bluuebunny/crossref_metadata_2025_split huggingface dataset:
The initial fetal human retinal vasculature develops by vasculogenesis
Authors: McLeod D. Scott , Hasegawa Takuya , Prow Tarl , Merges Carol , Lutty Gerard 
Published: October 2006

AbstractThere is increasing evidence that the hemangioblast, a common progenitor for hematopoietic cells and endothelial cells, participates in embryonic and extra‐embryonic vasculogenesis in some organs. Whether resident angioblasts or endothelial progenitor cells (EPCs) contribute to human retinal vasculogenesis is still a matter of controversy. To address this controversy, fetal human retinas of 6–23 weeks gestation (WG) were examined using immunohistochemistry and a panel of antibodies against endothelial cell markers (CD34, CD31), a marker for retinal angioblasts and endothelium (CD39/ecto‐ADPase), and a marker for precursors and hemangioblasts (CXCR4). Confocal microscopic spectral analysis and double labeling with Ki67 was used to identify the proliferating cell types. In the inner neuroblastic layer of the 6–8 WG retina and in the putative ganglion cell layer in avascular regions of older eyes (14 WG–20 WG), scattered CD39+ angioblasts were well in advance of forming vasculature. There was a layer of CXCR4+ cells in the inner retina that was reduced in size with development. As blood vessels formed, CD39+ cells were always well in advance of the vascular front and they expressed CXCR4. This demonstrates that a pool of resident angioblasts express CD39 and CXCR4 as they differentiate and participate in vasculogenesis in the fetal human. They retain expression of CD39 as endothelial cells in the newly formed retinal vasculature but they down‐regulate CXCR4 expression. Developmental Dynamics 235:3336–3347, 2006. © 2006 Wiley‐Liss, Inc.
Contribution to the Reactivity of N,N′‐Diaryl‐1,4‐diazabutadienes Aryl–N=CH–CH=N–Aryl (Aryl = 2,6‐Dimethylphenyl; 2,4,6‐Trimethylphenyl) Towards Boron Trichloride
Authors: Weber Lothar , Förster Jan , Stammler Hans‐Georg , Neumann Beate 
Published: October 2006

AbstractThe reaction of Aryl–N=CH–CH=N–Aryl (3a: Aryl = 2,6‐Me2C6H3; 3b: Aryl = 2,4,6‐Me3C6H2) with 2 equiv. BCl3 in a toluene/hexane mixture at –50 °C led to an inseparable mixture of borolium salts [Aryl–Na=CH–CH=N(Aryl)BCl2(Na–B)]+BCl4– (4a: Aryl = 2,6‐Me2C6H3; 9a: Aryl = 2,4,6‐Me3C6H2) and [Aryl–Na=CH–C(Cl)=N(Aryl)BCl2(Na–B)]+BCl4– (4b: Aryl = 2,6‐Me2C6H3; 9b: Aryl = 2,4,6‐Me3C6H2) and the bicyclic species [HCa=N(Aryl)BCl2N(Aryl)–Cb=(Ca–Cb)]2 (5: Aryl = 2,6‐Me2C6H3; 10: Aryl = 2,4,6‐Me3C6H2). Sodium amalgam reduction of borolium salts 4a,b and 9a,b afforded inseparable mixtures of the diazaboroles 2,6‐Me2C6H3NaCH=CR–Nb(2,6‐Me2C6H3)BCl(Na–B) (1: R = H; 6: R = Cl) and 2,4,6‐Me3C6H2NaCH=CR–Nb(2,4,6‐Me3C6H2)BCl(Na–B) (2: R = H; 11: R = Cl). In order to obtain pure 1 and 2, diazabutadienes 3a and 3b were slowly combined with 2 equiv. BCl3 in the same solvents at –78 °C. The acyclic adducts Cl3BN(Aryl)=CH–CH=N(Aryl)BCl3 (7a: Aryl = 2,6‐Me2C6H3; 7b: Aryl = 2,4,6‐Me3C6H2) were reduced with sodium amalgam to furnish the aminoboranes Cl2BN(Aryl)CH=CH–N(Aryl)BCl2 (8: Aryl = 2,6‐Me2C6H3; 12: Aryl = 2,4,6‐Me3C6H2). Stirring solutions of 8 and 12 in the presence of CaH2 cleanly gave the diazaboroles 1 and 2, respectively. The novel compounds were characterized by elemental analyses and 1H‐, 11B‐, 13C NMR and mass spectra. The molecular structures of 1, 4a, 5 and 8 were elucidated by single X‐ray diffraction analyses. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2006)
“Inhibition” of the Enzyme Model TpPh,MeZn–OH by Diketo Compounds
Authors: Tekeste Teame , Vahrenkamp Heinrich 
Published: October 2006

