bluuebunny/crossref_metadata_2025_split huggingface dataset:
Amino‐Substituted Ferra‐bis(tricarbollides) − Metallatricarbaboranes Designed for Linear Molecular Constructions
Authors: Grüner Bohumír , Bačkovský Jaroslav , Sillanpää Reijo , Kivekäs Raikko , Císařová Ivana , Teixidor Francesc , Viñas Clara , Štíbr Bohumil 
Published: March 2004

AbstractReactions between high purity FeCl2 and the anion [nido‐7‐(tBuHN)‐7,8,9‐C3B8H10)]− (1−) have been used for efficient syntheses of the twelve‐vertex double‐cluster metallatricarbollide complexes of the para,para (p,p) type [closo‐9,9′(RHN)2‐commo‐2,2′‐FeII‐1,7,9‐(C3B8H10)‐1′,7′,9′‐(C3B8H10)] (2) (2a, R = tBu and 2b, R = H) (yields 42−45% for 2a). Compound 2b, which contains two reactive amino substituents conveniently attached to the tricarbollide subclusters in p‐positions with respect to the metal center, was prepared via facile cleavage of the tBu substituent in 2a either by AlCl3 or by thermal means. The structure of 2b constitutes a good setting for the synthesis of building blocks for constructing linear metallatricarbollide rods of high stability. Two isomeric compounds of the para,meta (p,m) type 3, [closo‐9,10′‐(RHN)2‐commo‐2,2′‐Fe‐1,7,9‐(C3B8H10)‐1′,7′,10′‐(C3B8H10)] (where R = tBu 3a and/or H 3b), were isolated in smaller yields from reactions of high purity FeCl2 with 1− at higher temperatures. Also reported is the characterization of the m,m‐type complex, [closo‐10,10′‐(tBuHN)2‐commo‐2,2′‐FeII‐1,7,10‐(C3B8H10)‐1′,7′,10′‐(C3B8H10)] (4a), and the two zwitterionic species of the new 7‐L‐7,8,10‐C3B8H10 type (6) [L = Me3N 6a and tBu(Me)HN 6b] isolated in moderate yields from the reaction of reagent grade FeCl2 with 1−. The molecular structures of 2b, 3a, and 6b were determined by single‐crystal X‐ray diffraction studies. Multinuclear (1H and 11B), two‐dimensional [11B‐11B]‐COSY, and 1H{11B(selective)} magnetic resonance measurements enabled complete assignments of all resonances for all compounds and are in excellent agreement with the structures proposed. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2004)
Metal Telluride Clusters — From Small Molecules to Polyhedral Structures
Authors: Wachter Joachim 
Published: March 2004

AbstractNiobocene ditelluride complexes [(tBuC5H4)2Nb(Te2)H] (1) and [(C5Me5)2Nb(Te2H)] (2) are useful starting materials for the synthesis of heterometallic telluride complexes and clusters. The presence of free electron pairs, the propensity for Te−Te bond cleavage and the ability to eliminate Te ligands allow stepwise formation of polyhedral structures in reactions with binary transition metal carbonyl complexes or reactive organometallic fragments. Among the products are the first examples of organometallic derivatives of the elusive [MTe4]2− ion. Ligand cross‐transfer (CO versus Te) from one metal center to the other and subsequent charge separation lead to the formation of anionic metal telluride clusters and cationic carbonylniobocene species. The latter play a decisive role in tuning the electronic properties of the cluster units. Whereas the 17‐electron fragment (tBuC5H4)2Nb(CO) is directly anchored at the cluster cores by Te bridges, the 18‐electron cation [Cp*2Nb(CO)2]+ (Cp* = C5Me5) formed in situ is able to stabilize large and differently charged cluster anions. This is particularly the case in cobalt telluride cluster chemistry which is characterized by hexacapped cubic Co@Co8 or heptacapped pentagonal‐prismatic Co@Co10 polyhedra. These compounds exhibit pronounced electron‐sponge behavior, and crystallographic studies of differently charged clusters allow a correlation of different cluster charges and bond parameters important for understanding electronic structures. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2004)
Tissue‐specific expression of cre recombinase from the Pax8 locus
Authors: Bouchard Maxime , Souabni Abdallah , Busslinger Meinrad 
Published: March 2004

