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Zizania latifolia is a perennial plant native to East Asia. The swollen culm of Z. latifolia is a popular vegetable and traditional herbal medicine consumed in China and some other Asian countries. From 2019 to 2021, a sheath rot disease was found in Zhejiang Province of China. Symptoms mainly occurred in the leaf sheath showing as brown necrotic lesions surrounded by yellow halos. The pathogen fungal isolates were isolated from the affected sheaths. Ten representative isolates were selected for morphological and molecular identification by phylogenetic analyses of the translation elongation factor 1-α (TEF1) and the RNA polymerase II subunit beta (RPB2) gene regions. Based on the combined datasets, the fungal isolates were identified as Fusarium andiyazi. Koch’s postulates were confirmed by pathogenicity test, re-isolation and re-identification of the fungal isolates. To the best of our knowledge, this is the first report of sheath rot caused by F. andiyazi in Z. latifolia in China.

Cerebrovascular disorder-induced brain blood flow interruption or intracranial hemorrhage pose a great threaten to health. Emerging roles of long-noncoding RNAs (lncRNAs) in diagnosis and treatment of cardiovascular diseases have been recognized. However, whether and how lncRNAs modulate vascular homeostasis, especially network formation remain largely unknown. Here, we identified ECAL-1, a long non-coding RNA, as an important determinant for cerebrovascular homeostasis. Using the morpholino- and CRISPR /Cas9-based genetic modifications in combination with in vivo confocal imaging in zebrafish, we claimed that inactivation of ECAL-1 induced the apparent distortion of cerebral vascular pattern accompanied by intracranial hemorrhage. These cerebrovascular abnormalities were associated with decreased proliferation and anomalous interconnection of endothelial cells. Importantly, overexpression of Cldn5b, an endothelial cell-specific tight junction protein-encoding gene, could partially rescued the phenotype induced by ECAL-1 deficiency. Furthermore, bioinformatic analysis and experimental validation revealed that ECAL-1 sponged miR-23a, which targeted Cldn5b 3’UTR and modulated Cldn5b expression, to maintain cerebrovascular pattern formation and integrity. Our results presented here revealed that ECAL-1 specifically controls cerebrovascular network formation and integrity through targeting miR-23a-Cldn5b axis. These findings provide a new regulation modality for cerebrovascular patterning and the potential neurovascular disorders, and ECAL-1-miR-23a axis represents as an attractive therapeutic target for cerebrovascular diseases.

Background and objective Elevated pulse wave velocity (PWV) has been associated with higher mortality in the general population, chronic kidney disease (CKD) patients, and hemodialysis patients. However, in peritoneal dialysis (PD) patients, this association has received little attention. The aim of this study was to evaluate the association between baseline brachial-ankle PWV (baPWV) levels and total mortality in PD patients. Methods In this single-center retrospective cohort study, 254 incident PD patients with baseline baPWV were followed up from 1 January 2013 to 31 July 2016. Collected baseline data included demographic characteristics and clinical and laboratory measurements. The association of baseline baPWV levels with total mortality was assessed using multivariable-adjusted Cox models. Results Of 254 patients, mean age was 61.4 (±15.3) years, 61.4% of patients were men, and 22.4% of patients were diabetic. The mean baseline baPWV level was 17.6 (±5.84) m/s. During a mean 31.5 (±20.8) month follow-up period, 45 patients died, of which 13 deaths were caused by cardiovascular disease. After adjusting for sex, age, blood pressure (BP), body mass index (BMI), and hemoglobin, as well as serum albumin, calcium, phosphorus, intact parathyroid hormone (iPTH), uric acid, and medication use, the highest baPWV tertile was significantly associated with a hazard ratio (HR) for total mortality of 2.97 (95% confidence interval [CI], 1.23 – 7.16; p = 0.02). Each 1 m/s higher baseline baPWV level was associated with a 7% (95% CI, 1.03 – 1.12; p = 0.001) higher risk of total mortality. In sensitivity analyses, individuals with baPWV > 21.0 m/s had the highest adjusted risk for total death (HR, 3.22; 95% CI, 1.71 – 6.08; p < 0.001). Conclusion Higher baseline baPWV levels at the commencement of PD were independently associated with total mortality, which suggests that clinicians could use baPWV as a predictor of higher risk of mortality in PD patients.

