the neural plate, before closure of the neural tube. The β3 integrin gene was also strongly expressed in cephalic neural crest cells at the same stage in which they begin their migration but disappeared progressively in these cells along the route they take to the branchial arches. The gene was weakly expressed in the differentiating cranial neural crest cells. The αVβ3 integrin protein complex was also mainly detected in the migratory cephalic neural crest cells. However, during early mouse embryogenesis and in contrast to the chick, the β3 integrin gene was expressed in the foregut diverticulum and in the heart and not in the cephalic neural crest cells. Therefore, the difference in the β3 integrin expression suggests that mouse and chicken cranial neural crest cells may have distinct integrin requirements during their ontogenesis. Developmental Dynamics 227:309–313, 2003. © 2003 Wiley‐Liss, Inc.
Thyroid transcription factor (TTF) ‐1 regulates the expression of midkine (MK) during lung morphogenesis
Authors: Reynolds Paul R. , Mucenski Michael L. , Whitsett Jeffrey A. 
Published: May 2003

AbstractMidkine (MK) is a 13‐kDa heparin‐binding growth factor that is thought to mediate developmental processes, including vasculogenesis, cell migration, and proliferation in various organs. To determine whether MK plays a role during lung morphogenesis, immunostaining for MK was assessed in mouse lung from embryonic day (E) 13 to postnatal day (PN) 24. MK was detected in mesenchymal and respiratory epithelial cells of the peripheral mouse lung from E13.0 to E15.5. From E18.5 to PN1, MK was observed primarily in epithelial cells lining conducting airways and peripheral lung saccules. By PN10, expression was no longer observed in respiratory epithelial cells but was readily detected in small blood vessels in the alveolar region of the lung. Although most respiratory epithelial cells uniformly expressed MK before E13.0, MK was restricted to subsets of cells by E18.5, colocalizing with the Clara cell secretory protein (CCSP) marker in conducting airways and with pro‐SPC, a marker specific for alveolar type II pneumocytes. By PN10, MK was not detected in respiratory epithelial cells of the conducting airways and was closely associated with capillary networks. The sites of intense MK staining in the respiratory epithelial cells correlated with sites of expression of thyroid transcription factor (TTF) ‐1, a transcription factor regulating formation and gene expression in the lung parenchyma. TTF‐1 enhanced transcription of the mouse MK gene promoter, acting on TTF‐1 regulatory elements located in the 5′‐region of the gene. Furthermore, MK expression was not detected in lungs of TTF‐1 null mice. TTF‐1 regulates expression of MK in the lung. The temporal/spatial distribution of midkine is consistent with a potential role in paracrine signaling during lung morphogenesis. Developmental Dynamics 227:227–237, 2003. © 2003 Wiley‐Liss, Inc.
Enantiomerically Pure (R)‐ and (S)‐15‐Hydroxy[2.2]paracyclophane‐4‐carbaldehyde (iso‐FHPC): A Novel Parent Compound for Planar Chiral Ligands
Authors: Rozenberg Valeria I. , Antonov Dmitrii Yu. , Sergeeva Elena V. , Vorontsov Evgenii V. , Starikova Zoya A. , Fedyanin Ivan V. , Schulz Christian , Hopf Henning 
Published: May 2003

AbstractThe planar chiral 15‐hydroxy[2.2]paracyclophane‐4‐carbaldehyde (2, iso‐FHPC) was synthesized and resolved via its Schiff bases 8 by using the enantiomers of α‐phenylethylamine. The absolute configurations of the enantiomers of 2 were determined by a combined X‐ray diffraction and chemical correlation study. Derivatives 9, the first representatives of cyclophane‐derived aminophenols with a pseudo‐gem arrangement of the functional groups were synthesized. All new chiral compounds can be regarded as prospective ligands for asymmetric synthesis and catalysis. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2003)
Laser Flash Photolysis of Disulfonyldiazomethanes: Partitioning between Hetero‐Wolff Rearrangement and Intramolecular Carbene Oxidation by a Sulfonyl Group
Authors: Bucher Götz , Strehl Anja , Sander Wolfram 
Published: May 2003

