Applied Biochemistry and Biotechnology最新文献

Combustion power generation is still the main way of lignite utilization, but lignite combustion will produce a lot of toxic gases, so how to make lignite clean utilization has become an urgent problem to be solved. Hydrogen is an environmentally friendly, zero-carbon emission clean energy because microorganisms can degrade brown coal to produce hydrogen. Therefore, in this experiment, the anaerobic hydrogen production experiment of lignite was carried out, and the influence of different concentrations of benzyl alcohol on hydrogen production of lignite was studied. The results showed that the addition of 500 mg/L benzyl alcohol had the most significant effect on the hydrogen production of lignite, and the total hydrogen production reached 1.70 mL/g, which was 47.83% higher than that of the blank group. The addition of benzyl alcohol extended the peak time of hydrogen production in lignite fermentation. The peak hydrogen production time of 500 mg/L benzyl alcohol in the middle and late stage was 8 days, 5 days longer than that in the blank group. The peak hydrogen production of 500 mg/L benzyl alcohol in the middle and late stage was 0.11 mL/g, which was 2.75 times that of 0.04 mL/g in the blank group. Hydrogen production of lignite is mainly produced by acetic acid and propionic acid fermentation, which is different from butyric acid metabolic pathway of biomass microbial transformation such as crop straw and kitchen waste. This also provides a new way and theoretical basis for the fermentation of lignite to produce hydrogen.

Chlorella sorokiniana holds significant industrial relevance owing to its lipid profile. Consequently, the objective of this investigation was to enhance growth, lipid content, and photosynthetic pigment production through the application of UV-C irradiation. The growth parameters of microalgae demonstrated an increase in response to concentration. After 35 days of incubation, cells exposed to UV-C for 8 min produced the most biomass at 2.2 g/l. Additionally, the chlorophyll content demonstrated a comparable pattern, with the highest concentrations of chlorophyll a (4.99 mg/l), chlorophyll b (6.22 mg/l), and total chlorophyll (11.21 mg/l) observed in cells incubated for 35 days and exposed to UV-C for 8 min. The lipid profile, nevertheless, demonstrated minor fluctuations. Specifically, the relative abundance of frequently occurring lipid compounds was found to be greater in cells treated with UV-C compared to the control group, and the most significant increase was obtained in 15-day culture exposed to UV-C for 8 min. However, after 35 days of incubation, this abundance decreased in cells exposed to UV-C for more than 4 min. Additionally, the observation of specific lipid compounds presented solely in cells obtained from algal cultures treated with UV-C was made. Consequently, drawing from the results obtained in the current investigation, it is possible to deduce that UV-C can be utilised to augment the overall development and yield of significant metabolites in microalgae. Furthermore, these microalgae can be converted into single-cell bioreactors to facilitate the production of lipids utilised in a variety of applications, a process that could be refined to cater to industrial demands.

Dickkopf-1 (DKK1) is a secretory antagonist that can bind with the Wnt coreceptor to desensitize cells to canonical Wnt ligands. DKN-01 is a specific antibody targeting secreted DKK1, which has been investigated as a monotherapy or combination therapy for various malignant tumors, including gastric cancer (GC). Tumor-associated macrophages (TAMs) with high plasticity usually present M2 phenotype, which can promote tumor progression. The aim of this study was to investigate the effect of DKN-01 on macrophage polarization in GC and the underlying molecular mechanism. To ascertain the effect of DKN-01 on GC tumor growth, we established a tumor-bearing mouse model and found that DKN-01 treatment suppressed tumor growth efficiently. Through RNA-seq and pathway enrichment analysis, we identified that the differentially expressed genes after DKN-01 treatment are associated with tumor immune-related pathways. Macrophage polarization was assessed using immunohistochemistry and quantitative real-time polymerase chain reaction. DKN-01 and knockdown of DKK1 promoted M1 polarization and inhibited M2 polarization of macrophages, while DKK1 overexpression got the opposite results. Moreover, DKN-01 activated the cGAS/STING pathway, while the inactivation of cGAS-STING pathway using RU.521 reversed the inhibition of tumor growth in vivo and macrophage M2 polarization caused by DKN-01. This study reveals that DKN-01 suppresses GC tumor growth through activating cGAS-STING pathway to block macrophage M2 polarization.

Cardiovascular diseases are disorders of the heart and vascular system that cause high mortality rates worldwide. Vascular endothelial cell (VEC) injury caused by oxidative stress (OS) is an important event in the development of various cardiovascular diseases, including ischemic heart disease. This study aimed to investigate the critical roles and molecular mechanisms of long non-coding RNA (lncRNA) SNHG16 in regulating vascular endothelial cell injury under oxidative stress. We demonstrated that SNHG16 was significantly downregulated and miRNA-23a-3p was notably induced in human vascular endothelial cells under OS. Overexpressing SNHG16 or silencing miR-23a-3p effectively mitigated the OS-induced VEC injury. Additionally, glutamine metabolism of VECs was suppressed under OS. SNHG16 protected the OS-suppressed glutamine metabolism, while miR-23a-3p functioned oppositely in VECs. Furthermore, SNHG16 downregulated miR-23a-3p by sponging miR-23a-3p, which direct targeted the glutamine metabolism enzyme, GLS. Finally, restoring miR-23a-3p in SNHG16-overexpressing VECs successfully reversed the protective effect of SNHG16 on vascular endothelial cell injury under OS. In summary, our results revealed the roles and molecular mechanisms of the SNHG16-mediated protection against VEC injury under OS by modulating the miR-23a-3p-GLS pathway.