AbstractThe transcription factor Pax8 is expressed in the developing thyroid gland, inner ear, kidney, and mid‐hindbrain region. Pax8 mutant mice die only postnatally due to a thyroid gland defect. Here we report the generation and expression analysis of a Pax8cre allele. Cre recombinase activity was detected in known Pax8 expression domains of Pax8cre/+ and Pax8cre/cre embryos carrying the Z/AP transgene, which expresses alkaline phosphatase only after Cre‐mediated excision of lacZ sequences. Alkaline phosphatase expression was additionally detected in the adrenal gland and in the facial, vestibulocochlear, and cuneate nerves, which have so far not been associated with Pax8 expression. Our data indicate that the Pax8cre allele provides a novel important tool for conditional gene manipulation and lineage tracing in different Pax8 expression domains. genesis 38:105–109, 2004. © 2004 Wiley‐Liss, Inc.
Dorsal telencephalon‐specific expression of Cre recombinase in PAC transgenic mice
Authors: Iwasato Takuji , Nomura Ryochi , Ando Reiko , Ikeda Toshio , Tanaka Mika , Itohara Shigeyoshi 
Published: March 2004

AbstractThe ability to restrict gene expression or disruption to specific regions of the brain would enhance understanding of the molecular basis for brain development and function. For this purpose, brain region‐restricted promoters are essential. Here we report the isolation of a DNA fragment containing the Emx1 gene promoter, which is responsible for dorsal telencephalon‐specific expression. The Cre recombinase gene was inserted into a mouse PAC (P1‐derived artificial chromosome) Emx1‐locus clone (PAC‐Emx1#1 clone) and utilized to generate three transgenic mouse lines. In all three lines, especially Tg3, Cre‐mediated recombination was highly restricted to Emx1‐expressing cell lineages, from embryonic stages to adulthood. Immunohistochemical analyses showed that Cre protein is expressed in the dorsal telencephalon in all three lines in adulthood. Thus, the PAC‐Emx1#1 clone contains essentially all regulatory elements necessary for Emx1 gene expression. Our results suggest that Emx1‐Cre Tg3 mice and the PAC‐Emx1#1 clone constitute powerful tools for dorsal telencephalon‐specific gene manipulation. genesis 38:130–138, 2004. © 2004 Wiley‐Liss, Inc.
Conditional gene deletion in primary nociceptive neurons of trigeminal ganglia and dorsal root ganglia
Authors: Agarwal Nitin , Offermanns Stefan , Kuner Rohini 
Published: March 2004

AbstractThe use of Cre‐loxP technology for conditional mutagenesis in pain pathways had been restricted by the unavailability of mice expressing Cre recombinase selectively in functionally distinct components of the nociceptive system. Here we describe the generation of transgenic mouse lines which express Cre recombinase selectively in sensory ganglia using promoter elements of the Nav1.8 gene (Scn10a). Cre‐mediated recombination was greatly evident in all nociceptive and thermoreceptive neurons of the dorsal root ganglia and trigeminal ganglia, but only in a small proportion of proprioceptive neurons. Cre‐mediated recombination was not detectable in the brain, spinal cord, or any nonneural tissues and began perinatally after invasion of primary afferents into the developing spinal cord. Thus, these mice enable selective deletion of genes in subsets of sensory neurons and offer a wide scope for studying potential functions of genes in pain perception, independent of secondary effects arising from developmental defects or global gene ablation. genesis 38:122–129, 2004. © 2004 Wiley‐Liss, Inc.
A reliable lacZ expression reporter cassette for multipurpose, knockout‐first alleles
Authors: Testa Giuseppe , Schaft Julia , van der Hoeven Frank , Glaser Stefan , Anastassiadis Konstantinos , Zhang Youming , Hermann Thomas , Stremmel Wolfgang , Stewart A. Francis 
Published: March 2004

