bluuebunny/crossref_metadata_2025_split huggingface dataset:
Photoelectron Spectra and Electronic Structures of Some Cyanocyclopropanes
Authors: Rademacher Paul 
Published: March 2004

AbstractThe molecular structures of four cyanocyclopropanes 1−4 have been investigated by DFT B3LYP calculations. PE spectra of trans‐ and cis‐1,2‐dicyanocyclopropane (3 and 4) have been measured and analysed by semiempirical PM3 and B3LYP calculations. For compounds 1−4 a linear relationship, ΔIPψ = 0.218 Δr, between ΔIPψ (in eV), the difference in the IPs associated with the Walsh orbitals ψS and ψA of the three‐membered ring, and Δr (in pm), the difference of vicinal and distal C−C bond lengths, is established. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2004)
δ‐Galactonolactone: Synthesis, Isolation, and Comparative Structure and Stability Analysis of an Elusive Sugar Derivative
Authors: Bierenstiel Matthias , Schlaf Marcel 
Published: March 2004

Abstractδ‐D‐Gluconolactone, δ‐D‐mannonolactone, and — for the first time — the thermodynamically unstable δ‐D‐galactonolactone have been prepared and isolated from DMF solution by oxidizing the corresponding sugars with Shvo’s catalyst [(C4Ph4CO)(CO)2Ru]2 and a hydrogen acceptor. The preferred conformation of δ‐D‐galactonolactone in [D6]DMSO solution has been determined by 1H NMR spectroscopy experiments and DFT calculations to be 4H3 and is compared to those of the previously established conformations of δ‐D‐gluconolactone (4H3) and δ‐D‐mannonolactone (B2,5). The conformations of the lactones suggest an explanation for their relative rates of isomerization to their respective γ‐D‐lactones by an intramolecular mechanism. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2004)
Acid‐Promoted Retro‐Mannich Reaction of N‐Protected Tropenones to 2‐Substituted Pyrroles
Authors: Cramer Nicolai , Juretschke Jeannette , Laschat Sabine , Baro Angelika , Frey Wolfgang 
Published: March 2004

AbstractN‐protected tropenone 4 undergoes highly regioselective retro‐Mannich reactions to 2‐pyrrolyl ketones 5 and 7 in the presence of Lewis or Brønsted acids. Analogously, the pyrrole derivative 8a was obtained by using subsequent nucleophilic trapping with TMSCN. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2004)
Cover Picture: Effect of Substituents on the Complexation of Aromatic and Quinoid Substrates with Molecular Tweezers and Clips (Eur. J. Org. Chem. 7/2004)
Authors: Klärner Frank‐Gerrit , Polkowska Jolanta , Panitzky Jens , Seelbach Uta P. , Burkert Ulrich , Kamieth Markus , Baumann Michael , Wigger Arne E. , Boese Roland , Bläser Dieter 
Published: March 2004

AbstractThe cover picture shows the structures of the empty dimethoxy‐substituted clip and the host−guest complex between the hydroquinone clip and 1,2,4,5‐tetracyanobenzene (TCNB) calculated by force field. The calculations are in good agreement with single‐crystal structure analyses. The compression of the naphthalene sidewalls of the clip by 2.2 A? during the complexation, which is necessary to obtain binding arene−arene interactions in the complex, is calculated to be a low‐energy process. The complementary nature of the electrostatic potential surface (EPS) of the tetramethylene‐bridged naphthalene tweezer and TCNB (calculated by AM1) explains the high selectivity of this class of receptors toward electron‐deficient substrates. Details are discussed in the article by F.‐G. Klärner et al. on p. 1405 ff. Cover art by Björn Kahlert.
Negative BOLD in the visual cortex: Evidence against blood stealing
Authors: Smith Andrew T. , Williams Adrian L. , Singh Krishna D. 
Published: March 2004

