Patients with relapsed/refractory AL amyloidosis (RRAL) have poor prognosis, but emerging data shows promising results with the use daratumumab. We evaluated daratumumab treatment in RRAL in real-world setting. A retrospective multisite study of RRAL patients treated with daratumumab alone and in combinations. Forty-nine patients, diagnosed between 1.1.2008 and 1.2.2018 were included; 27% also had multiple myeloma (MM). Revised Mayo score was≥3 in 67%. Hematologic overall response rate was 81%, 64% achieved very good partial response (VGPR) or better. Concurrent active MM was associated with lower rates of VGPR (OR 0.19, 95% CI 0.04-0.81; P=.03) in a multi-variate analysis. Cardiac and renal responses were 74% and 73%, respectively. Median progression-free survival (PFS) was 28.4months and median overall survival (OS) was not reached; 2-year PFS and OS were 68.6±7.5% and 90.4±4.6%, respectively. Hematologic response correlated with prolonged PFS and OS. Daratumumab was safe and well tolerated, no patients discontinued therapy due to toxicity. Our data was aligned with outcomes from a systematic literature review, which identified 10 case series (n=517) and 2 clinical trials (n=62) meeting prespecified criteria. Our data support favorable safety tolerability and efficacy of daratumumab among non-selective RRAL patients in a real-world setting.Our data support favorable safety tolerability and efficacy of daratumumab among non-selective RRAL patients in a real-world setting.Iatrogenic nerve injury during surgery is a major source of concern for both patients and surgeons. This study aimed to identify the nerves most commonly injured during surgery, along with the commonly associated operative procedures. A literature search was conducted using the PubMed database to identify nerves commonly injured during surgery, along with the surgical procedure associated with the injury. The following 11 nerves, ranked in order with their associated surgical procedures, were found to be the most commonly injured (a) intercostobrachial nerve in axillary lymph node dissections and transaxillary breast augmentations, (b) vestibulocochlear nerve in cerebellopontine tumor resections and vestibular schwannoma removals, c) facial nerve in surgeries of the inner ear and cheek region, (d) long thoracic nerve in axillary lymph node dissections, (e) spinal accessory nerve in surgeries of the posterior triangle of the neck and cervical lymph node biopsies, (f) recurrent laryngeal nerve in thyroid surgeries, (g) genitofemoral nerve in inguinal hernia and varicocele surgeries, (h) sciatic nerve in acetabular fracture repairs and osteotomies, (i) median nerve in carpal tunnel release surgeries, (j) common fibular nerve in varicose vein and short saphenous vein surgeries, and (k) ulnar nerve in supracondylar fracture surgeries. Although the root cause of iatrogenic nerve injury differs for each nerve, there are four unifying factors that could potentially decrease this risk for all peripheral nerves. These four influencing factors include knowledge of potential anatomical variations, visual identification of at-risk nerves during the procedure, intraoperative nerve monitoring, and expertise of the surgeon.Emerging evidence suggests that miR-143 plays an important role in the regulation of tumor sensitivity to chemotherapeutic agents. The study explores the underlying mechanism of miR-143 in reversing cisplatin resistance in ovarian cancer. The cisplatin-resistant ovarian cancer cell line A2780/CDDP was induced and established via treating A2780 cells by gradually increasing cisplatin concentrations. The IC50 values of A2780/CDDP and A2780 to cisplatin were 218.10 ± 1.12 and 21.99 ± 1.12 μM, respectively. Quantitative real-time polymerase chain reaction (qRT-PCR) results showed that miR-143 was significantly decreased in A2780/CDDP cells compared with A2780 cells. miR-143 overexpression decreased cisplatin resistance in A2780/CDDP, and miR-143 inhibition decreased A2780 sensitivity to cisplatin. Results of qRT-PCR, Western blot analysis, and luciferase reporter assay indicated that the direct target of miR-143 was DNMT3A, which, in turn, was upregulated in A2780/CDDP. AF353 DNMT3A overexpression antagonized the sensitizing effect of miR-143 on A2780/CDDP to cisplatin. Knocking down of DNMT3A reduced cisplatin resistance in A2780/CDDP, while overexpression of DNMT3A increased cisplatin resistance in A2780. Methylation-specific polymerase chain reaction results showed that the methylation level in the promoter region of the miR-143 precursor gene was higher in A2780/CDDP cells than in A2780 cells. DNMT3A mediated the hypermethylation of the miR-143 precursor gene, resulting in miR-143 downregulation in A2780/CDDP. miR-143 inhibited cell growth of A2780/CDDP cell in nude mice. Our findings indicated the negative feedback between miR-143 and DNMT3A as a crucial epigenetic modifier of cisplatin resistance in ovarian cancer.Thymoquinone (TQ), the main active constituent of Nigella sativa seeds, has been shown to play a role in antioxidation, anti-inflammation, and antitumor. Recent studies have demonstrated that TQ contributes to the suppression of liver fibrosis. Abnormal activated epithelial-mesenchymal transition (EMT) promotes the activation of hepatic stellate cells (HSCs). However, whether the antifibrotic effects of TQ occur through inhibiting EMT is largely unknown. In this study, it was found that TQ ameliorated liver fibrosis and collagen accumulation in carbon tetrachloride (CCl4) mice. In vitro, TQ inhibited HSC activation including reduced proliferation, α-smooth muscle actin, and collagen. In addition, TQ markedly suppressed the EMT process, with enhanced E-cadherin and reduced desmin. Notably, snail family transcriptional repressor 1 (Snai1), the EMT master transcription factor, was obviously inhibited by TQ in vivo and in vitro. Further studies demonstrated that Snai1 was a target of microRNA-30a (miR-30a), which was upregulated by TQ. Interestingly, the effects of TQ on HSC activation and EMT were almost inhibited by miR-30a inhibitor. Collectively, we demonstrate that TQ inhibits HSC activation, at least in part, via regulation of miR-30a and Snai1. TQ upregulates miR-30a expression, resulting in a reduced Snai1 level as well as EMT process inactivation, which contributes to the inhibition of HSC activation. TQ may be a potential therapeutic agent for liver fibrosis.