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A callus line of manila grass [Zoysia matrella (L.) Merr.] has been maintained for 8 years in our laboratory. The present study investigated changes in ultrastructure and antioxidant enzyme activity during regeneration of the callus and examined the correlation between these changes and regeneration ability. The changes in fresh weight and diameter of the callus over time could be described by a sigmoidal growth curve with different stages. Electron microscopy revealed small embryonic callus cells, isodiametric in shape, with large, obvious nuclei, and dense cytoplasm. The cellular structures and morphology changed dramatically as regeneration proceeded. Of particular note was the formation of folded scutellum-like embryos at 14 d, which might be the turning point for morphological differentiation. Catalase (CAT) and peroxidase (POD) activities were the lowest at 14 d, the same time when superoxide dismutase (SOD) activity was highest. Thus, we speculate that the formation of the scutellum-like structures is associated with higher activity of SOD and lower activities of CAT and POD.

BackgroundThe intake of certain food and nutrients may play a crucial role in cognitive health. However, research on the relationship between dietary patterns and cognitive function is limited. This study aims to investigate the associations between dietary patterns and multi-dimensional cognitive functions, such as global cognitive status and related domain profiles, mild cognitive impairment (MCI), and four major subtypes of Chinese adults.MethodsUsing the baseline data from the Community-based Cohort Study on Nervous System Diseases (2018–2019), we selected 4,309 Chinese adults aged 55 years and older as subjects with complete diet, cognition, and other related data. We collected food data for the past 12 months with a valid semi-quantitative food frequency questionnaire. Diving 49 food items into 13 subgroups, we used factor analysis to derive the main dietary patterns. We evaluated cognitive functions based on the scores of the Montreal Cognitive Assessment (MoCA) and used quantile regression and multivariable logistic regression to examine the relationship between dietary patterns and cognitive-related outcomes.ResultsWe identified four dietary patterns, explaining 50.11% of the total variance: “meat-preferred” pattern, “plant-preferred” pattern, “eggs- and dairy-preferred” pattern, and “grain-preferred” pattern. After adjusting for all potential confounders, the “meat-preferred” pattern and the “plant-preferred” pattern were associated with higher scores of global cognition and several cognitive domains (p p p p p p-trend AOR) = 1.34, 95% CI: 1.11–1.63, p-trend = 0.003].ConclusionsAdhering to the “plant-preferred” pattern and the “meat-preferred” pattern may help improve the multi-dimensional cognitive functions; on the contrary, adhering to the “grain-preferred” pattern may worse cognitive health. More prospective studies in this field are needed to strengthen the evidence.

Pathogenic leucine-rich repeat kinase 2 (LRRK2) mutations are recognized as the most common cause of familial Parkinson's disease in certain populations. Recently, LRRK2 mutations were shown to be associated with a higher risk of hormone-related cancers. However, how LRRK2 itself contributes to cancer risk remains unknown. DNA damage causes cancer, and DNA damage responses are among the most important pathways in cancer biology. To understand the role of LRRK2 in DNA damage response pathway, we induced DNA damage by applying genotoxic stress to the cells with Adriamycin. We found that DNA damage enhances LRRK2 phosphorylation at Serine 910, Serine 935 and Serine 1292. We further showed that LRRK2 phosphorylation is abolished in the absence of ATM, suggesting that LRRK2 phosphorylation requires ATM. It should also be noted that LRRK2 interacts with ATM. In contrast, overexpression or knockdown of LRRK2 does not affect ATM phosphorylation, indicating that LRRK2 is the downstream target of ATM in response to DNA damage. Moreover, we demonstrated that LRRK2 increases the expression of p53 and p21 by increasing the Mdm2 phosphorylation in response to DNA damage. Loss-of-function in LRRK2 has the opposite effect to that of LRRK2. In addition, FACS analysis revealed that LRRK2 enhances cell cycle progression into S phase in response to DNA damage, a finding that was confirmed by 5-bromo-2'-deoxyuridine immunostaining. Taken together, our findings demonstrate that LRRK2 plays an important role in the ATM-Mdm2-p53 pathway that regulates cell proliferation in response to DNA damage.