AbstractIn order to gain a structural understanding of zinc enzyme inhibition, the model complex TpPh,MeZn–OH was treated with various diketo compounds. α‐Keto carboxylic acids were attached to the zinc ion as anionic O,O‐chelate ligands, of which benzoylformate was oxidatively decarboxylated in air to form the benzoate complex. Two functionalized β‐diketones did not use their functionality in forming the β‐diketonate complexes. Of the α‐diketones, 2,3‐pentanedione formed the α‐keto enolate complex, while 1‐phenyl‐1,2‐propanedione underwent oxidative C–C coupling resulting in a red dinuclear bis(α‐keto enolato) complex. Of the diaryl‐α‐diketones, benzil did not react, but pyridil underwent hydrolytic cleavage to pyridine‐2‐carbaldehyde and picolinate, of which the latter was bound to the zinc ion as an N,O‐chelate ligand.(© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2006)
Recoverable Homogeneous Palladium(0) Catalyst for Cross‐Coupling Reactions of Arenediazonium Salts with Potassium Organotrifluoroborates: Detection of Catalytic Intermediates by Electrospray Ionization Mass Spectrometry
Authors: Masllorens Judit , González Iván , Roglans Anna 
Published: October 2006

AbstractFifteen‐membered triolefinic macrocyclic palladium(0) complex 1, (E,E,E)‐1‐ferrocenylsulfonyl‐6,11‐bis[(4‐methylphenyl)sulfonyl]‐1,6,11‐triazacyclopentadeca‐3,8,13‐trienepalladium(0), is an active and recoverable catalyst for Suzuki–Miyaura cross‐couplings between arenediazonium salts and potassium organotrifluoroborates. The reactions were performed under aerobic conditions at room temperature and without added base. Use of electrospray ionization mass spectrometry (ESI‐MS) allowed the direct detection and identification of several intermediates, which furthers the study of the mechanistic aspects of the Suzuki–Miyaura reaction. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2007)
Restoring nature in mining areas of the Silesian Upland (Poland)
Authors: Pełka‐Gościniak Jolanta 
Published: October 2006

AbstractThe Silesian Upland is one of the most degraded areas in Poland owing to the long‐lasting influence of mining and metallurgy. Mining influences every component of the environment in significant and diverse ways. But even in such a devastated terrain there is evidence of the proper management of post‐mining areas and natural self‐restoration, which paradoxically, owing to mining, appear in the most intensively used economic areas. Copyright © 2006 John Wiley & Sons, Ltd.
The Effect of NaCl in the Cathode Air Stream on PEMFC Performance
Authors: Mikkola M. S. , Rockward T. , Uribe F. A. , Pivovar B. S. 
Published: October 2006

AbstractIn this contribution, the effects of sodium chloride in the cathode side air stream of a polymer electrolyte membrane fuel cell were studied, since it is present in the atmosphere in many fuel cell operating environments, especially at coastal regions and on roads where NaCl is used as a deicer. The effect on PEMFC performance was investigated by injecting NaCl solution into the cathode side air stream of an operating fuel cell. The most significant effect of NaCl under test conditions is the replacement of H+ by Na+ in the ionomer, lowering performance by reducing proton conductivity. In addition, NaCl was found to absorb into the graphite components, making them a potential long‐term NaCl source after the initial exposure. In contrast to expectations, chloride ions did not appear to effect performance of the cell and the overall magnitude of the effects due to NaCl introduction were smaller than expected.
Common fragile site FRA11G and rare fragile site FRA11B at 11q23.3 encompass distinct genomic regions
Authors: Fechter Anne , Buettel Isabel , Kuehnel Elisabeth , Savelyeva Larissa , Schwab Manfred 
Published: October 2006

AbstractFragile sites are specific genomic loci that are particularly prone to chromosomal breakage. Based on their incidence in the human population, they are divided into rare fragile sites occurring in less than 5% of all individuals and common fragile sites being a constitutional feature of the genome of probably all individuals. In this study, cloning of unstable DNA sequences, which have been previously genetically tagged with a marker gene, was the basis for defining the genomic localization of the common fragile site FRA11G at 11q23.3. Mapping of the fragile site with six‐color fluorescence in situ hybridization (FISH) resulted in the precise genomic localization of FRA11G to a 4.5 Mb region. The chromosomal subband 11q23.3 harbors both the common fragile site FRA11G and the rare fragile site FRA11B. Here, we show that FRA11G maps 0.8 Mb proximal to the genomic region previously defined to be affected by expression of FRA11B; thus, the common and the rare fragile sites at 11q23.3 encompass distinct genomic regions. The region of FRA11G is known to be involved in somatic and germline recurrent aberrations, and it is conceivable that genetic damage resulting from this fragile site might contribute to clinical phenotypes. © 2006 Wiley‐Liss, Inc.
Chemical fragments in real space: Definitions, properties, and energetic decompositions
Authors: Pendás A. Martín , Blanco M. A. , Francisco E. 
Published: October 2006

