Lineage-specific evolution of Aquibium, a close relative of Mesorhizobium, during habitat adaptation.

The novel genus Aquibium that lacks nitrogenase was recently reclassified from the Mesorhizobium genus. The genomes of Aquibium species isolated from water were smaller and had higher GC contents than those of Mesorhizobium species. Six Mesorhizobium species lacking nitrogenase were found to exhibit low similarity in the average nucleotide identity values to the other 24 Mesorhizobium species. Therefore, they were classified as the non-N2-fixing Mesorhizobium lineage (N-ML), an evolutionary intermediate species. The results of our phylogenomic analyses and the loss of Rhizobiales-specific fur/mur indicated that Mesorhizobium species may have evolved from Aquibium species through an ecological transition. Halotolerant and alkali-resistant Aquibium and Mesorhizobium microcysteis belonging to N-ML possessed many tripartite ATP-independent periplasmic transporter and sodium/proton antiporter subunits composed of seven genes (mrpABCDEFG). These genes were not present in the N2-fixing Mesorhizobium lineage (ML), suggesting that genes acquired for adaptation to highly saline and alkaline environments were lost during the evolution of ML as the habitat changed to soil. Land-to-water habitat changes in Aquibium species, close relatives of Mesorhizobium species, could have influenced their genomic evolution by the gain and loss of genes. Our study indicated that lineage-specific evolution could have played a significant role in shaping their genome architecture and conferring their ability to thrive in different habitats.IMPORTANCEPhylogenetic analyses revealed that the Aquibium lineage (AL) and non-N2-fixing Mesorhizobium lineage (N-ML) were monophyletically grouped into distinct clusters separate from the N2-fixing Mesorhizobium lineage (ML). The N-ML, an evolutionary intermediate species having characteristics of both ancestral and descendant species, could provide a genomic snapshot of the genetic changes that occur during adaptation. Genomic analyses of AL, N-ML, and ML revealed that changes in the levels of genes related to transporters, chemotaxis, and nitrogen fixation likely reflect adaptations to different environmental conditions. Our study sheds light on the complex and dynamic nature of the evolution of rhizobia in response to changes in their environment and highlights the crucial role of genomic analysis in understanding these processes.

Kaistella rhinocerotis sp. nov., isolated from the faeces of rhinoceros and reclassification of Chryseobacterium faecale as Kaistella faecalis comb. nov.

Strain Ran72T, a novel Gram-stain-negative, obligately aerobic, non-motile, and rod-shaped bacterium, was isolated from the faeces of the rhinoceros species Ceratotherium simum. The novel bacterial strain grew optimally in Reasoner's 2A medium under the following conditions: 0 % (w/v) NaCl, pH 7.5, and 30 °C. Based on phylogenetic analysis using 16S rRNA gene sequencing, strain Ran72T was found to be most closely related to Chryseobacterium faecale F4T (98.4 %), Kaistella soli DKR-2T (98.0 %), and Kaistella haifensis H38T (97.4 %). A comprehensive genome-level comparison between strain Ran72T with C. faecale F4T, K. soli DKR-2T, and K. haifensis H38T revealed average nucleotide identity, digital DNA-DNA hybridization, and average amino acid identity values of ≤74.9, ≤19.3, and ≤78.7 %, respectively. The major fatty acids were anteiso-C15 : 0 (22.3 %), with MK-6 being the predominant respiratory quinone. The major polar lipids of strain Ran72T were phosphatidylethanolamine, four unidentified aminolipids, and two unidentified lipids. Based on our chemotaxonomic, genotypic, and phenotype characterizations, strain Ran72T was identified as representing a novel species in the genus Kaistella, for which the name Kaistella rhinocerotis sp. nov. is proposed, with the type strain Ran72T (=KACC 23136T=JCM 36038T). Based on the outcomes of our phylogenomic study, Chryseobacterium faecale should be reclassified under the genus Kaistella as Kaistella faecalis comb. nov.