AbstractThe positive BOLD (blood oxygen level‐dependent) response elicited in human visual cortex by a localized visual stimulus is accompanied by a reduction in the BOLD response in regions of the visual cortex that represent unstimulated locations in the visual field. We have suggested previously that this negative BOLD reflects attention‐related suppression of neural activity, but it might also be explained in terms of “blood stealing,” i.e., hemodynamic changes that have no neural correlate. We distinguish two possible hemodynamic effects of this type: (1) blood flow reduction caused by locally reduced pressure in vessels that share their blood supply with nearby dilated vessels; and (2) blood flow reduction caused by active constriction of vessels under neural control. The first is ruled out as an explanation of negative BOLD by showing that a visual stimulus that stimulates primary visual cortex in one hemisphere can cause extensive suppression in the other hemisphere i.e., it is not a local phenomenon. Negative BOLD most likely reflects suppression of neural activity, but could also reflect an active blood flow control system. Hum. Brain Mapping 21:213–220, 2004. © 2004 Wiley‐Liss, Inc.
Some cyclic BIBDs with block size four
Authors: Chang Yanxun 
Published: March 2004

AbstractIn this paper we give some results on cyclic BIBDs with block size 4. It is proved that a cyclic B(4,1;4n u) exists where u is a product of primes congruent to 1 modulo 6 and n is a positive integer and n ≥ 3. In the case of n = 2, we also give some partial results on the existence of a cyclic B(4,1;42u) where u is a product of primes congruent to 1 modulo 6. © 2004 Wiley Periodicals, Inc.
An updated table of binary/ternary mixed covering codes
Authors: Bertolo Riccardo , Östergård Patric R. J. , Weakley William D. 
Published: March 2004

AbstractAn updated table of K2,3(b,t;R)—the minimum cardinality of a code with b binary coordinates, t ternary coordinates, and covering radius R—is presented for b + t ≤ 13, R ≤ 3. The results include new explanations of short binary and ternary covering codes, several new constructions and codes, and a general lower bound for R = 1. © 2004 Wiley Periodicals, Inc.
A classification result on weighted {δ (p3 + 1), δ; 3, p3}‐minihypers
Authors: Ferret S. , Storme L. 
Published: March 2004

AbstractWe classify all {δ (p3 + 1), δ; 3, p3}‐minihypers, $\delta \leq 2p^2-4p, p=p_0^{h}\geq 9, h \geq 1$, for a prime number p0 ≥ 7, with excess e ≤ p3. Such a minihyper is a sum of lines and of possibly one projected subgeometry PG(5, p), or a sum of lines and a minihyper which is a projected subgeometry PG(5, p) minus one line. When p is a square, also (possibly projected) Baer subgeometries PG(3, p3/2) can occur. © 2004 Wiley Periodicals, Inc.
Bile canalicular formation in hepatic organoid reconstructed by rat small hepatocytes and nonparenchymal cells
Authors: Sudo Ryo , Ikeda Shinichiro , Sugimoto Shinichi , Harada Keisuke , Hirata Koichi , Tanishita Kazuo , Mochizuki Yohichi , Mitaka Toshihiro 
Published: March 2004