AbstractAlteration of the mouse genome through homologous recombination in embryonic stem (ES) cells is the most accurate and versatile way to dissect gene function in a vertebrate model. Most often, a selectable marker is used to create a knockout allele by replacing an essential part of the gene. However, knockout strategies are limited because the mutation is present constitutively. Conditional approaches based on the Cre‐loxP site‐specific recombination (SSR) system address this limitation; however, it requires that all parts of the targeted gene remain in ES cells. Here we report success with a “knockout‐first” strategy that ablates gene function by insertion of RNA processing signals without deletion of any of the target gene. Incorporation of site‐specific recombination target sites creates a multipurpose allele for both knockout and conditional applications. genesis 38:151–158, 2004. © 2004 Wiley‐Liss, Inc.
p38/SAPK2 controls gap junction closure in astrocytes
Authors: Zvalova Darina , Cordier Jocelyne , Mesnil Marc , Junier Marie‐Pierre , Chneiweiss Hervé 
Published: March 2004

AbstractAstrocyte gap junction communication (GJC) is thought to contribute to death signal propagation following central nervous system injury, noteworthy in some ischemia/anoxia models. The inhibition of p38/stress‐activated protein kinase 2 (p38/SAPK2) by a pyrimidyl imidazole derivative has been reported to reduce the extent of the lesion area after cerebral ischemia. Therefore, interleukin‐1β (IL‐1β), which contributes to stroke‐induced brain injury and activates p38/SAPK2, and hyperosmolarity induced by sorbitol, a potent stimulus of p38/SAPK2 in non‐neuronal cells, were used to investigate a possible involvement of p38/SAPK2 in GJC modulation in mouse cultured astrocytes. Both stimuli inhibited dye coupling within minutes. The IL‐1β effect was transient, while that of sorbitol lasted up to 90 min. Both stimuli induced a rapid p38/SAPK2 activation, the kinetic of which matched that of induction of dye coupling inhibition. Immunocytochemical studies showed that IL‐1β and sorbitol induced a p38/SAPK2 translocation from the nucleus to the cytoplasm. The pharmacological agent SB203580 specifically blocked p38/SAPK2 activation, cytoplasmic translocation and reversed the IL‐1β and sorbitol‐induced inhibition of GJC. Further characterization of the p38/SAPK2 mode of action on GJC, performed with sorbitol, revealed an increased phosphorylation of protein kinase C (PKC) substrates abolished by both PKC inhibitors and SB203580. Expression and serine phosphorylation of connexin 43, the main component of astrocyte gap junctions, were unchanged, suggesting the existence of additional intracellular signaling mechanisms modulating the channel gating. Altogether, these results demonstrate that p38/SAPK2 is a central mediator of IL‐1β and sorbitol inhibitory actions on GJC and establish PKC among the distal effectors of p38/SAPK2. © 2004 Wiley‐Liss, Inc.
Triethyltin‐induced stress responses and apoptotic cell death in cultured oligodendrocytes
Authors: Stahnke Thomas , Richter‐Landsberg Christiane 
Published: March 2004