AbstractThe physical and chemical meaning of real space molecular fragments resulting from arbitrary partitions of the density is reviewed under a common unifying formalism. Both fuzzy (interpenetrating) and non‐fuzzy (exhaustive) decompositions are treated on an equal basis. Density decompositions are consistently generalized to compatible density matrix partitions by using Li and Parr's ideas (Li and Parr J Chem Phys 1986, 84, 1704), and these are carried onto an energy partition. It is argued that the merits of a given decomposition should be judged against both the charge and the energetic image it provides. Atomic partitions are used to show how the interacting quantum atoms approach (IQA) allows us to cope with the most important energy cancellations of quantum chemistry. Binding results from a trade‐off between atomic (or fragment) energy deformations with respect to a reference and interatomic (interfragment) interactions. Deformation energies are divided into charge transfer and redistribution terms and their relative roles are analyzed. A number of systems are compared against the fuzziness of different density decompositions. The results consistently show that fuzzy partitions tend to give low atomic net charges and enhanced covalency, while exhaustive partitions generate larger net charges and smaller covalencies, across a wide range of bonding regimes. © 2006 Wiley Periodicals, Inc. J Comput Chem, 2007
A survey of recent developments in ab initio valence bond theory
Authors: Hiberty Philippe C. , Shaik Sason 
Published: October 2006

AbstractStarting from the 1980s and onwards, Valence Bond theory has been enjoying renaissance that is characterized by the development of a growing number of ab initio methods, and by many applications to chemical reactivity and to the central paradigms of chemistry. Owing the increase of computational power of modern computers and to significant advances in the methodology, valence bond theory begins to offer a sound and attractive alternative to Molecular Orbital theory. This review aims at summarizing the most important developments of ab initio valence bond methods during the last two or three decades, and is primarily devoted to a description of what the various methods can actually achieve within their specific scopes and limitations. Key available softwares are surveyed. © 2006 Wiley Periodicals, Inc. J Comput Chem, 2007
Hamilton cycle decomposition of 6‐regular circulants of odd order
Authors: Dean Matthew 
Published: October 2006

AbstractThe circulant G = C(n,S), where $S\subseteq Z_n\setminus\{0\}$, is the graph with vertex set Zn and edge set $E(G)= \{\{x,x+s\}|x \in Z_n,s \in S\}$. It is shown that for n odd, every 6‐regular connected circulant C(n, S) is decomposable into Hamilton cycles. © 2006 Wiley Periodicals, Inc. J Combin Designs
Asymmetric ERM activation at the Schwann cell process tip is required in Axon‐Associated motility
Authors: Gatto Cheryl L. , Walker Barbara J. , Lambert Stephen 
Published: October 2006

AbstractAxon‐associated Schwann cell (SC) motility and process dynamics are crucial in the development and regeneration of the peripheral nervous system (PNS). The bipolar morphology of SCs represents an unexplored conundrum in terms of directed motility. Using fluorescence time‐lapse microscopy of transfected SCs within myelinating dorsal root ganglion (DRG) explants, we demonstrate cycling of SCs between bipolar and highly motile, unipolar morphologies as a result of asymmetric process retraction and extension. Unipolar SC motility appears nucleotaxic in nature, similar to the movement of neurons on radial glia during cortical development. We also show that asymmetric process retraction is associated with the activation of ERM (ezrin/radixin/moesin) proteins and subsequent recruitment of ezrin‐binding phospho‐protein 50 kDa (EBP50) at the retracting process tip. This activation occurs in response to localized synthesis of phosphatidylinositol (4,5)‐bisphosphate (PIP2) at this site. Finally, we demonstrate that the activation of ERM proteins at the SC process tip is essential for motility and the maintenance of SC polarity, as ERM disruption yields a dysfunctional, multi‐polar cell. These results demonstrate that specializations at the tips of SC processes regulate their dynamics, which in turn is associated with directed motility in these cells. J. Cell. Physiol. 210: 122–132, 2007. © 2006 Wiley‐Liss, Inc.
Molecular determinants of FGF‐21 activity—synergy and cross‐talk with PPARγ signaling
Authors: Moyers Julie S. , Shiyanova Tatiyana L. , Mehrbod Farrokh , Dunbar James D. , Noblitt Timothy W. , Otto Keith A. , Reifel‐Miller Anne , Kharitonenkov Alexei 
Published: October 2006

