This article reports a case of a male patient， aged 60 years， who developed pyrrolizidine alkaloid-induced hepatic sinusoidal obstruction syndrome （PA-HSOS） due to ingestion of Gynura segetum （Lour.） Merr. The patient presented with ascites and abnormal liver function， and a confirmed diagnosis was made based on radiological examination and liver biopsy. Since the patient was allergic to low-molecular-weight heparin and had no response to supportive therapy， low-dose defibrotide was administered as rescue treatment. After treatment， the patient achieved rapid regression of ascites and recovery of liver function， and liver biopsy reexamination showed alleviation of sinusoidal congestion and hepatocyte regeneration. Self-resolving conjunctival hemorrhage occurred during treatment. This case suggests that for patients with contraindications to standard anticoagulation therapy or those showing no response to such treatment， low-dose defibrotide may be used as an effective and relatively safe alternative treatment regimen.

Benign metastasizing leiomyomatosis is a rare clinical entity characterized by benign leiomyomas occur-ring outside the uterus,with the lungs being the most commonly involved site,thus termed pulmonary benign metastasi-zing leiomyomatosis.Fumarate hydratase(FH)-deficient leiomyoma represents a rare pathological variant of uterine leiomyoma,which is of great significance for screening hereditary leiomyomatosis and renal cell carcinoma syndrome.Although there have been reports of FH-deficient leiomyomas involving the lungs,studies on FH-deficient pulmonary benign metastasizing leiomyoma in this context remain limited.This article offers a comprehensive review of existing studies on FH-deficient pulmonary benign metastasizing leiomyoma by integrating the epidemiology,clinical manifesta-tions,pathological features,diagnosis,differential diagnosis,and therapeutic advancements of primary uterine FH-de-ficient leiomyoma.

Benign metastasizing leiomyomatosis is a rare clinical entity characterized by benign leiomyomas occur-ring outside the uterus,with the lungs being the most commonly involved site,thus termed pulmonary benign metastasi-zing leiomyomatosis.Fumarate hydratase(FH)-deficient leiomyoma represents a rare pathological variant of uterine leiomyoma,which is of great significance for screening hereditary leiomyomatosis and renal cell carcinoma syndrome.Although there have been reports of FH-deficient leiomyomas involving the lungs,studies on FH-deficient pulmonary benign metastasizing leiomyoma in this context remain limited.This article offers a comprehensive review of existing studies on FH-deficient pulmonary benign metastasizing leiomyoma by integrating the epidemiology,clinical manifesta-tions,pathological features,diagnosis,differential diagnosis,and therapeutic advancements of primary uterine FH-de-ficient leiomyoma.

[This corrects the article DOI: 10.1016/j.apsb.2021.03.043.].

Serine/arginine-rich splicing factor 7 (SRSF7), a known splicing factor, has been revealed to play oncogenic roles in multiple cancers. However, the mechanisms underlying its oncogenic roles have not been well addressed. Here, based on N⁶-methyladenosine (m⁶A) co-methylation network analysis across diverse cell lines, we find that the gene expression of SRSF7 is positively correlated with glioblastoma (GBM) cell-specific m⁶A methylation. We then indicate that SRSF7 is a novel m⁶A regulator, which specifically facilitates the m⁶A methylation near its binding sites on the mRNAs involved in cell proliferation and migration, through recruiting the methyltransferase complex. Moreover, SRSF7 promotes the proliferation and migration of GBM cells largely dependent on the presence of the m⁶A methyltransferase. The two m⁶A sites on the mRNA for PDZ-binding kinase (PBK) are regulated by SRSF7 and partially mediate the effects of SRSF7 in GBM cells through recognition by insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2). Together, our discovery reveals a novel role of SRSF7 in regulating m⁶A and validates the presence and functional importance of temporal- and spatial-specific regulation of m⁶A mediated by RNA-binding proteins (RBPs).
Humans ; Cell Line, Tumor ; Cell Proliferation ; Gene Expression Regulation, Neoplastic ; Glioblastoma/genetics* ; Methyltransferases/metabolism* ; RNA Splicing Factors/metabolism* ; RNA, Messenger/genetics* ; RNA-Binding Proteins/metabolism* ; Serine-Arginine Splicing Factors/metabolism* ; RNA Methylation/genetics*

Objective To summarize the electrophysiological indexes and scales used for evaluation of post-stroke spasticity, for integration of clinical management of spasms. Methods Literatures on identification and evaluation of post-stroke spasticity from databases of Web of Science, PubMed, CNKI, and Wanfang Data up to May 15, 2021 were retrieved and the indicators related to post-stroke spasticity were extracted for a scoping review. Results The scales of modified Asworth Scale, Comprehensive Spasticity Scale and modified Tardieu Scale; the electrophysiological indexes of F wave, H reflex, motor evoked potentials, visual-startle reaction time and vestibular evoked myogenic potentials were used to identify and evaluate post-stroke spasticity. Conclusion More clinical researches are needed to explore earlier identification and evaluation of post-stroke spasticity more objectively and accurately.

