Table_1_Intraoperative hypotension in non-emergency decompression surgery for cervical spondylosis: The role of chronic arterial hypertension.DOCX

BackgroundCervical spondylotic myelopathy and chronic hypertension show a cause-effect relationship. Hypertension increases cardiovascular risk and is associated with intraoperative hypotension. We aimed to evaluate intraoperative hypotension in patients undergoing non-emergency decompression surgery for cervical spondylosis and its association with clinical myelopathy and chronic arterial hypertension.MethodsThis retrospective cohort study used healthcare data of adult patients undergoing cervical spine surgeries at Taipei Veterans General Hospital from 2015 to 2019. The primary outcomes were the incidence of intraoperative hypotension and predictive factors, and the secondary outcomes were the association of intraoperative hypotension and postoperative adverse outcomes in the surgical population.ResultsAmong the 1833 patients analyzed, 795 (43.4%) required vasopressor treatment and 342 (18.7%) showed persistent hypotension. Factors independent associated with hypotension after anesthetic induction were age [odds ratio (OR), 1.15; 95% confidence interval (CI), 1.07-1.23 per 5 years, P ConclusionIntraoperative hypotension is common even in non-emergency cervical spine surgery. A history of hypertension independently predicted intraoperative hypotension. Prompt assessments for identifiable features can help ameliorate intraoperative hypotension.</p

Local Delivery of High-Dose Chondroitinase ABC in the Sub-Acute Stage Promotes Axonal Outgrowth and Functional Recovery after Complete Spinal Cord Transection

<div><p>Chondroitin sulfate proteoglycans (CSPGs) are glial scar-associated molecules considered axonal regeneration inhibitors and can be digested by chondroitinase ABC (ChABC) to promote axonal regeneration after spinal cord injury (SCI). We previously demonstrated that intrathecal delivery of low-dose ChABC (1 U) in the acute stage of SCI promoted axonal regrowth and functional recovery. In this study, high-dose ChABC (50 U) introduced via intrathecal delivery induced subarachnoid hemorrhage and death within 48 h. However, most SCI patients are treated in the sub-acute or chronic stages, when the dense glial scar has formed and is minimally digested by intrathecal delivery of ChABC at the injury site. The present study investigated whether intraparenchymal delivery of ChABC in the sub-acute stage of complete spinal cord transection would promote axonal outgrowth and improve functional recovery. We observed no functional recovery following the low-dose ChABC (1 U or 5 U) treatments. Furthermore, animals treated with high-dose ChABC (50 U or 100 U) showed decreased CSPGs levels. The extent and area of the lesion were also dramatically decreased after ChABC treatment. The outgrowth of the regenerating axons was significantly increased, and some partially crossed the lesion site in the ChABC-treated groups. In addition, retrograde Fluoro-Gold (FG) labeling showed that the outgrowing axons could cross the lesion site and reach several brain stem nuclei involved in sensory and motor functions. The Basso, Beattie and Bresnahan (BBB) open field locomotor scores revealed that the ChABC treatment significantly improved functional recovery compared to the control group at eight weeks after treatment. Our study demonstrates that high-dose ChABC treatment in the sub-acute stage of SCI effectively improves glial scar digestion by reducing the lesion size and increasing axonal regrowth to the related functional nuclei, which promotes locomotor recovery. Thus, our results will aid in the treatment of spinal cord injury.</p></div

Fluoro-Gold (FG) retrogradely labeled neurons in the spinal cord.

<p>The presence of FG-positive neurons in the rostral stumps suggested that FG, which was injected at the T13 level, was absorbed by the anterogradely regenerating axons crossing the transection gap. In the control group, there were virtually no FG-positive neurons beyond the rostral stumps, demonstrating an absence of axonal regeneration (A, magnifications in A’-A”’). In contrast, there were many FG-positive neurons in the 50 U (B, magnifications in B’-B”’) and 100 U (C, magnifications in C’-C”’) ChABC-treated groups, showing that the ChABC treatment could promote axons to regenerate and cross the transection gap. Mean number of FG-positive neurons in the rostral spinal cord stump (D). There were no labeled neurons in the rostral spinal cord from the control groups. (n = 3 per group; *<i>p</i><0.05, one-way ANOVA, Tukey’s post hoc test). The error bars denote the SEM. Scale bars: A, B, C = 1000 μm; A’-A”‘, B’-B”’, C’-C”’ = 100 μm.</p

MOESM3 of The superiority of conditioned medium derived from rapidly expanded mesenchymal stem cells for neural repair

Additional file 3: Figure S2. The expression levels of 120 proteins in the CM of BM-MSCs by cytokine array analysis. Bar diagrams represent the ratio of the mean spot pixel density/positive-control spot pixel density. Antibody arrays were performed on two types of MSC-CM from each of three patients. The results are presented as the mean ± SEM

Flow diagram of the search process and search results.

Flow diagram of the search process and search results.</p

MOESM1 of The superiority of conditioned medium derived from rapidly expanded mesenchymal stem cells for neural repair

Additional file 1: Table S1. The list for BM-MSC from clinical patients

MOESM2 of The superiority of conditioned medium derived from rapidly expanded mesenchymal stem cells for neural repair

Additional file 2: Figure S1. Characterization of clinical/commercial BM-MSCs expanded in MSCGM or NLRM. (A) The bar chart shows the percentage of cell surface marker expression in MSCGM- or NRLM-expanded MSCs; the dotted line indicates 90%. (B) MSCs were cultured in chondrogenesis medium for 14 days, and alcian blue staining was used to detect matrix proteoglycan. MSCs were cultured in osteogenesis medium for 10 days, and the expression of alkaline phosphatase was detected by alkaline phosphatase substrate (Blue AP Substrate Kit SK-5300, Vector)

Forest plot for comparisons of pain scores during positioning before spinal anesthesia (within 30 min) subgroup by time from intervention to spinal anesthesia.

Forest plot for comparisons of pain scores during positioning before spinal anesthesia (within 30 min) subgroup by time from intervention to spinal anesthesia.</p

Time course of functional recovery in the high-dose ChABC-treated and control groups.

<p>The dotted line indicates the intraparenchymal injection of high-dose ChABC at 2 weeks after spinal cord transection. The BBB score shows that there was no significant improvement of the BBB score in the control group. In contrast, locomotion mildly improved with the 50 U and 100 U ChABC treatments. Statistical analysis demonstrated that locomotion significantly improved at 6 (50 U), 8 and 10 weeks (50 U and 100 U) compared to the control group, but there was no significant difference between the 50 U and 100 U ChABC-treated groups (A). After spinal cord contusive injury, there was no significant functional recovery in the ChABC-treated groups compared to the control group (B) (for transection, n = 6 per group; for contusion, n = 4 per group, *<i>p</i><0.05 for 50 U compared to the control; #<i>p</i><0.05 for 100 U compared to the control, two-way ANOVA, Tukey’s post hoc test). The error bars denote the SEM.</p

Characteristics of the included studies.

Characteristics of the included studies.</p