Tendon-to-bone healing after repairing full-thickness rotator cuff tear with a triple-loaded single-row method in young patients.

BACKGROUND: Arthroscopic repair is recommended for young patients with full-thickness rotator cuff tears (RCTs), but the healing rates have raised concerns. The Southern California Orthopedic Institute (SCOI) row method has been developed based on greater than 3 decades of experience with excellent clinical outcomes; however, studies with a focus on the younger patient population are limited in number. The current study assessed the short-term clinical outcome and the initial tendon-to-bone healing in a young cohort after repair of a full-thickness RCT using the SCOI row method. METHODS: A retrospective cohort study was performed. Patients < 55 years of age who had a full-thickness RCT and underwent an arthroscopic repair using the SCOI row method were reviewed. Clinical outcomes were assessed at baseline, and 3 and 6 months post-operatively. The visual analog scale (VAS), University of California at Los Angeles (UCLA) scale, and Constant-Murley score were completed to assess pain and function. Active range of motion was also examined, including abduction and flexion of the involved shoulder. A preoperative MRI was obtained to assess the condition of the torn tendon, while 3- and 6-month postoperative MRIs were obtained to assess tendon-to-bone healing. Repeated measurement ANOVA and chi-square tests were used as indicated. RESULTS: Eighty-nine patients (57 males and 32 females) with a mean age of 44.1 ± 8.6 years who met the criteria were included in the study. Compared with baseline, clinical outcomes were significantly improved 3 and 6 months postoperatively based on improvement in the VAS, UCLA score, and Constant-Murley score, as well as range of motion. Greater improvement was also noted at the 6-month postoperative assessment compared to the 3-month postoperative assessment. Three- and six-month postoperative MRIs demonstrated intact repairs in all shoulders and footprint regeneration, which supported satisfactory tendon-to-bone healing. The mean thickness of regeneration tissue was 7.35 ± 0.76 and 7.75 ± 0.79 mm as measured from the 3- and 6-month MRI (P = 0.002). The total satisfactory rate was 93.3 %. CONCLUSIONS: Arthroscopic primary rotator cuff repair of a full-thickness RCT using the SCOI row method in patients < 55 years of age yields favorable clinical outcomes and early footprint regeneration.

Tianma Gouteng Decoction Exerts Cardiovascular Protection by Upregulating OPG and TRAIL in Spontaneously Hypertensive Rats.

Tianma Gouteng Decoction (TGD) is widely used in traditional Chinese medicine for the treatment of hypertension and its related complications, but its mechanisms remain incompletely defined. We now aim to assess the protective effect of TGD against cardiovascular damage and to investigate its characteristics and underlying mechanisms. Blood pressure was determined in TGD-treated spontaneously hypertensive rats (SHR) by noninvasive measurements. Echocardiography was performed to assess cardiac function and structure and sirius red staining to evaluate cardiac fibrosis, and the degree of vascular remodeling was evaluated. Additionally, vasoconstriction and relaxation factor expression changes were examined by means of ELISA. Protein expression changes were verified by western blot. Compared with untreated SHR, TGD-treated SHR exhibited cardiovascular traits more akin to those of the normotensive Wistar Kyoto (WKY) rats. That is, they had lower diastolic blood pressure, systolic blood pressure and mean BP, and increased expression of vasodilation factor. We also found that TGD reduces ventricular and vascular remodeling and improves cardiac function in SHR. Finally, we tested the antiapoptosis effect TGD exerts in SHR, ostensibly by upregulating the expression of OPG, TRAIL, and death receptor 5 (DR5) and downregulating caspases 8, 7, and 3. TRAIL may also exert antiapoptotic and prosurvival effects by upregulating AKT expression. Therefore, TGD may reverse cardiovascular remodeling in SHR by upregulating the expression of OPG and TRAIL, upregulating AKT, and inhibiting apoptosis, at least in part. For the first time, we have shown that OPG and TRAIL play complimentary cardioprotective roles in SHR.

A Simple Scoring Model for Prediction of Rupture Risk of Anterior Communicating Artery Aneurysms.

Background: The rupture risk of anterior communicating artery aneurysms (ACoAAs) has been known to be higher than that of aneurysms at other locations. Thus, the aim of this study is to investigate the clinical and morphological characteristics associated with risk factors for the rupture of ACoAAs. Methods: In total, 361 consecutive patients with 361 ACoAAs between August 2011 and December 2017 were retrospectively reviewed. Patients and ACoAAs were divided into ruptured and unruptured groups. In addition to clinical characteristics, ACoAA characteristics were evaluated by CT angiography (CTA). A multiple logistic regression analysis was used to identify the independent risk factors associated with ACoAA rupture. The assignment score of these variables depends on the ß coefficient. A receiver operating characteristic (ROC) curve analysis was used to calculate the optimal thresholds. Results: The multiple logistic regression model revealed that A1 dominance [odds ratio (OR) 3.034], an irregular shape (OR 3.358), and an aspect ratio ≥1.19 (AR; OR 3.163) increased the risk of rupture, while cerebral atherosclerosis (OR 0.080), and mean diameters ≥2.48 mm (OR 0.474) were negatively correlated with ACoAA rupture. Incorporating these five factors, the ROC analysis revealed that the threshold value of the multifactors was one, the sensitivity was 88.3%, and the specificity was 66.0%. Conclusions: The scoring model is a simple method that is based on A1 dominance, irregular shape, aspect ratio, cerebral atherosclerosis, and mean diameters from CTA and is of great value in the prediction of the rupture risk of ACoAAs.

Effects of the Long Non-Coding RNA HOST2 On the Proliferation, Migration, Invasion and Apoptosis of Human Osteosarcoma Cells.

BACKGROUND/AIMS: This study aimed to explore the effects of the long non-coding RNA HOST2 (lnc-HOST2) on the proliferation, migration, invasion and apoptosis of osteosarcoma cells. METHODS: Osteosarcoma tissues and adjacent normal tissues from 52 patients were selected. Human osteosarcoma cell lines (SaOS2, HOS, U2OS and MG-63) were collected and cultured; MG-63 cells had the highest lnc-HOST2 expression and thus were used in subsequent experiments. Then, MG-63 cells were transfected and divided into the blank (no transfection), si-CON (transfected with negative control siRNA) and si-lnc-HOST2 (transfected with small interference lnc-HOST2 siRNA) groups. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to determine the expression of lnc-HOST2 in primary tissues and cells. Cell growth was detected using the CCK-8 and colony formation assays. Cell doubling time was detected. Cell migration and invasion were observed using the scratch test and Transwell assays. Cell apoptosis and cell cycle progression of osteosarcoma cells were detected using flow cytometry with annexin V/PI double staining and PI staining, respectively. RESULTS: The level of lnc-HOST2 expression in the si-lnc-HOST2 group was significantly decreased compared to that in the blank and si-CON groups. The OD values in the si-lnc-HOST2 group were significantly lower than those in the blank and si-CON groups. Compared to the blank and si-CON groups, the si-lnc-HOST2 group presented significant decreases in the colony number and healing rates after scratching. The number of invasive cells in the si-lnc-HOST2 group was significantly less than that in the blank and si-CON groups. In the si-lnc-HOST2 group, the cell cycle was mainly halted in the G1 phase, and the apoptosis rate and doubling time in this group were significantly higher than those in the blank group and si-CON group. CONCLUSIONS: Inhibition of lnc-HOST2 could suppress the proliferation, migration, and invasion and promote the apoptosis of osteosarcoma cells.