Abstract:Fragrant rosewood (Dalbergia odorifera T.C. Chen) is a highly-valued species suffering from vulnerability due to over-development for wood and medicine. In this study, Fragrant rosewood seedlings were cultured with chitosan oligosaccharide (CO) addition at rates of 0 and 1/800 (v/v) under artificial lightings by 200-W high-pressure sodium (HPS) lamps and 280-W light-emitting diode (LED) panels for a 15 h daily photoperiod and a natural illumination as the control. The LEDs were designed to emit lights in 85% of red (600-700 nm), 15% of green(500-600 nm), and 5% of blue (400-500 nm). The height of artificial lightings was elevated every five to seven days to keep the mean photosynthetic photon flux density (PPFD) of 72-73 µmol m −2 s −1 of artificial lighting at shoot-tips. Seedlings under LED lighting with CO addition had the greatest diameter growth and leaf biomass, as well as the highest nutrient utilization and evaluated quality, while those under HPS lighting had a higher stem sugar concentration but unchanged shoot growth and biomass compared to the control. In conclusion, we recommend Fragrant rosewood seedlings to be cultured with CO addition under LED lighting to efficiently promote synthetic quality and nutrient utilization.

Autism spectrum disorder (ASD) is a common neurodevelopmental disorder. The mechanisms underlying ASD are unclear. Astrocyte alterations are noted in ASD patients and animal models. However, whether astrocyte dysfunction is causal or consequential to ASD-like phenotypes in mice is unresolved. Type 2 inositol 1,4,5-trisphosphate 6 receptors (IP3R2)-mediated Ca2+ release from intracellular Ca2+ stores results in the activation of astrocytes. Mutations of the IP3R2 gene are associated with ASD. Here, we show that both IP3R2-null mutant mice and astrocyte-specific IP3R2 conditional knockout mice display ASD-like behaviors, such as atypical social interaction and repetitive behavior. Furthermore, we show that astrocyte-derived ATP modulates ASD-like behavior through the P2X2 receptors in the prefrontal cortex and possibly through GABAergic synaptic transmission. These findings identify astrocyte-derived ATP as a potential molecular player in the pathophysiology of ASD.

Astrocytes are key components of the niche for neural stem cells (NSCs) in the adult hippocampus and play a vital role in regulating NSC proliferation and differentiation. However, the exact molecular mechanisms by which astrocytes modulate NSC proliferation have not been identified. Here, we identified adenosine 5 0 -triphosphate (ATP) as a proliferative factor required for astrocyte-mediated proliferation of NSCs in the adult hippocampus. Our results indicate that ATP is necessary and sufficient for astrocytes to promote NSC proliferation in vitro. The lack of inositol 1,4,5-trisphosphate receptor type 2 and transgenic blockage of vesicular gliotransmission induced deficient ATP release from astrocytes. This deficiency led to a dysfunction in NSC proliferation that could be rescued via the administration of exogenous ATP. Moreover, P2Y1-mediated purinergic signaling is involved in the astrocyte promotion of NSC proliferation. As adult hippocampal neurogenesis is potentially involved in major mood disorder, our results might offer mechanistic insights into this disease.

cn. than 0.05 was considered statistically significant. All data were analyzed with SPSS software (IBM). Study approvalEthics approval for this study was obtained from the ethics board for animal research of Southern Medical University (Guangzhou, China). The animals were handled in accordance with the Chinese Council on Animal Care Guidelines. Efforts were made to minimize animal suffering and to reduce the number of animals used.

Because of the high expression of MAPK1 in the cervical cancer tissue, the interference in the expression of MAPK1 can significantly inhibit the invasion and metastasis of cervical cancer HeLa cells, which is related to the interference in the expression of MMPs/TIMP and Snail-mediated generation of EMT.

No abstract

Glioblastoma (GBM) is the most frequent and aggressive primary adult brain tumor with poor prognosis. Epidermal growth factor receptor variant III (EGFRvIII) is the most common and highly oncogenic EGFR mutant in GBM. With the aim to generate specific molecular probes able to target EGFRvIII with high affinity, we selected four DNA aptamers (U2, U8, U19 and U31) specifically bound to U87-EGFRvIII cells that over expressed EGFRvIII with K d values in the nanomole range by a cell-based systematic evolution of ligands by exponential enrichment (cell-SELEX) process. U87MG cells were introduced as control cells for counter selection. We further affirmed U2 and U8 identified EGFRvIII on the surface of target cells specifically. Then we radiolabeled U2 with 188Re to serve as a molecular imaging probe and observed 188Re -labeled U2 significantly targeted EGFRvIII over-expressing glioblastoma exnografts in mice. In conclusion, aptamers obtained from whole cell-SELEX strategy have great potential as molecular imaging probes that are probably beneficial to GBM diagnoses.

No abstract