Mapping of the APE1 domains responsible for GSNO-induced nuclear export

<p><b>Copyright information:</b></p><p>Taken from "Nitric oxide controls nuclear export of APE1/Ref-1 through S-nitrosation of Cysteines 93 and 310"</p><p></p><p>Nucleic Acids Research 2007;35(8):2522-2532.</p><p>Published online 1 Apr 2007</p><p>PMCID:PMC1885639.</p><p>© 2007 The Author(s)</p> () Immunofluorescence images depicting the subcellular localization of APE1 truncated mutants in transfected HEK293 cells. () Schematic representation of the N-terminal and C-terminal truncated mutants of APE1. The NLS and the predicted NES and MTS within the full-length protein are indicated. C, cytoplasmic staining; N, nuclear staining; M, mitochondrial staining. () The subcellular distribution of HA-APE1(Δ64-80) and HA-APE1(1-305) determined by immunofluorescence in the presence of GSNO treatment. () Three-dimensional localization of the B1 (amino acids 61–69) and B2 (amino acids 311–317) beta-strands and the S-nitrosation sites C93 and C310 in the closed conformation of APE1. B1 and B2 form an antiparallel beta-fold. C93 and C310 are close to B1 and B2, respectively

Nitric-oxide-repressed classical importin-mediated nuclear import pathway

<p><b>Copyright information:</b></p><p>Taken from "Nitric oxide controls nuclear export of APE1/Ref-1 through S-nitrosation of Cysteines 93 and 310"</p><p></p><p>Nucleic Acids Research 2007;35(8):2522-2532.</p><p>Published online 1 Apr 2007</p><p>PMCID:PMC1885639.</p><p>© 2007 The Author(s)</p> () Left: Schematic presentation of the NLS-containing APE1(1-64) mutant. Right: Immunofluorescence images depicting the localization of APE1(1-64)-Myc in HEK293 cells challenged with or without 1 mM GSNO for 4 h. () Confocal images depicting the localization of (GFP)2-NLS and (GFP)2-M9 in HEK293 cells treated with GSNO for 4 h. () Left: Schematic presentation of the NLS-truncated mutant APE1(43-318)-Myc Right: Immunofluorescence images depicting the localization of APE1(43-318)-Myc in HEK293 cells challenged with or without 1 mM GSNO for 4 h

The effects of CHX and LMB on GSNO-induced cytosolic translocation of APE1

<p><b>Copyright information:</b></p><p>Taken from "Nitric oxide controls nuclear export of APE1/Ref-1 through S-nitrosation of Cysteines 93 and 310"</p><p></p><p>Nucleic Acids Research 2007;35(8):2522-2532.</p><p>Published online 1 Apr 2007</p><p>PMCID:PMC1885639.</p><p>© 2007 The Author(s)</p> () Effect of CHX. 30 h after transfection, cells were treated with 1 mM GSNO for 4 h in the presence or absence of CHX, and then fixed and immunostained by HA antibody and a Texas-red labeled secondary antibody, counterstained with Hoechst 33342, and analyzed by fluorescence microscopy. () Effect of LMB. HEK293 cells transfected with HA-APE1 were treated with 5 ng/ml LMB for 4 h, followed by 1 mM GSNO for another 4 h, and then the subcellular distribution of HA-APE1 was determined. () Positive control of the effect of LMB on the localization of GFP-IκB expressed in HEK293 cells

A model for nuclear-cytosolic translocation of APE1 in response to NO stimulation

