Bis(4-amino­benzene­sulfonato-κN)diaqua­bis(dimethyl­formamide-κO)nickel(II) dihydrate

In the title compound, [Ni(C6H6NO3S)2(C3H7NO)2(H2O)2]·2H2O, the NiII ion (site symmetry ) is coordinated by two –NH2 groups from two 4-amino­benzene­sulfonate anions, two O atoms from two dimethyl­formamide mol­ecules and two water mol­ecules, forming a slightly distorted trans-NiN2O4 octa­hedral geometry. In the crystal structure, inter­molecular O—H⋯O, O—H⋯(O,O) and N—H⋯O hydrogen bonds link the components into a three-dimensional network. The O atoms of the sulfonate group are disordered over two sets of sites in a 0.833 (4):0.167 (4) ratio and the O atom of the uncoordinated water mol­ecule is disordered over two sites in a 0.637 (18):0.363 (18) ratio

catena-Poly[[[tetra­aqua­iron(II)]-μ-5,5′-diazenediylditetra­zolido] dihydrate]

In the title compound, {[Fe(C2N10)(H2O)4]·2H2O}n, the coordin­ation geometry around the Fe(II) atom, which lies on a center of inversion, is distorted octa­hedral, with bonds to four O atoms and two N atoms. The azotetra­zolate ligand displays a bridging coordination mode, forming an infinite zigzag chain. Inter­molecular O—H⋯O and O—H⋯N hydrogen bonding and offset face-to-face π–π stacking inter­actions [centroid–centroid distance = 3.4738 (13) Å] lead to a three-dimensional network

(R)-7-Bromo-2,3,4,4a-tetra­hydro-1H-xanthen-1-one

The title compound, C13H11BrO2, contains a tricyclic ring system with one chiral center which exhibits an R configuration. The crystal structure is devoid of any classical hydrogen bonding

NG2 cells response to axonal alteration in the spinal cord white matter in mice with genetic disruption of neurofilament light subunit expression

<p>Abstract</p> <p>Background</p> <p>Chondroitin sulphate proteoglycan (NG2) expressing cells, morphologically characterized by multi-branched processes and small cell bodies, are the 4^thcommonest cell population of non-neuronal cell type in the central nervous system (CNS). They can interact with nodes of Ranvier, receive synaptic input, generate action potential and respond to some pathological stimuli, but the function of the cells is still unclear. We assumed the NG2 cells may play an active role in neuropathogenesis and aimed to determine if NG2 cells could sense and response to the alterations in the axonal contents caused by disruption of neurofilament light subunit (NFL) expression.</p> <p>Results</p> <p>In the early neuropathological development stage, our study showed that the diameter of axons of upper motor neurons of NFL-/- mice decreased significantly while the thickness of their myelin sheath increased remarkably. Although there was an obvious morphological distortion in axons with occasionally partial demyelination, no obvious changes in expression of myelin proteins was detected. Parallel to these changes in the axons and their myelination, the processes of NG2 cells were disconnected from the nodes of Ranvier and extended further, suggesting that these cells in the spinal cord white matter could sense the alteration in axonal contents caused by disruption of NFL expression before astrocytic and microglial activation.</p> <p>Conclusion</p> <p>The structural configuration determined by the NFL gene may be important for maintenance of normal morphology of myelinated axons. The NG2 cells might serve as an early sensor for the delivery of information from impaired neurons to the local environment.</p

Non-receptor tyrosine kinase Src is required for ischemia-stimulated neuronal cell proliferation via Raf/ERK/CREB activation in the dentate gyrus

<p>Abstract</p> <p>Background</p> <p>Neurogenesis in the adult mammalian hippocampus may contribute to repairing the brain after injury. However, Molecular mechanisms that regulate neuronal cell proliferation in the dentate gyrus (DG) following ischemic stroke insult are poorly understood. This study was designed to investigate the potential regulatory capacity of non-receptor tyrosine kinase Src on ischemia-stimulated cell proliferation in the adult DG and its underlying mechanism.</p> <p>Results</p> <p>Src kinase activated continuously in the DG 24 h and 72 h after transient global ischemia, while SU6656, the Src kinase inhibitor significantly decreased the number of bromodeoxyuridine (BrdU) labeling-positive cells of rats 7 days after cerebral ischemia in the DG, as well as down-regulated Raf phosphorylation at Tyr(340/341) site, and its down-stream signaling molecules ERK and CREB expression followed by 24 h and 72 h of reperfusion, suggesting a role of Src kinase as an enhancer on neuronal cell proliferation in the DG via modifying the Raf/ERK/CREB cascade. This hypothesis is supported by further findings that U0126, the ERK inhibitor, induced a reduction of adult hippocampal progenitor cells in DG after cerebral ischemia and down-regulated phospho-ERK and phospho-CREB expression, but no effect was detected on the activities of Src and Raf.</p> <p>Conclusion</p> <p>Src kinase increase numbers of newborn neuronal cells in the DG via the activation of Raf/ERK/CREB signaling cascade after cerebral ischemia.</p