MOESM1 of Herpes zoster sciatica mimicking lumbar canal stenosis: a case report

Additional file 1. The present manuscript confirmed to CARE checklist

Locomotor recovery.

<p>Assessment of hind limb function with the Basso, Beattie and Bresnahan (BBB) locomotor scale (A, B). Time course of recovery of hindlimb function (A) and comparison of final motor function scores (B). Rats from the G-CSF group (closed circle) showed significant recovery compared to rats from the vehicle group (open circle) (A; Repeated measures ANOVA, p<0.05). The final motor function score six weeks after surgery in the G-CSF group (average 12.8; B, closed circle) was significantly higher than that in the vehicle group (average 9.7; B, open circle, p<0.01). The average score in the inclined plane test ten weeks after surgery in the G-CSF group (average 50 degrees; C, closed column) was significantly higher than that in the vehicle group (average 31.7 degrees; C, open column, p<0.01). Values are mean±S.E.M. *p<0.05, **p<0.01.</p

Granulocyte colony-stimulating factor receptor (G-CSFR) expression.

<p>Immunofluorescent double labeling for G-CSFR and cell-specific markers 1 week after surgery in vehicle-treated rats. Double-positive cells for G-CSFR and glial fibrillary acidic protein (GFAP, marker for astrocytes; A–C) and G-CSFR and myelin oligodendrocyte specific protein (MOSP, marker for oligodendrocytes; D–G) were detected. To show co-localization precisely, positive signal for G-CSFR/GFAP and G-CSFR/MOSP were detected using confocal laser microscopy (A–F) and 3-dimensional image was reconstructed (G). Bars = 50 µm.</p

MOESM1 of Resolution of low back symptoms after corrective surgery for dropped-head syndrome: a report of two cases

Additional file 1: CARE checklist for case reports. The present manuscript confirmed to CARE checklist

Granulocyte Colony-Stimulating Factor (G-CSF) Protects Oligpdendrocyte and Promotes Hindlimb Functional Recovery after Spinal Cord Injury in Rats

<div><h3>Background</h3><p>Granulocyte colony-stimulating factor (G-CSF) is a protein that stimulates differentiation, proliferation, and survival of cells in the granulocytic lineage. Recently, a neuroprotective effect of G-CSF was reported in a model of cerebral infarction and we previously reported the same effect in studies of murine spinal cord injury (SCI). The aim of the present study was to elucidate the potential therapeutic effect of G-CSF for SCI in rats.</p> <h3>Methods</h3><p>Adult female Sprague-Dawley rats were used in the present study. Contusive SCI was introduced using the Infinite Horizon Impactor (magnitude: 200 kilodyne). Recombinant human G-CSF (15.0 µg/kg) was administered by tail vein injection at 1 h after surgery and daily the next four days. The vehicle control rats received equal volumes of normal saline at the same time points.</p> <h3>Results</h3><p>Using a contusive SCI model to examine the neuroprotective potential of G-CSF, we found that G-CSF suppressed the expression of pro-inflammatory cytokine (IL-1 beta and TNF- alpha) in mRNA and protein levels. Histological assessment with luxol fast blue staining revealed that the area of white matter spared in the injured spinal cord was significantly larger in G-CSF-treated rats. Immunohistochemical analysis showed that G-CSF promoted up-regulation of anti-apoptotic protein Bcl-Xl on oligpodendrocytes and suppressed apoptosis of oligodendrocytes after SCI. Moreover, administration of G-CSF promoted better functional recovery of hind limbs.</p> <h3>Conclusions</h3><p>G-CSF protects oligodendrocyte from SCI-induced cell death via the suppression of inflammatory cytokines and up-regulation of anti-apoptotic protein. As a result, G-CSF attenuates white matter loss and promotes hindlimb functional recovery.</p> </div

G-CSF suppressed pro-inflammatory cytokine expression.

<p>Real time quantitative PCR and western blot analysis were performed to quantify mRNA and protein expression of pro-inflammatory cytokines in the acute phase of spinal cord injury. Values obtained were normalized to value of 18S ribosomal RNA expression and were expressed as the fold-increase over values of the G-CSF group 12 hours after surgery. The expression of interleukin-1 beta (IL-1 β, A) and tumor necrosis factor-alpha (TNF-α, B) mRNA was significantly suppressed in the G-CSF group (closed column) compared with the vehicle group (open column) 12 hours after surgery. Western blot analysis revealed that G-CSF suppressed the expression level of IL-1 β (C, upper row right, D, closed column, p<0.05) and TNF-α (C, middle row right, D, closed column, p<0.05). There was no significant difference between the vehicle and G-CSF groups in mRNA expression of FAS, FASL, IFN-γ, MMP-2 and MMP-9. Values are mean±SEM. *p<0.05.</p

G-CSF attenuated degeneration of white matter myelin.

<p>Luxol Fast Blue (LFB) staining and immunofluoresent staining for myelin basic protein (MBP) were performed to quantify spared myelin in the chronic phase of SCI. Figures show LFB staining of the spinal cord 4 mm caudal to the epicenter. Higher magnification revealed better myelin integrity in rats from the G-CSF group (D) than the vehicle group (C). The extent of loss of myelin in the chronic phase of injury (six weeks after surgery) was analyzed (Fig. 4–E). Gray matter of each sample was subtracted from the whole area of the slice to reveal the area of white matter. The actual area of normal-appearing myelin was divided by the white matter to determine the percentage of normal-appearing myelin. The percentage of normal appearing myelin was significantly larger in the G-CSF group (E; closed column) than the vehicle group (E; open column). Immunofluorescence showed that the number of MBP-positive myelin sheath was larger in the G-CSF group than that in the vehicle group (L). Bars = 1 mm (F–H), 500 µm (A, B) and 100 µm (C, D, I–K), values are mean±SEM. *p<0.05, **p<0.01. Values are mean±SEM. *p<0.05.</p

G-CSF suppressed apoptosis of oligodendrocytes <i>and promoted anti-apoptotic protein Bcl-Xl on oligodendrocytes.</i>

<p>Immunohistochemistry for adenomatous polyposis coli (APC; a marker for oligodendrocytes) and activated caspase 3 (a marker for apoptotic cells) in the acute phase of spinal cord injury. Representative figure of cells double-positive for APC and activated caspase 3 in the vehicle group 4 mm rostral to the lesion epicenter 1 week after injury is shown (A–C, arrowheads). The percentage of apoptotic oligoendrocytes was significantly smaller in the G-CSF group (closed column) than that in the vehicle group (open column) 72 hours (D) and one week (E) after surgery. <i>In vehice-treated control rats, Bcl-Xl/APC doubler-positive cells were not detected (I–K). In contrast, Bcl-Xl/APC doubler-positive Bcl-Xl expressing oligodendrocytes were observed in the spinal cord of G-CSF-treated rats (F–H).</i> Bars = 50 µm (A–C) and 100 µm (F–K). Values are mean±SEM. *p<0.05, **p<0.01.</p

G-CSF decreased the number of IL- β expressing leukocytes.

<p>Immunohistochemistry for IL-1β and myeloperoxidase (MPO) in the acute phase of injury. Near the lesion epicenter, IL-1β-positive round cells were also positive for MPO, a marker for leukocytes (A–C, arrowheads). The number of double positive cells for IL-1β and MPO was significantly smaller in the G-CSF group (D, closed column) than in the vehicle group (D, open column). Bars = 50 µm Values are mean±SEM. *p<0.05.</p