The Microstructure and Thermal Conductive Behavior of Three-Dimensional Carbon/Carbon Composites with Ultrahigh Thermal Conductivity.

Carbon-based composite materials, denoted as C/C composites and possessing high thermal conductivity, were synthesized utilizing a three-dimensional (3D) preform methodology. This involved the orthogonal weaving of mesophase pitch-based fibers in an X (Y) direction derived from low-temperature carbonization, and commercial PAN-based carbon fibers in a Z direction. The 3D preforms were saturated with mesophase pitch in their raw state through a hot-pressing process, which was executed under relatively low pressure at a predetermined temperature. Further densification was achieved by successive stages of mesophase pitch impregnation (MPI), followed by impregnation with coal pitch under high pressure (IPI). The microstructure and thermal conductivity of the C/C composites were systematically examined using a suite of analytical techniques, including Scanning Electron Microscopy (SEM), X-ray Diffraction (XRD), and PLM, amongst others. The findings suggest that the volumetric fraction of fibers and the directional alignment of the mesophase pitch molecules can be enhanced via hot pressing. The high graphitization degree of the mesophase pitch matrix results in an increased microcrystalline size and thus improved thermal conductivity of the C/C composite. Conversely, the orientation of the medium-temperature coal pitch matrix is relatively low, which compensates for the structural inadequacies of the composite material, albeit contributing minimally to the thermal conductivity of the resultant C/C composites. Following several stages of impregnation with mesophase pitch and subsequent impregnation with medium-temperature coal pitch, the 3D C/C composites yielded a density of 1.83 and 2.02 g/cm3. The thermal conductivity in the X (Y) direction was found to be 358 and 400 W/(m·K), respectively.

Antibiotic resistance genes in constructed wetlands: Driving indicators and risk assessment.

Constructed wetlands (CWs) were responsible for the in-depth purification of wastewater, providing an ideal environment for the transport, acquisition, and dissemination of antibiotic resistance genes (ARGs). A better understanding of influencing factors and risks of ARGs in CWs was deemed indispensable. In this research, the abundance of ARGs and mobile genetic elements (MGEs) was determined to be higher in summer and spring, ranging from 53.7 to 8.51 × 106 and 30.9-6.02 × 106 copies/mL, respectively. Seasonal variation significantly influenced the abundance of ARGs and MGEs, as well as the co-occurrence patterns among ARGs, MGEs and bacteria. However, the environmental gradients, from the influent (CW01) to the effluent (CW10), did not impose significant effects on the abundance of ARGs and MGEs. Furthermore, the ratios of pathogenic bacteria to ARG hosts and ARG risks index decreased by 50.4% and 88.54% along with the environmental gradients, indicating that CWs could act as barriers to the transfer of ARGs. Partial least squares-path modeling (PLSPM) revealed that temperature was the main driving factor of ARGs, followed by MGEs, stable and differential bacteria. This finding effectively and innovatively explored the driving indicators for the variations and risks of ARGs caused by spatial-temporal variations, providing new insights into the evaluation and control of ARGs in CWs.

Fate of antibiotic resistance genes and bacteria in a coupled water-processing system with wastewater treatment plants and constructed wetlands in coastal eco-industrial parks.

