N-Benzyl­idenenordehydro­abietylamine

The title compound [systematic name: (1R,4aS,10aR,E)-N-benzyl­idene-7-isopropyl-1,4a-dimethyl-1,2,3,4,4a,9,10,10a-octa­hydro­phenanthren-1-amine], C26H33N, has been synthesized from nor-dehydro­abietylamine and benzaldehyde. The two cyclo­hexane rings form a trans ring junction with classic chair and half-chair conformations, respectively, the two methyl groups are on the same side of tricyclic hydro­phenanthrene structure. The dihedral angle between two benzene rings is 44.2 (4)°. The C=N bond is in an E configuration

Dehydro­abietic acid

The title compound [systematic name: (1R,4aS,10aR)-7-iso­prop­yl-1,4a-dimethyl-1,2,3,4,4a,9,10,10a-octa­hydro­phen­anthrene-1-carboxylic acid], C20H28O2, has been isolated from disproportionated rosin which is obtained by isomerizing gum rosin with a Pd-C catalyst.. Two crystallographically independent mol­ecules exist in the asymmetric unit. In each mol­ecule, there are three six-membered rings, which adopt planar, half-chair and chair conformations. The two cyclo­hexane rings form a trans ring junction with the two methyl groups in axial positions. The crystal structure is stabilized by inter­molecular O—H⋯O hydrogen bonds

15-Hydroxy­ethyl-19-isopropyl-5,9-dimethyl-14,16-dioxo-15-aza­penta­cyclo­[10.5.2.01,10.04,9.013,17]nona­dec-18-ene-5-carboxylic acid

The title compound, C26H37NO5, which was synthesized from monoethano­lamine and maleopimaric acid, consists of two fused and unbridged cyclo­hexane rings. They form a trans ring junction with a chair conformation. The two methyl groups are in axial positions. In the crystal, inter­molecular O—H⋯O hydrogen bonds link adjacent mol­ecules into a layer structure. Two C—H⋯O interactions are also present

N-(2-Pyridylmethyleneamino)dehydro­abietylamine

The title compound {systematic name: 1-[(1R,4aS,10aR)-7-isopropyl-1,2,3,4,4a,9,10,10a-octa­hydro­phenanthren-1-yl]-N-[(E)-2-pyridylmethyleneamino]methanamine}, C26H33N2, has been synthesized from dehydro­abietylamine. The two cyclo­hexane rings form a trans ring junction with classic chair and half-chair conformations, respectively, whereas the benzene and pyridine rings are almost planar, and the dihedral angle between them is 80.4°. The two methyl groups directly attached to the tricyclic nucleus are on the same side of the tricyclic hydro­phenanthrene structure

7-Isopropyl-1,4a-dimethyl-1,2,3,4,4a,5,6,7,8,9,10,10a-dodeca­hydro­phenan­threne-1-carboxylic acid

The title compound, C20H32O2, has been isolated from hydrogenated rosin. There are two independent mol­ecules in the asymmetric unit. In each mol­ecule, the cyclo­hexane ring assumes a chair conformation, while the two cyclo­hexene rings adopt half-chair and envelope conformations. Inter­molecular O—H⋯O hydrogen bonding between carboxyl groups links pairs of independent mol­ecules into dimers

Poly[[di-μ3-nicotinato-hemi-μ4-oxalato-hemi-μ2-oxalato-neodymium(III)silver(I)] dihydrate]

The asymmetric unit of the title compound, {[AgNd(C6H4NO2)2(C2O4)]·2H2O}n, contains one NdIII atom, one AgI atom, one oxalate ligand, two nicotinate ligands and two uncoordinated water mol­ecules. The NdIII atom is eight-coordinated in a distorted square-anti­prismatic coordination geometry by four O atoms from two oxalate ligands and four O atoms from four nicotinate ligands. The AgI atom has a T-shaped configuration, defined by two N atoms from two nicotinate ligands and one O atom from one oxalate ligand. The nicotinate and oxalate ligands link the Nd and Ag atoms into a three-dimensional coordination framework. O—H⋯O and O—H⋯N hydrogen bonds donated by water mol­ecules are observed in the crystal

Co-localization of two-color rAAV2-retro confirms the dispersion characteristics of efferent projections of mitral cells in mouse accessory olfactory bulb

The accessory olfactory bulb (AOB), located at the posterior dorsal aspect of the main olfactory bulb (MOB), is the first brain relay of the accessory olfactory system (AOS), which can parallelly detect and process volatile and nonvolatile social chemosignals and mediate different sexual and social behaviors with the main olfactory system (MOS). However, due to its anatomical location and absence of specific markers, there is a lack of research on the internal and external neural circuits of the AOB. This issue was addressed by single-color labeling and fluorescent double labeling using retrograde rAAVs injected into the bed nucleus of the stria terminalis (BST), anterior cortical amygdalar area (ACo), medial amygdaloid nucleus (MeA), and posteromedial cortical amygdaloid area (PMCo) in mice. We demonstrated the effectiveness of this AOB projection neuron labeling method and showed that the mitral cells of the AOB exhibited efferent projection dispersion characteristics similar to those of the MOB. Moreover, there were significant differences in the number of neurons projected to different brain regions, which indicated that each mitral cell in the AOB could project to a different number of neurons in different cortices. These results provide a circuitry basis to help understand the mechanism by which pheromone information is encoded and decoded in the AOS

Amelioration of the neuroinhibitory local environment after ischemic injury through in situ astrocyte-to-neuron conversion

Ischemic injury in central nervous system (CNS) often causes severe neuronal loss and activates glial cells. We showed earlier that NeuroD1-mediated astrocyte-to-neuron (AtN) conversion can regenerate a substantial proportion of neurons (~40% of the total) and reconstruct the ischemic injured neural circuits. In this study, we focus on glial changes and blood vessel recovery following AtN conversion. Specifically, we found that ectopic expression of NeuroD1 in the reactive astrocytes after ischemic injury significantly reduced glial reactivity, as shown by less hypertrophic morphology, along with reduced secretion of neuroinhibitory factors such as CSPG and LCN2. As for microglia, we found less amoeboid shape of reactive microglia with reduced inflammatory factors such as IL-1β, TNFα. Moreover, blood vessels in the injured areas were repaired after AtN conversion and the blood-brain-barrier structure was restored. Whole tissue transcriptome sequencing identified significantly reduced reactive astrocyte genes and proinflammatory genes, as well as an upregulation of neurogenesis pathway and angiogenesis genes. Together, we demonstrate that NeuroD1-mediated astrocyte-to-neuron (AtN) conversion can alleviate glial scarring and inflammation to create a more neuropermissive micro-environment for functional recovery