AbstractThe morphogenesis and movement of bile canaliculi (BC) are not well understood. This is because culture of hepatocytes that maintain polarity of cell membranes and possess highly differentiated functions has never been successful. We found that small hepatocytes (SHs), which are known to be hepatic progenitor cells, could proliferate and differentiate into mature hepatocytes and that BC‐like structures developed between rising/piled‐up cells. We investigated how BC‐like structures developed with maturation of SHs and whether the structures were functionally active as BC. Hepatic cells, including SHs, were isolated from an adult rat liver and cultured. Immunocytochemistry and immunoblotting for BC proteins, such as ectoATPase, 5′‐nucleotidase, dipeptidylpeptidase IV, and multidrug‐resistance associated protein 2, were examined and time‐lapse microscopy was used for the observation of BC contractions. Secretion of bilirubin into the reconstructed BC was also observed. The results of immunocytochemistry, immunoblots, and immunoelectron micrographs revealed that BC proteins were localized in the intercellular space that coincided with BC‐like structures reconstructed between rising/piled‐up cells. Tight junction‐associated protein ZO‐1 was also expressed along the BC‐like structures. Bilirubin added to the medium were secreted into BC‐like structure and accumulated without leakage. Time‐lapse microscopy showed continuous contractions of reconstructed BC. In conclusion, BC‐like structures reconstructed by SHs may be functional with membrane polarity, secretory ability, and motility. These results show that this culture system may suitable for investigating the mechanism of the formation of BC and their functions. J. Cell. Physiol. 199: 252–261, 2004© 2003 Wiley‐Liss, Inc.
Regulation of mesangial cell Na+/Ca2+ exchanger isoforms
Authors: Williams I. , Williams C. , Siroky B. , Bates E. , Kovacs G. , Peti‐Peterdi J. , Unlap M.T. , Bell P.D. 
Published: March 2004

AbstractAn isoform of the Na+/Ca2+ exchanger (SDNCX1.10) was cloned from mesangial cells of Sprague–Dawley rat. Regulation of this isoform was compared to two other clones that were derived from the Dahl/Rapp salt sensitive (SNCX) and salt resistant rat (RNCX). All isoforms differ at the alternative splice site and at amino acid 218 for SNCX. PKC activates RNCX but not SNCX while SDNCX1.10 was also activated by PKC. Regulation of exchanger activities by intracellular calcium ([Ca2+]i), pH, and kinases was assessed using Na‐dependent 45Ca2+ uptake assays in OK‐PTH cells expressing the vector, RNCX, SNCX, or SDNCX1.10. [Ca2+]i was elevated from 50 to 125 nM (n = 4) with thapsigargin (40 nM) and reduced from 50 to 29 nM (n = 4) and 18 nM (n = 4) with 10 or 20 μM BAPTA, respectively. RNCX was active at all three [Ca2+]i while SNCX and SDNCX1.10 were only active at lower [Ca2+]i. Varying extracellular pH (pHe, without nigericin) or pHe and intracellular pH (pHi, with 10 μM nigericin) from pH 7.4 to 6.2, 6.8, or 8.0 showed that SNCX activity was attenuated at both low and high pHs. SDNCX1.10 activity was attenuated only at pH 6.2 and 6.8 (with or without nigericin) while RNCX activity was attenuated at pH 6.2 (with or without nigericin) and pH 6.8 (with nigericin). Finally, only SDNCX1.10 activity was stimulated by 250 μM CPT‐cAMP or 250 μM DB‐cGMP treatment. Thus the differential regulation of [Ca2+]i by these exchangers is dependent upon the pattern of cellular Na+/Ca2+ exchanger isoform expression. J. Cell. Physiol. 199: 181–193, 2004© 2003 Wiley‐Liss, Inc.
Biallelic IgH rearrangements in patients with indolent lymphoproliferative disorders: Molecular and practical implications
Authors: Cerny Jan , Slavickova Alena , Krepelova Anna , Trneny Marek , Karban Josef , Klener Pavel 
Published: March 2004