In coastal eco-industrial zones, wastewater treatment plants (WWTPs) and constructed wetlands (CWs) can alleviate the challenge of water shortage and the negative effect of sewage discharge, while the problems of antibiotic resistance genes (ARGs) have not attracted enough attention. In this research, the Wafergen SmartChip system was adopted to investigate the ARG profiles in a coupled system combined WWTPs and CWs in a coastal industrial park. Potential risks of antibiotic resistance in chemical industrial wastewater were confirmed due to the higher abundance of target ARGs (> 107 copies/mL). General decline with partial enrichment in absolute and relative abundance of ARGs from the WWTPs to CWs revealed the effective removal of ARGs in the coupled system, while the fate of different ARG types varied greatly. Aminoglycoside and sulfonamide ARGs were detected with higher abundance (up to 5.34 ×107 and 3.61 ×107 copies/mL), especially aac(6')-Ib and sul1. Denitrification, secondary sedimentation, and acid hydrolysis contributed to the removal of aminoglycoside, sulfonamide, ß-lactamase, chloramphenicol, and multidrug ARGs. Catalytic ozonation contributed to the removal of tetracycline and MLSB ARGs. Subsurface CWs worked effectively for the removal of sulfonamide, tetracycline, and multidrug ARGs, especially tetX, cphA, tetG, and strB. Close correlations between ARGs and MGEs emphasized the vital roles of anthropogenic pollutants and horizontal gene transfer on the diffusion of ARGs. Actinobacteria, Bacteroidota, and Cyanobacteria were dominant in the CWs, while Proteobacteria, Firmicutes, and Planctomycetota were prevalent in the WWTPs. Redundancy analysis and variance partitioning analysis indicated that transposase and water quality posed greater influences on the distribution of ARGs. Co-occurrence network revealed that potential multiple antibiotic resistant pathogenic bacteria decreased in the CWs. The coupled system has a limited effect on the reduction of ARGs and potential ARG hosts, providing a comprehensive insight into the fate of ARGs in conventional water-processing systems.

SOD1 Gene Silencing Promotes Apoptosis and Suppresses Proliferation of Heat-Stressed Bovine Granulosa Cells via Induction of Oxidative Stress.

Heat stress (HS) compromises dairy cattle reproduction by altering the follicular dynamics, oocyte maturation, and normal physiological function of ovarian granulosa cells (GCs), eventually resulting in oxidative damage and cell apoptosis. To protect the cells from oxidative damage, the Superoxide dismutase-1 (SOD1) degraded the hydrogen peroxide (H2O2) to oxygen (O2) and water. The objective of the current study was to investigate the impact of SOD1 silencing on intracellular ROS accumulation, cell viability, MMP, hormone synthesis (P4, E2), cell proliferation, and apoptosis in GCs under HS. The mechanistic role of SOD1 regulation in the heat-stressed GCs was explored. SOD1 gene was successfully silenced in GCs and confirmed at both transcriptional and translational levels. We found that silencing of SOD1 using siRNA under HS aggravated intracellular accumulation of reactive oxygen species, apoptosis, disrupted the mitochondrial membrane potential (MMP), altered transition of the cell cycle, and impaired synthesis of progesterone (P4) and estrogen (E2) in GCs. The associative apoptotic, steroidogenic, and cell cycle genes (BAX, Caspase-3, STAR, Cyp11A1, HSP70, PCNA, and CyclinB1) were used to confirm the results. These results identify a novel role of SOD1 in the modulation of bovine ovarian GC apoptosis, which provides a target for improving the fertility of heat-stressed dairy cows in summer.

Unique bacterial communities and potential function along the vertical gradient in the deepest marine blue hole.

The Sansha Yongle Blue Hole is the deepest blue hole in the world discovered so far, while its great potential and values have not been fully exploited regarding microbial communities. A large-scale sampling was performed at different depths (0-270 m) inside the blue hole. Based on high-throughput sequencing, the diversity and richness of bacterial communities were relatively higher in oxic and euphotic layer, and at depths of 180-230 m in anoxic layer. Proteobacteria was dominant with mean relative abundance of 64.7%. As the representative genera, Thiomicrospira and Arcobacter were detected with higher abundances up to 96.1% and 31.5% in the anaerobic environment. Principal co-ordinates analysis, one-way ANOVA and network analysis highlighted the distinctive species at different depths. Correlation analysis illustrated the significant correlations between the bacteria and environmental elements of dissolved oxygen, temperature, salinity, pH, sulphur and nutrient. Phylogenetic analysis indicated that the microbial ecosystem was characterized with infrequent and unidentified microorganisms in the deep layer. This research revealed the unique microbial ecosystem and potential functions in regulating ecosystem productivity and cycling of carbon, sulphur and nitrogen. Comprehensive and long-term investigations in the Sansha Blue Hole should be taken to conserve the peculiar ecosystem.

RNAi-Mediated Silencing of Catalase Gene Promotes Apoptosis and Impairs Proliferation of Bovine Granulosa Cells under Heat Stress.