Gastrointestinal mucositis is one of the most debilitating side effects of the chemotherapeutic agent irinotecan (CPT-11). Andrographolide, a natural bicyclic diterpenoid lactone, has been reported to possess anti-colitis activity. In this study, andrographolide treatment was found to significantly relieve CPT-11-induced colitis in tumor-bearing mice without decreasing the tumor suppression effect of CPT-11. CPT-11 causes DNA damage and the release of double-stranded DNA (dsDNA) from the intestine, leading to cyclic-GMP-AMP synthase (cGAS)‒stimulator of interferon genes (STING)-mediated colitis, which was significantly decreased by andrographolide both in vivo and in vitro. Mechanistic studies revealed that andrographolide could promote homologous recombination (HR) repair and downregulate dsDNA‒cGAS‒STING signaling and contribute to the improvement of CPT-11-induced gastrointestinal mucositis. These results suggest that andrographolide may be a novel agent to relieve gastrointestinal mucositis caused by CPT-11.

Objective:To explore the expression and clinical significance of miR-143 in papillary thyroid cancer (PTC) .Methods:Tumor samples and adjacent tissues from 52 patients with PTC were obtained from Jan. 1st, 2018 to Mar. 31st, 2018 in Thyroid Surgery Department of the Affiliated Yantai Yuhuangding Hospital of Qingdao University. Quantitative reverse-transcriptase PCR (RT-qPCR) was used to measure the expression of miR-143 in those subjects. In addition, the relationship between the expression levels of miR-143 and the clinicopathological characteristics was analyzed.Results:RT-qPCR indicated that the expression of miR-143 was down-regulated in PTC, which was significantly lower than that in adjacent tissues ( t=-21.39, 95% CI: 18.20-15.07, P<0.001) . Low expression of miR-143 was related to the number of lymph node metastasis ≥3 in central compartment ( t=10.13, P=0.012) and lateral neck lymph node metastasis ( t=-4.67, P<0.001) . Conclusion:Downregulation of miR-143 in PTC is linked to the metastasis of PTC and may be a potential target for therapeutic intervention.

Objective:To explore the clinical significance of recurrent laryngeal nerve inlet zone(RLNIZ) lymph node metastasis in papillary thyroid cancer(PTC).Methods:The clinical data of the clinicopathologic characteristics of 738 cases with papillary thyroid cancer at our centers from Jul 2017 to Jun 2018 was retrospectively reviewed. 108 cases with RLNIZ lymph node dissection for pathological examination were included. The relationship between metastasis of RLNIZ lymph node and clinicopathologic characteristics was analyzed.Results:RLNIZ lymph node was detected in 12.3%(91/738)cases, the mean lymph node number in RLNIZ was 1.5±0.7, and 30.8%(28/91) cases suffered RLNIZ lymph node metastasis. RLNIZ lymph node metastasis(LNM) is associated with tumor size( P=0.028), capsular invasion( P=0.019), No. of central compartment LNM( P<0.001) and lateral neck LNM( P<0.001). No. of central compartment LNM was found to be the independent risk factor of RLNIZ lymph node metastasis. The incidence of dysphagia and inferior parathyroid damage was 0.9%(1/108)respectively. Conclusions:RLNIZ lymph node metastasis is common among PTC patients , therefore, RLNIZ lymph node should be routinely removed especially in patients with tumor size over 1cm、suspected capsular invasion and lateral neck lymph node metastasis confirmed by preoperative imaging examination.

Stroke is an acute cerebro-vascular disease with high incidence and poor prognosis, most commonly ischemic in nature. In recent years, increasing attention has been paid to inflammatory reactions as symptoms of a stroke. However, the role of inflammation in stroke and its underlying mechanisms require exploration. In this study, we evaluated the inflammatory reactions induced by acute ischemia and found that pyroptosis occurred after acute ischemia both in vivo and in vitro, as determined by interleukin-1β, apoptosis-associated speck-like protein, and caspase-1. The early inflammation resulted in irreversible ischemic injury, indicating that it deserves thorough investigation. Meanwhile, acute ischemia decreased the Sirtuin 1 (Sirt1) protein levels, and increased the TRAF6 (TNF receptor associated factor 6) protein and reactive oxygen species (ROS) levels. In further exploration, both Sirt1 suppression and TRAF6 activation were found to contribute to this pyroptosis. Reduced Sirt1 levels were responsible for the production of ROS and increased TRAF6 protein levels after ischemic exposure. Moreover, N-acetyl-L-cysteine, an ROS scavenger, suppressed the TRAF6 accumulation induced by oxygen-glucose deprivation via suppression of ROS bursts. These phenomena indicate that Sirt1 is upstream of ROS, and ROS bursts result in increased TRAF6 levels. Further, the activation of Sirt1 during the period of ischemia reduced ischemia-induced injury after 72 h of reperfusion in mice with middle cerebral artery occlusion. In sum, these results indicate that pyroptosis-dependent machinery contributes to the neural injury during acute ischemia via the Sirt1-ROS-TRAF6 signaling pathway. We propose that inflammatory reactions occur soon after oxidative stress and are detrimental to neuronal survival; this provides a promising therapeutic target against ischemic injuries such as a stroke.