Role of social media to improve job performance with mediating role of transactive memory capability and employee creativity.

The increased usage of social media in organizational settings has raised questions about its effect on job performance. This study explains the interplay between social media usage, transactive memory capability, employee creativity, and job performance within the Chinese organizational context. The rationale for this study stems from the need to understand how social media usage can enhance job performance through cognitive and creative processes within teams. On the basis of earlier literature, the survey questionnaire was designed to collect data and the survey included validated scales to measure these constructs. The data is collected from 816 employees in China via online resources like social media and emails and then Structural Equation Modeling is used for empirical analysis through AMOS software. The findings show the positive impact of social media on job performance while transactive memory capability and employee creativity mediates this relationship. These findings contribute to a better understanding of how social media can be leveraged to improve job performance. Practical implications highlight the importance of fostering transactive memory capability through social media platforms, facilitating employee creativity, and ultimately, bolstering job performance. Additionally, this study underscores the need for organizations to strategically harness the potential of social media as a catalyst for innovation and knowledge sharing, thus optimizing workforce performance in the digital era.

Sulforaphane suppresses cell proliferation and induces apoptosis in glioma via the ACTL6A/PGK1 axis.

This study aimed to examine the expression and biological functions of ACTL6A in glioma cells (U251), the effects of sulforaphane on the growth of U251 cells and the involvement of the ACTL6A/PGK1 pathway in those effects. The U251 cell line was transfected with ACTL6A over-expression plasmids to upregulate the protein, or with ACTL6A inhibitor to underexpress it, then treated with different concentrations of sulforaphane. Cell viability, proliferation, and apoptosis were assessed using standard assays, and levels of mRNAs encoding ACTL6A, PGK1, cyclin D1, Myc, Bax or Bcl-2 were measured using quantitative real-time polymerase chain reaction (qRT-PCR). ACTL6A and PGK1 were expressed at higher levels in glioma cell lines than in normal HEB cells. ACTL6A overexpression upregulated PGK1, whereas ACTL6A inhibition had the opposite effect. ACTL6A overexpression induced proliferation, whereas its inhibition repressed proliferation, enhanced apoptosis, and halted the cell cycle. Moreover, sulforaphane suppressed the growth of U251 cells by inactivating the ACTL6A/PGK1 axis. ACTL6A acts via PGK1 to play a critical role in glioma cell survival and proliferation, and sulforaphane targets it to inhibit glioma.

Microfluidic Liver-on-a-Chip for Preclinical Drug Discovery.

Drug discovery is an expensive, long, and complex process, usually with a high degree of uncertainty. In order to improve the efficiency of drug development, effective methods are demanded to screen lead molecules and eliminate toxic compounds in the preclinical pipeline. Drug metabolism is crucial in determining the efficacy and potential side effects, mainly in the liver. Recently, the liver-on-a-chip (LoC) platform based on microfluidic technology has attracted widespread attention. LoC systems can be applied to predict drug metabolism and hepatotoxicity or to investigate PK/PD (pharmacokinetics/pharmacodynamics) performance when combined with other artificial organ-on-chips. This review discusses the liver physiological microenvironment simulated by LoC, especially the cell compositions and roles. We summarize the current methods of constructing LoC and the pharmacological and toxicological application of LoC in preclinical research. In conclusion, we also discussed the limitations of LoC in drug discovery and proposed a direction for improvement, which may provide an agenda for further research.

Exosomes Derived from SW480-Resistant Colon Cancer Cells Are Promote Angiogenesis via BMP-2/Smad5 Signaling Pathway.

Background: Multidrug resistance is the main cause of tumor recurrence and metastasis. Therefore, it is urgent to explore the mechanism and treatment of drug resistance of tumor cells. We aim to investigate the relationship between drug resistance and angiogenesis in SW480 colon cancer cells and the possible underlying mechanism. Methods: Exosomes were extracted from SW480-sensitive or SW480-resistant colon cancer cells (SW480/oxaliplatin). The CCK-8 assay, migration assay, tube formation assay, qPCR, and Western blotting were performed in human umbilical vein endothelial cells (HUVECs). The underlying mechanisms were detected by Western blotting assays and BMP-2 si-RNA silencing assay in vitro and in vivo. Results: The conditioned medium and exosomes of SW480/oxaliplatin cells promoted proliferation, migration, and tube formation of HUVECs. The expression of BMP-2 released by SW480/oxaliplatin exosomes was 2.3-folds higher than that by SW480 exosomes. Additionally, exosomal BMP-2 inhibiting the Smad signaling pathway induced the expression of vascular endothelial growth factor and CD31. Silencing of BMP-2 partly blocks the promoting effect of SW480/oxaliplatin exosomes on angiogenesis. Moreover, SW480/oxaliplatin cells increased the BMP-2 expression, consequently promoting angiogenesis in vivo. Conclusions: SW480-resistant colon cancer exosomes promoted angiogenesis via the BMP-2/Smad signaling pathway, which is potential for the novel treatment for antiangiogenic therapies in colon cancer.