Antagonistic actions of Paucibacter aquatile B51 and its lasso peptide paucinodin toward cyanobacterial bloom-forming Microcystis aeruginosa PCC7806.

Superior antagonistic activity against axenic Microcystis aeruginosa PCC7806 was observed with Paucibacter sp. B51 isolated from cyanobacterial bloom samples among 43 tested freshwater bacterial species. Complete genome sequencing, analyzing average nucleotide identity and digital DNA-DNA hybridization, designated the B51 strain as Paucibacter aquatile. Electron and fluorescence microscopic image analyses revealed the presence of the B51 strain in the vicinity of M. aeruginosa cells, which might provoke direct inhibition of the photosynthetic activity of the PCC7806 cells, leading to perturbation of cellular metabolisms and consequent cell death. Our speculation was supported by the findings that growth failure of the PCC7806 cells led to low pH conditions with fewer chlorophylls and down-regulation of photosystem genes (e.g., psbD and psaB) during their 48-h co-culture condition. Interestingly, the concentrated ethyl acetate extracts obtained from B51-grown supernatant exhibited a growth-inhibitory effect on PCC7806. The physical separation of both strains by a filter system led to no inhibitory activity of the B51 cells, suggesting that contact-mediated anti-cyanobacterial compounds might also be responsible for hampering the growth of the PCC7806 cells. Bioinformatic tools identified 12 gene clusters that possibly produce secondary metabolites, including a class II lasso peptide in the B51 genome. Further chemical analysis demonstrated anti-cyanobacterial activity from fractionated samples having a rubrivinodin-like lasso peptide, named paucinodin. Taken together, both contact-mediated inhibition of photosynthesis and the lasso peptide secretion of the B51 strain are responsible for the anti-cyanobacterial activity of P. aquatile B51.

Sustainable control of Microcystis aeruginosa, a harmful cyanobacterium, using Selaginella tamariscina extracts.

Eco-friendly reagents derived from plants represent a promising strategy to mitigate the occurrence of toxic cyanobacterial blooms. The use of an amentoflavone-containing Selaginella tamariscina extract (STE) markedly decreased the number of Microcystis aeruginosa cells, thus demonstrating significant anti-cyanobacterial activity. In particular, the Microcystis-killing fraction obtained from pulverized S. tamariscina using hot-water-based extraction at temperatures of 40 °C induced cell disruption in both axenic and xenic M. aeruginosa. Liquid chromatographic analysis was also conducted to measure the concentration of amentoflavone in the STE, thus supporting the potential M. aeruginosa-specific killing effects of STE. Bacterial community analysis revealed that STE treatment led to a reduction in the relative abundance of Microcystis species while also increasing the 16S rRNA gene copy number in both xenic M. aeruginosa NIBR18 and cyanobacterial bloom samples isolated from a freshwater environment. Subsequent testing on bacteria, cyanobacteria, and algae isolated from freshwater revealed that STE was not toxic for other taxa. Furthermore, ecotoxicology assessment involving Aliivibrio fischeri, Daphnia magna, and Danio rerio found that high STE doses immobilized D. magna but did not impact the other organisms, while there was no change in the water quality. Overall, due to its effective Microcystis-killing capability and low ecotoxicity, aqueous STE represents a promising practical alternative for the management of Microcystis blooms.

Effects of TiO2 Nanotubes and Reduced Graphene Oxide on Streptococcus mutans and Preosteoblastic Cells at an Early Stage.

The effects of TiO2 nanotube (TNT) and reduced graphene oxide (rGO) deposition onto titanium, which is widely used in dental implants, on Streptococcus mutans (S. mutans) and preosteoblastic cells were evaluated. TNTs were formed through anodic oxidation on pure titanium, and rGO was deposited using an atmospheric plasma generator. The specimens used were divided into a control group of titanium specimens and three experimental groups: Group N (specimens with TNT formation), Group G (rGO-deposited specimens), and Group NG (specimens under rGO deposition after TNT formation). Adhesion of S. mutans to the surface was assessed after 24 h of culture using a crystal violet assay, while adhesion and proliferation of MC3T3-E1 cells, a mouse preosteoblastic cell line, were evaluated after 24 and 72 h through a water-soluble tetrazolium salt assay. TNT formation and rGO deposition on titanium decreased S. mutans adhesion (p < 0.05) and increased MC3T3-E1 cell adhesion and proliferation (p < 0.0083). In Group NG, S. mutans adhesion was the lowest (p < 0.05), while MC3T3-E1 cell proliferation was the highest (p < 0.0083). In this study, TNT formation and rGO deposition on a pure titanium surface inhibited the adhesion of S. mutans at an early stage and increased the initial adhesion and proliferation of preosteoblastic cells.

