2D MoB MBene: An Efficient Co-Catalyst for Photocatalytic Hydrogen Production under Visible Light.

Highly active and low-cost co-catalysts have a positive effect on the enhancement of solar H2 production. Here, we employ two-dimensional (2D) MBene as a noble-metal-free co-catalyst to boost semiconductor for photocatalytic H2 production. MoB MBene is a 2D nanoboride, which is directly made from MoAlB by a facile hydrothermal etching and manual scraping off process. The as-synthesized MoB MBene with purity >95 wt % is treated by ultrasonic cell pulverization to obtain ultrathin 2D MoB MBene nanosheets (∼0.61 nm) and integrated with CdS via an electrostatic interaction strategy. The CdS/MoB composites exhibit an ultrahigh photocatalytic H2 production activity of 16,892 µmol g-1 h-1 under visible light, surpassing that of pure CdS by an exciting factor of ≈1135%. Theoretical calculations and various measurements account for the high performance in terms of Gibbs free energy, work functions, and photoelectrochemical properties. This work discovers the huge potential of these promising 2D MBene family materials as high-efficiency and low-cost co-catalysts for photocatalytic H2 production.

Staggered Assembly of a Dimeric Au13 Cluster: Impacts on Coupling of Geometric Isomerism.

The specific states of aggregation of metal atoms in sub-nanometer-sized gold clusters are related to the different quantum confinement volumes of electrons, leading to novel optical and electronic properties. These volumes can be tuned by changing the relative positions of the gold atoms to generate isomers. Studying the isomeric gold core and the electron coupling between the basic units is fundamentally important for nanoelectronic devices and luminescence; however, appropriate cases are lacking. In this study, the structure of the first staggered di-superatomic Au25 -S was solved using single-crystal X-ray diffraction. The optical properties of Au25 -S were studied by comparing with eclipsed Au25 -E. From Au25 -E to Au25 -S, changes in the electronic structures occurred, resulting in significantly different optical absorptions originating from the coupling between the two Au13 modules. Au25 -S shows a longer electron decay lifetime of 307.7 ps before populating the lowest triplet emissive state, compared to 1.29 ps for Au25 -E. The experimental and theoretical results show that variations in the geometric isomerism lead to distinct photophysical processes owing to isomerism-dependent electronic coupling. This study offers new insights into the connection between the geometric isomerism of nanosized building blocks and the optical properties of their assemblies, opening new possibilities for constructing function-specific nanomaterials.

Effect of electroacupuncture on myocardial electrical remodeling in rats with acute myocardial infarction. / ç”µé’ˆå¯¹æ€¥æ€§å¿ƒè‚Œæ¢—æ­»å¤§é¼ å¿ƒè‚Œç”µé‡æž„çš„å½±å“åŠå ¶æœºåˆ¶ç ”ç©¶.

OBJECTIVES: To investigate the mechanism of electroacupuncture (EA) at "Neiguan" (PC6) in impro-ving myocardial electrical remodeling in rats with acute myocardial infarction (AMI) by enhancing transient outward potassium current. METHODS: A total of 30 male SD rats were randomly divided into control, model and EA groups, with 10 rats in each group. The AMI model was established by subcutaneous injection with isoprenaline (ISO, 85 mg/kg). EA was applied to left PC6 for 20 min, once daily for 5 days. Electrocardiogram (ECG) was recorded after treatment. TTC staining was used to observe myocardial necrosis. HE staining was used to observe the pathological morphology of myocardial tissue and measure the cross-sectional area of myocardium. Potassium ion-related genes in myocardial tissue were detected by RNA sequencing. The mRNA and protein expressions of Kchip2 and Kv4.2 in myocardial tissue were detected by real-time fluorescence quantitative PCR and Western blot, respectively. RESULTS: Compared with the control group, cardiomyocyte cross-sectional area in the model group was significantly increased (P<0.01), the ST segment was significantly elevated (P<0.01), and QT, QTc, QTd and QTcd were all significantly increased (P<0.05, P<0.01). After EA treatment, cardiomyocyte cross-sectional area was significantly decreased (P<0.01), the ST segment was significantly reduced (P<0.01), and the QT, QTc, QTcd and QTd were significantly decreased (P<0.01, P<0.05). RNA sequencing results showed that a total of 20 potassium ion-related genes co-expressed by the 3 groups were identified. Among them, Kchip2 expression was up-regulated most notablely in the EA group. Compared with the control group, the mRNA and protein expressions of Kchip2 and Kv4.2 in the myocardial tissue of the model group were significantly decreased (P<0.01, P<0.05), while those were increased in the EA group (P<0.01, P<0.05). CONCLUSIONS: EA may improve myocardial electrical remodeling in rats with myocardial infarction, which may be related to its functions in up-regulating the expressions of Kchip2 and Kv4.2.