Obtaining help by standing higher: The mediating role of moral reputation.

Drawing on the social cognitive chain of being (SCCB) theory and heuristic perspective, the present study explored whether and how social targets' vertical spatial position influences the help the social targets can get from others. Study 1 demonstrated that individuals would be more likely to help social targets who were presented on a higher vertical spatial position than those who were presented on a lower vertical spatial position. In Study 2, an experimental-causal-chain design was adopted for further testing the mediating role of moral reputation between the social targets' vertical spatial position and the amount of help that the social targets obtain from others. Study 3 cross-validated this mediating process by a measurement-of-mediation design. Those three studies help us comprehend how helping behavior occurs from the characteristics of help recipients as well as extend the influence of vertical spatial metaphor of morality from cognitive connection to action-relevant outcomes.

Escherichia coli PagP Enzyme-Based De Novo Design and In Vitro Activity of Antibacterial Peptide LL-37.

BACKGROUND The aim of this study was to investigate the antimicrobial property of peptide LL-37 sequences. MATERIAL AND METHODS Humanized antibacterial peptide LL-37 and the mutant were prepared by chemical synthesis. The physicochemical properties of antibacterial peptide LL-37 were analyzed by SWISS-MODEL online prediction tool. Molecular docking between antibacterial peptide LL-37 fragments and palmitoyl transferase PagP was made with Lamarckian genetic algorithm by AutoDock1.5.6. RESULTS The systems contacted each other at 8.75 picosec. After 20 picsec, the system had no trend of dissociation, and the bond energy of weak bond -C-O-H…NH2-CH2- was calculated. The hydrophobic groups were important factors that led to contact and merged the two parts. The contacted weak bond -C-O-H…NH2-CH2- was the bridge for contacting LL-37 with palmitoyl transferase PagP. The binding sites of antibacterial peptide LL-37 and palmitoyl transferase PagP mainly included LYS8, GLU11, LEU28, LYS12, PHE27, ILE13, and PHE6 of antibacterial peptide LL-37 and ARG94, TRP89, ASN65, SER3, GLU90, GLU90, ASN100, HIS102, and THR92 of palmitoyl transferase PagP. CONCLUSIONS Antibacterial peptide LL-37 had stronger antibacterial effect via inhibition of activity of PagP.

Thermosensitive AB4 four-armed star PNIPAM-b-HTPB multiblock copolymer micelles for camptothecin drug release.

Thermo-sensitive poly(N-isoproplacrylamide)m-block-hydroxyl-terminated polybutadiene-block-poly(N-isoproplacrylamide)m (PNIPAMm-b-HTPB-b-PNIPAMm, m = 1 or 2) block copolymers, AB4 four-armed star multiblock and linear triblock copolymers, were synthesized by ATRP with HTPB as central blocks, and characterization was performed by (1)H NMR, Fourier transform infrared, and size exclusion chromatography. The multiblock copolymers could spontaneously assemble into more regular spherical core-shell nanoscale micelles than the linear triblock copolymer. The physicochemical properties were detected by a surface tension, nanoparticle analyzer, transmission electron microscope (TEM), dynamic light scattering, and UV-vis measurements. The multiblock copolymer micelles had lower critical micelle concentration than the linear counterpart, TEM size from 100 to 120 nm, and the hydrodynamic diameters below 150 nm. The micelles exhibited thermo-dependent size change, with low critical solution temperature of about 33-35 °C. The characteristic parameters were affected by the composition ratios, length of PNIPAM blocks, and molecular architectures. The camptothecin release demonstrated that the drug release was thermo-responsive, accompanied by the temperature-induced structural changes of the micelles. MTT assays were performed to evaluate the biocompatibility or cytotoxicity of the prepared copolymer micelles.