AbstractFibroblast growth factor (FGF)‐21 is a novel regulator of insulin‐independent glucose transport in 3T3‐L1 adipocytes and has glucose and triglyceride lowering effects in rodent models of diabetes. The precise mechanisms whereby FGF‐21 regulates metabolism remain to be determined. Here we describe the early signaling events triggered by FGF‐21 treatment of 3T3‐L1 adipocytes and reveal a functional interplay between FGF‐21 and peroxisome proliferator‐activated receptor gamma (PPARγ) pathways that leads to a marked stimulation of glucose transport. While the early actions of FGF‐21 on 3T3‐L1 adipocytes involve rapid accumulation of intracellular calcium and phosphorylation of Akt, GSK‐3, p70S6K, SHP‐2, MEK1/2, and Stat3, continuous treatment for 72 h induces an increase in PPARγ protein expression. Moreover, chronic activation of the PPARγ pathway in 3T3‐L1 adipocytes with the PPARγ agonist and anti‐diabetic agent, rosiglitazone (BRL 49653), enhances FGF‐21 action to induce tyrosine phosphorylation of FGF receptor‐2. Strikingly, treatment of cells with FGF‐21 and rosiglitazone in combination leads to a pronounced increase in expression of the GLUT1 glucose transporter and a marked synergy in stimulation of glucose transport. Together these results reveal a novel synergy between two regulators of glucose homeostasis, FGF‐21 and PPARγ, and further define FGF‐21 mechanism of action. J. Cell. Physiol. 210: 1–6, 2007. © 2006 Wiley‐Liss, Inc.
Fragmentation behavior of glycated peptides derived from D‐glucose, D‐fructose and D‐ribose in tandem mass spectrometry
Authors: Frolov Andrej , Hoffmann Peter , Hoffmann Ralf 
Published: October 2006

AbstractNonenzymatic glycosylation (or glycation) is a common nonenzymatic side‐chain specific sequence‐independent posttranslational modification formed by the reaction of reducing carbohydrates with free amino groups. Thus, proteins can react with aldoses or ketoses to yield Amadori or Heynes compounds, respectively. Here, the fragmentation behavior of D‐glucose and D‐ribose‐derived Amadori peptides as well as D‐fructose‐derived Heynes peptides were studied by collision‐induced fragmentation (CID) after electrospray (ESI) or matrix‐assisted laser desorption/ionization (MALDI) mass spectrometry (MS). All three sugar moieties displayed characteristic fragmentation patterns accompanying the parent and the fragment ions, which could be explained by consecutive losses of water and formaldehyde. Glucose‐derived Amadori parent and fragment ions displayed losses of 18, 36, 54, 72, and 84 u at a characteristic intensity distribution compared with losses of 18, 36, 54, 72, 84, and 96 u for D‐fructose‐derived ions and losses of 18, 36, and 54 u for ribose‐derived ions. Furthermore, each sugar moiety produced indicative lysine‐derived immonium ions that were successfully used in a precursor ion scan analysis to identify Amadori peptides in a tryptic digest of bovine serum albumin (BSA) glycated with D‐glucose. BSA was modified on lysine residues at positions 36, 160, 235, 256, 401, and 548. Copyright © 2006 John Wiley & Sons, Ltd.
Kinetics of inflammatory response of astrocytes induced by TLR 3 and TLR4 ligation
Authors: Krasowska‐Zoladek Alicja , Banaszewska Monika , Kraszpulski Michal , Konat Gregory W. 
Published: October 2006

