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Background: The aim of this randomised prospective study is to compare the outcomes of traditional open trigger digit release versus ultrasound-guided modified small needle-knife (SNK) percutaneous release in the treatment of trigger digits. Methods: Patients with grade 2 and above trigger digits were enrolled into the study and randomly assigned to traditional open surgery (OS) or ultrasound-guided modified SNK percutaneous release group. The patients were followed up for 7, 30 and 180 days after treatment and data with regard to visual analogue scale (VAS) score and Quinnell grading (QG) was collected and compared between the two groups. Results: A total of 72 patients were enrolled in the study with 30 in the OS group and 42 in the SNK group. VAS scores and QG of the two groups significantly decreased at 7 days and 30 days after treatment compared to before treatment, but there was no significant difference between the two groups. There was also no differences between the two groups at 180 days and between the values at 30 days and 180 days. Conclusions: The outcomes of ultrasound-guided SNK percutaneous release is similar to traditional OS. Level of Evidence: Level II (Therapeutic)

In recent years, plentiful studies have uncovered the long noncoding RNA’s (lncRNA’s) momentous functions in osteonecrosis of the femoral head (ONFH), but the specific mechanism has not been fully illustrated. The study was to figure out lncRNA Zinc finger antisense 1 (LncZFAS1)’s biological function and its latent downstream molecular mechanism in glucocorticoid- (GC-) induced ONFH. The results manifested LncZFAS1 and transforming growth factor type III receptor (TGFBR3) were elevated, while microRNA- (miR-) 124-3p was reduced in ONFH tissues and cells. Knockdown LncZFA1 reduced rat femoral cell apoptosis, perfected bone microstructure and bone density, and accelerated osteogenic proteins bone morphogenetic protein- (BMP-) 9, BMP-3, and osteocalcin. In vitro studies manifested knockdown LncZFAS1 prevented GC-induced reduction in osteoblast advancement with facilitating osteoblast calcification capacity, ALP activity, and osteogenic proteins. Elevation of LncZFAS1 further aggravated GC-induced osteoblast injury, but this effect was turned around by enhancement of miR-124-3p or knockdown of TGFBR3. Mechanistically, LncZFAS1 performed as a sponge for miR-124-3p to mediate TGFBR3 expression to motivate GC-induced ONFH. All in all, the results of this study indicate the LncZFAS1/miR-124-3p/TGFBR3 axis is supposed to be a latent therapeutic molecular target for GC-induced ONFH.

Rationale: Rectal ectopic pregnancy is an extremely rare abdominal pregnancy. This article presents a female underwent an unsuccessful in vitro fertilization which was misdiagnosed by serum beta-human chorionic gonadotropin (β-hCG) test and transvaginal ultrasonography. Twenty days later, a ruptured rectal ectopic pregnancy was confirmed by laparoscopy then the gestational tissue removed successfully.Patient concerns: A 32-year-old Chinese female was admitted to our hospital with complaining of symptoms, like gradual worsening of lower abdominal pain and dysuria. The abdominal ultrasonography revealed a sac-like mass in the posterior area to the uterus and a moderate amount of free fluid in the pelvic cavity. Forty days ago, she underwent a frozen embryo transfer. Twenty days ago, her serum β-hCG level was <5 mIU/mL and neither intrauterine nor ectopic pregnancy was detected by transvaginal ultrasonography. Then the procedure was thought to have resulted in biochemical pregnancy failure.

Exosomes (Exo) originated from bone marrow mesenchymal stem cells (BMSCs) have therapeutic impacts on osteonecrosis of the femoral head (ONFH), and microRNA (miR)-532-5p has been confirmed to participate in ONFH progression. In the research, it was figured out whether BMSCs-Exo could relieve ONFH by delivering miR-532-5p. MG-63 cells were treated with DEX to construct an ONFH cell model in vitro. The effects of Exo and miR-532-5p on the cell viability, lactate dehydrogenase (LDH) content, and apoptosis of BMSCs were detected. The ONFH rat model was established, and the effect of BMSCs-Exo delivering miR-532-5p on the pathological damage of ONFH rats was evaluated. Changes in nuclear receptor coactivator-3 (NCOA3) and apoptotic proteins were assessed by western blot. The relationship between miR-532-5p and NCOA3 was verified by dual luciferase reporter experiments. miR-532-5p was elevated in vivo and in vitro ONFH-models, while NCOA3 expression was reduced. Overexpression of miR-532-5p aggravated DEX toxicity in osteoblasts, decreased cell viability, and promoted apoptosis. Knockdown of miR-532-5p made Exo further attenuate the toxic effect of DEX on osteoblasts and inhibited apoptosis. The protective effect of miR-532-5p-delivering Exo on osteoblasts was reversed by NCOA3 silencing. In addition, in vivo experiments also confirmed that knockdown of miR-532-5p enhanced the therapeutic effect of Exo on ONFH rats. This study demonstrates that miR-532-5p-delivering BMSCs-Exo inhibits osteoblast viability and promote apoptosis by targeting NCOA3, thereby aggravating ONFH development.