Standardized procedures important for improving single-component ceramic fuel cell technology

Standardized procedures important for improving single-component ceramic fuel cell technolog

Table2_A real-world pharmacovigilance analysis of FDA adverse event reporting system database for upadacitinib.DOCX

Objective: To mine the adverse drug event (ADE) signals of upadacitinib based on the Food and Drug Administration (FDA) Adverse Event Reporting System (FAERS) database to provide a reference for the safe clinical use of the drug.Methods: The ADE data for upadacitinib from Q1 2004 to Q1 2023 in the FAERS database were retrieved, and data mining was performed using the reporting odds ratio and proportional reporting ratio.Results: A total of 21,213 ADE reports for the primary suspect drug upadacitinib were obtained, involving 444 ADEs. Patients aged ≥60 years (21.48%) and female (70.11%) patients were at a higher risk of ADEs with upadacitinib. After data cleaning, 182 ADE signals from 19 system organ classes (SOCs) were obtained. Six of these SOCs that occurred more frequently and were not mentioned in the drug labeling information included renal and urinary system (1.09%), reproductive and breast diseases (1.14%), ear and labyrinth disorders (0.57%), psychiatric disease (0.57%), blood and lymphatic system disorders (0.57%), and endocrine disorders (0.57%). The top ten most frequent ADE signals reported for upadacitinib were mainly related to: infections and infestations (7), investigations (2), and skin and subcutaneous tissue disorders (1). The top 10 ADEs in signal intensity ranking were lip neoplasm, ureteral neoplasm, eczema herpeticum, vulvar dysplasia, mediastinum neoplasm, eosinopenia, herpes zoster cutaneous disseminated, eye ulcer, acne cystic, and Moraxella infection. The top 10 high-frequency events leading to serious adverse events were urinary tract infection (2.74%), herpes zoster (1.63%), diverticulitis (1.19%), bronchitis (0.68%), nasopharyngitis (0.68%), localised infection (0.66%), nephrolithiasis (0.66%), pulmonary thrombosis (0.66%), blood cholesterol increased (0.55%), and Pneumocystis jirovecii pneumonia (0.53%).Conclusion: Clinicians should be vigilant to upadacitinib-induced events in systems not covered in the drug labeling information and to new and highly signaled ADEs to ensure the safe and effective use of upadacitinib.</p

Table1_A real-world pharmacovigilance analysis of FDA adverse event reporting system database for upadacitinib.DOCX

Objective: To mine the adverse drug event (ADE) signals of upadacitinib based on the Food and Drug Administration (FDA) Adverse Event Reporting System (FAERS) database to provide a reference for the safe clinical use of the drug.Methods: The ADE data for upadacitinib from Q1 2004 to Q1 2023 in the FAERS database were retrieved, and data mining was performed using the reporting odds ratio and proportional reporting ratio.Results: A total of 21,213 ADE reports for the primary suspect drug upadacitinib were obtained, involving 444 ADEs. Patients aged ≥60 years (21.48%) and female (70.11%) patients were at a higher risk of ADEs with upadacitinib. After data cleaning, 182 ADE signals from 19 system organ classes (SOCs) were obtained. Six of these SOCs that occurred more frequently and were not mentioned in the drug labeling information included renal and urinary system (1.09%), reproductive and breast diseases (1.14%), ear and labyrinth disorders (0.57%), psychiatric disease (0.57%), blood and lymphatic system disorders (0.57%), and endocrine disorders (0.57%). The top ten most frequent ADE signals reported for upadacitinib were mainly related to: infections and infestations (7), investigations (2), and skin and subcutaneous tissue disorders (1). The top 10 ADEs in signal intensity ranking were lip neoplasm, ureteral neoplasm, eczema herpeticum, vulvar dysplasia, mediastinum neoplasm, eosinopenia, herpes zoster cutaneous disseminated, eye ulcer, acne cystic, and Moraxella infection. The top 10 high-frequency events leading to serious adverse events were urinary tract infection (2.74%), herpes zoster (1.63%), diverticulitis (1.19%), bronchitis (0.68%), nasopharyngitis (0.68%), localised infection (0.66%), nephrolithiasis (0.66%), pulmonary thrombosis (0.66%), blood cholesterol increased (0.55%), and Pneumocystis jirovecii pneumonia (0.53%).Conclusion: Clinicians should be vigilant to upadacitinib-induced events in systems not covered in the drug labeling information and to new and highly signaled ADEs to ensure the safe and effective use of upadacitinib.</p

The schematic diagram of crosstalk between RhoC and IQGAP1 in gastric cancer.

