Table_1_Midgut Transcriptional Variation of Chilo suppressalis Larvae Induced by Feeding on the Dead-End Trap Plant, Vetiveria zizanioides.DOC

<p>Chilo supprressalis is one of the most important rice pests that causes serious damage to production in the rice growth area of Asia. Vetiver grass (Vetiveria zizanioides) was previously found to effectively attract female adults of C. suppressalis laying eggs on vetiver leaves, while the larvae cannot complete their life cycles by feeding on vetiver, indicating a potential means of controlling this pest. In the present study, the transcriptomes of midguts of rice-fed and vetiver-fed C. suppressalis larvae were profiled, which aimed to clarify the molecular mechanism of vetiver as a dead-end trap plant preliminarily. We found that ingestion of vetiver provoked a robust transcriptional response in the larval midguts, and a total of 1,849 differentially expressed UniGenes were identified. We focused on 12 digestion-related genes, four immune-related genes and three detoxification-related genes. Most of these genes were significantly down regulated in the larval midguts at 6, 8, and 10 days after feeding on vetiver compared to on rice. Transcriptional dynamics suggested that these genes might be involved in toxicity responses following exposure to vetiver. Taken together, this study provides an initial molecular framework for developing biological control strategies for C. suppressalis in an effort to protect economically important rice crops.</p

Temperature- and pH-Responsive Benzoboroxole-Based Polymers for Flocculation and Enhanced Dewatering of Fine Particle Suspensions

Random copolymers based on <i>N</i>-isopropylacrylamide (NIPAAm) containing 2-aminoethyl methacrylamide hydrochloride (AEMA) and 5-methacrylamido-1,2-benzoboroxole (MAAmBo) were synthesized and subsequently evaluated for their performance in solid–liquid separation at various pH and temperatures. The strong interactions between benzoboroxole residues and kaolin hydroxyl groups were evaluated for the first time in the flocculation of fine particle suspensions. The lower critical solution temperatures (LCSTs) of PAMN decreases because of the hydrophobic nature of the benzoboroxole moieties, resulting in strong hydrophobic interaction at temperatures higher than the LCSTs. Temperature and pH responsive polymer, P­(AEMA₅₁-<i>st</i>-MAAmBo₇₆-<i>st</i>-NIPAM₃₈₁) (denoted as PAMN) shows the ability to induce fastest settling at a low dosage of 25 ppm and under the condition of pH 9 and 50 °C. The accelerated settling rate is considered to be due to the strong adhesion of benzoboroxole residues to the kaolin hydroxyl groups, the electrical double layer force, and the hydrophobic force. During condensation phase, increasing the pH of sediment to pH 11 could attain the most compact structure. Random copolymers containing benzoboroxole groups act as dispersants (due to pH-responsive character) rather than flocculants at pH 11, providing repulsive force that enables particles to rearrange their position and consolidate well. Through a two-step solid–liquid separation including settling phase and consolidation phase, rapid settling and compact sediment are feasible simultaneously

Measuring Charge-Separation Dynamics via Oligomer Length Variation

We study the optically induced charge-transfer dynamics in donor–acceptor oligomers of different chain lengths. The combination of systematic synthesis, electrochemical measurements, and ultrafast transient absorption spectroscopy allows us to determine the charge-transfer properties and dynamics in donor–acceptor systems of confined lengths. Calculations within Marcus and Jortner electron-transfer theory explain the different charge-recombination times. For compounds in which complete charge separation can occur we deduce fast equilibration between different charge-transfer configurations prior to charge recombination. Thus, monoexponential charge-recombination kinetics are observed, as only the smallest-barrier configuration leads to relaxation to the ground state. The systematic oligomer length variation along with time-resolved spectroscopy allows us to determine how far apart charges can be separated in multichromophore donor–acceptor systems. Such information is relevant for understanding on a microscopic level the charge carrier mobility in materials for organic electronics and photovoltaics

table_4_Denervated mouse CA1 pyramidal neurons express homeostatic synaptic plasticity following entorhinal cortex lesion.xlsx