Toll-Like Receptor 5 Promotes the Neurogenesis From Embryonic Stem Cells and Adult Hippocampal Neural Stem Cells in Mice.

Toll-like receptors (TLRs) make a crucial contribution to the innate immune response. TLR5 was expressed in embryoid body derived from mouse embryonic stem cells (mESCs) and ßIII-tubulin-positive cells under all-trans retinoic acid-treated condition. TLR5 was upregulated during neural differentiation from mESCs and augmented the neural differentiation of mESCs via nuclear factor-κB and interleukin 6/CREB pathways. Besides, TLR5 was expressed in SOX2- or doublecortin-positive cells in the subgranular zone of the hippocampal dentate gyrus where adult neurogenesis occurs. TLR5 inhibited the proliferation of adult hippocampal neural stem cells (NSCs) by regulating the cell cycle and facilitated the neural differentiation from the adult hippocampal NSCs via JNK pathway. Also, TLR5 deficiency impaired fear memory performance in mice. Our data suggest that TLR5 is a crucial modulator of neurogenesis from mESCs and adult hippocampal NSCs in mice and represents a new therapeutic target in neurological disorders related to cognitive function.

Aquibium microcysteis gen. nov., sp. nov., isolated from a Microcystis aeruginosa culture and reclassification of Mesorhizobium carbonis as Aquibium carbonis comb. nov. and Mesorhizobium oceanicum as Aquibium oceanicum comb. nov.

A novel bacterial strain, NIBR3T, was isolated from a Microcystis aeruginosa culture. Strain NIBR3T was characterized as Gram-negative, rod-shaped, catalase- and oxidase-positive, and aerobic. The 16S rRNA gene sequence analysis showed that strain NIBR3T was most closely related to Mesorhizobium carbonis B2.3T (=KCTC 52461), Mesorhizobium oceanicum B7T (=KCTC 42783) and Mesorhizobium qingshengii CCBAU 33460T (=HAMBI 3277), at 98.7, 97.2 and 97.2% similarity, respectively. Our phylogenetic analyses revealed that three strains [strain NIBR3T with the previously reported two Mesorhizobium species (M. carbonis B2.3T and M. oceanicum B7T)] formed a distinct cluster from other Mesorhizobium type strains. The average nucleotide identity of strain NIBR3T relative to M. carbonis B2.3T , M. oceanicum B7T, and M. qingshengii CCBAU 33460T was found to be 84.3, 79.4 and 75.8 %, with average amino-acid identities of 85.1, 74.8 and 64.3 %, and digital DNA-DNA hybridization values of 27.6, 22.6 and 20.7 %, respectively. The genome size and genomic DNA G+C content of NIBR3T were 6.1 Mbp and 67.9 mol%, respectively. Growth of strain NIBR3T was observed at 23-45 °C (optimum, 33 °C), at pH 6-11 (optimum, 8) and in the presence of 0-4 % (w/v) NaCl (optimum, 0 %). The major polar lipids in this novel strain were phosphatidylethanolamine, phosphatidylcholine and phosphatidylmethylethanolamine. The predominant respiratory quinone was Q-10. Summed feature 8 (C18 : 1 ω7c and/or C18 : 1 ω6c) was the most abundant cellular fatty acid in strain NIBR3T. Based on genotypic characteristics using our genomic data, strain NIBR3T was identified as a member of new genus, Aquibium gen. nov., with the two aforementioned stains. The type strain f the novel species, Aquibium microcysteis sp. nov., is NIBR3T (=KACC 22092T=HAMBI 3738T). We also reclassified Mesorhizobium carbonis and M. oceanicum as Aquibium carbonis comb. nov. and A. oceanicum comb. nov., respectively.