AbstractLaser flash photolysis of bis(phenylsulfonyl)diazomethane (1a) and ditosyldiazomethane (1b) leads to the formation of sulfonylsulfenes 8a/8b (λmax = 310 nm). Non‐first‐order kinetics and non‐linear Stern−Volmer behavior suggest the formation of another transient species also absorbing at λ = 310 nm. Based on the results of DFT calculations, these species are tentatively identified as dithiocarbonate S,S,S′‐trioxides 12a/b, which are formed from the oxathiirene S‐oxides 9a/b. The latter compounds bear the characteristics of masked carbenes (τ estimated as 700 ps) and are quenched by methanol and cyclooctene. Singlet disulfonylcarbenes 2a/b are not predicted to be minima, since all attempts at optimizing the geometry of 2a led to 9a instead. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2003)
Propyne Iminium Salts and Phosphorus(III) Nucleophiles: Synthesis of (3‐Morpholinoallenyl)phosphanes and ‐phosphane Oxides or 1‐(Morpholinopropargyl)phosphanes and ‐phosphonates
Authors: Reisser Martin , Maier Alexandra , Maas Gerhard 
Published: May 2003

AbstractTreatment of 4‐(1,3‐diphenyl‐l‐propynylidene)morpholinium triflate (1a) with the neutral phosphorus nucleophiles Me3Si−PPh2, Me3Si−P(Ph)C5H11, and Me3SiO−PPh2 affords (3‐morpholinoallenyl)phosphanes 4 and 5 and (3‐morpholinoallenyl)phosphane oxide 11, respectively. In contrast to these conjugate addition reactions at the ambident propyne iminium moiety of 1a, nucleophilic attack by Me3Si−PEt2 and Me3SiO−P(OEt)2 takes place at the iminium function and gives (1‐morpholinopropargyl)phosphane 6 and (1‐morpholinopropargyl)phosphonate 12, respectively. Propyne iminium salt 1b reacts with Me3Si−PPh2 to form (3‐morpholino‐1,3‐butadienyl)phosphane oxide 8. The bis(donor)‐substituted allene 4 is transformed by oxidation of the phosphorus substituent into the push‐pull substituted allenylphosphane oxide 11. Treatment of allene 4 with elemental sulfur results in the formation of betaine 16, which undergoes [3+2] cycloaddition reactions with acetylenic esters to afford 5‐benzylidene‐4,5‐dihydrothiophenes 17 and 18. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2003)
Signaling to and from radial glia
Authors: Campbell Kenneth 
Published: May 2003

AbstractRadial glia represent the major glial cell type in the developing CNS and perform many essential functions, which range from acting as neural precursors to providing physical substrates for newborn neurons to migrate on. Previous work has shown that cell‐cell signaling is important for the development of the radial glial phenotype. In particular, signals from newborn neurons appear to contribute significantly to the formation of this cell type. In addition, radial glia may be involved in reciprocal signaling roles that contribute to regional patterning and differentiation in the developing CNS. GLIA 43:44–46, 2003. © 2003 Wiley‐Liss, Inc.
Astrocytes as support for axonal regeneration in the central nervous system of mammals
Authors: Privat A. 
Published: May 2003

AbstractReactive astrocytes are one of the main impediments for axonal regeneration in the central nervous system of mammals. Using mice KO for GFAP and vimentin, we show that reinnervation occurs after an hemisection of the spinal cord, mainly through sprouting of controlateral intact serotoninergic and cortico‐spinal axons, thanks to the absence of glial reactivity. This reinnervation is paralleled by the restoration of impaired locomotion of the ipselateral hindleg. Future applications to spinal cord injured patients are discussed. GLIA 43:91–93, 2003. © 2003 Wiley‐Liss, Inc.
Fibrin as a matrix for grafting 2‐hydroxyethyl methacrylate: Preparation and characterization of the graft and its in vivo evaluation for wound healing
Authors: Sathian J. , Sastry T. P. , Suguna L. , Lakshminarayana Y. , Radhakrishnan G. 
Published: May 2003