AbstractTriethyltin (TET)‐induced neurotoxicity in the brain causes the formation of myelin edema and loss. Myelin deficits produced by early postnatal exposure to TET are permanent and cannot be repaired as the brain matures. The underlying causes have not been resolved. To investigate whether TET directly affects oligodendrocytes, the myelin‐forming cells of the central nervous system, cultured rat brain oligodendrocytes were prepared and treated with TET. The data show that TET was cytotoxic for oligodendrocytes and led to the onset of programmed cell death, as indicated by DNA fragmentation. Cellular membranous extensions were severely damaged, and the nuclei appeared to be condensed and fragmented. Concomitantly, the small heat shock protein HSP32, also known as heme oxygenase‐1 (HO‐1), and an indicator of oxidative stress, as well as the activation of extracellular signal‐regulated kinases 1 and 2 (ERK1,2), were observed. ERK1,2 have been implicated to participate in the regulation of cell death and survival. Myelin‐specific proteins MBP and CNP were not affected. In TET‐treated cells mitochondria redistributed from the processes to the cell somata near the nucleus, possibly as a consequence of microtubule disorganization. A disturbance of the mitochondrial membrane potential and mitochondrial fragmentation occurred. Hence, it might be hypothesized that oligodendroglial PCD, rather than axonal degeneration, contributes to myelin damage and deficits observed in rats after treatment with TET in vivo. © 2004 Wiley‐Liss, Inc.
Prostaglandin E2 and 6‐keto‐prostaglandin F1α production is elevated following traumatic injury to sciatic nerve†
Authors: Muja Naser , DeVries George H. 
Published: March 2004

AbstractSciatic nerve explants cultured either alone or in the presence of peritoneal macrophages were used to study prostaglandin E2 (PGE2) and 6‐keto‐PGF1α production following traumatic peripheral nerve injury. Although barely detectable at early time points (1–3 h in vitro), the production of PGE2 and 6‐keto‐PGF1α by sciatic nerve explants increased significantly after 18 h and remained elevated for up to 96 h. The cyclooxygenase‐2 (COX‐2) selective inhibitor, NS‐398, inhibited PGE2 and 6‐keto‐PGF1α production by injured sciatic nerve in a dose‐dependent manner. Consistent with the observed effect of NS‐398, peripheral nerve explants, as well as Schwann cells and perineural fibroblasts cultured from neonatal sciatic nerve, each contained COX‐2 immunoreactivity after 24 h in vitro. Both Schwann cells and perineural fibroblasts produced significant amounts of PGE2 and 6‐keto‐PGF1α; but only in the presence of arachidonic acid. As observed for injured sciatic nerve, the production of PGE2 and 6‐keto‐PGF1α by primary Schwann cells and perineural fibroblasts was completely inhibited by NS‐398. Compared to macrophages cultured alone, macrophages cultured in the presence of sciatic nerve explants produced large amounts of PGE2, whereas the level of 6‐keto‐PGF1α was unchanged. In contrast, macrophages treated with adult sciatic nerve homogenate did not produce significant amounts of either PGE2 or 6‐keto‐PGF1α during the entire course of treatment. We conclude that injured sciatic nerves produce PGE2 and 6‐keto‐PGF1α by a mechanism involving COX‐2 activity and that macrophages produce large amounts of PGE2 in response to soluble factors produced by injured nerve but not during the phagocytosis of peripheral nerve debris. Published 2004 Wiley‐Liss, Inc.
BDNF‐dependent stimulation of dopamine D5 receptor expression in developing striatal astrocytes involves PI3‐kinase signaling
Authors: Brito Veronica , Beyer Cordian , Küppers Eva 
Published: March 2004

AbstractIt is well known that brain‐derived neurotrophic factor (BDNF) and the early nigrostriatal dopaminergic input are implicated in the regulation of developmental processes in the neostriatum. There is growing evidence that interactions between these developmental signals rather than singular actions are critical for cellular differentiation and compartmentation of the striatum. In the present report, our goal is to identify striatal target cells for BDNF and dopamine. Using primary neuronal and astroglial cell cultures, we have demonstrated that BDNF selectively regulates D5 but not D1 receptor expression in astrocytes. This effect was not observed in neurons. Pharmacological approaches indicated that BDNF effects on dopamine D5 receptor expression were mediated at the intracellular level by an activation of the PI3‐ but not MAP‐kinase cascade. FACS analysis and confocal laser microscopy revealed that the newly synthesized D5 receptors were integrated into the plasma membrane of astrocytes. Our findings clearly show that developing striatal astrocytes are targets for BDNF. Furthermore, BDNF appears to regulate the dopamine responsiveness of astrocytes. This implicates that functional interactions between BDNF, dopamine, and astrocytes are necessary to warrant proper differentiation of the striatal anlage. © 2004 Wiley‐Liss, Inc.
Microglia expressing interleukin‐13 undergo cell death and contribute to neuronal survival in vivo
Authors: Shin Won Ho , Lee Da‐Yong , Park Keun Woo , Kim Seung Up , Yang Myung‐Soon , Joe Eun‐Hye , Jin Byung Kwan 
Published: March 2004