Epigallocatechin Gallate Protects against Hypoxia-Induced Inflammation in Microglia via NF-κB Suppression and Nrf-2/HO-1 Activation.

Hypoxia-induced neuroinflammation in stroke, neonatal hypoxic encephalopathy, and other diseases subsequently contributes to neurological damage and neuronal diseases. Microglia are the primary neuroimmune cells that play a crucial role in cerebral inflammation. Epigallocatechin gallate (EGCG) has a protective antioxidant and anti-inflammatory effects against neuroinflammation. However, the effects of EGCG on hypoxia-induced inflammation in microglia and the underlying mechanism remain unclear. In this study, we investigated whether EGCG might have a protective effect against hypoxia injury in microglia by treatment with CoCl2 to establish a hypoxic model of BV2 microglia cells following EGCG pre-treatment. An exposure of cells to CoCl2 caused an increase in inflammatory mediator interleukin (IL)-6, inducible nitric oxide synthase (iNOS), and cyclooxygenase (COX)-2 expression, which were significantly ameliorated by EGCG via inhibition of NF-κB pathway. In addition, EGCG attenuated the expression of hypoxia-inducible factor (HIF)-1α and the generation of ROS in hypoxic BV2 cells. Furthermore, the suppression of hypoxia-induced IL-6 production by EGCG was mediated via the inhibition of HIF-1α expression and the suppression of ROS generation in BV2 cells. Notably, EGCG increased the Nrf-2 levels and HO-1 levels in the presence of CoCl2. Additionally, EGCG suppressed hypoxia-induced apoptosis of BV2 microglia with cleavage of poly (ADP-ribose) polymerase (PARP) and caspase-3. In summary, EGCG protects microglia from hypoxia-induced inflammation and oxidative stress via abrogating the NF-κB pathway as well as activating the Nrf-2/HO-1 pathway.

Discrete Infomax Codes for Supervised Representation Learning.

For high-dimensional data such as images, learning an encoder that can output a compact yet informative representation is a key task on its own, in addition to facilitating subsequent processing of data. We present a model that produces discrete infomax codes (DIMCO); we train a probabilistic encoder that yields k-way d-dimensional codes associated with input data. Our model maximizes the mutual information between codes and ground-truth class labels, with a regularization which encourages entries of a codeword to be statistically independent. In this context, we show that the infomax principle also justifies existing loss functions, such as cross-entropy as its special cases. Our analysis also shows that using shorter codes reduces overfitting in the context of few-shot classification, and our various experiments show this implicit task-level regularization effect of DIMCO. Furthermore, we show that the codes learned by DIMCO are efficient in terms of both memory and retrieval time compared to prior methods.

Roseococcus microcysteis sp. nov., isolated from a Microcystis aeruginosa culture sample.

Strain NIBR12T (=KACC 22094T=HAMBI 3739T), a novel Gram-stain-negative, obligate aerobic, non-spore-forming, non-motile and coccobacillus-shaped bacterium, was isolated from a cyanobacterial sample culture (Microcysitis aeruginosa NIBRCYC000000452). The newly identified bacterial strain grew optimally in modified Reasoner's 2A medium under the following conditions: 0 % (w/v) NaCl, pH 7.5 and 35 °C. Phylogenetic analysis using the 16S rRNA gene sequence confirmed that strain NIBR12T belongs to the genus Roseococcus, with its closest neighbours being Roseococcus suduntuyensis SHETT (98.8%), Roseococcus thiosulfatophilus RB-3T (97.7%), "Sediminicoccus rosea" R-30T (95.7 %) and Rubritepida flocculans H-8T (95.0 %). Genomic comparison of strain NIBR12T with type species in the genus Roseococcus was conducted using digital DNA-DNA hybridization, average nucleotide identity and average amino acid identity analyses, resulting in values of ≤53.7, ≤93.7 and ≤96.1 %, respectively. The genomic DNA G+C content of strain NIBR12T was 70.9 mol%. The major fatty acids of strain NIBR12T were summed feature 8 (C18 : 1 ω7c and/or C18:1 ω6c) and summed feature 3 (C16 : 1 ω6c/C16 : 1 ω7c). Q-9 was its major respiratory quinone. Moreover, the major polar lipids of strain NIBR12T were diphosphatidylglycerol, phosphatidylglycerol, phosphatidylethanolamine and phosphatidylcholine. Based on our chemotaxonomic, genotypic and phenotype analyses, strain NIBR12T is identified as represeting a novel species of the genus Roseococcus, for which the name Roseococcus microcysteis sp. nov. is proposed.

