ESI-MS/MS analysis of lipoprotein loaded macrophages and native LDL, oxLDL and eLDL.

<p>(A) eLDL induced significant accumulation of mono- and polyunsaturated lipid species in macrophages. oxLDL only elevated levels of monounsaturated species. (B) Lipid compositional analysis of lipoproteins. oxLDL showed substantially decreased levels of mono- and polyunsaturated lipids compared to native LDL. Saturated lipid species were decreased in eLDL, but increased in oxLDL. Mean and standard deviation of six (A) or eleven (B) replicates from different donors. Mann-Whitney <i>U</i> test: *p<0.05, **p<0.01.</p

Changes in NMR-visible lipids as consequence of loading macrophages with modified LDL.

<p>(A) Moderate mobile lipid signals were present in NMR spectra of native macrophages (control). Loading with native LDL or oxLDL did not result in any significant increase of mobile lipid intensities, whereas eLDL loading gave rise to a dominant lipid signal increase. NMR spectral parameters: 800 MHz spectrometer frequency, gradient-based water suppression pulse sequence (zgesgp) with additional water presaturation, 3.7 s repetition time, temperature: 5°C. Spectra were normalized to protein and/or glutathione (GSH) signal intensities. Spectral annotation according to dominant contributions to NMR signals. (B) The NMR-visible lipid content, i.e. the integral in arbitrary units over the deconvolved NMR signal of the terminal methyl group of fatty acid chains. (C) The average percentage of <i>bis-</i>allylic methylene per fatty acid chain in control macrophages and macrophages loaded with native LDL, oxLDL and eLDL, i.e. the ratio of NMR-visible <i>bis-</i>allylic methylene groups and methyl groups. Deconvolved peaks of (-CH = CH-CH₂-CH = CH-)- and (-CH₃)-protons were integrated. Mean and standard deviation of five samples from different donors, N = 5 except for “LDL” (N = 4). Mann-Whitney <i>U</i> test: **p<0.01.</p

Risk of glioma in patients using etodoloac, meloxicam, celecoxib, rofecoxib, etoricoxib, valdecoxib, lumiracoxib or diclofenac.

<p>Risk of glioma in patients using etodoloac, meloxicam, celecoxib, rofecoxib, etoricoxib, valdecoxib, lumiracoxib or diclofenac.</p

Human in vitro reporter model of neuronal development and early differentiation processes-2

could induce the expression of the DCX-promoter-EGFP reporter (A-H). NTERA-2cells inducing the expression of EGFP upon retinoic acid treatment (I), also expressed DCX (J) and frequently Map2 (K). Parallel upregulation of the EGFP reporter and DCX mRNAs (M) and proteins (N) upon retinoic acid differentiation could also be detected in NTERA-2 clones, but not in HeLa clones. Induction of a neurogenic differentiation program following transient transfection of mouse Ngn2 also resulted in a significant induction of DCX-promoter-luciferase reporter in NTERA-2 clones, but not in HeLa clones (O).<p><b>Copyright information:</b></p><p>Taken from "Human in vitro reporter model of neuronal development and early differentiation processes"</p><p>http://www.biomedcentral.com/1471-2202/9/31</p><p>BMC Neuroscience 2008;9():31-31.</p><p>Published online 29 Feb 2008</p><p>PMCID:PMC2270856.</p><p></p

Characteristics of glioma cases and controls.

<p>Characteristics of glioma cases and controls.</p

Spontaneous recovery of locomotion.

<p>Postoperative assessment of the modified 12-point BBB open field locomotor rating scale in 8 adult rats after a 200 kDyn mid-thoracic spinal cord contusion. Animals were monitored weekly starting day 1 post-injury until post-op day 40.</p

Human in vitro reporter model of neuronal development and early differentiation processes-3

ERA-2 cells (A . G) and D283 cells (B . H) showed a morphological response to retinoic acid. PC12 cells treated with NGF developed a complex network of cellular processes (I inset). Scale bar in L = 100 μm.<p><b>Copyright information:</b></p><p>Taken from "Human in vitro reporter model of neuronal development and early differentiation processes"</p><p>http://www.biomedcentral.com/1471-2202/9/31</p><p>BMC Neuroscience 2008;9():31-31.</p><p>Published online 29 Feb 2008</p><p>PMCID:PMC2270856.</p><p></p

Post SCI cell renewal in motor cortex, subventricular zone, corpus callosum and hippocampus.

<p>(A, D, G, J) Quantification of BrdU positive cells in control (Intact) versus spinal cord injured (SCI) animals in the motor cortex (MC; A), subventricular zone (SVZ; D), corpus callosum (CC; G) and hippocampus (HC; H). Brightfield micrographs display cell renewal represented by BrdU immunoreactive nuclei in the MC (B, C), SVZ (E, F), CC (H, I) and HC (K, L) of control (Intact; B, E, H, K) and injured animals (C, F, I, L). Scale bar: 50 µm in (L).</p

Characteristics of meningioma cases and controls.

<p>Characteristics of meningioma cases and controls.</p

Post SCI cell renewal in the cervical spinal cord.

<p>Coronal spinal cord sections were analyzed in the parenchyma and around the central canal. (A) Quantification of BrdU positive surviving newborn cells in the spinal parenchyma and around the central canal of intact and SCI animals. BrdU positive nuclei in the lateral white matter (B, C) and in the ependymal layer of the central canal (D, E) of intact and injured animals (SCI). (F) Quantification of BrdU positive cells expressing GFAP representing astroglia; BrdU positive cells co-localizing with APC, but negative for GFAP, were counted as oligodendrocytes. (G-J) Immunofluorescent labeling for (G) BrdU (red), (H) APC (green) and (I) GFAP (blue) in a coronal cervical spinal cord section of an injured animal taken from the ventral gray matter. (J) Merged image of (G-I). Co-localization of BrdU with GFAP indicates astroglial differentiation (arrow), whereas BrdU/APC positive cells that are GFAP-negative represent oligodendrocytes (arrowhead). Scale bars: 100 µm in (C), 50 µm in (E), 34.1 µm in (J).</p