Objective To evaluate the value of the Bedside Index for Severity in Acute Pancreatitis (BISAP) in diagnosing severe acute pancreatitis. Methods Sixty-eight patients with suspected diagnosis of severe acute pancreatitis were collected and were scored by BISAP, APACHE Ⅱ , Ranson and CTSI scoring systems, respectively. BISAP scoring system included the blood urea nitrogen, impaired mental status,systemic inflammatory response syndrome, age, and pleural effusion. The diagnosis criteria of severe acute pancreatitis was BISAP ≥ 3 points or APACHE IⅡ ≥ 8 points, Ranson ≥ 3 points, CTSI ≥ 3 points. The diagnostic accuracy of SAP of these scoring systems was calculated. Results Among these 68 cases, 63.2％(43/68) were graded ≥ 3 points in BISAP scoring system;60.3％ (41/68) were marked ≥8 points in APACHE Ⅱ scoring system; 60.3％ (41/68) were scored ≥ 3 points in Ranson scoring system; and 67.6％(46/68) were scored ≥3 points in CTSI scoring system. There was no statistical difference between BISAP scoring system and other three scoring systems in diagnosing severe acute pancreatitis. Conclusions As a new and simple scoring system, BISAP scoring system can be widely used in the diagnosis of severe acute pancreatitis.

Ubiquitin specific protease 33 (USP33) is a multifunctional protein regulating diverse cellular processes. The expression and role of USP33 in lung cancer remain unexplored. In this study, we show that USP33 is down-regulated in multiple cohorts of lung cancer patients and that low expression of USP33 is associated with poor prognosis. USP33 mediates Slit-Robo signaling in lung cancer cell migration. Downregulation of USP33 reduces the protein stability of Robo1 in lung cancer cells, providing a previously unknown mechanism for USP33 function in mediating Slit activity in lung cancer cells. Taken together, USP33 is a new player in lung cancer that regulates Slit-Robo signaling. Our data suggest that USP33 may be a candidate tumor suppressor for lung cancer with potential as a prognostic marker.
Blotting, Western ; Cell Line, Tumor ; Cell Movement ; genetics ; physiology ; Cohort Studies ; Down-Regulation ; Female ; Gene Expression Regulation, Neoplastic ; HEK293 Cells ; Humans ; Immunohistochemistry ; Intercellular Signaling Peptides and Proteins ; metabolism ; Kaplan-Meier Estimate ; Lung Neoplasms ; genetics ; metabolism ; pathology ; Male ; Middle Aged ; Nerve Tissue Proteins ; metabolism ; Prognosis ; RNA Interference ; Receptors, Immunologic ; metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction ; genetics ; physiology ; Ubiquitin Thiolesterase ; genetics ; metabolism

Despite the advancement of treatments, adults with relapsed/refractory (R/R) B-lineage acute lymphoblastic leukemia (B-ALL) have poor prognosis, with an expected five-year overall survival (OS) rate of 10%‒20% (Nguyen et al., 2008; Oriol et al., 2010). Extramedullary relapse of B-ALL is regarded as a high-risk factor generally associated with poor survival, occurring in about 15% to 20% of all relapsed patients (Ding et al., 2017; Sun et al., 2018). The central nervous system (CNS) and the testes are the most common sites of extramedullary relapse of B-ALL. In addition, extramedullary leukemia can appear in the skin, eyes, breasts, bones, muscles, and abdominal organs. The prognosis of relapsed extramedullary B-ALL after allogeneic hematopoietic stem cell transplantation (allo-HSCT) is extremely poor (Spyridonidis et al., 2012; Dahlberg et al., 2019). Conventional chemotherapy or radiation is often ineffective in such patients. At present, there are no optimal treatment strategies for treating extramedullary leukemia after allo-HSCT.
Adult ; Antigens, CD19 ; Hematopoietic Stem Cell Transplantation ; Humans ; Immunotherapy, Adoptive/adverse effects* ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/therapy* ; Receptors, Chimeric Antigen ; Recurrence

Aberrant regulation of miRNA genes contributes to pathogenesis of a wide range of human diseases, including cancer. The TAR DNA binding protein 43 (TDP-43), a RNA/DNA binding protein associated with neurodegeneration, is involved in miRNA biogenesis. Here, we systematically examined miRNAs regulated by TDP-43 using RNA-Seq coupled with an siRNA-mediated knockdown approach. TDP-43 knockdown affected the expression of a number of miRNAs. In addition, TDP-43 down-regulation led to alterations in the patterns of different isoforms of miRNAs (isomiRs) and miRNA arm selection, suggesting a previously unknown role of TDP-43 in miRNA processing. A number of TDP-43 associated miRNAs, and their candidate target genes, are associated with human cancers. Our data reveal highly complex roles of TDP-43 in regulating different miRNAs and their target genes. Our results suggest that TDP-43 may promote migration of lung cancer cells by regulating miR-423-3p. In contrast, TDP-43 increases miR-500a-3p expression and binds to the mature miR-500a-3p sequence. Reduced expression of miR-500a-3p is associated with poor survival of lung cancer patients, suggesting that TDP-43 may have a suppressive role in cancer by regulating miR-500a-3p. Cancer-associated genes LIF and PAPPA are possible targets of miR-500a-3p. Our work suggests that TDP-43-regulated miRNAs may play multifaceted roles in the pathogenesis of cancer.
Animals ; Cells, Cultured ; DNA-Binding Proteins ; metabolism ; Electrophoretic Mobility Shift Assay ; Humans ; Immunoprecipitation ; Mice ; MicroRNAs ; genetics ; metabolism ; Neoplasms ; genetics ; metabolism