537 research outputs found
4-{[5-(4-Chlorophenyl)-1-(4-fluorophenyl)-1H-pyrazol-3-yl]carbonyl}-N-ethylpiperazine-1-carboxamide
The asymmetric unit of the title compound, C23H23ClFN5O2, contains two crystallographically independent molecules. In one molecule, the pyrazole ring makes dihedral angles of 43.93 (7) and 35.82 (7)°, respectively, with the fluoro- and chloro-substituted benzene rings, while the corresponding angles in the other molecule are 52.26 (8) and 36.85 (7)°. The piperazine rings adopt chair conformations. In the crystal, adjacent molecules are connected via intermolecular N—H⋯O, C—H⋯F, C—H⋯N and C—H⋯O hydrogen bonds, forming a two-dimensional network parallel to the bc plane. The crystal structure is further stabilized by a weak π–π interaction with a centroid–centroid distance of 3.6610 (8) Å and by C—H⋯π interactions
1,3-Dimethyl-4-phenylsulfanyl-1H-pyrazol-5-ol
In the title compound, C11H12N2OS, the pyrazole ring makes a dihedral angle of 85.40 (8)° with the phenyl ring. In the crystal, intermolecular N—H⋯O and C—H⋯O hydrogen bonds link molecules into a two-dimensional network parallel to the bc plane
4-Methyl-5-phenyl-1H-pyrazol-3-ol
The title compound, C10H10N2O, crystallizes with two independent molecules in the asymmetric unit, having closely comparable geometries. The dihedral angles between the 1H-pyrazole and benzene rings in the two molecules are 39.57 (14) and 41.95 (13)°. The two molecules are each connected to neighbouring molecules by pairs of intermolecular O—H⋯N hydrogen bonds, forming dimers with R
2
2(8) ring motifs. These dimers are further linked into R
4
4(10) ring motifs by intermolecular N—H⋯O hydrogen bonds, forming chains along [101]. The crystal structure is further stabilized by a C—H⋯π interaction
4-{2-[5-(4-Chlorophenyl)-1-(4-fluorophenyl)-1H-pyrazol-3-yl]thiazol-4-yl}benzonitrile
The asymmetric unit of the title compound, C25H14ClFN4S, contains two independent molecules (A and B). Each molecule consists of five rings, namely chlorophenyl, fluorophenyl, 1H-pyrazole, thiazole and benzonitrile. In molecule A, the 1H-pyrazole ring makes dihedral angles of 52.54 (8), 35.96 (8) and 15.43 (8)° with respect to the attached chlorophenyl, fluorophenyl and thiazole rings. The corresponding values in molecule B are 51.65 (8), 37.26 (8) and 8.32 (8)°. In the crystal, molecules are linked into dimers by C—H⋯N hydrogen bonds, generating R
2
2(10) ring motifs. These dimers are further linked into two-dimensional arrays parallel to the ab plane via intermolecular weak C—H⋯N and C—H⋯F hydrogen bonds. The crystal structure is further stabilized by weak π-π interactions [with centroid–centroid distances of 3.4303 (9) and 3.6826 (9) Å] and weak C—H⋯π interactions
3-(2,5-Dimethylfuran-3-yl)-1H-pyrazol-5-ol–ethyl 3-(propan-2-ylidene)carbazate (1/1). Corrigendum
Corrigendum to Acta Cryst. (2010), E66, o3020–o3021
Antioxidant activity of the methanolic extracts of some species of Phlomis and Stachys on sunflower oil
Antioxidant effects of the methanolic extract of Phlomis bruguieri, P. herba-venti, P. olivieri, Stachys byzantina, S. inflata, S. lavandulifolia and S. laxa were tested in sunflower oil stored at 70ºC, by measuring peroxide values after regular intervals and compared with rosemary-, green tea- and BHAcontaining samples. The methanolic extracts of P. bruguieri and S. laxa were found to be most effective in stabilizing sunflower oil
Tau aggregation and progressive neuronal degeneration in the absence of changes in spine density and morphology after targeted expression of Alzheimer's disease-relevant tau constructs in organotypic hippocampal slices