Structural, functional, and molecular reorganization of denervated neural networks is often observed in neurological conditions. The loss of input is accompanied by homeostatic synaptic adaptations, which can affect the reorganization process. A major challenge of denervation-induced homeostatic plasticity operating in complex neural networks is the specialization of neuronal inputs. It remains unclear whether neurons respond similarly to the loss of distinct inputs. Here, we used in vitro entorhinal cortex lesion (ECL) and Schaffer collateral lesion (SCL) in mouse organotypic entorhino-hippocampal tissue cultures to study denervation-induced plasticity of CA1 pyramidal neurons. We observed microglia accumulation, presynaptic bouton degeneration, and a reduction in dendritic spine numbers in the denervated layers 3 days after SCL and ECL. Transcriptome analysis of the CA1 region revealed complex changes in differential gene expression following SCL and ECL compared to non-lesioned controls with a specific enrichment of differentially expressed synapse-related genes observed after ECL. Consistent with this finding, denervation-induced homeostatic plasticity of excitatory synapses was observed 3 days after ECL but not after SCL. Chemogenetic silencing of the EC but not CA3 confirmed the pathway-specific induction of homeostatic synaptic plasticity in CA1. Additionally, increased RNA oxidation was observed after SCL and ECL. These results reveal important commonalities and differences between distinct pathway lesions and demonstrate a pathway-specific induction of denervation-induced homeostatic synaptic plasticity.</p

table_5_Denervated mouse CA1 pyramidal neurons express homeostatic synaptic plasticity following entorhinal cortex lesion.xlsx

Structural, functional, and molecular reorganization of denervated neural networks is often observed in neurological conditions. The loss of input is accompanied by homeostatic synaptic adaptations, which can affect the reorganization process. A major challenge of denervation-induced homeostatic plasticity operating in complex neural networks is the specialization of neuronal inputs. It remains unclear whether neurons respond similarly to the loss of distinct inputs. Here, we used in vitro entorhinal cortex lesion (ECL) and Schaffer collateral lesion (SCL) in mouse organotypic entorhino-hippocampal tissue cultures to study denervation-induced plasticity of CA1 pyramidal neurons. We observed microglia accumulation, presynaptic bouton degeneration, and a reduction in dendritic spine numbers in the denervated layers 3 days after SCL and ECL. Transcriptome analysis of the CA1 region revealed complex changes in differential gene expression following SCL and ECL compared to non-lesioned controls with a specific enrichment of differentially expressed synapse-related genes observed after ECL. Consistent with this finding, denervation-induced homeostatic plasticity of excitatory synapses was observed 3 days after ECL but not after SCL. Chemogenetic silencing of the EC but not CA3 confirmed the pathway-specific induction of homeostatic synaptic plasticity in CA1. Additionally, increased RNA oxidation was observed after SCL and ECL. These results reveal important commonalities and differences between distinct pathway lesions and demonstrate a pathway-specific induction of denervation-induced homeostatic synaptic plasticity.</p

table_1_Denervated mouse CA1 pyramidal neurons express homeostatic synaptic plasticity following entorhinal cortex lesion.xlsx

Structural, functional, and molecular reorganization of denervated neural networks is often observed in neurological conditions. The loss of input is accompanied by homeostatic synaptic adaptations, which can affect the reorganization process. A major challenge of denervation-induced homeostatic plasticity operating in complex neural networks is the specialization of neuronal inputs. It remains unclear whether neurons respond similarly to the loss of distinct inputs. Here, we used in vitro entorhinal cortex lesion (ECL) and Schaffer collateral lesion (SCL) in mouse organotypic entorhino-hippocampal tissue cultures to study denervation-induced plasticity of CA1 pyramidal neurons. We observed microglia accumulation, presynaptic bouton degeneration, and a reduction in dendritic spine numbers in the denervated layers 3 days after SCL and ECL. Transcriptome analysis of the CA1 region revealed complex changes in differential gene expression following SCL and ECL compared to non-lesioned controls with a specific enrichment of differentially expressed synapse-related genes observed after ECL. Consistent with this finding, denervation-induced homeostatic plasticity of excitatory synapses was observed 3 days after ECL but not after SCL. Chemogenetic silencing of the EC but not CA3 confirmed the pathway-specific induction of homeostatic synaptic plasticity in CA1. Additionally, increased RNA oxidation was observed after SCL and ECL. These results reveal important commonalities and differences between distinct pathway lesions and demonstrate a pathway-specific induction of denervation-induced homeostatic synaptic plasticity.</p

table_3_Denervated mouse CA1 pyramidal neurons express homeostatic synaptic plasticity following entorhinal cortex lesion.xlsx