Killing effect of deinoxanthins on cyanobloom-forming Microcystis aeruginosa: Eco-friendly production and specific activity of deinoxanthins.

Cyanobacterial blooms caused mainly by Microcystis aeruginosa could be controlled using chemical and biological agents such as H2O2, antagonistic bacteria, and enzymes. Little is known about the possible toxic effects of bacterial membrane pigments on M. aeruginosa cells. Deinococcus metallilatus MA1002 cultured under light increased the production of several carotenoid-like compounds by upregulating two deinoxanthin biosynthesis genes: crtO and cruC. The deinoxanthin compounds were identified using thin-layer chromatography, high-performance liquid chromatography, and liquid chromatography-mass spectrometry. D. metallilatus was cultured with agricultural by-products under light to produce the deinoxanthin compounds. Soybean meal, from six tested agricultural by-products, was selected as the single factor for making an economical medium to produce deinoxanthin compounds. The growth of axenic M. aeruginosa PCC7806, as well as other xenic cyanobacteria such as Cyanobium gracile, Trichormus variabilis, and Dolichospermum circinale, were inhibited by the deinoxanthin compounds. Scanning electron microscopic images showed the complete collapse of M. aeruginosa cells under deinoxanthin treatment, probably due to its interference with cyanobacterial membrane synthesis during cellular elongation. Deinoxanthins appeared to be nontoxic to other non-cyanobacteria such as Acinetobacter, Pseudomonas, Methylobacterium, and Bacillus species, suggesting that it can be a novel candidate for preventing cyanobacterial blooms through its specific activity against cyanobacteria.

Mineral trioxide aggregate-induced AMPK activation stimulates odontoblastic differentiation of human dental pulp cells.

AIM: To investigate the role of autophagy in MTA-induced odontoblastic differentiation of human dental pulp cells (HDPCs). METHODOLOGY: In MTA-treated HDPCs, odontoblastic differentiation was assessed based on expression levels of dentine sialophosphoprotein (DSPP) and dentine matrix protein 1 (DMP1), alkaline phosphatase activity (ALP) activity by ALP staining and the formation of mineralized nodule by Alizarin red S staining. Expression of microtubule-associated protein 1A/1B-light chain3 (LC3), adenosine monophosphate-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) signalling molecules and autophagy-related genes was analysed by Western blot analysis and Acridine orange staining was used to detect autophagic lysosome. For in vivo experiments, tooth cavity preparation models on rat molars were established and the expression of proteins-related odontogenesis and autophagy markers was observed by Immunohistochemistry and Western blot analysis. Kruskal-Wallis with Dunn's multiple comparison was used for statistical analysis. RESULTS: Mineral trioxide aggregate (MTA) promoted odontoblastic differentiation of HDPCs, accompanied by autophagy induction, including formation of autophagic lysosome and cleavage of LC3 to LC3II (P < 0.05). Conversely, inhibition of autophagy through 3MA significantly attenuated the expression level of DSPP (P < 0.05) and DMP1 (P < 0.05) as well as formation of mineralized nodules (P < 0.05), indicating the functional significance of autophagy in MTA-induced odontoblastic differentiation. Also, MTA increased the activity of AMPK (P < 0.01), whereas inhibition of AMPK by compound C downregulated DSPP (P < 0.01) and DMP1 (P < 0.05), but increased the phosphorylation of mTOR (P < 0.05), p70S6 (P < 0.01) and Unc-51-like kinases 1 (ULK1) (ser757) (P < 0.01), explaining the involvement of AMPK pathway in MTA-induced odontoblast differentiation. In vivo study, MTA treatment after tooth cavity preparation on rat molars upregulated DMP-1 and DSPP as well as autophagy-related proteins LC3II and p62, and enhanced the phosphorylation of AMPK. CONCLUSION: MTA induced odontoblastic differentiation and mineralization by modulating autophagy with AMPK activation in HDPCs. Autophagy regulation is a new insight on regenerative endodontic therapy using MTA treatment.

