Search

Objective The study aims to optimize the conditions for constructing orthotopic nude mouse models of liver cancer by injecting human liver tumor cell lines and to explore appropriate timings for drug administration. Methods Human hepatocellular carcinoma Hep3B and hepatoblastoma HepG2 cell lines, which stably expressing the luciferase reporter gene (LUC), were selected. The linear correlation between the luciferase luminescence intensity and the number of liver tumor cells was analyzed using a Small Animal In Vivo Imaging system to verify the luminescent efficiency of the human liver tumor cells. Different concentrations (8×106, 2.4×107, 7.2×107 cells/mL) and resuspension media (PBS, Matrigel) of human liver tumor cell suspensions HepG2-LUC and Hep3B-LUC were orthotopically inoculated into the liver lobes of 5-week-old female BALB/c nude mice (12 groups, 7 mice each) to construct human liver tumor nude mouse orthotopic cancer models. Every 7 days, the weights of mice were recorded, and the growth of orthotopic tumors was monitored using the Small Animal In Vivo Imaging system. On day 35 post-cell inoculation, mouse livers were dissected, and pathological slices were prepared for HE staining to observe histopathological changes in liver tissues. Results The luminescence intensity of human liver tumor cell lines was positively correlated with the number of cells (R2=0.983 1, R2=0.970 5), indicating their suitability for orthotopic model construction. Successful modeling was achieved in the high-concentration groups of HepG2-LUC, the low-, medium-, and high-concentration groups of HepG2-LUC+Matrigel, the medium- and high-concentration groups of Hep3B-LUC, and the low-, medium-, and high-concentration groups of Hep3B-LUC+Matrigel. For both HepG2-LUC+Matrigel and Hep3B-LUC+Matrigel groups, mice in the high-concentration groups exhibited significantly reduced body weight compared to the low- and medium-concentration groups (both with P0.950 0), and reached a minimum of 1.0×107 p/(s·cm²·sr) by day 14 post-transplantation. Mice in the low- and medium-concentration groups of HepG2-LUC and the low-concentration group of Hep3B-LUC showed no significant pathological changes, while the other groups exhibited evident liver tumors and hepatocyte lesions. Conclusion For the HepG2-LUC cell line, the recommended injection volume is 50 µL with a cell density of 2.4×107 cells/mL, resuspended with Matrigel, followed by drug administration or prognostic measures on day 7 post-modeling. For the Hep3B-LUC cell line, the recommended injection volume is 50 µL with a cell density of 7.2×107 cells/mL, not resuspended with Matrigel, with administration or prognostic measures on day 14 post-modeling.

Using rectorite as raw material, REC is modified by nitric acid, TiO2 is attached to the surface of the acidized modified REC tablet to form modified REC-TiO2 composite materials by the sol-gel method, and its adsorption performance and photocatalytic properties were studied. The results show that the adsorption of REC, modified REC, modified REC-TiO2 composite materialtoporads to methylene blue increased with the increase of equilibrium concentration. The process of adsorption MB of modified REC-TiO2 composite materials is an endothermic process. The adsorption of REC, modified REC, modified REC-TiO2 composite materials to MB increased with the increase of temperature. When the temperature is 25 degree, the maximum adsorption capacity of REC is 93.985 mg/g, the maximum adsorption capacity of modified REC is 107.006 mg/g, and the maximum adsorption capacity of modified REC-TiO2 is 120.773 mg/g. The degradation rate of MB and p-nitrophenol by modified REC-TiO2 composite under illumination are 99% and 98%, respectively. The decontamination rate of MB and 4-NP of modified REC-TiO2 composites under darkness was 50% and 0.8%, respectively. Under light conditions, the degradation rate of MB and 4-NP in modified REC-TiO2 composite materials is improved.

The genus Camphora encompasses species of significant ecological and economic importance, such as C. parthenoxylon and C. officinarum, which exhibit distinct phenotypic traits and stress responses. This study seeks to elucidate the molecular basis of cold tolerance through comparative transcriptomic analysis complemented by physiological characterization. RNA sequencing revealed 6123 differentially expressed genes between the two species, with enriched pathways related to cold stress, oxidative stress, carotenoid biosynthesis, and photosynthesis. Key genes, such as annexin D5, chlorophyll a/b-binding protein, early light-induced protein 1, 9-cis-epoxycarotenoid dioxygenase, were identified as critical regulators of frost resistance, photosynthetic efficiency, and carotenoid biosynthesis. Functional enrichment analyses highlighted the involvement of signal transduction, membrane stabilization, and secondary metabolism in adaptive responses. Physiological assays supported these findings, showing higher chlorophyll and carotenoid content and enhanced antioxidative enzyme activities in C. parthenoxylon. These results provide valuable insights into the genetic and biochemical mechanisms underlying stress adaptation in Camphora species and offer promising targets for enhancing resilience in economically valuable plants. [ABSTRACT FROM AUTHOR]

African swine fever virus (ASFV) is the causative agent of African swine fever (ASF), a severe hemorrhagic disease with a mortality rate reaching 100%. Despite extensive research on ASFV mechanisms, no safe and effective vaccines or antiviral treatments have been developed. Live attenuated vaccines generated via gene deletion are considered to be highly promising. We developed a novel recombinant ASFV strain by deleting MGF360-10L and MGF505-7R, significantly reducing virulence in pigs. In the inoculation experiment, pigs were infected with 104 50% hemadsorption doses (HAD50) of the mutant strain. All the animals survived the observation period without showing ASF-related clinical signs. Importantly, no significant viral infections were detected in the cohabitating pigs. In the virus challenge experiment, all pigs succumbed after being challenged with the parent strain. RNA-seq analysis showed that the recombinant virus induced slightly higher expression of natural immune factors than the parent ASFV; however, this level was insufficient to provide immune protection. In conclusion, our study demonstrates that deleting MGF360-10L and MGF505-7R from ASFV CN/GS/2018 significantly reduces virulence but fails to provide protection against the parent strain. [ABSTRACT FROM AUTHOR]