<p>When RhoC is stimulated by extracelluar or intracelluar signals, it binds with the scaffold protein IQGAP1, influences the expression of cell cycle-related proteins such as cyclin D1 and cyclin B, affects G1-S transitions in the cell cycle, and then causes the change in cell proliferation. The signal transduction event through which IQGAP1 affects the expression of cyclin still needs to be elucidated.</p

The proliferation-stimulating effect of RhoC was blocked by IQGAP1 siRNA.

<p>(<b>A</b>) The protein expression levels of IQGAP1, IQGAP1-C and RhoC in BGC-823 cells. BGC-823 cells were transiently transfected with IQGAP1 siRNA or RhoC siRNA for 24 h. The transfected cells were afterwards infected with Ad-RhoC-V14, Ad-IQGAP1-C or Ad-IQGAP1 for additional 48 h followed by Western blotting. (<b>B</b>) RhoC depletion did not significantly affect IQGAP1 or IQGAP1-C induced proliferation of BGC-823 cells. (<b>C</b>) The silencing of IQGAP1 by siRNA markedly inhibited the RhoC-induced cell proliferation in BGC-823 cells. (MTT assay, *P<0.05; **P<0.01). The data are the means ± SD from three independent experiments each performed in duplicate.</p

Novel Aptasensor Platform Based on Ratiometric Surface-Enhanced Raman Spectroscopy

A novel aptasensor platform has been developed for quantitative detection of adenosine triphosphate (ATP) based on a ratiometric surface-enhanced Raman scattering (SERS) strategy. The thiolated 3′-Rox-labeled complementary DNA (cDNA) is first immobilized on the gold nanoparticle (AuNP) surface and then hybridizes with the 3′-Cy5-labeled ATP-binding aptamer probe (Cy5-aptamer) to form a rigid double-stranded DNA (dsDNA), in which the Cy5 and Rox Raman labels are used to produce the ratiometric Raman signals. In the presence of ATP, the Cy5-aptamer is triggered the switching of aptamer to form the aptamer–ATP complex, leading to the dissociation of dsDNA, and the cDNA is then formed a hairpin structure. As a result, the Rox labels are close to the AuNP surface while the Cy5 labels are away from. Therefore, the intensity of SERS signal from Rox labels increases while that from Cy5 labels decreases. The results show that the ratio between the Raman intensities of Rox labels and Cy5 labels is well linear with the ATP concentrations in the range from 0.1 to 100 nM, and the limit of detection reaches 20 pM, which is much lower than that of other methods for ATP detection and is also lower than that of SERS aptasensor for ATP detection. The proposed strategy provides a new reliable platform for the construction of SERS biosensing methods and has great potential to be a general method for other aptamer systems

The effect of IQGAP1 on proliferation of BGC-823 cells.

<p>(<b>A</b>) Western blot analysis of IQGAP1 expression in gastric cancer cell BGC-823 lines infected with Ad-LacZ, Ad-IQGAP1-C, Ad-IQGAP1-N or Ad-IQGAP1. (<b>B</b>) In the MTT assay, IQGAP1-C and IQGAP1 over expression cells both have more proliferation activity than control group (*P<0.05, compared to Ad-LacZ group). (<b>C</b>) The protein expression level of IQGAP1 in gastric cancer cell line BGC-823 transfected with IQGAP1 siRNA. (<b>D</b>) The proliferation of BGC-823 cells transfected with IQGAP1 siRNA were examined by MTT assay. (*P<0.05, compared to Control siRNA group). (<b>E</b>) BGC-823 cells were transiently transfected with plasmids Flag-IQGAP1, Flag-IQGAP1-C, or Flag-IQGAP1-N for 48 h. Western blotting showed the expression of IQGAP1, IQGAP1-N, and IQGAP1-C constructs in BGC-823 cell lines. Equal amounts of cell lysate from each group were loaded and blotted with anti-IQGAP1 antibodies (against C-terminal fragment or N- terminal fragment). (<b>F</b>) BrdU assay was used for analysis cell proliferation. Representative images of BGC-823 cells expressing the indicated IQGAP1 constructs were stained with antibodies against BrdU (second panels red) and Hoechst 33342 for nuclei (first panel, blue). The percentage of cells with BrdU incorporation was calculated. The mean ± SD of three independent experiments is presented (*P<0.05).</p