AbstractHow to minimize brain inflammation is pathophysiologically important, since inflammation induced by microglial activation can exacerbate brain damage. In the present report, we show that injection of lipopolysaccharide (LPS) into the rat cortex led to increased levels of interleukin‐13 (IL‐13) and to IL‐13 immunoreactivity, followed by the substantial loss of microglia at 3 days post‐LPS. IL‐13 levels in LPS‐injected cortex reached a peak at 12 h post‐injection, remained elevated at 24 h, and returned to basal levels at day 4. In parallel, IL‐13 immunoreactivity was detected as early as 12 h post‐LPS and maintained up to 24 h; it disappeared at 4 days. Surprisingly, IL‐13 immunoreactivity was detected exclusively in microglia, but not in neurons or astrocytes. Following treatment with LPS in vitro, IL‐13 expression was also induced in microglia in the presence of neurons, but not in the presence of astrocytes or in cultured pure microglia alone. In experiments designed to determine the involvement of IL‐13 in microglia cell death, IL‐13‐neutralizing antibodies significantly increased survival of activated microglia at 3 days post‐LPS. Consistent with these results, the expression of inducible nitric oxide synthase (iNOS) and tumor necrosis factor‐α (TNF‐α) was sustained in activated microglia and neuronal cell death was consequently increased. Taken together, the present study is the first to demonstrate the endogenous expression of IL‐13 in LPS‐activated microglia in vivo, and to demonstrate that neurons may be required for IL‐13 expression in microglia. Our data strongly suggest that IL‐13 may control brain inflammation by inducing the death of activated microglia in vivo, resulting in an enhancement of neuronal survival. © 2004 Wiley‐Liss, Inc.
IGF‐I prevents glutamate‐mediated bax translocation and cytochrome C release in O4+oligodendrocyte progenitors
Authors: Ness Jennifer K. , Scaduto Russell C. , Wood Teresa L. 
Published: March 2004

AbstractOligodendroglial death due to overactivation of the AMPA/kainate glutamate receptors is implicated in white matter damage in multiple CNS disorders. We previously demonstrated that glutamate induces caspase‐3 activation and death of the late oligodendrocyte progenitor known as the pro‐oligodendroblast (pro‐OL) via activation of the AMPA/kainate glutamate receptors. We also demonstrated that IGF‐I had the unique ability to sustain activation of Akt in the pro‐OL and provide long‐term protection of these cells from glutamate‐mediated apoptosis. The goal of these studies was to investigate the mechanisms of glutamate toxicity and IGF‐I‐mediated survival in the pro‐OL. IGF‐I prevented glutamate‐induced loss of mitochondrial membrane potential, cytochrome c release, and caspase‐9 activation. In contrast to IGF‐I mediated survival mechanisms in neurons, IGF‐I had no effect on the influx or recovery of intracellular calcium levels or on levels of major pro‐ and anti‐apoptotic molecules including Bax or Bcl‐xL. Rather, IGF‐I prevented the glutamate‐induced translocation of Bax to the mitochondria. Moreover, IGF‐I prevented caspase‐3 activation in pro‐OLs as long as 8 h after exposure of the cells to glutamate, suggesting that delayed activation of IGF‐I‐mediated survival pathways can block glutamate‐mediated apoptosis in pro‐OLs. The results of these experiments define the mechanisms by which glutamate kills oligodendrocyte progenitor cells and by which IGF‐I blocks glutamate‐induced apoptosis in these cells. The data also demonstrate that IGF‐I disrupts the glutamate‐mediated apoptotic pathway in the pro‐OL through mechanisms that are distinct from its survival‐promoting actions in neurons. © 2004 Wiley‐Liss, Inc.
Diverse microglial motility behaviors during clearance of dead cells in hippocampal slices
Authors: Petersen Mark A. , Dailey Michael E. 
Published: March 2004

