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Background The retro superior costotransverse ligament space (RSS) block, reported as a novel target in paraspinal block, involves the spreading of local anesthetics into the thoracic paravertebral space through slits around the superior costotransverse ligament. This blocks not only the dorsal rami but also the ventral rami, achieving a reliable complete sensory blockade. Case We performed an RSS block at the T5, T7, and T9 levels on both sides for postoperative analgesia in two patients who underwent laparoscopic gastrectomy. Both patients showed complete sensory blockade from T4 to L1 on the anterior, lateral, and posterior chest walls in the recovery room. The resting and dynamic pain scores were 0 at 30 min and 6 h postoperatively. The pain score consistently remained below 3 throughout postoperative period. Conclusions The RSS block provided effective postoperative analgesia in laparoscopic gastrectomy through definitive complete sensory blockade.

Objectives This study aimed to investigate the epidemiology of intravenous midazolam-induced postoperative expressive aphasia (EA). Methods The incidence rate, risk ratio, and contributing factors to intravenous midazolam-induced postoperative EA were analyzed retrospectively in 6756 orthopedic patients. A telephone interview was conducted with patients with EA after surgery. Results Patients were allocated to either the midazolam group (n = 6178) or no-midazolam group (n = 578). Twelve patients developed EA in the midazolam group, with an incidence of 0.19%, and no patient developed EA in the no-midazolam group. The mean age of EA patients was 70 years, and 92% were women. Among them, 75% received general anesthesia, and the mean dose of midazolam was 1.8 mg. EA was reversed in nine of 12 (75%) patients within 4 minutes of flumazenil administration, and >60 minutes were required to reverse EA in the other three patients (25%). Conclusion Intravenous midazolam administration for preoperative sedation caused transient EA in 0.19% of patients, especially elderly women who received general anesthesia, and EA could be reversed by flumazenil.

Background: Although case reports have suggested that the erector spinae plane block (ESPB) may help analgesia for patients after breast surgery, no study to date has assessed its effectiveness. This retrospective observational study analyzed the analgesic effects of the ESPB after total mastectomy. Methods: Forty-eight patients were divided into an ESPB group (n = 20) and a control group (n = 28). Twenty patients in the control group were selected by their propensity score matching the twenty patients in the ESPB group. Patients in the ESPB group were injected with 30 mL 0.375% ropivacaine, followed by catheter insertion for further injections of local anesthetics every 12 hours. Primarily, total fentanyl consumption was compared between the two groups during the first 24 hours postoperatively. Secondary outcomes included pain intensity levels (visual analogue scale) and incidence of postoperative nausea and vomiting (PONV). Results: Median cumulative fentanyl consumption during the first 24 hours was significantly lower in the ESPB (33.0 g; interquartile range [IQR], 27.0-69.5 g) than in the control group (92.8 g; IQR, 40.0-155.0 g) (P = 0.004). Pain level in the early postoperative stage (＜3 hr) and incidence of PONV (0% vs. 55%) were also significantly lower in the ESPB group compared to the control (P = 0.001). Conclusions: Intermittent ESPB after total mastectomy reduces fentanyl consumption and early postoperative pain. ESPB is a good option for multimodal analgesia after breast surgery. [ABSTRACT FROM AUTHOR]

Epigenetic regulation by the type II protein arginine methyltransferase, PRMT5, plays an essential role in the control of cancer cell proliferation and tumorigenesis. In this report, we investigate the relationship between PRMT5 and WNT/β- CATENIN as well as AKT/GSK3β proliferative signaling in three different types of non-Hodgkin's lymphoma cell lines, clinical samples, and mouse primary lymphoma cells. We show that PRMT5 stimulates WNT/β-CATENIN signaling through direct epigenetic silencing of pathway antagonists, AXIN2 and WIF1, and indirect activation of AKT/GSK3β signaling.PRMT5 inhibition with either shRNA-mediated knockdown or a specific small molecule PRMT5 inhibitor, CMP-5, not only leads to derepression ofWNTantagonists and decreased levels of active phospho-AKT (Thr-450 and Ser-473) and inactive phospho- GSK3β (Ser-9) but also results in decreased transcription of WNT/β-CATENIN target genes, CYCLIN D1, c-MYC, and SURVIVIN, and enhanced lymphoma cell death. Furthermore, PRMT5inhibition leads to reduced recruitment of co-activators CBP, p300, and MLL1, as well as enhanced recruitment of co-repressors HDAC2 and LSD1 to the WNT/β-CATENIN target gene promoters. These results indicate that PRMT5 governs expression of prosurvival genes by promoting WNT/β- CATENIN and AKT/GSK3β proliferative signaling and that its inhibition induces lymphoma cell death, which warrants further clinical evaluation. [ABSTRACT FROM AUTHOR]

Background: PRMT5, PRC2, and cyclin D1 are overexpressed in non-Hodgkin lymphoma (NHL). Results: PRMT5 expression inversely correlates with levels of hypophospho-RB1 and RBL2. Conclusion: PRMT5 inhibition reactivates RB1 and RBL2 and silences PRC2 and cyclin D1. Significance: PRMT5 inhibition results in NHL growth arrest and cell death. [ABSTRACT FROM AUTHOR]

Protein arginine methyltransferase-5 (PRMT5) is overexpressed in aggressive B-cell non-Hodgkin's lymphomas, including mantle cell lymphoma and diffuse large B-cell lymphoma, and supports constitutive expression of CYCLIN D1 and c-MYC. Here, we combined ChIP analysis with next-generation sequencing to identify microRNA (miRNA) genes that are targeted by PRMT5 in aggressive lymphoma cell lines. We identified enrichment of histone 3 dimethylation at Arg-8 (H3(Me2)R8) in the promoter regions of miR33b, miR96, and miR503. PRMT5 knockdown de-repressed transcription of all three miRNAs, accompanied by loss of recruitment of epigenetic repressor complexes containing PRMT5 and either histone deacetylase 2 (HDAC2) or HDAC3, enhanced binding of co-activator complexes containing p300 or CREB-binding protein (CBP), and increased acetylation of specific histones, including H2BK12, H3K9, H3K14, and H4K8 at the miRNA promoters. Re-expression of individual miRNAs in B-cell lymphoma cells down-regulated expression of PRMT5, CYCLIN D1, and c-MYC, which are all predicted targets of these miRNAs, and reduced lymphoma cell survival. Luciferase reporter assays with WT and mutant 3'UTRs of CYCLIN D1 and c-MYC mRNAs revealed that binding sites for miR33b, miR96, and miR503 are critical for translational regulation of the transcripts of these two genes. Our findings link altered PRMT5 expression to transcriptional silencing of tumor-suppressing miRNAs in lymphoma cells and reinforce PRMT5's relevance for promoting lymphoma cell growth and survival. [ABSTRACT FROM AUTHOR]