AbstractIn this work, fibrin was used as a substrate to graft 2‐hydroxyethyl methacrylate (HEMA) by free radical polymerization using potassium persulfate and sodium metabisulfite as redox initiators. The extent of grafting the synthetic polymer on the biopolymer was studied under various experimental conditions, and the optimum factors for affording maximum grafting were standardized. The graft, fib‐g‐p[HEMA], was characterized by Fourier transform infrared, scanning electron microscopy, and X‐ray diffraction studies. The graft exhibited a higher shelf life than native fibrin. The biocompatibility of the graft has been tested by in vivo studies and the results, in terms of collagen formation and wound size, proved its suitability for wound healing. © 2003 Wiley Periodicals, Inc. J Biomed Mater Res 65A: 435–440, 2003
Gas plasma etching of PEO/PBT segmented block copolymer films
Authors: Olde Riekerink M. B. , Claase M. B. , Engbers G. H. M. , Grijpma D. W. , Feijen J. 
Published: May 2003

AbstractA series of poly(ethylene oxide)/poly(butylene terephthalate) (PEO/PBT) segmented block copolymer films was treated with a radio‐frequency carbon dioxide (CO2) or with argon (Ar) plasma. The effects of (preferential) etching on surface structure, topography, chemistry, and wettability were studied by scanning electron microscopy, atomic force microscopy, X‐ray photoelectron spectroscopy, and contact angle measurements. In all cases, a granular‐type nanostructure was formed after prolonged CO2 plasma etching. Ar plasma etching generally did not lead to significant changes in surface structure. Regarding surface chemistry, CO2 plasma treatment caused surface oxidation and oxidative degradation of the films while Ar plasma etching resulted mainly in the preferential removal of PEO blocks. The wettability of all films significantly increased after plasma treatment because of the creation of polar functional groups at the surface. Preliminary goat bone‐marrow cell compatibility experiments have shown that all plasma‐treated PEO/PBT films induced a greatly enhanced cell adhesion and/or growth compared to untreated biomaterials. This improvement was attributed to changes in surface chemistry during plasma etching rather than to changes in surface structure. These results show that plasma‐treated PEO/PBT copolymers have a high potential as scaffolds for bone tissue regeneration. © 2003 Wiley Periodicals, Inc. J Biomed Mater Res 65A: 417–428, 2003
Relationship between damage accumulation and mechanical property degradation in cortical bone: Microcrack orientation is important
Authors: Akkus Ozan , Knott David F. , Jepsen Karl J. , Davy Dwight T. , Rimnac Clare M. 
Published: May 2003

AbstractThe accumulation of damage and the associated degradation of the mechanical properties of cortical bone are postulated to contribute to age‐, disease‐, overuse‐, and disuse‐related skeletal fragilities. Therefore, gaining insight into the relationship between damage and degradation processes is essential in understanding the etiology of skeletal fractures. In investigating this relationship, the damage measure ideally needs to account for the size, the distribution density, and the orientation of microcracks. Existing measures of damage address the size and distribution density of microcracks; however, the orientation of cracks has not been well‐investigated. Because the overall orientation of microcracks determines the material axis along which the greatest degradation will be experienced, we hypothesized that the incorporation of the relative orientation between microcracks and loading direction will improve the significance of the relationship between damage accumulation and material property degradation. A three‐cycle damage protocol was used to induce tensile damage and to quantify the degradation of the elastic modulus of specimens from human donor femoral cortical bone (a 24‐year‐old and a 72‐year‐old man). Microcracks were evaluated by en bloc basic fuchsin staining of specimens after testing. The length (Li) and the orientation with respect to the loading direction (βi) of each crack were quantified by a video microscopy system. Three damage measures were quantified for each specimen: the number of linear microcracks (Cr #), the sum of the crack lengths (ΣLi) accounting for the microcrack size alone, and the sum of the projected crack length [ΣLPi = ΣLicos(βi)] accounting for both crack size and orientation. Inclusion of the orientation parameter improved the coefficient of determination between damage accumulation and the degradation of the elastic modulus: the coefficient of determination of the sum of the projected crack length (R2 = 0.239) was 60% greater than that of the sum the projected crack length (R2 = 0.149) and 33% greater than that of the number of linear microcracks (R2 = 0.180). We conclude that microcrack orientation is an essential physical variable in the relationship between damage accumulation and degradation of mechanical properties of cortical bone tissue. © 2003 Wiley Periodicals, Inc. J Biomed Mater Res 65A: 482–488, 2003
Identification, characterization, and expression of a novel α‐tropomyosin isoform in cardiac tissues in developing chicken
Authors: Zajdel Robert W. , Denz Christopher R. , Lee Sung , Dube Syamalima , Ehler Elisabeth , Perriard Evylene , Perriard Jean‐Claude , Dube Dipak K. 
Published: May 2003