Antioxidant hesperetin improves the quality of porcine oocytes during aging in vitro.

The citrus flavonoid hesperetin has a variety of pharmacological actions, including antioxidant, antiinflammatory, and anticancer activities. This study investigated whether hesperetin prevents aging of oocytes in vitro in which it determined the maturation of nuclear and cytoplasm and the developmental capacity of embryo by modulating the reactive oxygen species (ROS) level. Porcine oocytes were matured in vitro for 44 hr (control) and for an additional 24 hr in the presence of 0, 1, 10, 100, and 250 µM hesperetin (aging, H-1, H-10, H-100, and H-250, respectively). Although there was no difference in the rate of maturation among all the groups, both the control and H-100 groups significantly increased in the rate of cleavage and blastocyst formation compared to the aging group. The H-100 group significantly decreased ROS activity and increases the level of glutathione (GSH) and expression of the antioxidant genes (PRDX5, NFE2L, SOD1, and SOD2) compared with the aging group. The H-100 groups prevented aberrant spindle organization and chromosomal misalignment, blocked the decrease in the level of phosphorylated-p44/42 mitogen-activated protein kinase and increased the messenger RNA expression of cytoplasmic maturation factor genes (GDF9, CCNB1, BMP15, and MOS). Subsequently, both the control and H-100 groups significantly increased the total cell number and decreased the apoptosis cells at the blastocyst stage compared with aging group. The results indicate that hesperetin improves the quality of porcine oocytes by protecting them against oxidative stress during aging in vitro.

Pioglitazone improves porcine oocyte maturation and subsequent parthenogenetic embryo development in vitro by increasing lipid metabolism.

Optimization of culture conditions is important to improve oocyte maturation and subsequent embryo development. In particular, this study analyzed the effects of increasing concentrations of PIO in the maturation medium on spindle formation and chromosome alignment, glutathione, and intracellular ROS levels and expression of selected genes related to maternal markers, apoptosis, and lipid metabolism. The percentage of oocytes displaying normal spindle formation and chromosome alignment was higher in the 1 µM PIO (1 PIO)-treated group than in the control group. The glutathione level was significantly higher in the 1 PIO-treated group than in the control group, while the reactive oxygen species level did not differ. Expression of maternal marker (MOS and GDF9), antiapoptotic (BIRC5), and lipid metabolism-related (ACADS, CPT2, SREBF1, and PPARG) genes was higher in the 1 PIO-treated group than in the control group, while expression of a proapoptotic gene (CASP3) was lower. The blastocyst formation rate and the percentage of blastocysts that reached at least the hatching stage on Days 6 and 7, and the percentage of blastocysts containing more than 128 cells were significantly higher in the 1 PIO-treated group than in the control group. These results indicate that PIO treatment during in vitro maturation improves porcine oocyte maturation and subsequent parthenogenetic embryo development mainly by enhancing lipid metabolism and antioxidant defense in oocytes.

Autophagy induction plays a protective role against hypoxic stress in human dental pulp cells.