AbstractWe report a group of patients (pts) with indolent lymphoproliferative disorder who had both alleles for the immunoglobulin heavy chain genes rearranged (biIgH). This group of 17 pts consisted of 9 small lymphocytic lymphomas (SLL) and 8 chronic lymphocytic leukemia (CLL). The polymerase chain reaction (PCR) amplification of clonal immunoglobulin heavy (IgH) rearrangement using the complementarity determining region III (CDRIII) constantly retrieved two distinct bands in all PCR informative samples of those pts. To rule out biclonality, we evaluated samples by fluorescein activated cell sorting (FACS) analysis and sequenced the PCR products. We were able to obtain both IgH sequences from 12 patients. FACS suggested biclonality in one case, which also correlated with sequencing results as both IgH rearrangements were in‐frame. Recently, we reported a patient who sustained transformation into an aggressive disease after biIgH was detected in the setting of monoclonal disease (Cerny et al., 2003b, Haematologica 88(05):ECR15 B.). We decided to compare clinical characteristics and prognosis of 17 pts with biIgH and 37 pts with monoIgH rearrangements. Although we found some minor differences in disease characteristics between both groups, these did not translate into a significantly different overall survival. Our findings suggest that true biclonal cases of CLL are rare. J. Cell. Physiol. 199: 217–226, 2004© 2003 Wiley‐Liss, Inc.
S100B causes apoptosis in a myoblast cell line in a RAGE‐independent manner
Authors: Sorci Guglielmo , Riuzzi Francesca , Agneletti Anna Lisa , Marchetti Cristina , Donato Rosario 
Published: March 2004

AbstractS100B, a Ca2+‐modulated protein with both intracellular and extracellular regulatory roles, is most abundant in astrocytes, is expressed in various amounts in several non‐nervous cells and is also found in normal serum. Astrocytes secrete S100B, and extracellular S100B exerts trophic and toxic effects on neurons depending on its concentration, in part by interacting with the receptor for advanced glycation end products (RAGE). The presence of S100B in normal serum and elevation of its serum concentration in several non‐nervous pathological conditions suggest that S100B‐expressing cells outside the brain might release the protein and S100B might affect non‐nervous cells. Recently we reported that at picomolar to nanomolar doses S100B inhibits rat L6 myoblast differentiation via inactivation of p38 kinase in a RAGE‐independent manner. We show here that at ≥5 nM in the absence of and at >100 nM in the presence of serum S100B causes myoblast apoptosis via stimulation of reactive oxygen species (ROS) production and inhibition of the pro‐survival kinase, extracellular signal‐regulated kinase (ERK)1/2, again in a RAGE‐independent manner. Together with our previous data, the present results suggest that S100B might participate in the regulation of muscle development and regeneration by two independent mechanism, i.e., by inhibiting crucial steps of the myogenic program at the physiological levels found in serum and by causing elevation of ROS production and myoblast apoptosis following accumulation in serum and/or muscle extracellular space. Our data also suggest that RAGE has no role in the transduction of S100B effects on myoblasts, implying that S100B can interact with more than one receptor to affect its target cells. J. Cell. Physiol. 199: 274–283, 2004© 2003 Wiley‐Liss, Inc.
NO induced apoptosis of vascular smooth muscle cells accompanied by ceramide increase
Authors: Pilane Cyril M. , LaBelle Edward F. 
Published: March 2004

AbstractWe have shown previously that nitric‐oxide (NO) can induce apoptosis of vascular smooth muscle cells (VSMCs) and that the NO‐induced apoptosis is accompanied by an increase in arachidonic acid release via cytoplasmic Ca2+‐dependent phospholipase A2 (cPLA2). We have evidence that during NO‐induced apoptosis there is an increase in ceramide synthesis. The use of inhibitors of ceramide synthesis, namely, fumonisin B1 and desipramine, which block ceramide synthase and sphingomyelinase, respectively revealed that the ceramide was produced via the sphingomyelinase pathway. Inhibition of acid sphingomyelinase by desipramine was shown to inhibit NO‐induced apoptosis while fumonisin B1 failed to inhibit this process. C2‐ceramide could induce apoptosis in cultured VSMCs. Apoptosis in smooth muscle cells was accompanied by the increased activity of DNA fragmentation factor‐40 and the secretion of cathepsin D from the cells. In this study, ceramide appears to function as a mediator of apoptosis. J. Cell. Physiol. 199: 310–315, 2004© 2003 Wiley‐Liss, Inc.
p27/Kip1 mediates retinoic acid‐induced suppression of ovarian carcinoma cell growth
Authors: Vuocolo Scott , Soprano Dianne Robert , Soprano Kenneth J. 
Published: March 2004