The epidermal growth factor receptor (EGFR) has been extensively studied for its critical role in the development and progression of various malignancies. In this comprehensive pan-cancer analysis, we investigated the potential of EGFR as a biomarker across multiple tumor types; a comprehensive analysis of EGFR gene mutation and copy number variation was conducted using cBioPortal and other tools. Utilizing multi-omics datasets from The Cancer Genome Atlas (TCGA), we analyzed EGFR's expression patterns, prognostic implications, genetic mutations, and molecular interactions in different cancers. Our findings revealed frequent dysregulation of EGFR in several tumor types, including lung cancers and glioblastoma multiforme. High EGFR expression was consistently associated with poor clinical outcomes, such as reduced overall survival, disease-free survival, and progression-free survival. Genetic alteration analysis indicated a high frequency of EGFR mutations and copy number variations, particularly in glioblastoma multiforme. Additionally, our study suggests a complex relationship between EGFR expression and cancer-associated fibroblast infiltration, which may contribute to an immunosuppressive tumor microenvironment. These findings underscore the clinical relevance of EGFR as a prognostic biomarker and therapeutic target, emphasizing the need for further research and the development of targeted therapies to enhance patient outcomes in cancers with EGFR alterations. The co-expression network of EGFR with genes and proteins involved in cell cycle regulation and mitotic control provided insights into the molecular mechanisms of oncogenesis.

The aim of the present work was to partially purify and characterize an Antarctic polygalacturonase and to determine the enzyme's potential in pectin extraction and vegetal maceration at 20 °C. Polygalacturonase was purified by chromatography to obtain an enzymatic preparation of specific activity 30.3 U.mg^-1. Optimal conditions for the polygalacturonase activity were 45 °C and pH 5.0-6.0, and the activation energy for the reaction was 41.8 kJ.mol^-1. Of the enzyme activity, 100% was retained after 3 h at 40 °C. The enzyme was remarkably stable for an hour over a wide range of pH (2.0-12.0). Polygalacturonase activity was slightly reduced in the presence of Ca⁺², Fe⁺³, K⁺, Mn⁺², and Zn⁺², whereas Hg⁺² reduced the activity by 60%, suggesting a thiol-dependent catalysis. The apparent molecular weight of the enzyme was 33 kDa. The kinetic constants evaluated against polygalacturonic acid were 0.17 mg.ml^-1 (K_m), 480 s^-1 (K_cat), and 7.9 µmol.mg^-1.min^-1 (V_max). The enzyme was active against different pectic substrates. Thin-layer chromatography revealed an endo-mechanism of action. Polygalacturonase digested lime pomace to aid the extraction of high-methoxylated pectin at 20 °C and increased the vegetal maceration of Capsicum annuum by 24% over the control values.

In the current research, a chitosan/broccoli extract/ZnO nanoparticle (CH/BE/ZnO) bionanocomposite was created. The physicochemical properties of CH/BE/ZnO bionanocomposite were investigated using a variety of methods, including field emission scanning electron microscopy (FESEM), elemental analysis (CHN-O), X-ray diffraction (XRD), Fourier transform infrared spectrum (FTIR), Brunauer-Emmett-Teller (BET), and transmission electron microscopy (TEM). The CH/BE/ZnO bionanocomposite's biological activity was assessed by examining its cytotoxicity capabilities against a bone cancer cell line (MG63). The total pore volume and specific surface area of CH/BE/ZnO are 0.134 cm³/g and 16.99 m²/g, respectively. The IC50 results for CH/BE/ZnO bionanocomposite in bone cancer investigations using the MTT test against the MG63 cell line was 115 μg/mL. The results indicate that the CH/BE/ZnO bionanocomposite is an effective chemotherapeutic agent against human osteosarcoma. The CH/BE/ZnO bionanocomposite showed high performance and structure, which means innovating nanomaterial agents for biological applications in the future.

This study aimed to evaluate the antimicrobial effect of coated orthodontic molar tubes (COMT) with zinc oxide nanoparticles (ZnO NPs) using an electrophoretic deposition method (EPD) and to evaluate the orthodontic molar tubes (OMT) bond failure rate. Seventy-two orthodontic molar tubes (OMTs) for second molars were divided into two groups 36 each; one group coated with ZnO NPs and the other control negative uncoated. The OMT was coated using the EPD method with ZnO NPs in a concentration of 10 g/l. The OMTs were randomly allocated using a split-mouth, cross-quadrant design. After 2 weeks of appliance placement, swabs were taken from the surface of the OMTs for microbial assessment against Streptococcus mutans, Lactobacillus acidophilus, and total bacterial counts; additionally, plaque and gingival indices were assessed. The patient was followed for 3 months to evaluate the bond failure rate. The COMT showed a statistically significant reduction in total bacterial accounts, S. mutans, and L. acidophilus compared to UOMT (P < 0.001). Furthermore, the plaque and gingival indices near COMT were significantly less than that of UOMT. The bond failure rate was not significant between the COMT and UOMT. The COMT with ZnO NPs has potent antibacterial activity against the tested pathogens with a reduction in the amount of plaque accumulation. The use of the EPD method was feasible without adverse effects on the orthodontic molar tubes bond failure rate.