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Camellia oleifera, a key economic forestry species in southern China, struggles with low productivity due to suboptimal planting management. Recently, transforming old or unadopted varieties of C. oleifera plantations has been recognized as a means to enhance economic benefits and production. However, the impact of these transformations on soil properties and fungal communities has received little attention. In this study, we targeted pre-renewal old C. oleifera and post-renewal young C. oleifera, Pinus massoniana, and Cunninghamia lanceolata. Through field sampling and soil physicochemical property analysis, we developed a soil quality evaluation system that effectively analyzes fungal community structures and identifies key arbuscular mycorrhizal fungi (AMF) species for soil health. We found that the soil quality evaluation system for this region comprises pH, TK, AK, NO3−, PO4− BG, ACP, F.simpson, AMF.shannon, and AMF.ace, which collectively indicated significant improvements in soil quality following transformation. Notably, the nutritional characteristics of the dominant fungal communities underwent marked changes, with an increase in pathogenic fungi in young C. oleifera and an expansion of ectomycorrhizal fungi in P. massoniana forests. The AMF communities in all four types of forest exhibited aggregation, and Scutellospora and Diversispora emerged as key species in the AMF community of C. oleifera. Additionally, Mortierella and Trichoderma were found to enhance plant resistance to pathogenic fungi. This study demonstrates that forestland transformation positively impacts soil quality and fungal community structure in C. oleifera, which provides valuable insights for future soil management in the region, both in terms of soil quality evaluation and fungal conservation. [ABSTRACT FROM AUTHOR]

Simple Summary: Chinese soft-shell turtle (Pelidiscus sinensis) is a widely farmed aquatic reptile in China. It has of high nutritional, pharmaceutical, and economic value, but wild Chinese soft-shell turtle has been faced with an extreme decline of populations. Thus, it is of great significance to study the germ cells biology and develop the techniques for turtle breeding and genetic resource preserving. Nanog is a homeodomain-containing transcription factor, and it plays a vital role in maintaining the pluripotency of embryonic stem cells; there is a lack of reporting on the Nanog gene in reptile. In this study, the cDNA sequence and promoter of a Nanog gene was identified in P. sinensis, designed as PsNanog. PsNanog gene products were mainly expressed in gonads and were especially rich in ovary. Particularly, PsNanog mRNA and protein was exclusively expressed in germ cells in ovary and testis. Collectively, this is the first report on the gene structure and expression of Nanog in turtle, which may lay a foundation for further functional analysis of the Nanog in turtle, even in the reptiles. Further, PsNanog probably has the conserved and divergent function in regulating cell pluripotency and germ cell development in turtle, compared with other species, including teleosts and mammals. Nanog is a homeodomain-containing transcription factor, and it plays a vital role in maintaining the pluripotency of embryonic stem cells. Nanog's function has been well studied in many species. However, there is lack of reporting on the Nanog gene in reptile. Here, we identified a 1032 bp cDNA sequence of a Nanog gene in Pelidiscus sinensis, known as PsNanog. PsNanog has a highly conserved HD domain and shares a high identity with that of Chelonia mydas and the lowest identity with Oryzias latipes. Similarly, PsNanog presented a tight cluster with C. mydas Nanog, but was far from those of teleosts. Additionally, we cloned a length of 1870 bp PsNanog promoter. Dual luciferase assay showed that the DNA fragment of −1560 to +1 exhibited a high promoter activity. The RT-PCR and RT-qPCR results showed that PsNanog was predominantly expressed in ovary, and then in testis. The in situ hybridization and immunohistochemical analysis showed that PsNanog was expressed in the early primary oocytes and the cytoplasm of the cortical region of stage VIII oocytes in ovary, and distributed in most stages of germ cells in testis. Collectively, the results imply that PsNanog probably has the conserved function in regulating germ cell development across phyla and is also a pluripotent cell gene and expressed in germ cells, which is similar to that in teleosts and mammals. [ABSTRACT FROM AUTHOR]

Cancer stem cells (CSCs) can form new tumors and contribute to post-operative recurrence and metastasis. We showed that CD133CD13 hepatocytes isolated from HuH7 cells and primary HCC cells display biochemical and functional characteristics typical of CSCs, suggesting that CD133CD13 hepatocytes in primary HCC tumors function as CSCs. We also found that arsenite treatment reduced the viability and stemness of CD133CD13 hepatocytes, enhanced the sensitivity of HuH7 cells to pirarubicin, and reduced the tumorigenicity of CD133CD13 hepatocytes xenografts in mice. The effects of sodium arsenite treatment in CD133CD13 hepatocytes were mediated by the post-transcriptional suppression of PML expression and the inhibition of Oct4, Sox2, and Klf4 expression at the transcriptional level. Incomplete rescue of Oct4 expression in arsenic-treated cells ectopically expressing an siRNA-resistant PML transcript suggested that OCT4 regulation in liver CSCs involves other factors in addition to PML. Our findings provide evidence of a specific role for PML in regulating Oct4 levels in liver CSCs and highlight the clinical importance of arsenic for improving the efficacy of other chemotherapeutic agents and the prevention of post-operative HCC recurrence and metastasis. [ABSTRACT FROM AUTHOR]