AbstractWe used two‐channel three‐dimensional time‐lapse fluorescence confocal imaging in live rat hippocampal slice cultures (1–7 days in vitro) to determine the motility behaviors of activated microglia as they engage dead and dying cells following traumatic brain tissue injury. Live microglia were labeled with a fluorescently conjugated lectin (IB4), and dead neurons were labeled with a membrane‐impermeant fluorescent DNA‐binding dye (Sytox Orange or To‐Pro‐3). Tissue injury during the slicing procedure induced neuronal death and microglial activation, but the density of dead cells diminished ∼ 10‐fold by 7 days in vitro as resident microglia cleared dead cells. In time‐lapse movies (4–20 h long), activated microglia exhibited varying levels of motile and locomotory activity. The motility of microglia could change abruptly following contact by other microglia or death of nearby cells. When neighboring cells died, some microglia rapidly moved toward or extended a process to engulf the dead cell, consistent with a chemotactic signaling response. Dead cell nuclei usually were engulfed and carried along by highly motile and locomoting microglia. The mean time to engulfment was ∼ 5 times faster for newly deceased cells (33 min) than for extant dead cells (160 min), suggesting that the efficacy of microglial phagocytosis in situ might vary with time after cell death or mode of cell death. These observations demonstrate that activated microglia are heterogeneous with respect to motile activity following traumatic tissue injury and further indicate that cell motility in situ is temporally regulated at the single cell level, possibly by direct cell‐cell contact and by diffusible substances emanating from nearby dead cells. © 2004 Wiley‐Liss, Inc.
Transient upregulation of Nkx2.2 expression in oligodendrocyte lineage cells during remyelination
Authors: Watanabe Masahiko , Hadzic Tarik , Nishiyama Akiko 
Published: March 2004

AbstractWhile numerous oligodendrocyte progenitor cells (OPCs) exist in the adult central nervous system (CNS), the molecular signals that promote or inhibit their differentiation into mature oligodendrocytes (OLs) are not known. To investigate whether remyelination in the adult CNS is regulated by the same mechanisms that promote developmental myelination, we used an acute demyelinating/remyelinating lesion in the adult rat spinal cord to examine the expression of the homeodomain transcription factor Nkx2.2, which has previously been implicated in oligodendrocyte differentiation during embryonic development. After a demyelinating insult, Nkx2.2 expression was upregulated first in NG2‐expressing OPCs surrounding the lesion and subsequently in both precursors and OLs that appeared inside the lesion prior to the onset of remyelination. The temporal and spatial pattern of Nkx2.2 upregulation coincided with that of oligodendrocyte differentiation characterized in our previous study (Watanabe et al., J Neurosci Res 69:826–836, 2002). A similar increase in the level of Nkx2.2 expression was observed in the postnatal developing optic nerve in a wave from the proximal to the distal retinal end. In vitro Nkx2.2 was expressed in OPCs and immature OLs isolated from postnatal rat spinal cord but was absent from mature OLs. These observations indicate that the process of generating new OLs in a remyelinating lesion recapitulates the developmental program involving activation of the Nkx2.2 gene, which may trigger the existing NG2‐expressing precursors in the adult CNS to undergo terminal differentiation into remyelinating OLs. © 2004 Wiley‐Liss, Inc.