Heat stress in dairy cattle is recognized to compromise fertility by altering the functions of ovarian follicle-enclosed cells, e.g., oocyte and granulosa cells (GCs). Catalase is an antioxidant enzyme that plays a significant role in cellular protection against oxidative damage by the degradation of hydrogen peroxide to oxygen and water. In this study, the role and mechanism of CAT on the heat stress (HS)-induced apoptosis and altered proliferation of bovine GCs were studied. The catalase gene was knocked-down successfully in bovine GCs at both the transcriptional and translational levels. After a successful knockdown using siRNA, GCs were divided into HS (40 °C + NC and 40 °C + CAT siRNA) and 38 °C + NC (NC) groups. The GCs were then examined for ROS, viability, mitochondrial membrane potential (MMP), cell cycle, and biosynthesis of progesterone (P4) and estrogen (E2) hormones. The results indicated that CAT silencing promoted ROS production and apoptosis by up-regulating the Bcl-2-associated X protein (BAX) and Caspase-3 genes both at the transcriptional and translational levels. Furthermore, the knockdown of CAT markedly disrupted the MMP, impaired the production of P4 and E2, altered the progression of the G1 phase of the cell cycle, and decreased the number of cells in the S phase. This was further verified by the down-regulation of proliferating cell nuclear antigen (PCNA), CyclinB1, steroidogenic acute regulatory protein (STAR), and cytochrome P450 family 11 subfamily A member 1 (Cyp11A1) genes. Our study presented a novel strategy to characterize how CAT can regulate cell proliferation and apoptosis in GCs under HS. We concluded that CAT is a broad regulatory marker in GCs by regulating apoptosis, cellular progression, and simultaneously by vital fluctuations in hormonal signaling. Our findings infer a crucial evidence of how to boost the fertility of heat-stressed cows.

Impact of Microstructure on the Electrochemical Performance of Round-Shaped Pitch-Based Graphite Fibers.

In this study, three kinds of round-shaped pitch-based graphite fiber with different microstructural features (crystallinity and carbon layer orientation) were fabricated by melt-spinning, preoxidation, carbonization and graphitization. The morphology, crystalline size and carbon layer orientation of carbon fibers from different pitch precursors and spinning rates were characterized through X-ray diffraction, scanning electron microscopy and transmission electron analyses. The correlation of the electrochemical performance and microstructure of graphite fibers as anode materials for lithium-ion batteries was investigated. The results suggest that large-diameter anisotropic graphite fibers (L-AF3000) with a radial texture of the transverse section are more favorable for lithium intercalation storage. The discharge capacity of L-AF3000 is 319.1 mAh∙g-1 at 0.1 C (current density). Nevertheless, the capacity drops to 209.9 mAh∙g-1 at a high current density of 1 C, and the capacity retention is only 82.2% over 100 cycles at 0.1 C. Small-diameter anisotropic graphite fibers (S-AF3000) with a spiral-shaped wrinkle texture of the transverse section possess discharge capacities of 284.1 mAh∙g-1 at 0.1 C and 260.2 mAh∙g-1 at a high current density of 1 C. Meanwhile, the best capacity retention of the fibers is 101.6% over 100 cycles at 0.1 C. The results suggest that the disordered carbon layers in S-AF3000 can retain the structural integrity of fibers as anode material for lithium-ion batteries and thus obtain excellent cycle stability. In addition, larger crystalline sizes of fibers correspond to higher discharge capacity, and a smaller diameter is beneficial to the fast insertion and extraction of lithium-ion in fibers.

Effects of Inhibin A on Apoptosis and Proliferation of Bovine Granulosa Cells.