AbstractToll‐like receptors (TLRs) are sentinels of the innate immune system that recognize an array of exogenous and endogenous pathogenic molecules. The ligation of the receptors triggers inflammatory response necessary for pathogen elimination and for the healing process. In the present study we examined inflammatory response of astrocytes elicited by the ligation of TLR3 and TLR4. Astrocytic cultures established from newborn rat brains were exposed to double stranded RNA (dsRNA) and lipopolysaccharide (LPS), the ligands for TLR3 and TLR4, respectively. The expression of cytokine genes was determined by RNase protection assay, and the generation of nitric oxide (NO) was measured by Griess technique. Both ligands upregulated the expression of several cytokines (i.e., IL‐1α, IL‐1β, IL‐6, TNFα, GM‐CSF, LTβ, and TGFβ3) and downregulated the expression of MIF, but have no effect on the expression of IL‐2, IL‐3, IL‐4, IL‐5, IL‐10, TGFβ1, TGFβ2, TNFβ, and IFNγ. Although dsRNA upregulated the expression of IFNβ, LPS did not indicating that the TRIF‐dependent branch of TLR4 signaling is inactive in astrocytes. Proinflammatory response as seen from upregulated cytokine expression and NO generation reached a peak within the first day of exposure, and was subsequently abrogated. The cells also became refractory to subsequent stimulation by the ligands indicating the existence of negative feedback mechanisms that control proinflammatory response in astrocytes. © 2006 Wiley‐Liss, Inc.
Oral administration of metal chelator ameliorates motor dysfunction after a small hemorrhage near the internal capsule in rat
Authors: Masuda Tadashi , Hida Hideki , Kanda Yoshie , Aihara Noritaka , Ohta Kengo , Yamada Kazuo , Nishino Hitoo 
Published: October 2006

AbstractCerebral hemorrhage leads to local production of free iron, radicals, cytokines, etc. To investigate whether a decrease of iron‐mediated radical production influences functional recovery after intracerebral hemorrhage (ICH), a modified ICH rat model with a small hemorrhage near the internal capsule (IC) accompanied with relatively severe motor dysfunction was first developed. Then clioquinol (CQ), an iron chelator that reduces hydroxyl radical production, was orally administrated. Injection of different doses of Type IV collagenase (1.4 μl 1–200 U/ml) into the left striatum near the IC in Wistar rats showed that injection of 7.5 U/ml collagenase resulted in a small hemorrhoidal lesion near the IC with relatively severe motor dysfunction (IC model). Retrograde labeling of neurons in the sensory‐motor cortex and axons in the corticospinal tract using Fluoro‐gold (FG) injection into the spinal cord (C3–C4) showed that few labeled neurons in the sensory‐motor cortex were detected in the IC model, FG‐labeled axons disappeared, and FG‐including ED‐1‐positive cells appeared within 24 hr in the IC. Assessments of behavior and histologic analysis after oral administration of CQ in the IC model indicated that oral administration of CQ prevented a decrease of FG‐labeled neurons, and resulted in better motor‐function recovery. CQ inhibited hydrogen peroxide‐induced cell toxicity in oligodendrocytes in vitro, but not in neurons. Our data suggests that CQ ameliorated motor dysfunction after a small hemorrhage near the IC by a mechanism that is related to reduction of chain‐reactive hydroxyl radical production in oligodendrocytes. © 2006 Wiley‐Liss, Inc.
VEGF overexpression enhances striatal neurogenesis in brain of adult rat after a transient middle cerebral artery occlusion
Authors: Wang Yong‐Quan , Guo Xin , Qiu Mei‐Hong , Feng Xiao‐Yuan , Sun Feng‐Yan 
Published: October 2006

AbstractTo elucidate whether vascular endothelial growth factor (VEGF) improves stroke‐induced striatal neurogenesis, we intraventricularly injected human VEGF165‐expressive plasmid (phVEGF) mixed with liposome into adult rats after a transient middle cerebral artery occlusion (MCAO). The results showed that EGFP, a reporter protein, positive cells appeared at 2 hr, further enhanced at 4 hr, reached the maximum at 3 days and still remained at 14 days after a single injection. Treatment with phVEGF increased angiogenesis, as indicated by double staining of vWF, a marker of endothelial cells, and 5′‐bromodeoxyuridine (BrdU), a marker of cell proliferation. The phVEGF treatment dose‐dependently reduced infarct volume of brain at 2 weeks after MCAO. The neuroprotection by VEGF could be obtained when the plasmid was injected within 2 hr after stroke. Moreover, VEGF overexpression significantly increased cell proliferation in the ipsilateral SVZ and the numbers of BrdU+‐CRMP‐4+ and BrdU+‐Tuj1+, two markers of immature newborn neurons, and BrdU+‐MAP‐2+, a marker of mature newborn neurons, cells in the ipsilateral striatum to MCAO. Present results show that VEGF plasmid treatment after stroke can significantly reduce infarct volume and enhance striatal neurogenesis in adult rat brain. This suggests that VEGF overexpression acquires significant functions of neuronal protection and repair in the injured brain, which provides a possibility to develop a novel therapeutic strategy for the patients with stroke. © 2006 Wiley‐Liss, Inc.