Additional file 2: Table S2. of Pneumococcal meningitis: Clinical-pathological correlations (meningene-path)

Summary of statistical analysis of pathological findings in relation to clinical characteristics. (DOC 42 kb

GFAP⁺¹ cross-reactivity with neurofilament-L is removed by affinity purification.

<p>A Western blot on human spinal cord filaments revealed two bands (∼50 kDa and ∼70 kDa) when stained with the unpurified GFAP⁺¹ antibody (A, unpur). After affinity purification of the antibody only the lower band was left (A, pur). On a western blot that was double-stained for different GFAP⁺¹ antisera (green) and NF-L (red), the 70 kDa unpurified GFAP⁺¹ band showed co-localization with NF-L (B, up, yellow band). This was gone with the purified antibody, which only stained one GFAP⁺¹ band at 50 kDa (B, pur, green band). With the pre-immune serum of the GFAP⁺¹ immunized rabbit, no staining was detected (B, pi). The original unpurified GFAP⁺¹ antibody stained both neurons and astrocytes in the hippocampus of an AD brain (C, NBB 93-040). These GFAP⁺¹ (green) neurons often co-localized with NF-L (red) (D, NBB 01-125), but the astrocytes did not (E, NBB 01-119). The purified GFAP⁺¹ antibody only stained a subpopulation of astrocytes (F, NBB 95-102). Scale bars represent 100 µm (C, F), 50 µm (D–E).</p

Detailed donor information.

<p>NBB = Netherlands Brain bank; AMC = Amsterdam Medical Center; SVZ = Subventricular zone; N.A. = Not Available.</p

Sequence homology between neurofilament-L and the GFAP⁺¹ antibody epitope.

<p>Some homology (green and yellow highlights) was found between the tail domain of NF-L (red letters) and the GFAP⁺¹ antibody epitope (blue letters).</p

Dimensional transmutation in quantum theory

This work deals with two models - from the quantum eld theory it is the massless scalar electrodynamics (the so-called Coleman-Weinberg model) and from quantum mechanics it is the contact (-function) potential (in two dimensions) - that are apparently invariant under some sort of scale transformations and thus they, in suitably chosen units, contain only dimensionless parameters. It turns out that even in the quantum-mechanical case one has to add an additional procedure to the formal denition of the model and that the use of dierent physical regulators leads to the same results, that furthermore agree with the predictions of the mathematically rigorous method of self-adjoint operator extensions. In this work, we present detailed calculations supporting this result. Contrary to the common literature, we do so in a straightforward manner, which can be followed step by step (with all the necessary elements of functional analysis summarised in the Appendix). In quantum eld theory we apply a similar approach, when we "rediscover" the results of the abstract functional methods in the ordinary perturbation theory. In its framework, we further show how to obtain predictions also for other quantities than particle masses

GFAP⁺¹ expressing astrocytes in different areas of the human CNS.

<p>No GFAP⁺¹ expression is detected in the developing hippocampus of a 16 week old human fetus (A), or in the hippocampus of a 39 year old healthy female, neither in the dentate gyrus/hilus (B) nor in CA1 (C) or CA3 (D) regions. The purified GFAP⁺¹ antibody clearly stained a subpopulation of astrocytes throughout the brain, e.g. in the caudate/putamen (E–F), along the subventricular zone of the lateral ventricle beneath the cingulate gyrus (G) and in the most posterior part of the lateral ventricle (H). Often cells were found contacting blood vessels (E–F, arrows). A relatively large number of GFAP⁺¹ expressing cells was detected in the human spinal cord (I–J). Most expression was found near the meninges (arrowheads), in the anterior horn (arrow) and in the grey commissure around the central canal (asterix) as shown in half of a transverse section (I). A GFAP⁺¹ expressing cell and surrounding processes are shown in more detail in a longitudinal section (J). Pan-GFAP staining reveals many reactive astrocytes in the hippocampus (K), which clearly show intense GFAP expression and hypertrophic cell bodies in a magnified image of the squared area (K'). GFAP⁺¹ staining in the same area of an adjacent section shows no staining at all (L), indicating GFAP⁺¹ does not generally mark reactive astrocytes. NBB 01-021 (E), NBB 02-013 (F), NBB 07-006 (G-H), AMC 06/9 (I–J), NBB 05-083 (K–L). Scale bars represent 500 µm (A–B, K–L), 200 µm (C–D),100 µm (E, G–H, J, 50 µm (B, K'), 1 mm (I).</p

