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)

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

Incidences of spinal cord injury (1998–2008).

†<p>per 100,000 person-year.</p

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

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

Adjusted incidence ratios in pediatric spinal cord injury (n = 4949).

<p>Pre-school age: 0–5 years; School age: 6–12 years; Teenagers: 13–18 years; Young adults: 19 years and above.</p

Proportional composition of traumatic causes of spinal cord injury.

<p>C, cervical; T, thoracic; L, lumbar.</p

Highly Sensitive Ammonia Sensor with Organic Vertical Nanojunctions for Noninvasive Detection of Hepatic Injury

We successfully demonstrate the first solid-state sensor to have reliable responses to breath ammonia of rat. For thioacetamide (TAA)-induced hepatopathy rats, we observe that the proposed sensor can detect liver that undergoes acute–moderate hepatopathy with a <i>p</i>-value less than 0.05. The proposed sensor is an organic diode with vertical nanojunctions produced by using low-cost colloidal lithography. Its simple structure and low production cost facilitates the development of point-of-care technology. We also anticipate that the study is a starting point for investigating sophisticated breath-ammonia-related disease models

Characteristics of the spinal cord injury group versus the comparison cohort.

<p>Pre-school age: 0–5 years; School age: 6–12 years; Teenagers: 13–18 years.</p