Percutaneous Curved Vertebroplasty Versus Unilateral Percutaneous Vertebroplasty for Osteoporotic Vertebral Compression Fractures: A Systematic Review and Meta-Analysis.

BACKGROUND: Percutaneous curved vertebroplasty (PCVP), a modified traditional unilateral percutaneous vertebroplasty (UPVP) technique, is increasingly being used to treat osteoporotic vertebral compression fractures (OVCFs); however, its advantages remain controversial. This meta-analysis was conducted to determine whether PCVP is superior to traditional UPVP in treating OVCFs. METHODS: Six databases were searched for studies comparing the clinical efficacy of PCVP and UPVP in treating patients with OVCFs published until March 2023. After study selection, data extraction, and risk of bias evaluation, a meta-analysis was conducted. The study protocol was registered in the PROSPERO platform (registration number: CRD42023417190). RESULTS: Eight studies (6 randomized controlled trials and 2 cohort studies) were eligible for the final analysis. The pooled results revealed no between-group differences in operation time (P = 0.85), intraoperative fluoroscopy (P = 0.58), or postoperative short-term visual analog scale scores (P = 0.15). However, PCVP was associated with more injected cement (P = 0.003), a lower cement leakage rate (P = 0.006), and a lower final follow-up visual analog scale score (P < 0.0001). CONCLUSIONS: PCVP was superior to UPVP in terms of reducing the bone cement leakage rate and providing long-term pain relief. Further trials with larger sample sizes and longer follow-up periods are required to verify these findings owing to the potential risk of bias.

Long non-coding RNA-small nucleolar RNA host gene 7 regulates inflammatory responses following spinal cord injury by regulating the microRNA-449a/TNF-α-induced protein 3-interacting protein 2 axis.

The current study aimed to explore the anti-inflammatory effects of long non-coding RNA-small nucleolar RNA host gene 7 (lncRNA-SNHG7) and its mechanism in spinal cord injury (SCI) models. SCI models were established both in vivo and in vitro. Reverse transcription-quantitative PCR was performed to determine the expression levels of lncRNA-SNHG7 in SCI models. Bioinformatics analysis and dual-luciferase reporter assays were carried out to confirm the interaction between lncRNA-SNHG7 with microRNA (miR)-499a and TNF-α-induced protein 3-interacting protein 2 (TNIP2). In addition, cell viability, apoptosis, and the secretion of inflammatory cytokines were assessed by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay, flow cytometric analysis, and enzyme linked immunosorbent assay (ELISA), respectively. The results showed that lncRNA-SNHG7 was markedly downregulated in the SCI model group. LncRNA-SNHG7 directly bound to miR-499a, which in turn directly targeted TNIP2. In addition, TNIP2 was significantly decreased in SCI rats and lipopolysaccharide (LPS)-treated PC-12 cells. The in vitro results in PC-12 cells revealed that lncRNA-SNHG7 overexpression attenuated neuronal cell death and SCI-mediated inflammatory responses by regulating miR-449a expression. Furthermore, miR-499a knockdown inhibited LPS-induced PC-12 cell injury by targeting TNIP2. In conclusion, lncRNA-SNHG7 modulates the apoptosis and inflammation of PC-12 cells by regulating the miR-449a/TNIP2/NF-κB signaling pathway.

Leiomyoma of the prostate: A case report and systematic review.

Purpose: It is rare to find a large leiomyoma in the prostate, especially in that of a young man. This case report and systematic review provides additional information on the diagnosis, distinguishing features of imaging examinations, and treatment options. Patients and Methods: We report on the case of a thirty-year-old man with a large leiomyoma of the prostate. MRI of the prostate revealed a round mass in the posterior lobe, 8.0 × 8.0 × 5.5 cm in size. With the assistance of laparoscopy, we resected the prostate mass completely and spared this organ. A systematic review was conducted utilizing the Preferred Reporting Items for Systematic Reviews (PRISMA) including English language published reports, from 1970 to December 2021. Results: Urinary and erectile functioning was preserved postoperatively. After a year of follow-up, no evidence of recurrence emerged. A total of 21 studies were included for analysis. Conclusions: A medical history of no, or few, lower urinary tract symptoms; the characteristics of a benign tumor in imaging examinations; and negative tumor markers should be included in any differential diagnosis of leiomyoma of the prostrate. A prostate biopsy should be performed before the preparative radical prostatectomy and choose nonsurgical treatment to confirm the diagnosis. Nowadays, minimally invasive surgery is the preferred effective option for this disease. It is a rare recurrence after its removal by means of surgery.

Non Functioning Paraganglioma in the Urinary Bladder: a Case Report.

Paragangliomas are tumors that arise from autonomic nervous system. Non-functioning bladder paraganglioma is rare and usually misdiagnosed. Here we describe a case of a 45-year-old man with primary urinary bladder paraganglioma. The patient had no active signs and symptoms, and histological and immunohistological examinations of a transurethral resection specimen confirmed correct diagnosis. After successful transurethral resection of the tumors, the patient showed no signs of recurrence at one-year follow-up.

miR-101 Enhances Cisplatin-Induced DNA Damage Through Decreasing Nicotinamide Adenine Dinucleotide Phosphate Levels by Directly Repressing Tp53-Induced Glycolysis and Apoptosis Regulator Expression in Prostate Cancer Cells.

Tp53-induced glycolysis and apoptosis regulator (TIGAR) enhances the pentose phosphate pathway, thereby contributing directly to DNA repair due to generation of nicotinamide adenine dinucleotide phosphate (NADPH) and ribose-5-phosphate, two key precursors of DNA synthesis and repair. Targetscan database showed that miR-101 was predicted to potentially target TIGAR. Therefore, we speculated that miR-101 could enhance cisplatin-induced DNA damage by directly repressing TIGAR expression in prostate cancer cells. We found that upregulation of miR-101 inhibited viability, induced apoptosis, increased glycolysis rate and fructose-2,6-bisphosphate levels, decreased glucose-6-phosphate dehydrogenase expression and NADPH levels, and enhanced cisplatin-induced DNA damage in prostate cancer cells. We also demonstrated that TIGAR was a direct target of miR-101 by using luciferase activity assay. Furthermore, this study revealed that the roles of knockdown of TIGAR were similar to miR-101 upregulation in prostate cancer cells. Taken together, miR-101 inhibited viability, induced apoptosis, reprogramed glucose metabolism, and enhanced cisplatin-induced DNA damage through decreasing NADPH levels by directly suppressing the expression of TIGAR in prostate cancer cells.