Two-dimensional ß-MnOOH nanosheets with high oxidase-mimetic activity for smartphone-based colorimetric sensing.

Manganese (Mn) is a versatile transition element with diverse oxidation states and significant biological importance. Mn-based nanozymes have emerged as promising catalysts in various applications. However, the direct use of manganese oxides as oxidase mimics remains limited and requires further improvement. In this study, we focus on hydroxylated manganese (MnOOH), specifically the layered form ß-MnOOH which exhibits unique electronic and structural characteristics. The two-dimensional ß-MnOOH nanosheets were synthesized through a hydrothermal approach and showed remarkable oxidase-like activity. These nanosheets effectively converted the oxidase substrate, 3,3',5,5'-tetramethylbenzidine (TMB), into its oxidized form by initiating the conversion of dissolved oxygen into ·O2-, 1O2 and ·OH. However, in the presence of L-cysteine (L-Cys), the catalytic activity of ß-MnOOH was significantly inhibited, enabling highly sensitive detection of L-Cys. This sensing strategy was successfully applied for smartphone-based L-Cys assay, offering potential utility in the diagnosis of Cys-related diseases. The exploration of layered ß-MnOOH nanosheets as highly active oxidase mimics opens up new possibilities for catalytic and biomedical applications.

Seeded Growth of Size-Tunable Au@Ag Core-Shell Nano-Octahedra and Their Yolk-Shell Derivatives for Near Infrared Photothermal Conversion.

Gold-based nanostructures with well-defined morphologies and hollow interiors have significant potential as a versatile platform for various plasmonic applications including biomedical diagnostics and sensing. In this study, we report the synthesis of Au@Ag core-shell nanocrystals with perfect octahedral shapes and tunable edge lengths via seeded growth. These nanocrystals were then oxidatively carved into yolk-shell nanocages with a retained octahedral morphology. The increase in octahedral edge length and volume of the interior hollow cavity synergistically leads to a red-shift of the LSPR peak. As a result, the optimized Au@AuAg yolk-shell octahedral nanocages showed a remarkable temperature increase of 23 °C upon 15 min irradiation of an 808 nm laser at a power density of 1 W cm-2. This study provides a feasible strategy for creating octahedral AuAg nanostructures with tunable sizes and hollow interiors and validates their promising use in NIR photothermal conversion.

[The effect of suppressive oligodeoxynucleotides on interferon-γ and phosphorylation of signal transducers and activators of transcription 4 expression of silica-induced pulmonary inflammation in mice].

OBJECTIVE: To investigate the protective effect of suppressive oligodeoxynucleotides (Sup ODN) on interferon-γ (IFN-γ) and signal transducers and activators of transcription (pSTAT4) expression of Silica-induced pulmonary inflammation in Mice. METHODS: Sixty Balb/c mice were randomly divided into 4 groups, normal control group, silicious group, suppressive oligodeoxynucleotides (Sup ODN) group, control oligodeoxynucleotides (Con ODN) group. Except the normal control group injected normal saline, the rest groups were induced by the intratracheal instillation of 0.1 ml (5 g/L) of sterilized silica suspension. Sup ODN group and Con ODN group were treated by i.p. injection of 0.3 ml (1mg/mL) of suppressive or control ODN 3 h before silica administration. After 7 days, the animals were killed and levels of IFN-γ were detected by ELISA. The pathologic changes in lung tissues of mice were observed with HE staining. Expressions of IFN-γ and pSTAT4 in lung tissue were detected with immunohistochemistry and quantified by Image-Pro Plus 7.0. RESULTS: HE staining showed that the lung tissue of silicious group were damaged seriously than Sup ODN group. Compared with the normal control group (serum: (280.1±41.3) pg/ml, lung tissue: (0.249±0.373), IFN-γ increased in silicious group (serum: (886.3±81.7) pg/ml, lung tissue: (0.270±0.300) (P < 0.05). Compared with the normal control group and Con ODN group [(894.5±91.6) pg/ml], IFN-γ in the serum of Sup ODN group decreased significantly (P < 0.01). Compared with the silicious group , IFN-γ in lung tissue decreased in Sup ODN group (0.241±0.250) (P < 0.05). Compared with the normal control group (0.279±0.353), pSTAT4 in lung tissue increased significantly in silicious group (0.313±0.231) (P < 0.01). Compared with the silicious group, pSTAT4 in lung tissue decreased significantly in Sup ODN group (0.269±0.523) (P < 0.01). CONCLUSION: Sup ODN attained protective effect on Silica treated mice by suppressing expression of IFN-γ and pSTAT4.

[Correlation analysis between the exposure levels and the serum protein fingerprints in population exposure to silica].

OBJECTIVE: To explore the correlation between the exposure levels and serum protein fingerprints in population exposed to silica. METHODS: Liquid chip time-of-flight mass spectrometry technology was used to investigate the serum profiles in control group (30 cases), group exposed to silica (30 cases), silicosis group (I stage, 25 cases) and suspected silicosis group (30 cases), and screen the differential expression proteins. The correlation between the levels of the differential expression proteins and the exposure levels was performed. RESULTS: Five differential expression proteins were found among 4 groups, the expression of 5081 and 5066 proteins was upregulated, and the expression of 3954, 2021 and 1777 proteins was downregulated. There was no the correlation between the exposure levels and the peak with M/Z among those proteins. CONCLUSION: the results of present investigation indicated there was no correlation between the exposure levels and protein/peptide peak.