AbstractWe have investigated the mechanisms by which all‐trans retinoic acid (ATRA) causes growth inhibition of ovarian carcinoma cells. As a model, we have studied the CAOV3 cell line, which is sensitive to ATRA, and the SKOV3 cell line, which is resistant. We have found that treatment of CAOV3 cells with ATRA causes a 5–10 fold increase in the protein level of the cyclin dependent kinase inhibitor p27/Kip1. p27/Kip1 protein upregulation is important in ovarian carcinoma as primary tumors are frequently found lacking this protein. The increase in p27/Kip1 is detected by day 3 of ATRA treatment of CAOV3 cells, and is maximal by day 5. Messenger RNA levels of p27/Kip1 do not change in CAOV3 cells following ATRA treatment, however, we have shown that p27/Kip1 mRNA is more stable in ATRA treated CAOV3 cells. Conversely, the ATRA resistant cell line SKOV3 fails to show p27/Kip1 accumulation. Interestingly, the SCF component protein SKP2 appears to be decreased in CAOV3 cells treated with ATRA. We have also shown that the ATRA dependent increase in p27/kip1 protein in CAOV3 cells leads to a decrease in the kinase activity of cyclin dependent kinase 4 (CDK4) following ATRA treatment. Finally, we found that CAOV3 cells stably transfected with a p27/kip1antisense construct, which express lower levels of p27/kip1 following ATRA treatment, and have a higher CDK4 kinase activity are less sensitive to ATRA induced growth suppression. Taken together our data suggest ATRA‐induced growth inhibition in CAOV3 ovarian carcinoma cells involves modulation of the CDK inhibitor p27/kip1. J. Cell. Physiol. 199: 237–243, 2004© 2004 Wiley‐Liss, Inc.
From Cell–ECM interactions to tissue engineering
Authors: Rosso Francesco , Giordano Antonio , Barbarisi Manlio , Barbarisi Alfonso 
Published: March 2004

AbstractThe extracellular matrix (ECM) consists of a complex mixture of structural and functional macromolecules and serves an important role in tissue and organ morphogenesis and in the maintenance of cell and tissue structure and function. The great diversity observed in the morphology and composition of the ECM contributes enormously to the properties and function of each organ and tissue. The ECM is also important during growth, development, and wound repair: its own dynamic composition acts as a reservoir for soluble signaling molecules and mediates signals from other sources to migrating, proliferating, and differentiating cells. Approaches to tissue engineering center on the need to provide signals to cell populations to promote cell proliferation and differentiation. These “external signals” are generated from growth factors, cell–ECM, and cell–cell interactions, as well as from physical‐chemical and mechanical stimuli. This review considers recent advances in knowledge about cell–ECM interactions. A description of the main ECM molecules and cellular receptors with particular care to integrins and their role in stimulation of specific types of signal transduction pathways is also explained. The general principles of biomaterial design for tissue engineering are considered, with same examples. J. Cell. Physiol. 199: 174–180, 2004© 2003 Wiley‐Liss, Inc.
Intracellular redistribution and modification of proteins of the Mre11/Rad50/Nbs1 DNA repair complex following irradiation and heat‐shock
Authors: Seno Joshua D. , Dynlacht Joseph R. 
Published: March 2004