<p><b>Copyright information:</b></p><p>Taken from "Nitric oxide controls nuclear export of APE1/Ref-1 through S-nitrosation of Cysteines 93 and 310"</p><p></p><p>Nucleic Acids Research 2007;35(8):2522-2532.</p><p>Published online 1 Apr 2007</p><p>PMCID:PMC1885639.</p><p>© 2007 The Author(s)</p> APE1 carries an importin-dependent NLS at the N-terminal end (not shown). Two antiparellel beta-strands (B1 and B2) in close proximity to C93 and C310 are masked in the internal structure. In rested cells, APE1 resides in the nucleus due to the existence of NLS. Upon nitrosative stress, S-nitrosation of C93 and C310 contributes to unmasking of the B1 and/or B2 by changing conformation, which may facilitate the nuclear export of APE1 in a CRM1-independet manner (perhaps mediated by an unknown transport protein). At the same time, importin-dependent nuclear import pathway is repressed by NO insult, which may prevent the already exported cytosolic APE1 from re-import into the nucleus. However, once the intracellular environment becomes reductive (e.g. the increased reducing molecules such as DTT), both NO-elicited S-nitrosation of APE1 and NO-caused repression of importin can be abrogated; thus, the inducible nuclear export of APE1 by NO could be prevented or reversed

Microporous Cyanate Resins: Synthesis, Porous Structure, and Correlations with Gas and Vapor Adsorptions

Three silicon and nitrogen-centered cyanate monomers tetrakis­(4-cyanatophenyl)­silane, tetrakis­(4-cyanatobiphenyl)­silane, and tris­(4-cyanatobiphenyl)­amine were designed and synthesized, which were then polymerized via thermal cyclotrimerization reaction to create highly porous cyanate resin networks with systematically varied nodes and linking struts. The chemical structures of monomers and polymers were confirmed by ¹H NMR, FTIR, solid-state ¹³C CP/MAS NMR spectra, and elemental analysis. The products are amorphous with 5% weight-loss temperatures over 428 °C. The results based on N₂ and CO₂ adsorption isotherms show that the pores in these polymers mainly locate in the microporous region, and the BET surface areas are up to 960 m² g^–1, which is the highest value for the porous cyanate resin reported to date. The nitrogen- and oxygen-rich characteristics of cyanate resins lead to the networks strong affinity for CO₂ and thereby high CO₂ adsorption capacity of 11.1 wt % at 273 K and 1.0 bar. The adsorption behaviors of H₂, CO₂, benzene, <i>n</i>-hexane, and water vapors were investigated by correlating with the chemical composition and porosity parameters of the networks as well as the physicochemical nature of adsorbates

Table1_Service scheduling strategy for microservice and heterogeneous multi-cores-based edge computing apparatus in smart girds with high renewable energy penetration.DOCX

The microservice-based smart grid service (SGS) organization and the heterogeneous multi-cores-based computing resource supply are the development direction of edge computing in smart grid with high penetration of renewable energy sources and high market-oriented. However, their application also challenges the service schedule for edge computing apparatus (ECA), the physical carrier of edge computing. In the traditional scheduling strategy of SGS, an SGS usually corresponds to an independent application or component, and the heterogeneous multi-core computing environment is also not considered, making it difficult to cope with the above challenges. In this paper, we propose an SGS scheduling strategy for the ECA. Specifically, we first present an SGS scheduling framework of ECA and give the essential element of meeting SGS scheduling. Then, considering the deadline and importance attributes of the SGS, a microservice scheduling prioritizing module is proposed. On this basis, the inset-based method is used to allocate the microservice task to the heterogeneous multi-cores to utilize computing resources and reduce the service response time efficiently. Furthermore, we design the scheduling unit dividing module to balance the delay requirement between the service with early arrival time and the service with high importance in high concurrency scenarios. An emergency mechanism (EM) is also presented for the timely completion of urgent SGSs. Finally, the effectiveness of the proposed service scheduling strategy is verified in a typical SGS scenario in the smart distribution transformer area.</p

Table_1_Immune-related adverse events with severe pain and ureteral expansion as the main manifestations: a case report of tislelizumab-induced ureteritis/cystitis and review of the literature.docx

