BackgroundSome studies have shown significant functional improvement after rotator cuff (RC) repair in elderly patients. However, few studies have reported the healing potential of RC tears in elderly patients.MethodsTwenty-five patients aged ≥ 75 years who underwent RC repair were enrolled. The mean age at the time of surgery was 78.3 years (range, 75 to 88 years) while the mean follow-up was 36.3 months (range, 18 to 114 months). We evaluated clinical and structural outcomes after RC repair in the retear and healed groups.ResultsOf 25 patients, 16 (64%) had healed RC lesions and 9 (36%) had retorn cuff lesions. The retear rate increased significantly with increasing initial tear size (small to medium, 13%; large, 60%; massive, 80%; p = 0.024) but not with increasing age (p = 0.072). The mean visual analog scale (VAS), University of California Los Angeles (UCLA), and Constant scores significantly improved from 5.2, 15.8, and 49.3 preoperatively to 1.4, 31.1, and 71.9 in the healed group and from 6.0, 14.4, and 39.5 preoperatively to 2.4, 28.3, and 63.6 in the retear group at the final follow-up (p < 0.05, respectively). There were no significant differences in clinical outcomes between the 2 groups at the final follow-up. Retear was significantly correlated with initial tear size (p = 0.001; odds ratio [OR], 2.771; 95% confidence interval [CI], 1.394 to 5.509 for large to massive tears) (p = 0.001; OR, 0.183; 95% CI, 0.048 to 0.692 for small to medium tears).ConclusionsThere were significant improvements in clinical outcomes after RC repair in patients ≥ 75 years. Structural integrity after cuff repair did not affect the final clinical outcome. Even in elderly patients aged ≥ 75 years, healing of repaired RC can be expected in cases of small to medium tears. Although the retear rate was relatively high for large to massive tears, clinical outcomes still showed significant improvement.

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Oleic acid (OA) is released from brain phospholipids after cerebral ischaemia; however, its role in ischaemic injury remains unknown. We hypothesised that OA has neuroprotective effects after cerebral ischaemia, which may be exerted through peroxisome proliferator-activated receptor gamma (PPAR-γ) activation, since OA is an endogenous ligand of PPAR-γ. The effects of OA administration were evaluated in rodent models of middle cerebral artery occlusion (MCAO), photothrombosis, and four-vessel occlusion (4-VO). We determined the time window of therapeutic opportunity and examined the ability of the PPAR-γ antagonist GW9662 to reverse OA’s protective effects after MCAO. We found that OA administration decreased the MCAO-induced infarct volume and functional deficits, photothrombosis-induced infarct volume, and 4-VO-induced hippocampal neuronal death. Additionally, OA was highly efficacious when administered up to 3 h after MCAO. Pre-treatment with GW9662 abolished the inhibitory effects of OA on the infarct volume and immunoreactivity of key inflammatory mediators in the ischaemic cortex. Our results indicate that OA has neuroprotective effects against transient and permanent focal cerebral ischaemia, as well as global cerebral ischaemia. It may have therapeutic value for the ischaemic stroke treatment with a clinically feasible therapeutic window. The OA-mediated neuroprotection might be attributable to its anti-inflammatory actions through PPAR-γ activation.

Abstract:This study aimed to investigate the effects of Phlomis umbrosa root on bone growth and growth mediators in rats. Female adolescent rats were administered P. umbrosa extract, recombinant human growth hormone or vehicle for 10 days. Tetracycline was injected intraperitoneally to produce a glowing fluorescence band on the newly formed bone on day 8, and 5-bromo-2 1 -deoxyuridine was injected to label proliferating chondrocytes on days 8-10. To assess possible endocrine or autocrine/paracrine mechanisms, we evaluated insulin-like growth factor-1 (IGF-1), insulin-like growth factor binding protein-3 (IGFBP-3) or bone morphogenetic protein-2 (BMP-2) in response to P. umbrosa administration in either growth plate or serum. Oral administration of P. umbrosa significantly increased longitudinal bone growth rate, height of hypertrophic zone and chondrocyte proliferation of the proximal tibial growth plate. P. umbrosa also increased serum IGFBP-3 levels and upregulated the expressions of IGF-1 and BMP-2 in growth plate. In conclusion, P. umbrosa increases longitudinal bone growth rate by stimulating proliferation and hypertrophy of chondrocyte with the increment of circulating IGFBP-3. Regarding the immunohistochemical study, the effect of P. umbrosa may also be attributable to upregulation of local IGF-1 and BMP-2 expressions in the growth plate, which can be considered as a GH dependent autocrine/paracrine pathway.

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