AbstractMre11, Rad50, and Nbs1form a tight complex which is homogeneously distributed throughout the nuclei of mammalian cells. However, after irradiation, the Mre11/Rad50/Nbs1 (M/R/N) complex rapidly migrates to sites of double strand breaks (DSBs), forming foci which remain until DSB repair is complete. Mre11 and Rad50 play direct roles in DSB repair, while Nbs1 appears to be involved in damage signaling. Hyperthermia sensitizes mammalian cells to ionizing radiation. Radiosensitization by heat shock is believed to be mediated by an inhibition of DSB repair. While the mechanism of inhibition of repair by heat shock remains to be elucidated, recent reports suggest that the M/R/N complex may be a target for inhibition of DSB repair and radiosensitization by heat. We now demonstrate that when human U‐1 melanoma cells are heated at 42.5 or 45.5°C, Mre11, Rad50, and Nbs1 are rapidly translocated from the nucleus to the cytoplasm. Interestingly, when cells were exposed to ionizing radiation (12 Gy of X‐rays) prior to heat treatment, the extent and kinetics of translocation were increased when nuclear and cytoplasmic fractions of protein were analyzed immediately after treatment. The kinetics of the translocation and subsequent relocalization back into the nucleus when cells were incubated at 37°C from 30 min to 7 h following treatment were different for each protein, which suggests that the proteins redistribute independently. However, a significant fraction of the translocated proteins exist as a triple complex in the cytoplasm. Treatment with leptomycin B (LMB) inhibits the translocation of Mre11, Rad50, and Nbs1 to the cytoplasm, leading us to speculate that the relocalization of the proteins to the cytoplasm occurs via CRM1‐mediated nuclear export. In addition, while Nbs1 is rapidly phosphorylated in the nuclei of irradiated cells and is critical for a normal DNA damage response, we have found that Nbs1 is rapidly phosphorylated in the cytoplasm, but not in the nucleus, of heated irradiated cells. The phosphorylation of cytoplasmic Nbs1, which cannot be inhibited by wortmannin, appears to be a unique post‐translational modification in heated, irradiated cells, and coupled with our novel observations that Mre11, Rad50, and Nbs1 translocate to the cytoplasm, lend further support for a role of the M/R/N complex in thermal radiosensitization and inhibition of DSB repair. J. Cell. Physiol. 199: 157–170, 2004© 2004 Wiley‐Liss, Inc.
Rab3D redistribution and function in rat parotid acini
Authors: Ngyen Danielle , Jones Antoinette , Ojakian George K. , Raffaniello Robert D. 
Published: March 2004

AbstractThe original article to which this Erratum refers was published in J. Cell. Physiol. (2003) 197(3) 400–408 .Rab3D is a low molecular weight GTP‐binding protein believed to be involved with regulated secretion in many cell types. In parotid, Rab3D is localized to secretory granule membranes or present in the cytosol as a complex with Rab escort protein. In the present study, we examined the redistribution of membrane‐associated Rab3D during secretion in permeabilized parotid acini. When permeabilized acini were stimulated with calcium and cAMP, amylase release increased greater than twofold over basal. Quantitative immunoblotting of subcellular fractions revealed that Rab3D did not dissociate from parotid membranes during secretion. Immunohistochemical staining demonstrated that Rab3D co‐localizes with amylase containing granules that are found in the apical pole of the cell. Upon stimulation with calcium and cAMP, Rab3D and amylase immunostaining of granules appeared to be more dispersed. However, Rab3D immunostaining was not observed on the plasma membrane and appeared to reside in the apical cytoplasm. To examine the role of Rab3D in amylase release, cytosolic extracts containing myc‐tagged Rab3D and Rab3DQ81L, a GTP‐binding mutant, were prepared and incubated with streptolysin O‐permeabilized acini. Rab3D, but not Rab3DQ81L, bound to parotid membranes suggesting that Rab3D‐binding to parotid membranes is guanine nucleotide‐dependent. Moreover, wild‐type and mutant Rab3D inhibited agonist‐induced amylase release from permeabilized parotid acini. These observations indicate that in parotid acini, Rab3D does not dissociate from parotid membranes or redistribute to the plasma membrane during secretion, and may play an inhibitory role in regulated secretion. The fact that both wild‐type Rab3D and the GTP‐binding mutant inhibit amylase release suggests that binding of Rab3D to the membrane is not essential for secretory inhibition. J. Cell. Physiol. 199: 316, 2004© 2004 Wiley‐Liss, Inc.