Current advances of chlorinated organics degradation by bioelectrochemical systems: a review.

Chlorinated organic compounds (COCs) are typical refractory organic compounds, having high biological toxicity. These compounds are a type of pervasive pollutants that can be present in polluted soil, air, and various types of waterways, such as groundwater, rivers, and lakes, posing a significant threat to the ecological environment and human health. Bioelectrochemical systems (BESs) are an effective strategy for the degradation of bio-refractory compounds. BESs improve the waste treatment efficiency through the application of weak electrical stimulation. This review discusses the processes of BESs configurations and degradation performances in different environmental media including wastewater, soil, waste gas and groundwater. In addition, the degradation mechanisms and performance-enhancing additives are summarized. The future challenges and perspectives on the development of BES for COCs removal are briefly discussed.

Effect of weak electrical stimulation on m-dichlorobenzene biodegradation in biotrickling filters: Insights from performance and microbial community analysis.

The microbial electrolysis cell coupled with the biotrickling filters (MEC-BTF) was developed for enhancing the biodegradation of gaseous m-dichlorobenzene (m-DCB) through weak electrical stimulation. The maximum removal efficiency and elimination capacity in MEC-BTF were 1.48 and 1.65 times higher than those in open-circuit BTF (OC-BTF), respectively. Weak electrical stimulation had a positive impact on the characteristics of the biofilm. Additionally, microbial community analysis revealed that weak electrical stimulation increased the abundance of key functional genera (e.g., Rhodanobacter and Bacillus) and genes (e.g., catA/E and E1.3.1.32), thereby accelerating reductive dechlorination and ring-opening of m-DCB. Macrogenomic sequencing further revealed that electron transfer pathway in MEC-BTF might be mediated through extracellular electroactive mediators and cytochromes.

Analysis of prognostic factors and construction of prognostic models for triple-positive breast cancer.

Objective: By identifying the clinicopathological characteristics and prognostic influences of patients with triple-positive breast cancer (TPBC) at Xijing Hospital in China compared with those in the United States, this study aims to construct a nomogram model to forecast the overall survival rate (OS) of TPBC patients. Method: The Surveillance, Epidemiology, and End Results (SEER) database was used to screen 5769 patients as the training cohort, and 191 patients from Xijing Hospital were used as the validation cohort. Cox risk-proportional model was applied to select variables and the nomogram model was constructed based on the training cohort. The performance of the model was evaluated by calculating the C-index and generating calibration plots in the training and validation cohorts. Results: Cox multifactorial analysis showed that age, chemotherapy, radiotherapy, M-stage, T-stage, N-stage, and the mode of surgery were all independent risk factors for the prognosis of TPBC patients (all P<0.05). With this premise, the nomogram model was constructed and evaluated. The C-index value of the nomogram model was 0.830 in the training group and 0.914 in the validation group. Moreover, both the calibration and ROC curves for the proposed model exhibited reliable performance, and the clinical decision curve analysis showed that the proposed model can bring clinical benefits. Conclusions: The constructed nomogram can accurately predict individual survival probabilities and may serve as a clinical decision support tool for clinicians to optimize treatment in individuals.

Glutamatergic synapses from the insular cortex to the basolateral amygdala encode observational pain.

Empathic pain has attracted the interest of a substantial number of researchers studying the social transfer of pain in the sociological, psychological, and neuroscience fields. However, the neural mechanism of empathic pain remains elusive. Here, we establish a long-term observational pain model in mice and find that glutamatergic projection from the insular cortex (IC) to the basolateral amygdala (BLA) is critical for the formation of observational pain. The selective activation or inhibition of the IC-BLA projection pathway strengthens or weakens the intensity of observational pain, respectively. The synaptic molecules are screened, and the upregulated synaptotagmin-2 and RIM3 are identified as key signals in controlling the increased synaptic glutamate transmission from the IC to the BLA. Together, these results reveal the molecular and synaptic mechanisms of a previously unidentified neural pathway that regulates observational pain in mice.

SEPT7 Interacts with KIF20A and Regulates the Proliferative State of Neural Progenitor Cells During Cortical Development.

Balanced proliferation and differentiation of neural progenitor cells (NPCs) are critical for brain development, but how the process is regulated and what components of the cell division machinery is involved are not well understood. Here we report that SEPT7, a cell division regulator originally identified in Saccharomyces cerevisiae, interacts with KIF20A in the intercellular bridge of dividing NPCs and plays an essential role in maintaining the proliferative state of NPCs during cortical development. Knockdown of SEPT7 in NPCs results in displacement of KIF20A from the midbody and early neuronal differentiation. NPC-specific inducible knockout of Sept7 causes early cell cycle exit, precocious neuronal differentiation, and ventriculomegaly in the cortex, but surprisingly does not lead to noticeable cytokinesis defect. Our data uncover an interaction of SEPT7 and KIF20A during NPC divisions and demonstrate a crucial role of SEPT7 in cell fate determination. In addition, this study presents a functional approach for identifying additional cell fate regulators of the mammalian brain.