Protective effects of curcumin on desipramine-induced islet ß-cell damage via AKAP150/PKA/PP2B complex.

Tricyclic antidepressants (TCAs) are widely used to treat depression and anxiety-related mood disorders. But evidence shows that TCAs elevate blood glucose levels and inhibit insulin secretion, suggesting that TCAs are a risk factor, particularly for individuals with diabetes. Curcumin is a bioactive molecule from the rhizome of the Curcuma longa plant, which has shown both antidepressant and anti-diabetic activities. In the present study, we investigated the protective effect of curcumin against desipramine-induced apoptosis in ß cells and the underlying molecular mechanisms. In the mouse forced swimming test (FST), we found that lower doses of desipramine (5 and 10 mg/kg) or curcumin (2.5 mg/kg) alone did not affect the immobility time, whereas combined treatment with curcumin (2.5 mg/kg) and desipramine (5, 10 mg/kg) significantly decreased the immobility time. Furthermore, desipramine dose-dependently inhibited insulin secretion and elevated blood glucose levels, whereas the combined treatment normalized insulin secretion and blood glucose levels. In RIN-m5F pancreatic ß-cells, desipramine (10 µM) significantly reduced the cell viability, whereas desipramine combined with curcumin dose-dependently prevented the desipramine-induced impairment in glucose-induced insulin release, most effectively with curcumin (1 and 10 µM). We demonstrated that desipramine treatment promoted the cleavage and activation of Caspase 3 in RIN-m5F cells. Curcumin treatment inhibited desipramine-induced apoptosis, increased mitochondrial membrane potential and Bcl-2/Bax ratio. Desipramine increased the generation of reactive oxygen species, which was reversed by curcumin treatment. Curcumin also inhibited the translocation of forkhead box protein O1 (FOXO1) from the cytoplasm to the nucleus and suppressed the binding of A-kinase anchor protein 150 (AKAP150) to protein phosphatase 2B (PP2B, known as calcineurin) that was induced by desipramine. These results suggest that curcumin protects RIN-m5F pancreatic ß-cells against desipramine-induced apoptosis by inhibiting the phosphoinositide 3-kinase/AKT/FOXO1 pathway and the AKAP150/PKA/PP2B interaction. This study suggests that curcumin may have therapeutic potential as an adjunct to antidepressant treatment.

A Non-canonical Excitatory PV RGC-PV SC Visual Pathway for Mediating the Looming-evoked Innate Defensive Response.