[The effects of complement C3f segment on expression and secretion of collagen I, III and transforming growth factor-beta1 in human embryonic lung fibroblast].

OBJECTIVE: To observe the effects of complement fragment C3f on expression and secretion of collagen I, III and transforming growth factor( TGF)-beta1 in human embryonic lung fibroblast (MRC-5) cells. METHODS: MRC-5 cells were cultured with C3f (the synthetic 17 peptides fragments of complement C3). The extracellular and intracellular expression levels of type I, III collagens and TGF-beta1 in MRC-5 cultures were detected by ELISA and immunohistochemistry, respectively. RESULTS: The expression levels of type I, III collagen and TGF-beta1 in the supernatant of MRC-5 cultures decreased significantly with the concentrations of C3f as compared with controls (P < 0.05). Also the expression level of TGF-beta1 in MRC-5 cytoplasm reduced significantly as compared with controls (P < 0.05). CONCLUSION: The results of present in vitro study showed that the complement fragment C3f could reduce the formation of TGF-beta1 and type I, III collagens in MRC-5 cells, and inhibit the lung tissue fibrosis.

[The study of the differential gene expression profiles related to toxic effects in rats exposed to silica].

OBJECTIVE: To study the differential gene expression profiles related to toxic effects in rats exposed to silica. METHODS: Wistar rats exposed to SiO2 (50 mg/ml) and 1 ml normal saline by intratracheal injection served as the exposure and control groups, on the 14th day after exposure all rats were executed and the rat lung tissues were obtained. The differential gene expression profiles in the lung tissues of rats exposed to silica were detected using confocal fiber beads gene chip technique, and the differential expression profiling data were analyzed using the database for annotation, visualization and integrated discovery (DAVID) bioinformation analysis tool. RESULTS: The results of present study indicated that 1567 genes with differential expression were identified in 22107 genes of rat lung tissues in exposure group, including 765 up-regulated genes and 802 down-regulated genes as compared to control group. In the 461 genes related to toxic effects, 285 genes were up-regulated and 176 genes were down-regulated in exposure group. The trends of up-regulation of HMOX1 and SOD2 genes in RT-PCR assay were similar to those in gene chip technique. CONCLUSION: A large number of genes related to toxic effects in the rats with silica-induced pulmonary fibrosis appeared up-regulation or down-regulation. There may be a complex gene regulation network in the pulmonary fibrosis induced by SiO2, and the toxicological mechanism is an important part in the development of pulmonary fibrosis.

The cytoplasmic terminus of Kaposi's sarcoma-associated herpesvirus glycoprotein B is not essential for virion egress and infectivity.

Kaposi's sarcoma-associated herpesvirus (KSHV)-encoded glycoprotein B (gB) is an important determinant of viral infectivity and virion egress. A small interfering RNA (siRNA)-based strategy was devised to inhibit KSHV gB gene expression. Transient cotransfection of plasmids constitutively expressing gB and anti-gB siRNAs in 293 cells substantially inhibited gB mRNA levels and protein production. Similarly, transient expression of siRNAs into the primary effusion lymphoma cell line BCBL-1 caused a substantial reduction of gB transcripts and protein synthesis. TaqMan real-time PCR assays against the lytic KSHV gene ORF59 and infectivity assays on 293 cells were employed to assess the effect of inhibiting gB synthesis on virion egress from BCBL-1 cells and infectivity on 293 cells, respectively. These experiments showed that gB was essential for virion egress and infectivity. Transfection of a codon-optimized gB gene with the first 540 nucleotides altered, and therefore not recognized by anti-gB siRNAs that target the native but not the codon-optimized sequence, efficiently rescued virion egress and infectivity in BCBL-1 cells in the presence of siRNAs inhibiting wild-type gB expression. To assess the role of the cytoplasmic domain of gB in virion egress, mutant gB genes were generated specifying carboxyl terminal truncations of 25 and 58 amino acids disrupting two prominent predicted alpha-helical domains associated with virus-induced cell fusion. A third truncation removed the entire predicted cytoplasmic terminus of 84 amino acids, while a fourth truncation removed 110 amino acids, including the terminal most hydrophobic, intramembrane anchoring sequence. Virion egress experiments revealed that all truncated gBs facilitated virion egress from BCBL-1 cells, with the exception of the largest 110-amino-acid truncation, which removed the gB anchoring sequence. Importantly, the gB truncation that removed the entire predicted cytoplasmic domain increased virion egress, suggesting the presence of a egress regulation domain located proximal to the intramembrane sequence within the cytoplasmic domain of gB. All supernatant virions were infectious on 293 cells, indicating that the carboxyl terminus of gB is not essential for either virion egress or virus infectivity.