Inhibin A is well known for its inhibitory properties against follicle-stimulating hormone (FSH), released through a pituitary-gonadal negative feedback loop to regulate follicular development. Ovarian folliculogenesis, hormonal biosynthesis, and gametogenesis are dependent on inhibins, playing vital roles in promoting or inhibiting cell proliferation. The present study explored the physiological and molecular response of bovine granulosa cells (GCs) to different concentrations of inhibin A in vitro. We treated the primary GCs isolated from ovarian follicles (3-6 mm) with different levels of inhibin A (20, 50, and 100 ng/mL) along with the control (0 ng/mL) for 24 h. To evaluate the impact of inhibin A on GCs, several in vitro cellular parameters, including cell apoptosis, viability, cell cycle, and mitochondrial membrane potential (MMP) were detected. Besides, the transcriptional regulation of pro-apoptotic (BAX, Caspase-3) and cell proliferation (PCNA, CyclinB1) genes were also quantified. The results indicated a significant (p < 0.05) increase in the cell viability in a dose-dependent manner of inhibin A. Likewise, MMP was significantly (p < 0.05) enhanced when GCs were treated with high doses (50, 100 ng/mL) of inhibin A. Furthermore, inhibin A dose (100 ng/mL) markedly improved the progression of the G1 phase of the cell cycle and increased the cell number in the S phase, which was supported by the up-regulation of the proliferating cell nuclear antigen PCNA (20, 50, and 100ng/mL) and CyclinB (100 ng/mL) genes. In addition, higher doses of inhibin A (50 and 100 ng/mL) significantly (p < 0.05) decreased the apoptotic rate in GCs, which was manifested by down regulating BAX and Caspase-3 genes. Conclusively, our study presented a worthy strategy for the first time to characterize the cellular adaptation of bovine GCs under different concentrations of inhibin A. Our results conclude that inhibin A is a broad regulatory marker in GCs by regulating apoptosis and cellular progression.

Cellular and Molecular Adaptation of Bovine Granulosa Cells and Oocytes under Heat Stress.

Heat stress has long been recognized as a challenging issue that severely influences the reproductive functions of dairy cattle, disrupting oocyte development during fetal growth. These detrimental effects of heat stress are the result of either the hyperthermia associated with heat stress or the physiological adjustments made by the heat-stressed animal to regulate body temperature. In addition, elevated temperatures have been implicated in increasing the production of reactive oxygen species. Thus, understanding the impact of heat stress on reproductive functions, from a cellular to molecular level, might help in selecting heat-resilient dairy cattle and developing heat stress mitigation strategies. In the present paper, we have attempted to describe the changes in the reproductive system and function of dairy cattle in response to heat stress by reviewing the latest literature in this area. The review provides useful knowledge on the cellular and genetic basis of oocyte and granulosa cells in heat-stressed dairy cattle, which could be helpful for future research in this area.

No imprinted XIST expression in pigs: biallelic XIST expression in early embryos and random X inactivation in placentas.

Dosage compensation, which is achieved by X-chromosome inactivation (XCI) in female mammals, ensures balanced X-linked gene expression levels between the sexes. Although eutherian mammals commonly display random XCI in embryonic and adult tissues, imprinted XCI has also been identified in extraembryonic tissues of mouse, rat, and cow. Little is known about XCI in pigs. Here, we sequenced the porcine XIST gene and identified an insertion/deletion mutation between Asian- and Western-origin pig breeds. Allele-specific analysis revealed biallelic XIST expression in porcine ICSI blastocysts. To investigate the XCI pattern in porcine placentas, we performed allele-specific RNA sequencing analysis on individuals from reciprocal crosses between Duroc and Rongchang pigs. Our results were the first to reveal that random XCI occurs in the placentas of pigs. Next, we investigated the H3K27me3 histone pattern in porcine blastocysts, showing that only 17-31.8% cells have attained XCI. The hypomethylation status of an important XIST DMR (differentially methylated region) in gametes and early embryos demonstrated that no methylation is pre-deposited on XIST in pigs. Our findings reveal that the XCI regulation mechanism in pigs is different from that in mice and highlight the importance of further study of the mechanisms regulating XCI during early porcine embryo development.

Tumor-derived mesenchymal-stem-cell-secreted IL-6 enhances resistance to cisplatin via the STAT3 pathway in breast cancer.