Human dental pulp exposed to hypoxic conditions induces cell death accompanied by autophagy. However, the role of hypoxia-induced autophagy in human dental pulp cells (HDPCs) is unclear. The present study aimed to investigate the role of autophagy in hypoxia-induced apoptosis of HDPCs. Cobalt chloride (CoCl2 ) treated HDPCs, to mimic hypoxic conditions, decreased cell viability. Also, apoptosis-related signal molecules, cleaved caspase-3 and PARP levels, were enhanced in CoCl2 -treated HDPCs. HDPCs exposed to CoCl2 also promoted autophagy, showing upregulated p62 and microtubule-associated protein 1 light chain 3 (LC3)-II levels, typical autophagic markers, and increased acidic autophagolysosomal vacuoles. Autophagy inhibition by 3 methyladenine (3MA) or RNA interference of LC3B resulted in increased levels of cleaved PARP and caspase-3, and the release of cytochrome c from mitochondria into cytosol in the CoCl2 -treated HDPCs. However, autophagy activation by rapamycin enhanced the p62 and LC3-II levels, whereas it reduced PARP and caspase-3 cleavage induced by CoCl2. These results revealed that CoCl2 -activated autophagy showed survival effects against CoCl2 -induced apoptosis in the HDPCs. CoCl2 upregulated HIF-1α and decreased the phosphorylation of mTOR/p70S6K. HIF-1α inhibitor, YC-1 decreased p62 and LC3-II levels, whereas it augmented PARP and caspase-3 cleavage in response to CoCl2 . Also, YC-1 enhanced the phosphorylation of mTOR and p70S6K suppressed by CoCl2 , demonstrating that CoCl2 -induced autophagy via mTOR/p70S6K is mediated by HIF-1α. Taken together, these finding suggest that CoCl2 -induced autophagy mediated by the mTOR/p70S6K pathway plays a protective role against hypoxic stress in HDPCs.

Active synchronization and modulation of fiber lasers with a graphene electro-optic modulator.

We report the synchronization of two actively Q-switched fiber lasers operating at 1.5 µm and 2 µm with a shared broadband graphene electro-optic modulator. Two graphene monolayer sheets separated with a high-kHfO2 dielectric layer are configured to enable broadband light modulation. The graphene electro-optic modulator is shared by two optical fiber laser cavities (i.e., an erbium-doped fiber laser cavity and a thulium/holmium-codoped fiber laser cavity) to actively Q-switch the two lasers, resulting in stable synchronized pulses at 1.5 µm and 2 µm with a repetition rate ranging from 46 kHz to 56 kHz.

Antioxidant ß-cryptoxanthin enhances porcine oocyte maturation and subsequent embryo development in vitro.

Oxidative stress is partly responsible for the poor quality of IVM oocytes. The present study investigated the effects of the antioxidant ß-cryptoxanthin on the IVM of porcine oocytes and the in vitro development of the ensuing embryos. Oocytes were matured in IVM medium containing different concentrations of ß-cryptoxanthin (0, 0.1, 1, 10 or 100µM). Treatment with 1µM ß-cryptoxanthin (Group 1B) improved polar body extrusion and the expression of maturation-related genes in cumulus cells and oocytes compared with control. In addition, levels of reactive oxygen species decreased significantly in Group 1B, whereas there were significant increases in glutathione levels and expression of the antioxidant genes superoxide dismutase 1 and peroxiredoxin 5 in this group. After parthenogenetic activation, although the cleavage rate did not differ between the control and 1B groups, the blastocyst formation rate was higher in the latter. Moreover, the total number of cells per blastocyst and relative mRNA levels of pluripotency marker and antioxidant genes were significantly higher in the 1B compared with control group. These results demonstrate that ß-cryptoxanthin decreases oxidative stress in porcine oocytes and improves their quality and developmental potential.

Toll-like receptor 2 promotes neurogenesis from the dentate gyrus after photothrombotic cerebral ischemia in mice.