Background MicroRNAs (miRNAs) are short non-coding RNAs that are emerging as important post-transcriptional regulators of neuronal and synaptic development. The precise impact of miRNAs on presynaptic function and neurotransmission remains, however, poorly understood. Results Here, we identify miR-27b—an abundant neuronal miRNA implicated in neurological disorders—as a global regulator of the presynaptic transcriptome. miR-27b influences the expression of three quarters of genes associated with presynaptic function in cortical neurons. Contrary to expectation, a large majority of these genes are up-regulated by miR-27b. This stimulatory effect is mediated by miR-27b-directed silencing of several transcriptional repressors that cooperate to suppress the presynaptic transcriptome. The strongest repressive activity appears to be mediated by Bmi1, a component of the polycomb repressive complex implicated in self-renewal of neural stem cells. miR-27b knockdown leads to reduced synaptogenesis and to a marked decrease in neural network activity, which is fully restored by RNAi-mediated silencing of Bmi1. Conclusions We conclude that silencing of Bmi1 by miR-27b relieves repression of the presynaptic transcriptome and supports neurotransmission in cortical networks. These results expand the repressive activity of Bmi1 to genes involved in synaptic function and identify a unique post-transcriptional circuitry that stimulates expression of synaptic genes and promotes synapse differentiation. Electronic supplementary material The online version of this article (doi:10.1186/s12864-016-3139-7) contains supplementary material, which is available to authorized users.

A complete protocol of in vitro selection and greenhouse screening for glyphosate-tolerant variants in manilagrass (Zoysia matrella [L.] Merr) was established in this study. Newly subcultured calli of more than 5 years’ old were transferred to selection medium containing 2 mM glyphosate. After two rounds of selection, 220 calli survived out of 840 and were transferred to regeneration medium without glyphosate. Regenerated plantlets were then transferred to regeneration medium containing 0.5 mM glyphosate to select tolerant plantlets. After 1-month growth, there were plantlets remained green and new shoots formed beside or on discolored explants. These surviving organisms were then transferred to fresh regeneration medium for further growth. Fully developed plantlets were transferred to a green house and then subjected to greenhouse screening by foliar spraying with 0.05 % glyphosate solution. Six glyphosate-tolerant plantlets, TP1-TP6, were obtained and proliferated for determination of sod-tolerance using morphological and physiological measurements. Fourteen days after foliar application with 0.1 % glyphosate, only TP5 showed enhanced sod-tolerance. The dark green color index value of TP5 was significantly higher than CK2, demonstrating that TP5 suffered less injury from glyphosate than CK2. Different physiological characters were also observed in CK1, CK2 and TP5. Significantly higher chlorophyll a content and catalase activity were observed in TP5 than in CK1. Fourteen days after treatment (DAT), the ion leakage, proline content and ascorbate peroxidase activity of CK2 and TP5 increased significantly, but the ion leakage of TP5 was significantly lower than that of CK2. The guaiacol peroxidase activity of TP5 increased significantly 14 DAT, and was significantly higher than that of CK1 and CK2. No change in shikimate content was observed in CK2 or TP5 14 DAT.

To study growth in the presence of NaCl, in vitro plantlets regenerated from callus of manilagrass (Zoysia matrella [L.] Merr.) were cultured on regeneration medium supplemented with or without 0.3 M NaCl. The results indicated that growth was significantly inhibited by NaCl, with the leaves becoming relatively shorter and thicker. The differences of in vitro plantlets grown under NaCl stress provided specific criteria for the selection of salt tolerant variants. The 6-year maintained calli were treated with different doses (0, 5, 10, 20, 40, 80, 100, 150, 200, 250, and 300 Gy) of 60Co γ rays. Regeneration rate and regeneration capacity of the calli were highest after treatment with 20 Gy 60Co γ rays, 27.08 and 91.67% respectively. When the irradiation dose was increased to 100 Gy, 10.42% of the calli developed shoots, but at 150 Gy, both regeneration capacity and regeneration rate declined significantly, and no shoot was observed after 6 weeks of regeneration. Therefore, 100–150 Gy is the most appropriate irradiation span for inducing somaclonal variation. The irradiated calli were selected in vitro for NaCl tolerance. Five NaCl tolerant variant lines, Ze1, Fv1, Te1, Tw1, Fr1, were selected on subculture medium supplemented with 0.35 M NaCl, then transferred to regeneration medium containing 0.25 M NaCl, and grown in a greenhouse. The dark green colour index (DGCI) was used to identify the amount of injury caused by NaCl treatment. This was significantly higher in four of the lines, Ze1, Fv1, Te1, Fr1 (30.88, 31.17, 30.45 and 37.70%, respectively) compared to the control line (CK), which was regenerated from calli subcultured monthly (27.39%), indicating that watering with NaCl caused less injury in these four lines. These lines had lower proline contents than CK under salt stress. The superoxide dismutase (SOD) activity was higher in Ze1 under control condition and its peroxidase (POD) activity increased significantly under salt stress. With Fr1 catalase (CAT) activity was higher under salt stress. The higher activity of these antioxidant enzymes may contribute to the enhanced salt tolerance of the four plant lines.

In the future, Machine-to-Machine (M2M) technology will be popularly used to make the world more connected. M2M gateways play an important role in bridging locally networked devices to a wired or wireless connection. In this paper, classifications of M2M gateways are summarized, and the key technology of M2M gateway is mainly discussed such as complex event processing, protocol conversion, identification & addressing and security enhancement. At the same time, the architecture model of M2M gateway is also described in detail. In the end, the trends of M2M gateways are analyzed.