AbstractTropomyosins are present in various muscle (skeletal, cardiac, and smooth) and non‐muscle cells with different isoforms characteristic of specific cell types. We describe here a novel smooth/striated chimeric isoform that was expressed in developing chick heart in addition to the classically described TM‐4 type. This novel α‐Tm tropomyosin isoform, designated as α‐Tm‐2, contains exon 2a (in place of exon 2b). The known striated muscle isoform (α‐Tm‐1) was also expressed in embryonic hearts along with the striated muscle isoform of TM‐4. In adult heart, TM‐4 was expressed, however, expression of both α‐Tm‐1 and α‐Tm‐2 isoforms was drastically reduced or downregulated. Interestingly, we were unable to detect the expression of α‐Tm‐2 in embryonic and adult skeletal muscle, however, the α‐Tm‐1 isoform is expressed in embryonic and adult skeletal muscle. Examination of other possible isoforms of the α‐TM gene, i.e., α‐smooth muscle tropomyosin (α‐Sm), α‐Fibroblast‐1 (α‐F1), and α‐Fibroblast‐2 (α‐F2) revealed expression in embryonic hearts and a significant reduction of each of these isoforms in adult heart. In order to elucidate the role of the newly discovered tropomyosin isoform in chicken, we ectopically expressed the GFP fusion protein of α‐Tm‐1 and α‐Tm‐2 separately into cardiomyocytes isolated from neonatal rats. Each isoform was incorporated into organized myofibrils. Our results suggest that the α‐TM gene may undergo both positive and negative transcriptional control in chicken hearts during development. © 2003 Wiley‐Liss, Inc.
Thrombospondin‐1‐induced vascular smooth muscle cell chemotaxis: The role of the type 3 repeat and carboxyl terminal domains
Authors: Lee Taeseung , Nesselroth Susan M. , Olson Eric T. , Esemuede Nowokere , Lawler Jack , Sumpio Bauer E. , Gahtan Vivian 
Published: May 2003

AbstractThrombospondin‐1 (TSP‐1), an acute phase reactant implicated in vascular disease, is a matricellular glycoprotein with six domains that confer different functions. The authors have shown TSP‐1 induces vascular smooth muscle cell (VSMC) chemotaxis via extracellular signal‐regulated kinases‐1 and ‐2 (ERK) and p38 kinase (p38) and that a fusion protein of the carboxyl terminal (COOH) and type 3 repeat (T3) domains independently induce VSMC chemotaxis. The purpose of this study was to determine whether COOH‐, T3‐induced VSMC chemotaxis, or both, is dependent upon ERK or p38 activation. To determine if the T3, COOH, or type 2 repeat domain (T2, control domain not associated with chemotaxis) activate ERK, p38, or both, VSMCs were exposed to each fusion protein (20 μg/ml for 15, 30, 60, or 120 min), serum‐free media (SFM, negative control), or TSP‐1 (20 μg/ml for 30 min, positive control). Western immunoblotting was performed for activation studies. Using a microchemotaxis chamber, VSMCs pre‐incubated in SFM, DMSO (vehicle control), PD98059 (10 μM), or SB202190 (10 μM) were exposed to each domain, TSP‐1, or SFM. After 4 h (37°C), migrated VSMCs were recorded as cells/five fields (400 ×) and analyzed by paired t‐test. ERK was activated by T2, T3, and COOH. However, p38 was activated by T3 and COOH, but not T2. T3 and COOH‐induced VSMC chemotaxis were inhibited by PD98059 or SB202190, but more completely by SB202190. The T2 domain had no effect on VSMC chemotaxis. These results suggest activation of the p38 pathway may be more specific than ERK for COOH‐ and T3‐induced VSMC chemotaxis. © 2003 Wiley‐Liss, Inc.