The effects of RhoC and IQGAP1 on expression of cell cycle-related proteins.

<p>(<b>A</b>) BGC-823 cells were infected with Ad-IQGAP1, Ad-IQGAP1-C or Ad-RhoC-V14 for 48 h, and Western blot was used to analyze the expressions of cyclin E, cyclin D1 cyclin B and CDK. (<b>B</b>) BGC-823 cells were transfected with IQGAP1 siRNA or RhoC siRNA for 72 h, and the expressions of cyclin E, cyclin D1, cyclin B and CDK were analyzed by Western blotting. (<b>C</b>) The protein expressions of cyclin E, cyclin D1, cyclin B and CDK in BGC-823 cells which were transiently transfected with IQGAP1 siRNA or RhoC siRNA for 24 h and afterwards infected with Ad-RhoC-V14, Ad-IQGAP1-C or Ad-IQGAP1 for additional 48 h (Results of Western blotting).</p

Identification of the interaction between RhoC and IQGAP1.

<p>(<b>A</b>) BGC-823 cells growing on 100 mm plates were transiently co-infected with Ad-IQGAP1 and Ad-RhoC-V14, or Ad-IQGAP1-C and Ad-RhoC-V14 for 48 h. The cells were lysed and equal amounts of lysate protein were immunoprecipitated (IP) with anti-RhoC, anti-IQGAP1 antibodies or isotype-matched IgG. Whole cell lysate was used as a protein input control. (<b>B</b>) BGC-823 cells were transfected with above adenovirus for 24–48 h, and the co-localization of RhoC and IQGAP1 in cells were determined by Immunofluorescence microscopy using anti-RhoC and anti-IQGAP1 antibodies. Nuclei were stained by Hoechst 33342 (blue). (<b>C</b>) COS-7 cells were transiently co-infected with Ad-IQGAP1-C/Ad-IQGAP1 and Ad-RhoC-V14 for 48 h. The cells were undergoing the same Co-IP procedure described above. (<b>D</b>) COS-7 cells were transfected with above adenoviral vectors for 24–48 h, and the co-localization of RhoC and IQGAP1 in cells were shown by Immunofluorescence. The data are representative from three independent experiments with similar results.</p

Enhanced photocatalytic hydrogen production of S-scheme TiO2/g-C3N4 heterojunction loaded with single-atom Ni

S-scheme heterostructure photocatalysts can achieve highly efficient solar energy utilization. Here, single-atom Ni species were deposited onto TiO2/g-C3N4 (TCN) composite photocatalyst with an S-scheme heterojunction for highly efficient photocatalytic water splitting to produce hydrogen. Under solar irradiation, it realized the hydrogen production activity of 134 µmol g–1 h–1, about 5 times higher than the TCN without atomic Ni. In-situ Kelvin probe force microscopy characterization and the density functional calculation certify that by forming the S-scheme heterojunction, the photo-excited electrons from the TiO2 combine with the photogenerated holes at the coupled g-C3N4 driven by a built-in electric field. More importantly, the single-atom Ni species stabilized the photogenerated electrons from the g-C3N4 could effectively enhance the charge separation between the holes on the valence band of TiO2 and electrons at the conduction band of g-C3N4. Meanwhile, the Ni atoms act as the surface catalytic centers for the water reduction reaction, which greatly improves the reactivity of the photocatalyst. The present work provides a new approach for developing noble metal-free heterojunctions for high-efficiency photocatalysis.</p