Ultrasound-Guided Prolotherapy with Polydeoxyribonucleotide for Painful Rotator Cuff Tendinopathy.

Background: Rotator cuff tendinopathy is a primary cause of shoulder pain and dysfunction. Several effective nonsurgical treatment methods have been described for chronic rotator cuff tendinopathy. Prolotherapy with polydeoxyribonucleotide (PDRN), which consists of active deoxyribonucleotide polymers that stimulate tissue repair, is a nonsurgical regenerative injection that may be a viable treatment option. The objective of this study was to assess the efficacy of PDRN in the treatment of chronic rotator cuff tendinopathy. Method: The records of patients with chronic rotator cuff tendinopathy (n=131) were reviewed retrospectively, and the patients treated with PDRN prolotherapy (n=32) were selected. We measured the main outcome of the shoulder pain and disability index score on a numerical rating scale of average shoulder pain. Results: Compared with baseline data, significant improvements in the shoulder pain and disability index and pain visual analog scale scores were demonstrated at one week after the end of treatment, and at one month and three months later. Conclusions: PDRN prolotherapy may improve the conservative treatment of painful rotator cuff tendinopathy for a specific subset of patients.

The effects of etomidate and midazolam on adipose tissue-derived mesenchymal stem cell proliferation.

BACKGROUND: Stem cell therapy using adipose tissue-derived mesenchymal stem cells (ADSCs), which are capable of multipotent differentiation, is currently being investigated in the field of tissue regeneration and the treatment of patients in intensive care units. It is known that type-A γ-aminobutyric acid (GABAA) receptor activity has an influence on stem cell proliferation. Thus, we investigated the effects of the clinically available GABAA receptor agonists, etomidate and midazolam, on ADSC proliferation measured by the cell counting kit-8 assay. METHODS: ADSCs cultured in control medium or adipogenic differentiation medium for 15 days were divided into 5 treatment groups: non-medicated (Control) and 4 groups including treatment with etomidate or midazolam at 1 and 50 µM (n = 3 per group). The cell counting kit-8 assay was performed for determining the cell proliferation in both medium groups at day 0, 3, 6, 9, 12, and 15 in culture. The absorbance values at 450 nm were then measured by enzyme-linked immunosorbent assay reader and statistically compared among groups. RESULTS: There was no significant difference in cell proliferation profiles among the 5 groups at any time point in both control and adipogenic differentiation media. CONCLUSIONS: Etomidate and midazolam did not influence ADSC proliferation under both media when compared to the non-medicated group and there was no dose-dependent effect of etomidate and midazolam on ADSC viability.