Pan Liu,1,* Huapeng Lin,2,* Yuanyuan Chen,3 Yu-Shen Wu,4 Maocai Tang,5 Liang Lai1 1Department of Hepatobiliary Surgery, The First People’s Hospital of Neijiang, Sichuan, People’s Republic of China; 2Department of Intensive Care Unit, Affiliated Hangzhou First People’s Hospital, Zhejiang University School of Medicine, Zhejiang, People’s Republic of China; 3Department of Oncology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, People’s Republic of China; 4Chongqing Key Laboratory of Molecular Oncology and Epigenetics, The First Affiliated Hospital of Chongqing Medical University, Chongqing, People’s Republic of China; 5Department of Gastrointestinal Surgery, Chongqing University Cancer Hospital, Chongqing, People’s Republic of China *These authors contributed equally to this work Aim: To compare endoscopic papillary large balloon dilation (EPLBD) alone with EPLBD following endoscopic sphincterotomy (EST) in patients with large and/or multiple common bile duct stones.Methods: We conducted a comprehensive search of PubMed, EMBASE, and the Cochrane Library database to identify relevant available articles until July 19, 2018. Complete common bile duct stone (CBDS) removal rate, frequency of mechanical lithotripsy (ML) usage, total procedure time and intra- and postoperative adverse events were analyzed. We used RevMan 5.3 to perform the pooled analyses.Results: Seven RCTs matched the selection criteria. A total of 369 patients underwent EPLBD alone, and 367 patients underwent EPLBD following EST. Our meta-analysis revealed that there were no significant differences in terms of initial success rate (OR =0.69, 95% CI=0.44–1.09, P=0.11), frequency of ML usage (OR =1.18, 95% CI=0.68–2.05, P=0.55), rate of post-endoscopy pancreatitis (PEP) (OR =0.88, 95% CI=0.43–1.78, P=0.72), total procedure time (MD =1.52, 95% CI=-0.13–3.17, P=0.07), or other intra- and postoperative adverse events between the groups for patients with large and/or multiple CBDSs.Conclusions: EPLBD alone was comparable to EPLBD with prior EST in patients with large and/or multiple CBDSs. Further studies are required to confirm the mechanisms of PEP in patients who accept EPLBD during endoscopic retrograde cholangiopancreatography (ERCP). Keywords: endoscopic retrograde holangiopancreatography, ERCP, endoscopic papillary large balloon dilation, EPLBD, endoscopic sphincterotomy, EST, common bile duct stone, CBDS, meta-analysis

Podocyte apoptosis plays a pivotal role in the pathogenesis of diabetic nephropathy (DN). The main purpose of this study was to investigate the effects of perilipin2 on high glucose (HG)-induced podocyte apoptosis and associated mechanisms. Differentially expressed genes (DEGs) in BTBR ob/ob mice vs. nondiabetic mice kidneys were obtained from GSE106841 dataset and picked out using the 'limma' package. The protein-protein interaction (PPI) network was constructed using the Search Tool for the Retrieval of Interacting Genes (STRING) and was visualized by Cytoscape. Perilipin2 was a hub gene using the cytoHubba plug-in from Cytoscape. Gene ontology (GO) analysis revealed that the 126 overlapping DEGs were mainly enriched in 'oxidation reduction' [biological process, (BP)], metal ion binding' [molecular function, (MF)] and 'extracellular region' [cellular component, (CC)]. KEGG pathway analysis revealed that perilipin2 was mainly involved in 'PPAR signaling pathway'. DN inhibited perilipin2 expression and PPARγ expression, as by both in vitro and in vivo studies. In vitro experiments demonstrated that perilipin2 inhibition could not only reduced PPARγ expression in podocytes, it could also promote the apoptosis, and inhibit the viability in HG treated podocytes using western blot, CCK8 and flow cytometry assays. Perilipin2 overexpression reversed the effects of HG on inhibiting podocalyxin, nephrin, precursor (pro)-caspase-3/-9 and PPARγ protein expression and increasing cleaved caspase-3/-9 protein expression. Furthermore, the functions of perilipin2 overexpression reversing HG-induced podocyte apoptosis were inhibited by PPARγ inhibitor. In conclusion, the functions of DN-induced podocyte apoptosis were inhibited by activation of the PPARγ signaling pathway caused by perilipin2 overexpression.

SummaryPTPN12 is an important tumor suppressor that plays critical roles in various physiological processes. However, the molecular basis underlying the substrate specificity of PTPN12 remains uncertain. Here, enzymological and crystallographic studies have enabled us to identify two distinct structural features that are crucial determinants of PTPN12 substrate specificity: the pY+1 site binding pocket and specific basic charged residues along its surface loops. Key structurally plastic regions and specific residues in PTPN12 enabled recognition of different HER2 phosphorylation sites and regulated specific PTPN12 functions. In addition, the structure of PTPN12 revealed a CDK2 phosphorylation site in a specific PTPN12 loop. Taken together, our results not only provide the working mechanisms of PTPN12 for desphosphorylation of its substrates but will also help in designing specific inhibitors of PTPN12.