Cisplatin is used for the treatment of a range of solid malignant tumors; however, with prolonged treatment durations, the sensitivity of tumor cells to the drug decreases owing to an unclear mechanism of drug resistance. The present study aimed to investigate whether breast-cancer-tissue-derived mesenchymal stem cells (BC-MSCs) are involved in mediating the effects of cisplatin on breast cancer cells, and which component of the BC-MSC conditioned medium (BC-MSC-CM) exhibited an anti-apoptotic effect. Cytokines/chemokines in BC-MSC-CM were quantified using a Luminex immunoassay, and reverse transcription-quantitative polymerase chain reaction analysis detected interleukin-6 (IL-6) levels in MCF-7 cells following different treatments. MTT and flow cytometry analysis measured cell vitality and apoptosis, respectively, and activation of signal transduced and activator of transcription 3 (STAT3) was evaluated by western blotting. BC-MSCs reversed the pro-apoptotic effect of cisplatin and enhanced the proliferation of MCF-7 cells more potently than bone-marrow-derived MSCs. Further study revealed that BC-MSCs secreted IL-6 to protect MCF-7 cells from apoptosis and promote their survival. Neutralizing IL-6 with a specific antibody partially inhibited the IL-6/STAT3 signaling pathway and reversed the promoter role of BC-MSCs in MCF-7 cells. Taken together, the findings of the present study indicated that BC-MSCs decreased the level of cisplatin-induced apoptosis in MCF-7 cells by activating the IL-6/STAT3 pathway in cancer cells. BC-MSCs, as important cells in the tumor microenvironment, have a key role in the treatment of breast cancer.

Diphenyl ethers from a marine-derived isolate of Aspergillus sp. CUGB-F046.

One new diphenyl ether, diorcinol K (1), along with three known compounds, diorcinols D (2), F (3) and I (4) were isolated from the fermentation media of a marine-derived fungus Aspergillus sp. CUGB-F046 which was isolated from a sediment sample collected from the Bohai Sea, China. Their structures were elucidated by detailed spectroscopic methods. Compounds 1, 2 and 4 displayed significant antibacterial activities against Staphylococcus aureus and methicillin-resistant S. aureus with MIC values of 3.125, 6.25 and 6.25 µg/mL, respectively.

Human umbilical cord mesenchymal stem cells attenuate cisplatin-induced acute and chronic renal injury.

Mesenchymal stem cell is becoming a promising candidate in acute kidney injury (AKI). We first reported that human umbilical cord mesenchymal stem cells (hucMSCs) could ameliorate renal function in ischemic/reperfusion AKI rats, but the role of hucMSCs in cisplatin-induced acute and chronic injury has been demonstrated. More specifically, it is still unknown whether hucMSCs halt renal interstitial fibrosis. In this study, we investigated the effect of hucMSCs in cisplatin-induced kidney injury and explored the mechanism of action. Blood urea nitrogen (BUN) and creatinine (Cr) analyses showed amelioration of functional parameters in hucMSC-treated rats at early damage. Transplantation with hucMSCs promoted renal cell regeneration, inhibited cell apoptosis, abrogated inflammatory responses and protected mitochondria. Moreover, Masson's trichrome staining demonstrated reduced levels of fibrosis in kidney tissues of hucMSC-treated rats at six and eight weeks after cisplatin injection. These results were corroborated by reduced collagen deposit, the ratio of Bax to Bcl-2 and transforming growth factor ß mRNA expression. Furthermore, hucMSCs prevented the epithelial-mesenchymal transition (EMT) in injury renal tissues, leading to the attenuation of chronic renal interstitial fibrosis. Taken together, our findings suggested that hucMSCs could decrease the kidney from development of later renal interstitial fibrosis by amelioration of early AKI.

Human umbilical cord mesenchymal stem cells attenuate cisplatin-induced acute and chronic renal injury.

Mesenchymal stem cell is becoming a promising candidate in acute kidney injury (AKI). We first reported that human umbilical cord mesenchymal stem cells (hucMSCs) could ameliorate renal function in ischemic/reperfusion AKI rats, but the role of hucMSCs in cisplatin-induced acute and chronic injury has been demonstrated. More specifically, it is still unknown whether hucMSCs halt renal interstitial fibrosis. In this study, we investigated the effect of hucMSCs in cisplatin-induced kidney injury and explored the mechanism of action. Blood urea nitrogen (BUN) and creatinine (Cr) analyses showed amelioration of functional parameters in hucMSC-treated rats at early damage. Transplantation with hucMSCs promoted renal cell regeneration, inhibited cell apoptosis, abrogated inflammatory responses and protected mitochondria. Moreover, Masson's trichrome staining demonstrated reduced levels of fibrosis in kidney tissues of hucMSC-treated rats at six and eight weeks after cisplatin injection. These results were corroborated by reduced collagen deposit, the ratio of Bax to Bcl-2 and transforming growth factor ß mRNA expression. Furthermore, hucMSCs prevented the epithelial-mesenchymal transition (EMT) in injury renal tissues, leading to the attenuation of chronic renal interstitial fibrosis. Taken together, our findings suggested that hucMSCs could decrease the kidney from development of later renal interstitial fibrosis by amelioration of early AKI.