Alzheimer's disease (AD) is characterized by progressive loss of neurons in selected brain regions, extracellular accumulations of amyloid beta, and intracellular fibrils containing hyperphosphorylated tau. Tau mutations in familial tauopathies confirmed a central role of tau pathology; however, the role of tau alteration and the sequence of tau-dependent neurodegeneration in AD remain elusive. Using Sindbis virus-mediated expression of AD-relevant tau constructs in hippocampal slices, we show that disease-like tau modifications affect tau phosphorylation at selected sites, induce Alz50/MC1-reactive pathological tau conformation, cause accumulation of insoluble tau, and induce region-specific neurodegeneration. Live imaging demonstrates that tau-dependent degeneration is associated with the development of a "ballooned" phenotype, a distinct feature of cell death. Spine density and morphology is not altered as judged from algorithm-based evaluation of dendritic spines, suggesting that synaptic integrity is remarkably stable against tau-dependent degeneration. The data provide evidence that tau-induced cell death involves apoptotic as well as nonapoptotic mechanisms. Furthermore, they demonstrate that targeted expression of tau in hippocampal slices provides a novel model to analyze tau modification and spatiotemporal dynamics of tau-dependent neurodegeneration in an authentic CNS environment
The mammalian target of rapamycin (mTOR) kinase mediates haloperidol-induced cataleptic behavior.
The mammalian target of rapamycin (mTOR) is a ubiquitously expressed serine/threonine kinase protein complex (mTORC1 or mTORC2) that orchestrates diverse functions ranging from embryonic development to aging. However, its brain tissue-specific roles remain less explored. Here, we have identified that the depletion of the mTOR gene in the mice striatum completely prevented the extrapyramidal motor side effects (catalepsy) induced by the dopamine 2 receptor (D2R) antagonist haloperidol, which is the most widely used typical antipsychotic drug. Conversely, a lack of striatal mTOR in mice did not affect catalepsy triggered by the dopamine 1 receptor (D1R) antagonist SCH23390. Along with the lack of cataleptic effects, the administration of haloperidol in mTOR mutants failed to increase striatal phosphorylation levels of ribosomal protein pS6 (S235/236) as seen in control animals. To confirm the observations of the genetic approach, we used a pharmacological method and determined that the mTORC1 inhibitor rapamycin has a profound influence upon post-synaptic D2R-dependent functions. We consistently found that pretreatment with rapamycin entirely prevented (in a time-dependent manner) the haloperidol-induced catalepsy, and pS6K (T389) and pS6 (S235/236) signaling upregulation, in wild-type mice. Collectively, our data indicate that striatal mTORC1 blockade may offer therapeutic benefits with regard to the prevention of D2R-dependent extrapyramidal motor side effects of haloperidol in psychiatric illness
5-Ethyl-4-methyl-1H-pyrazol-3(2H)-one
In the title compound, C6H10N2O, the 2,3-dihydro-1H-pyrazole ring is approximately planar, with a maximum deviation of 0.013 (1) Å. Pairs of intermolecular N—H⋯O hydrogen bonds link neighboring molecules into dimers, generating R
2
2(8) ring motifs. These dimers are further linked into two-dimensional arrays parallel to the bc plane by intermolecular N—H⋯O hydrogen bonds. The crystal structure is further stabilized by C—H⋯π interactions
5-Pentyl-4-phenylsulfonyl-1H-pyrazol-3-ol
In the title compound, C14H18N2O3S, the 1H-pyrazole ring is approximately planar, with a maximum deviation of 0.005 (1) Å. The dihedral angle formed between the 1H-pyrazole and phenyl rings is 79.09 (5)°. Pairs of intermolecular N—H⋯O and O⋯H⋯N hydrogen bonds form dimers between neighboring molecules, generating R
2
2(10) ring motifs. These dimers are further linked by intermolecular N—H⋯O and O—H⋯N hydrogen bonds into two-dimensional arrays parallel to the ac plane. The crystal structure is also stabilized by C—H⋯π interactions
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