Brown adipose tissue (BAT) is specialized to burn lipids for heat generation as a natural defense against cold and obesity. Previous studies established microRNAs (miRNAs) as essential regulators of brown adipocyte differentiation, but whether miRNAs are required for the feature maintenance of mature brown adipocytes remains unknown. To address this question, we ablated Dgcr8, a key regulator of the miRNA biogenesis pathway, in mature brown as well as in white adipocytes. Adipose tissue–specific Dgcr8 knockout mice displayed enlarged but pale interscapular brown fat with decreased expression of genes characteristic of brown fat and were intolerant to cold exposure. Primary brown adipocyte cultures in vitro confirmed that miRNAs are required for marker gene expression in mature brown adipocytes. We also demonstrated that miRNAs are essential for the browning of subcutaneous white adipocytes in vitro and in vivo. Using this animal model, we performed miRNA expression profiling analysis and identified a set of BAT-specific miRNAs that are upregulated during brown adipocyte differentiation and enriched in brown fat compared with other organs. We identified miR-182 and miR-203 as new regulators of brown adipocyte development. Taken together, our study demonstrates an essential role of miRNAs in the maintenance as well as in the differentiation of brown adipocytes.

Previous studies reported that the polycomb group gene Bmi-1 is downregulated in the aging brain. The aim of this study was to investigate whether decreased Bmi-1 expression accelerates brain aging by analyzing the brain phenotype of adult Bmi-1 heterozygous knockout (Bmi-1(+/-)) mice. An 8-month-old Bmi-1(+/-) brains demonstrated mild oxidative stress, revealed by significant increases in hydroxy radical and nitrotyrosine, and nonsignificant increases in reactive oxygen species and malonaldehyde compared with the wild-type littermates. Bmi-1(+/-) hippocampus had high apoptotic percentage and lipofuscin deposition in pyramidal neurons associated with upregulation of cyclin-dependent kinase inhibitors p19, p27, and p53 and downregulation of anti-apoptotic protein Bcl-2. Mild activation of astrocytes was also observed in Bmi-1(+/-) hippocampus. Furthermore, Bmi-1(+/-) mice showed mild spatial memory impairment in the Morris Water Maze test. These results demonstrate that heterozygous Bmi-1 gene knockout causes an early onset of age-related brain changes, suggesting that Bmi-1 has a role in regulating brain aging.

There was an error in the Author Contributions section. The second contributions category should read: "Performed the experiments: GC MG MZ; GC and MG contributed equally to this work."

It has been demonstrated that the water channel protein aquaporin-4 (AQP4) plays an important role in astrocyte plasticity in response to a variety of injuries or stimuli. However, the potential role of AQP4 in astrocyte response to β-amyloid (Aβ) has not been studied. The purpose of this study was to investigate this issue. Compared to media control, the lower concentrations of Aβ 1–42 (0.1–1 μM) increased AQP4 expression in cultured mouse cortical astrocytes, while the higher concentrations of Aβ 1–42 (10 μM) decreased AQP4 expression. AQP4 gene knockout reduced Aβ 1–42 -induced astrocyte activation and apoptosis, which was associated with a reduction in the uptake of Aβ via decreased upregulation of low-density lipoprotein receptor related protein-1. Moreover, time-course and levels of Aβ 1–42 -induced mitogen-activated protein kinase phosphorylation were altered in AQP4 null astrocytes compared with wild-type controls. Our data reveal a novel role of AQP4 in the uptake of Aβ by astrocytes, indicating that AQP4 is a molecular target for Alzheimer's disease.

Previous studies reported that a subpopulation of mouse and rat trigeminal neurons express water channel aquaporin-1 (AQP1). In this study we make a comparative investigation of AQP1 localization in the human and mouse trigeminal systems. Immunohistochemistry and immunofluorescence results showed that AQP1 was localized to the cytoplasm and cell membrane of some medium and small-sized trigeminal neurons. Additionally, AQP1 was found in numerous peripheral trigeminal axons of humans and mice. In the central trigeminal root and brain stem, AQP1 was specifically expressed in astrocytes of humans, but was restricted to nerve fibers within the central trigeminal root and spinal trigeminal tract and nucleus in mice. Furthermore, AQP1 positive nerve fibers were present in the mucosal and submucosal layers of human and mouse oral tissues, but not in the muscular and subcutaneous layers. Fluorogold retrograde tracing demonstrated that AQP1 positive trigeminal neurons innervate the mucosa but not skin of cheek. These results reveal there are similarities and differences in the cellular localization of AQP1 between the human and mouse trigeminal systems. Selective expression of AQP1 in the trigeminal neurons innervating the oral mucosa indicates an involvement of AQP1 in oral sensory transduction.