Immune checkpoint inhibitor (ICI) is an up-to-date therapy for cancer with a promising efficacy, but it may cause unique immune-related adverse events (irAEs). Although irAEs could affect any organ, irAEs-induced whole urinary tract expansion was rarely reported. Herein, we reported a 27-year-old male patient with thymic carcinoma who received the treatment of tislelizumab, paclitaxel albumin and carboplatin. He was hospitalized for severe bellyache and lumbago after 6 courses of treatment. Antibiotic and antispasmodic treatment did not relieve his symptoms. The imaging examinations reported whole urinary tract expansion and cystitis. Therefore, we proposed that the patient’s pain was caused by tislelizumab-induced ureteritis/cystitis. After the discontinuation of tislelizumab and the administration of methylprednisolone, his symptoms were markedly alleviated. Herein, we reported a rare case of ICI-induced ureteritis/cystitis in the treatment of thymic cancer and reviewed other cases of immunotherapy-related cystitis and tislelizumab-related adverse events, which will provide a reference for the diagnosis and treatment of ICI-related irAEs.</p

Image_2_Immune-related adverse events with severe pain and ureteral expansion as the main manifestations: a case report of tislelizumab-induced ureteritis/cystitis and review of the literature.png

Immune checkpoint inhibitor (ICI) is an up-to-date therapy for cancer with a promising efficacy, but it may cause unique immune-related adverse events (irAEs). Although irAEs could affect any organ, irAEs-induced whole urinary tract expansion was rarely reported. Herein, we reported a 27-year-old male patient with thymic carcinoma who received the treatment of tislelizumab, paclitaxel albumin and carboplatin. He was hospitalized for severe bellyache and lumbago after 6 courses of treatment. Antibiotic and antispasmodic treatment did not relieve his symptoms. The imaging examinations reported whole urinary tract expansion and cystitis. Therefore, we proposed that the patient’s pain was caused by tislelizumab-induced ureteritis/cystitis. After the discontinuation of tislelizumab and the administration of methylprednisolone, his symptoms were markedly alleviated. Herein, we reported a rare case of ICI-induced ureteritis/cystitis in the treatment of thymic cancer and reviewed other cases of immunotherapy-related cystitis and tislelizumab-related adverse events, which will provide a reference for the diagnosis and treatment of ICI-related irAEs.</p

Image_1_Immune-related adverse events with severe pain and ureteral expansion as the main manifestations: a case report of tislelizumab-induced ureteritis/cystitis and review of the literature.jpeg

Immune checkpoint inhibitor (ICI) is an up-to-date therapy for cancer with a promising efficacy, but it may cause unique immune-related adverse events (irAEs). Although irAEs could affect any organ, irAEs-induced whole urinary tract expansion was rarely reported. Herein, we reported a 27-year-old male patient with thymic carcinoma who received the treatment of tislelizumab, paclitaxel albumin and carboplatin. He was hospitalized for severe bellyache and lumbago after 6 courses of treatment. Antibiotic and antispasmodic treatment did not relieve his symptoms. The imaging examinations reported whole urinary tract expansion and cystitis. Therefore, we proposed that the patient’s pain was caused by tislelizumab-induced ureteritis/cystitis. After the discontinuation of tislelizumab and the administration of methylprednisolone, his symptoms were markedly alleviated. Herein, we reported a rare case of ICI-induced ureteritis/cystitis in the treatment of thymic cancer and reviewed other cases of immunotherapy-related cystitis and tislelizumab-related adverse events, which will provide a reference for the diagnosis and treatment of ICI-related irAEs.</p

Eremophilane Sesquiterpenes and Polyketones Produced by an Endophytic <i>Guignardia</i> Fungus from the Toxic Plant <i>Gelsemium elegans</i>

A cultured endophytic fungus, <i>Guignardia mangiferae</i>, isolated from the toxic plant <i>Gelsemium elegans</i> yielded five new sesquiterpenes (<b>1</b>–<b>5</b>), two new polyketones (<b>6</b> and <b>7</b>), and two known terpene polyketones (<b>8</b> and <b>9</b>). Their structures were elucidated using spectroscopic methods. On the basis of circular dichroism, the absolute configurations of the new compounds were determined. Compounds <b>1</b>, <b>3</b>, <b>4</b>, and <b>9</b> inhibited lipopolysaccharide-induced NO production in BV2 cells with IC₅₀ values of 15.2, 6.4, 4.2, and 4.5 μM, respectively (positive control curcumin, IC₅₀ = 3.9 μM)