Introduction Hypertrophic scars, which are a consequence of alterations in the normal processes involved in wound healing of the skin, are characterized by the proliferation of dermal tissues accompanied by [...], The effects of long non-coding RNAs (lncRNAs) on the proliferation of hypertrophic scars have been described, however, the underlying mechanisms are not well characterized. The present study aimed to investigate the mechanisms of lncRNA H19 in hypertrophic scars. The effects of the lncRNA H19 on the proliferation and apoptosis of hypertrophic scar fibroblasts (HSFs) were analyzed using 5&apos;-ethynyl-2&apos;-deoxyuridine staining, flow cytometry, and 3-(4,5-dimethyl-2- thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT). The results revealed H19 promoted the proliferation and inhibited the apoptosis in HSF. In addition, the binding associations between H19 and microRNA-194 (miR-194), and miR-194 and insulin-like growth factor I receptor (IGF1R) were identified using bioinformatics screening and verified using dual-luciferase assays. Furthermore, the effects of the IGF1R knockdown on H19-induced HSF phenotypes and regulation over the p38 MAPK pathway were determined. Mechanistically, miR-194 was identified as the downstream effector of the H19-mediated phenotypes of HSFs through its ability to directly target IGF1R, thus modulating the p38 MAPK signaling pathway. In conclusion, the findings suggested that H19 may inhibit the apoptosis and promote the proliferation of HSFs through the miR-194/IGF1R/ p38 MAPK signaling axis, thereby contributing to the progression of hypertrophic scars. These findings may provide novel targets for the treatment of hypertrophic scars. Key words: long non-coding RNA H19 imprinted maternally expressed transcript, microRNA-194, insulin-like growth factor- I receptor, p38 MAPK signaling pathway, hypertrophic scar fibroblasts. Les effets des ARN longs non codants (ARNlnc) sur la proliferation des cicatrices hypertrophiques ont ete decrits. Cependant, les modes d&apos;action sous-jacents ne sont pas bien caracterises. La presente etude portait sur les modes d&apos;action de l&apos;ARNlnc H19 dans les cicatrices hypertrophiques. Nous avons etudie les effets de l&apos;ARNlnc H19 sur la proliferation et l&apos;apoptose de fibroblastes de cicatrices hypertrophiques (FCH) a l&apos;aide de la coloration par la 5&apos;-ethynyl-2&apos;-desoxyuridine, de la cytometrie en flux et du test 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT). Les resultats ont revele que le H19 favorisait la proliferation et entrainait une inhibition de l&apos;apoptose des FCH. De plus, nous avons etabli a l&apos;aide de criblage bioinformatique les associations de liaison entre l&apos;H19 et le microARN-194 (miR-194), et entre le miR-194 et les recepteurs de l&apos;IGF1 (pour << insulin-like growth factor-I >>), ce que nous avons verifie a l&apos;aide d&apos;epreuves de double luciferase. En outre, nous avons etabli les effets de la repression (<< knockdown >>) des recepteurs de l&apos;IGF1 sur les phenotypes de FCH induits par le H19, ainsi que la regulation au sein de la voie de signalisation p38 MAPK. Au point de vue des modes d&apos;action, nous avons caracterise le miR-194 comme etant l&apos;effecteur en aval du phenotype des FCH medies par le H19 par sa capacite de cibler directement les recepteurs de l&apos;IGF1, modulant par le fait meme la voie de signalisation p38 MAPK. En conclusion, les resultats laissaient entendre que le H19 pourrait entrainer une inhibition de l&apos;apoptose et favoriser la proliferation des FCH par l&apos;intermediaire de l&apos;axe de signalisation miR-194/ IGF1R/p38 MAPK, contribuant donc a l&apos;evolution des cicatrices hypertrophiques. Ces resultats pourraient donner acces a de nouvelles cibles dans le traitement des cicatrices hypertrophiques. [Traduit par la Redaction] Mots-cles: ARN long non codant, transcrit exprime par la mere impregne du H19, microARN-194, recepteurs de l&apos;IGF1, voie de signalisation p38 MAPK, fibroblastes des cicatrices hypertrophiques.

The co-benefit business model innovation is a potential business strategy for pursuing value creation for multiple stakeholders and sustainable business development. Corporate social responsibility (CSR) has significant implications for the co-benefit business model innovation during crises. Using a grounded coding approach in multiple cases, this study elaborates on how pure commercial CSR, normalized CSR, advanced CSR, and pure CSR constitute different CSR combinations, and how CSR combinations influence the co-benefit business model innovation and bring about the ultimate effects. Using a fuzzy-set qualitative comparative analysis, this study draws the following conclusions: As enterprises grow in size and the social environment improves, enterprises gradually shift their focus from pure commercial CSR to high-level CSR, eventually placing greater emphasis on advanced CSR and pure CSR. Enterprises with strong economic goals should drive co-benefit business model innovation through highly normalized CSR and advanced CSR. Enterprises with general economic goals should promote co-benefit business model innovation through highly advanced CSR. Enterprises with high economic expectations of co-benefit business model should consider both highly commercial CSR and normalized CSR, while enterprises with highly advanced CSR and co-benefit business model innovation tend to generate high social benefits. Finally, the study provides recommendations for enterprises on how to scientifically undertake CSR based on the resource endowment and staged development needs and strike to achieve the co-benefit targets. [ABSTRACT FROM AUTHOR]