Structural, functional, and molecular reorganization of denervated neural networks is often observed in neurological conditions. The loss of input is accompanied by homeostatic synaptic adaptations, which can affect the reorganization process. A major challenge of denervation-induced homeostatic plasticity operating in complex neural networks is the specialization of neuronal inputs. It remains unclear whether neurons respond similarly to the loss of distinct inputs. Here, we used in vitro entorhinal cortex lesion (ECL) and Schaffer collateral lesion (SCL) in mouse organotypic entorhino-hippocampal tissue cultures to study denervation-induced plasticity of CA1 pyramidal neurons. We observed microglia accumulation, presynaptic bouton degeneration, and a reduction in dendritic spine numbers in the denervated layers 3 days after SCL and ECL. Transcriptome analysis of the CA1 region revealed complex changes in differential gene expression following SCL and ECL compared to non-lesioned controls with a specific enrichment of differentially expressed synapse-related genes observed after ECL. Consistent with this finding, denervation-induced homeostatic plasticity of excitatory synapses was observed 3 days after ECL but not after SCL. Chemogenetic silencing of the EC but not CA3 confirmed the pathway-specific induction of homeostatic synaptic plasticity in CA1. Additionally, increased RNA oxidation was observed after SCL and ECL. These results reveal important commonalities and differences between distinct pathway lesions and demonstrate a pathway-specific induction of denervation-induced homeostatic synaptic plasticity.</p

table_2_Denervated mouse CA1 pyramidal neurons express homeostatic synaptic plasticity following entorhinal cortex lesion.xlsx

Structural, functional, and molecular reorganization of denervated neural networks is often observed in neurological conditions. The loss of input is accompanied by homeostatic synaptic adaptations, which can affect the reorganization process. A major challenge of denervation-induced homeostatic plasticity operating in complex neural networks is the specialization of neuronal inputs. It remains unclear whether neurons respond similarly to the loss of distinct inputs. Here, we used in vitro entorhinal cortex lesion (ECL) and Schaffer collateral lesion (SCL) in mouse organotypic entorhino-hippocampal tissue cultures to study denervation-induced plasticity of CA1 pyramidal neurons. We observed microglia accumulation, presynaptic bouton degeneration, and a reduction in dendritic spine numbers in the denervated layers 3 days after SCL and ECL. Transcriptome analysis of the CA1 region revealed complex changes in differential gene expression following SCL and ECL compared to non-lesioned controls with a specific enrichment of differentially expressed synapse-related genes observed after ECL. Consistent with this finding, denervation-induced homeostatic plasticity of excitatory synapses was observed 3 days after ECL but not after SCL. Chemogenetic silencing of the EC but not CA3 confirmed the pathway-specific induction of homeostatic synaptic plasticity in CA1. Additionally, increased RNA oxidation was observed after SCL and ECL. These results reveal important commonalities and differences between distinct pathway lesions and demonstrate a pathway-specific induction of denervation-induced homeostatic synaptic plasticity.</p

Robust Metal–Organic Framework Containing Benzoselenadiazole for Highly Efficient Aerobic Cross-dehydrogenative Coupling Reactions under Visible Light

A zirconium­(IV)-based UiO-topological metal–organic framework (UiO-68Se) containing benzoselenadiazole was synthesized by an approach of the mixed dicarboxylate struts, which show highly efficient and recycalable photocatalytic activity for aerobic cross-dehydrogenative coupling reactions between tertiary amines and various carbon nucleophiles under visible-light irradiation

image_1_v1_Denervated mouse CA1 pyramidal neurons express homeostatic synaptic plasticity following entorhinal cortex lesion.tif

Structural, functional, and molecular reorganization of denervated neural networks is often observed in neurological conditions. The loss of input is accompanied by homeostatic synaptic adaptations, which can affect the reorganization process. A major challenge of denervation-induced homeostatic plasticity operating in complex neural networks is the specialization of neuronal inputs. It remains unclear whether neurons respond similarly to the loss of distinct inputs. Here, we used in vitro entorhinal cortex lesion (ECL) and Schaffer collateral lesion (SCL) in mouse organotypic entorhino-hippocampal tissue cultures to study denervation-induced plasticity of CA1 pyramidal neurons. We observed microglia accumulation, presynaptic bouton degeneration, and a reduction in dendritic spine numbers in the denervated layers 3 days after SCL and ECL. Transcriptome analysis of the CA1 region revealed complex changes in differential gene expression following SCL and ECL compared to non-lesioned controls with a specific enrichment of differentially expressed synapse-related genes observed after ECL. Consistent with this finding, denervation-induced homeostatic plasticity of excitatory synapses was observed 3 days after ECL but not after SCL. Chemogenetic silencing of the EC but not CA3 confirmed the pathway-specific induction of homeostatic synaptic plasticity in CA1. Additionally, increased RNA oxidation was observed after SCL and ECL. These results reveal important commonalities and differences between distinct pathway lesions and demonstrate a pathway-specific induction of denervation-induced homeostatic synaptic plasticity.</p