Exosomes released by human umbilical cord mesenchymal stem cells protect against cisplatin-induced renal oxidative stress and apoptosis in vivo and in vitro.

INTRODUCTION: Administration of bone marrow mesenchymal stem cells (MSCs) or secreted microvesicles improves recovery from acute kidney injury (AKI). However, the potential roles and mechanisms are not well understood. In the current study, we focused on the protective effect of exosomes derived from human umbilical cord mesenchymal stem cells (hucMSC-ex) on cisplatin-induced nephrotoxicity in vivo and in vitro. METHODS: We constructed cisplatin-induced AKI rat models. At 24 h after treatment with cisplatin, hucMSC-ex were injected into the kidneys via the renal capsule; human lung fibroblast (HFL-1)-secreted exosomes (HFL-1-ex) were used as controls. All animals were killed at day 5 after administration of cisplatin. Renal function, histological changes, tubular apoptosis and proliferation, and degree of oxidative stress were evaluated. In vitro, rat renal tubular epithelial (NRK-52E) cells were treated with or without cisplatin and after 6 h treated with or without exosomes. Cells continued to be cultured for 24 h, and were then harvested for western blotting, apoptosis and detection of degree of oxidative stress. RESULTS: After administration of cisplatin, there was an increase in blood urea nitrogen (BUN) and creatinine (Cr) levels, apoptosis, necrosis of proximal kidney tubules and formation of abundant tubular protein casts and oxidative stress in rats. Cisplatin-induced AKI rats treated with hucMSC-ex, however, showed a significant reduction in all the above indexes. In vitro, treatment with cisplatin alone in NRK-52E cells resulted in an increase in the number of apoptotic cells, oxidative stress and activation of the p38 mitogen-activated protein kinase (p38MAPK) pathway followed by a rise in the expression of caspase 3, and a decrease in cell multiplication, while those results were reversed in the hucMSCs-ex-treated group. Furthermore, it was observed that hucMSC-ex promoted cell proliferation by activation of the extracellular-signal-regulated kinase (ERK)1/2 pathway. CONCLUSIONS: The results in the present study indicate that hucMSC-ex can repair cisplatin-induced AKI in rats and NRK-52E cell injury by ameliorating oxidative stress and cell apoptosis, promoting cell proliferation in vivo and in vitro. This suggests that hucMSC-ex could be exploited as a potential therapeutic tool in cisplatin-induced nephrotoxicity.

Mesenchymal stem cells relieve fibrosis of Schistosoma japonicum-induced mouse liver injury.

Mesenchymal stem cells (MSCs) have gained popularity for their potential as seed cells to treat various human diseases, including pathogenic infections. Schistosoma japonicum (S. japonicum) infection is characterized by formation of parasite egg granulomas and host liver fibrosis. MSCs have been proposed as useful treatments of S. japonicum infection, but the efficacy and underlying mechanisms remain unknown. Herein, we report that MSCs were able to ameliorate S. japonicum-induced liver injury in vivo and this effect was enhanced by combining MSCs with conventional drug praziquantel (PZQ). Kunming strains of mice were infected with S. japonicum and treated with vehicle, MSCs, PZQ or PZQ + MSCs. MSC treatment not only prolonged the survival time of infected mice but reduced egg granuloma diameter and decreased the concentrations of serum transforming growth factor-ß1 and hyaluronic acid. MSC treatment also inhibited collagen deposition and reduced the expression of collagen type 3, α-smooth muscle actin and vimentin in infected mouse liver tissues. Collectively, our findings suggest that MSC treatment represents a novel therapeutic approach for S. japonicum-induced liver injury and fibrosis.