Neuron-like staining by different GFAP antibodies.

<p>Neuron-like structures are stained by the GFAP⁺¹ (A), GFAP C-terminal (B) and GFAP N-terminal (C) antibody (arrows). The C-terminal and N-terminal antibodies also stain astrocytes (B–C, arrowheads). Double-labeling of pan-GFAP (black) and neurofilament (brown) (D–E) shows that neuron-like structures stained by GFAP (E, arrowheads) are surrounded by neurofilament positive neurons (E, arrow), but do not co-localize. NBB 96-058 (A–C), NBB 88-073 (D–E). Scale bars represent 100 µm (A–C), 200 µm (D), 25 µm (E).</p

Additional file 1: Figure S1. of Complement activation at the motor end-plates in amyotrophic lateral sclerosis

Representative confocal immunofluorescence for synaptophysin (SYN-Cy3) detecting the motor nerve terminal (A, B) or S100b (Cy3) detecting the terminal Schwann cells (C, D) double stained with anti-C1q (FITC) in control (A, C) and ALS (B, D) intercostal muscle shows C1q co-localizing with both synaptophysin and S100b (white arrow in B and D, respectively) but no C1q deposition in controls. (TIF 1461 kb

Additional file 4: Figure S4. of Complement activation at the motor end-plates in amyotrophic lateral sclerosis

Representative confocal immunofluorescence for synaptophysin (SYN-Cy3) detecting the motor nerve terminal (A, B) or S100b (Cy3) detecting the terminal Schwann cells (C, D) double stained with anti-CD55 (FITC) in control (A, C) and ALS (B, D) intercostal muscle shows CD55 co-localizing with both synaptophysin and S100b (white arrow in B and D, respectively) but no CD55 deposition in controls. (TIF 1271 kb

Expression levels of the miR-146a targets (IRAK-1, IRAK-2 and TRAF-6) after transfection with anti-miR-146a LNA or miR-146a mimic.

<p>(<b>A–C</b>) Quantitative real-time PCR of IRAK-1 (A), IRAK-2 (B) and TRAF-6 (C) expression 24 hours after exposure to IL-1β in U373 glioblastoma cell line transfected with LNA-antimiR-146a (25 nM) or miR-146a mimic (pre-mir-146a, 50 nM). (<b>D</b>) Quantitative real-time PCR of IRAK-1, 24 hours after exposure to IL-1β in cultured human astrocytes transfected with LNA anti-miR-146a (50 nM) or miR-146a mimic (pre-mir-146a, 50 nM). Data are expressed relative to the levels in unstimulated cells and are mean ± SEM from two separate experiments performed in triplicate (<b>E</b>) IRAK-1 protein expression 24 hours after exposure to IL-1β in glial cells transfected with LNA anti-miR-146a (50 nM) or miR-146a mimic (pre-mir-146a, 50 nM); Representative immunoblot (1 control; 2, IL-1β; 3, IL-1β + LNA-antimiR-146a; 4, IL-1β + LNA-antimiR-146a scramble; 5, IL-1β + mimic; 6, IL-1β + mimic scramble) and optical density measurements. Data are expressed relative to the levels in unstimulated cells and are mean ± SEM from two separate experiments (*p<0.05, compared to control; **p<0.05, LNA or mimic transfected cells stimulated with IL-1β compared to IL-1β alone).</p