The subgranular zone (SGZ) of hippocampal dentate gyrus (HDG) is a primary site of adult neurogenesis. Toll-like receptors (TLRs), are involved in neural system development of Drosophila and innate immune response of mammals. TLR2 is expressed abundantly in neurogenic niches such as adult mammalian hippocampus. It regulates adult hippocampal neurogenesis. However, the role of TLR2 in adult neurogenesis is not well studied in global or focal cerebral ischemia. Therefore, this study aimed to investigate the role of TLR2 in adult neurogenesis after photochemically induced cerebral ischemia. At 7 days after photothrombotic ischemic injury, the number of bromodeoxyuridine (BrdU)-positive cells was increased in both TLR2 knock-out (KO) mice and wild-type (WT) mice. However, the increment rate of BrdU-positive cells was lower in TLR2 KO mice compared to that in WT mice. The number of doublecortin (DCX) and neuronal nuclei (NeuN)-positive cells in HDG was decreased after photothrombotic ischemia in TLR2 KO mice compared to that in WT mice. The survival rate of cells in HDG was decreased in TLR2 KO mice compared to that in WT mice. In contrast, the number of cleaved-caspase 3 (apoptotic marker) and the number of GFAP (glia marker)/BrdU double-positive cells in TLR2 KO mice were higher than that in WT mice. These results suggest that TLR2 can promote adult neurogenesis from neural stem cell of hippocampal dentate gyrus through increasing proliferation, differentiation, and survival from neural stem cells after ischemic injury of the brain.

Ascorbic Acid Induces Necrosis in Human Laryngeal Squamous Cell Carcinoma via ROS, PKC, and Calcium Signaling.

Ascorbic acid induces apoptosis, autophagy, and necrotic cell death in cancer cells. We investigated the mechanisms by which ascorbic acid induces death in laryngeal squamous cell carcinoma Hep2 cells. Ascorbic acid markedly reduced cell viability and induced death without caspase activation and an increase in cytochrome c. Hep2 cells exposed to ascorbic acid exhibited membrane rupture and swelling, the morphological characteristics of necrotic cell death. The generation of reactive oxygen species (ROS) was increased in Hep2 cells treated with ascorbic acid, and pretreatment with N-acetylcysteine blocked ascorbic acid-induced cell death. Ascorbic acid also stimulated protein kinase C (PKC) signaling, especially PKC α/ß activation, and subsequently increased cytosolic calcium levels. However, ascorbic acid-induced necrotic cell death was inhibited by Ro-31-8425 (PKC inhibitor) and BAPTA-AM (cytosolic calcium-selective chelator). ROS scavenger NAC inhibited PKC activation induced by ascorbic acid and Ro-31-8425 suppressed the level of cytosolic calcium increased by ascorbic acid, indicating that ROS is represented as an upstream signal of PKC pathway and PKC activation leads to the release of calcium into the cytosol, which ultimately regulates the induction of necrosis in ascorbic acid-treated Hep2 cells. These data demonstrate that ascorbic acid induces necrotic cell death through ROS generation, PKC activation, and cytosolic calcium signaling in Hep2 cells. J. Cell. Physiol. 232: 417-425, 2017. © 2016 Wiley Periodicals, Inc.

Scaling of graphene field-effect transistors supported on hexagonal boron nitride: radio-frequency stability as a limiting factor.

The quality of graphene in nanodevices has increased hugely thanks to the use of hexagonal boron nitride as a supporting layer. This paper studies to which extent hBN together with channel length scaling can be exploited in graphene field-effect transistors (GFETs) to get a competitive radio-frequency (RF) performance. Carrier mobility and saturation velocity were obtained from an ensemble Monte Carlo simulator that accounted for the relevant scattering mechanisms (intrinsic phonons, scattering with impurities and defects, etc). This information is fed into a self-consistent simulator, which solves the drift-diffusion equation coupled with the two-dimensional Poisson's equation to take full account of short channel effects. Simulated GFET characteristics were benchmarked against experimental data from our fabricated devices. Our simulations show that scalability is supposed to bring to RF performance an improvement that is, however, highly limited by instability. Despite the possibility of a lower performance, a careful choice of the bias point can avoid instability. Nevertheless, maximum oscillation frequencies are still achievable in the THz region for channel lengths of a few hundreds of nanometers.