The traditional faulting distress detection method is a manual detection method, which is inefficient, less reliable and dangerous to use. To overcome these shortcomings, a new automatic detection method based on statistics values of vertical acceleration was proposed. Firstly, noise reduction was applied to acceleration signals by 5 layers Daubechies wavelet, acceleration sequence was put forward from the acceleration-gray map and a new joint location method based on the joint periodicity in the acceleration sequence was obtained. Secondly, three statistic parameters were adopted to analyze the acceleration variation near the joint, which included the position distribution of peak acceleration values (gm) as well as the accumulative mean of acceleration values (ge) and the accumulative absolute mean of acceleration values (ga) at the same position on each slab from the acceleration-gray map. Test results show that the position distribution of peak acceleration values (gm) on slabs is similar to random distribution, peak acceleration values have no relation with faulting distress. The position of peak values and the amplitude near each joint on curves of ge and ga have weak relation with faulting distress. The increment near each joint on the curve of ga has fair relation with faulting distress. Based on the analysis, a new acceleration statistic parameter (af) was put forward to estimate the faulting value, which had good relation with faulting distress. [ABSTRACT FROM AUTHOR]

Abstract: This paper reports the reactive ion etching (RIE) characteristics of benzocyclobutene (BCB) in sulfur hexafluoride/oxygen (SF6/O2) plasmas. The dependence of etching rate and etch anisotropy on the processing parameters, including RF power, chamber pressure, and SF6 concentration, are investigated comprehensively ranging from 50 to 200W, 22.5 to 270mTorr, and 0% to 80%, respectively. The BCB etching rate increases with chamber pressure and RF power in spite of nonlinearity, but decreases with the increase in SF6 concentration. Anisotropic etching can be achieved using low chamber pressure, large RF power, and high SF6 concentration. To avoid grass-like residue that happens at low pressure and large power fluorine-poor conditions, processing parameters with respect to residue-free etching are recommended. The etching mechanisms of the dependence of the etching characteristics on the processing parameters are discussed. Optimal processing parameters are presented as a guideline for isotropic etching of BCB as sacrificial layers to release structures and for anisotropic etching of BCB to precisely control etching dimensions and profiles. [Copyright &y& Elsevier]

Cancer stem cells (CSCs) can form new tumors and contribute to post-operative recurrence and metastasis. We showed that CD133 + CD13 + hepatocytes isolated from HuH7 cells and primary HCC cells display biochemical and functional characteristics typical of CSCs, suggesting that CD133 + CD13 + hepatocytes in primary HCC tumors function as CSCs. We also found that arsenite treatment reduced the viability and stemness of CD133 + CD13 + hepatocytes, enhanced the sensitivity of HuH7 cells to pirarubicin, and reduced the tumorigenicity of CD133 + CD13 + hepatocytes xenografts in mice. The effects of sodium arsenite treatment in CD133 + CD13 + hepatocytes were mediated by the post-transcriptional suppression of PML expression and the inhibition of Oct4, Sox2, and Klf4 expression at the transcriptional level. Incomplete rescue of Oct4 expression in arsenic-treated cells ectopically expressing an siRNA-resistant PML transcript suggested that OCT4 regulation in liver CSCs involves other factors in addition to PML. Our findings provide evidence of a specific role for PML in regulating Oct4 levels in liver CSCs and highlight the clinical importance of arsenic for improving the efficacy of other chemotherapeutic agents and the prevention of post-operative HCC recurrence and metastasis.

Background: Hyperglycemia, via peroxynitrite-mediated endothelial nitric oxide synthase (eNOS) enzymatic uncoupling, induced endothelial dysfunction. Propofol has been reported to improve high glucose-induced endothelial dysfunction. However, its mechanisms of action remain unclear. We hypothesized that propofol could improve hyperglycemia-induced endothelial dysfunction by decreasing the peroxynitrite level and thus restoring eNOS coupling., Methods: At the end of 3 days of incubation in medium with 30 mM glucose, human umbilical vein endothelial cells were treated with different concentrations (0.2, 1, 5, and 25 μM) of propofol for different times (0.5, 1, 2, and 4 hours). In parallel experiments, cells were cultured in 5 mM glucose for 3 days as a control. Nitric oxide (NO) production was measured with a nitrate reductase assay. Superoxide anion (O(2)(·-)) accumulation was measured with the reduction of ferricytochrome c and dihydroethidine fluorescence assay. The treatment that had maximal effect on 30 mM glucose-induced NO production and O(2)(·-) accumulation was applied in the following studies to examine the underlying signaling pathways. eNOS total protein, eNOS dimer and monomer expression, eNOS phosphorylation at Ser(1177), inducible NO synthase total protein, inducible NO synthase dimer and monomer expression, peroxynitrite, and guanosine triphosphate cyclohydrolase I expression were measured by Western blot. Tetrahydrobiopterin (BH(4)) level was measured with liquid chromatography-mass spectrometry., Results: Compared with 5 mM glucose treatment, 30 mM glucose significantly decreased NO production by 60% (P < 0.001) and increased O(2)(·-) accumulation by 175% (P = 0.0026), which were both attenuated by propofol in a concentration- and time-dependent manner. Compared with 5 mM glucose treatment, total eNOS protein expression was increased by 30 mM glucose (P < 0.001), whereas the ratio of eNOS dimer/monomer (P = 0.0001) and eNOS phosphorylation (P < 0.001) were decreased by 30 mM glucose. Propofol did not affect 30 mM glucose-induced total eNOS protein expression, but restored the ratio of eNOS dimer/monomer (P = 0.0005) and increased eNOS phosphorylation (P < 0.001). 30 mM glucose-induced O(2)(·-) accumulation was inhibited by the eNOS inhibitor hydrochloride. Furthermore, compared with 5 mM glucose treatment, 30 mM glucose decreased the BH(4) level (P = 0.0001) and guanosine triphosphate cyclohydrolase I expression (P < 0.001), whereas it increased peroxynitrite level (P = 0.0003), which could all be reversed by propofol (P = 0.0045, P < 0.001, P = 0.0001 vs 30 mM glucose treatment, respectively)., Conclusions: Propofol has beneficial effects on 30 mM glucose-induced NO reduction and O(2)(·-) accumulation in human umbilical vein endothelial cells. This may be mediated through inhibiting peroxynitrite-mediated BH(4) reduction, and restoring eNOS coupling.