KIF20A/MKLP2 regulates the division modes of neural progenitor cells during cortical development.

Balanced symmetric and asymmetric divisions of neural progenitor cells (NPCs) are crucial for brain development, but the underlying mechanisms are not fully understood. Here we report that mitotic kinesin KIF20A/MKLP2 interacts with RGS3 and plays a crucial role in controlling the division modes of NPCs during cortical neurogenesis. Knockdown of KIF20A in NPCs causes dislocation of RGS3 from the intercellular bridge (ICB), impairs the function of Ephrin-B-RGS cell fate signaling complex, and leads to a transition from proliferative to differentiative divisions. Germline and inducible knockout of KIF20A causes a loss of progenitor cells and neurons and results in thinner cortex and ventriculomegaly. Interestingly, loss of function of KIF20A induces early cell cycle exit and precocious neuronal differentiation without causing substantial cytokinesis defect or apoptosis. Our results identify a RGS-KIF20A axis in the regulation of cell division and suggest a potential link of the ICB to regulation of cell fate determination.

Alternative RNA Splicing Associated With Mammalian Neuronal Differentiation.

Alternative pre-mRNA splicing (AS) produces multiple isoforms of mRNAs and proteins from a single gene. It is most prevalent in the mammalian brain and is thought to contribute to the formation and/or maintenance of functional complexity of the brain. Increasing evidence has documented the significant changes of AS between different regions or different developmental stages of the brain, however, the dynamics of AS and the possible function of it during neural progenitor cell (NPC) differentiation is less well known. Here, using purified NPCs and their progeny neurons isolated from the embryonic mouse cerebral cortex, we characterized the global differences of AS events between the 2 cell types by deep sequencing. The sequencing results revealed cell type-specific AS in NPCs and neurons that are important for distinct functions pertinent to the corresponding cell type. Our data may serve as a resource useful for further understanding how AS contributes to molecular regulations in NPCs and neurons during cortical development.

Robo4 regulates the radial migration of newborn neurons in developing neocortex.

During the morphogenesis of neocortex, newborn neurons undergo radial migration from the ventricular zone toward the surface of the cortical plate to form an "inside-out" lamina structure. The spatiotemporal signals that control this stereotyped radial migration remain elusive. Here, we report that a recently identified Robo family member Robo4 (Magic Roundabout), which was considered to be solely expressed in endothelial cells, is expressed in developing brain and regulates the radial migration of newborn neurons in neocortex. Downregulation of Robo4 expression in cortical newborn neurons by using in utero electroporation, with either specific siRNAs in wild-type rodents or with Cre recombinase in floxed-robo4 mutant mice, led to severe defects in the radial migration of newborn neurons with misorientation of these neurons. Moreover, newborn neurons transfected with Robo4 siRNAs exhibited significantly lower motility in a transwell migration assay (Boyden chamber) in the absence of Slit and significantly higher sensitivity to the repulsive effect of Slit in both transwell migration assay and growth cone collapse assay. Overall, our results showed an important role of Robo4 in the regulation of cortical radial migration through Slit-dependent and -independent mechanisms.

PKCdelta regulates cortical radial migration by stabilizing the Cdk5 activator p35.

Cyclin-dependent kinase 5 (Cdk5) and its activator p35 are critical for radial migration and lamination of cortical neurons. However, how this kinase is regulated by extracellular and intracellular signals during cortical morphogenesis remains unclear. Here, we show that PKCdelta, a member of novel PKC expressing in cortical neurons, could stabilize p35 by direct phosphorylation. PKCdelta attenuated the degradation of p35 but not its mutant derivative, which could not be phosphorylated by PKCdelta. Down-regulation of PKCdelta by in utero electroporation of specific small interference RNA (siRNA) severely impaired the radial migration of cortical neurons. This migration defect was similar to that caused by down-regulation of p35 and could be prevented by cotransfection with the wild-type but not the mutant p35. Furthermore, PKCdelta could be activated by the promigratory factor brain-derived neurotrophic factor (BDNF) and was required for the activation of Cdk5 by BDNF. Both PKCdelta and p35 were required for the promigratory effect of BDNF on cultured newborn neurons. Thus, PKCdelta may promote cortical radial migration through maintaining the proper level of p35 in newborn neurons.