Epidural labor analgesia was associated with a decreased risk of postpartum depression. Further study with a large sample size is needed to evaluate the impact of epidural analgesia on the occurrence of postpartum depression.

Nanopore technology is a promising label-free detection method. However, challenges exist for its further application in sequencing, clinical diagnostics and ultra-sensitive single molecule detection. The development of DNA nanotechnology nonetheless provides possible solutions to current obstacles hindering nanopore sensing technologies. In this review, we summarize recent relevant research contributing to efforts for developing nanopore methods associated with DNA nanotechnology. For example, DNA carriers can capture specific targets at pre-designed sites and escort them from nanopores at suitable speeds, thereby greatly enhancing capability and resolution for the detection of specific target molecules. In addition, DNA origami structures can be constructed to fulfill various design specifications and one-pot assembly reactions, thus serving as functional nanopores. Moreover, based on DNA strand displacement, nanopores can also be utilized to characterize the outputs of DNA computing and to develop programmable smart diagnostic nanodevices. In summary, DNA assembly-based nanopore research can pave the way for the realization of impactful biological detection and diagnostic platforms via single-biomolecule analysis.

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Abstract. glioblastoma is the most aggressive form of primary brain tumor with a tendency to invade surrounding healthy brain tissues, rendering tumors of this type largely incurable. aquaporin-4 (aQP4) is a key molecule involved in maintaining water and ion homeostasis in the central nervous system and has been recently reported to play a role in cell migration in addition to its well-known function in brain edema. increased aQP4 expression has been demonstrated in glioblastoma multiforme (gBM), suggesting that it is also involved in malignant brain tumors. Here, we identify a novel role for aquaporin-4 in glioblastoma cell migration and invasion. in the present study, we used small-interference rna technology and a pharmacological inhibitor to knock down the expression of AQP4, which resulted in specific and massive impairment of glioblastoma cell migration and invasion in vitro and in vivo. in addition, we demonstrated the possible mechanisms by which aQP4 functions in the process of glioblastoma cell invasion. the downregulation of matrix metalloprotease-2 (MMP-2) expression in ln229 cells with aQP4 reduction coincided with decreased cell invasive ability. furthermore, our study showed that aQP4 may also be involved in the regulation of glioblastoma cell adhesion. The expression of β-catenin and connexin 43 were increased in aQP4-downregulated ln229 cells consistent with their enhanced cell-cell adhesion ability. in summary, our results indicate that aQP4 is involved in the control of glioblastoma cell migration and invasion and may be a potential therapeutic target for glioblastoma cell infiltration. Introductionglioblastomas are the most common malignant tumors of the adult central nervous system. these are highly invasive and infiltrative tumors which are associated with a poor prognosis and median patient survival of only one year (1,2). a major barrier to available malignant glioma treatment is the invasion of these cells into brain parenchyma. Because of this, local therapies such as surgery or radiation therapy are ineffective (3). glioma cells invade through the ecM of the brain by activating a number of coordinated cellular processes, which include those necessary for migration and invasion. therefore, a detailed understanding of the mechanisms underlying this invasive behavior is essential for the development of novel effective therapies. aQPs (aquaporins) are a family of water channel proteins that provide a major pathway for osmotically driven water transport through cell membranes. to date, 13 aquaporin isoforms (AQP0-AQP12) have been identified in mammalian species (4). Both aQP1 and aQP4 have been clearly identified in brain, and AQP4 is known to participate mainly in brain edema after injury or other brain diseases (5). aQP4 is primarily expressed at the border between brain parenchyma and major fluid compartments, including astrocyte foot processes and glia limitans, as well as ependymal cells and subependymal astrocytes (6). this distribution suggests that aQP4 controls water fluxes into an...

Botrytis cinerea is a necrotrophic fungus causing disease on many important agricultural crops. Two novel mycoviruses, namely Botrytis cinerea hypovirus 1 (BcHV1) and Botrytis cinerea fusarivirus 1 (BcFV1), were fully sequenced. The genome of BcHV1 is 10,214 nt long excluding a poly-A tail and possesses one large open reading frame (ORF) encoding a polyprotein possessing several conserved domains including RNA-dependent RNA polymerase (RdRp), showing homology to hypovirus-encoded polyproteins. Phylogenetic analysis indicated that BcHV1 may belong to the proposed genus Betahypovirus in the viral family Hypoviridae. The genome of BcFV1 is 8411 nt in length excluding the poly A tail and theoretically processes two major ORFs, namely ORF1 and ORF2. The larger ORF1 encoded polypeptide contains protein domains of an RdRp and a viral helicase, whereas the function of smaller ORF2 remains unknown. The BcFV1 was phylogenetically clustered with other fusariviruses forming an independent branch, indicating BcFV1 was a member in Fusariviridae. Both BcHV1 and BcFV1 were capable of being transmitted horizontally through hyphal anastomosis. Infection by BcHV1 alone caused attenuated virulence without affecting mycelial growth, significantly inhibited infection cushion (IC) formation, and altered expression of several IC-formation-associated genes. However, wound inoculation could fully rescue the virulence phenotype of the BcHV1 infected isolate. These results indicate the BcHV1-associated hypovirulence is caused by the viral influence on IC-formation-associated pathways.

Glioblastomas are the most aggressive forms of primary brain tumors due to their tendency to invade surrounding healthy brain tissues, rendering them largely incurable. The water channel protein, Aquaporin-4 (AQP4) is a key molecule for maintaining water and ion homeostasis in the central nervous system and has recently been reported with cell survival except for its well-known function in brain edema. An increased AQP4 expression has been demonstrated in glioblastoma multiforme (GBM), suggesting it is also involved in malignant brain tumors. In this study, we show that siRNA-mediated down regulation of AQP4 induced glioblastoma cell apoptosis in vitro and in vivo. We further show that several apoptotic key proteins, Cytochrome C, Bcl-2 and Bad are involved in AQP4 signaling pathways. Our results indicate that AQP4 may serve as an anti-apoptosis target for therapy of glioblastoma.