Background: Thoracic epidural anesthesia can contribute to facilitate the fast-track approach in lung surgery. However, data regarding the effects of thoracic epidural anesthesia on oxygenation during one-lung ventilation (OLV) are scarce and contradictory. Therefore, the authors conducted a prospective, randomized, double-blinded trial in patients undergoing lung surgery under spectral entropy-guided intravenous anesthesia to evaluate the effects of thoracic epidural anesthesia with different concentrations of ropivacaine on oxygenation, shunt fraction (Qs/Qt) during OLV, and maintenance doses of propofol., Methods: One hundred twenty patients scheduled for lung surgery were randomly divided into four groups to epidurally receive saline (Group S), 0.25% (Group R0.25), 0.50% (Group R0.50), and 0.75% (Group R0.75) ropivacaine. Ropivacaine was administered intraoperatively (6-8 ml of first bolus + 5 ml/h infusion). Arterial oxygen tension (Pao2) and Qs/Qt were measured before, during, and after OLV., Results: Pao2 was significantly lower in Group R0.75 compared with that in Group S and Group R0.25 10 min (170 +/- 61 vs. 229 +/- 68 mmHg, P = 0.01; 170 +/- 61 vs. 223 +/- 70 mmHg, P = 0.03) and 20 min after OLV (146 +/- 52 vs. 199 +/- 68 mmHg, P = 0.009; 146 +/- 52 vs. 192 +/- 67 mmHg, P = 0.03). During OLV, Qs/Qt was significantly higher in Group R0.75 compared with that in Group S and Group R0.25 (P < 0.05). Maintenance doses of propofol were significantly lower in Group R0.75. Vasopressor requirements were higher in Group R0.75., Conclusion: A decrease in oxygenation during OLV occurred only at the highest dose of epidural local anesthetic and not at lower doses. Higher doses of epidural medication required less propofol and more vasopressors.

Unlabelled: Bradykinin induces activation of phospholipase D (PLD) via B(2) receptors in neuronal cells. To demonstrate molecular mechanism(s) of local anesthetics, we examined whether and how local anesthetics affect bradykinin-induced PLD activation in PC12 cells. Using [(3)H]Palmitic acid-labeled PC12 cells stimulated with bradykinin, formation of [(3)H]phosphatidylbutanol was measured as a variable of PLD activity. Bradykinin-stimulated PLD activity seemed to peak at 2 min. Procaine, lidocaine, ropivacaine, bupivacaine, and tetracaine suppressed the bradykinin-induced PLD activation. We chose tetracaine, the most potent drug among the local anesthetics tested, to examine how local anesthetics affect phospholipase C, protein tyrosine kinase, and extracellular signal-regulated kinase, which are the molecules upstream of PLD. Tetracaine at clinically relevant concentrations (1 approximately 10 x 10(-4) M) inhibited the bradykinin-induced PLD activation in a dose- and time-dependent manner, but neither tetrodotoxin nor nifedipine affected the PLD activation. Tetracaine (5 x 10(-4) M) slightly potentiated brady-kinin-induced phospholipase C activation. Bradykinin-stimulated protein tyrosine-phosphorylation and extracellular signal-regulated kinase activation were not affected by tetracaine. Tetracaine significantly decreased PLD activity of membrane fraction in PC12 cells. These results indicate that local anesthetics depress bradykinin-induced lipid signaling pathway(s) and may provide some clues to understanding the molecular mechanisms of these drugs for anesthesia or analgesia., Implications: Local anesthetics depressed the bradykinin-induced activation of phospholipase D (PLD) in PC12 cells. The effects of tetracaine, the most potent among the anesthetics tested, on the bradykinin-induced intracellular signaling molecules were examined. The bradykinin-induced PLD activation could be one of the potential intracellular signaling molecular sites of local anesthetic action.