Parvalbumin-positive retinal ganglion cells (PV+ RGCs) are an essential subset of RGCs found in various species. However, their role in transmitting visual information remains unclear. Here, we characterized PV+ RGCs in the retina and explored the functions of the PV+ RGC-mediated visual pathway. By applying multiple viral tracing strategies, we investigated the downstream of PV+ RGCs across the whole brain. Interestingly, we found that the PV+ RGCs provided direct monosynaptic input to PV+ excitatory neurons in the superficial layers of the superior colliculus (SC). Ablation or suppression of SC-projecting PV+ RGCs abolished or severely impaired the flight response to looming visual stimuli in mice without affecting visual acuity. Furthermore, using transcriptome expression profiling of individual cells and immunofluorescence colocalization for RGCs, we found that PV+ RGCs are predominant glutamatergic neurons. Thus, our findings indicate the critical role of PV+ RGCs in an innate defensive response and suggest a non-canonical subcortical visual pathway from excitatory PV+ RGCs to PV+ SC neurons that regulates looming visual stimuli. These results provide a potential target for intervening and treating diseases related to this circuit, such as schizophrenia and autism.

Paraventricular Hypothalamic Nucleus Upregulates Intraocular Pressure Via Glutamatergic Neurons.

Purpose: The neuroregulatory center of intraocular pressure (IOP) is located in the hypothalamus. An efferent neural pathway exists between the hypothalamic nuclei and the autonomic nerve endings in the anterior chamber of the eye. This study was designed to investigate whether the paraventricular hypothalamic nucleus (PVH) regulates IOP as the other nuclei do. Methods: Optogenetic manipulation of PVH neurons was used in this study. Light stimulation was applied via an optical fiber embedded over the PVH to activate projection neurons after AAV2/9-CaMKIIα-hChR2-mCherry was injected into the right PVH of C57BL/6J mice. The same methods were used to inhibit projection neurons after AAV2/9-CaMKIIα-eNpHR3.0-mCherry was injected into the bilateral PVH of C57BL/6J mice. AAV2/9-EF1α-DIO-hChR2-mCherry was injected into the right PVH of Vglut2-Cre mice to elucidate the effect of glutamatergic neuron-specific activation. IOP was measured before and after light manipulation. Associated nuclei activation was clarified by c-Fos immunohistochemical staining. Only mice with accurate viral expression and fiber embedding were included in the statistical analysis. Results: Activation of projection neurons in the right PVH induced significant bilateral IOP elevation (n = 11, P < 0.001); the ipsilateral IOP increased more noticeably (n = 11, P < 0.05); Bilateral inhibition of PVH projection neurons did not significantly influence IOP (n = 5, P > 0.05). Specific activation of glutamatergic neurons among PVH projection neurons also induced IOP elevation in both eyes (n = 5, P < 0.001). The dorsomedial hypothalamic nucleus, ventromedial hypothalamic nucleus, locus coeruleus and basolateral amygdaloid nucleus responded to light stimulation of PVH in AAV-ChR2 mice. Conclusions: The PVH may play a role in IOP upregulation via glutamatergic neurons.

A direct spino-cortical circuit bypassing the thalamus modulates nociception.

Nociceptive signals are usually transmitted to layer 4 neurons in somatosensory cortex via the spinothalamic-thalamocortical pathway. The layer 5 corticospinal neurons in sensorimotor cortex are reported to receive the output of neurons in superficial layers; and their descending axons innervate the spinal cord to regulate basic sensorimotor functions. Here, we show that a subset of layer 5 neurons receives spinal inputs through a direct spino-cortical circuit bypassing the thalamus, and thus define these neurons as spino-cortical recipient neurons (SCRNs). Morphological studies revealed that the branches from spinal ascending axons formed a kind of disciform structure with the descending axons from SCRNs in the basilar pontine nucleus (BPN). Electron microscopy and calcium imaging further confirmed that the axon terminals from spinal ascending neurons and SCRNs made functional synaptic contacts in the BPN, linking the ascending sensory pathway to the descending motor control pathway. Furthermore, behavioral tests indicated that the spino-cortical connection in the BPN was involved in nociceptive responses. In vivo calcium imaging showed that SCRNs responded to peripheral noxious stimuli faster than neighboring layer 4 cortical neurons in awake mice. Manipulating activities of SCRNs could modulate nociceptive behaviors. Therefore, this direct spino-cortical circuit represents a noncanonical pathway, allowing a fast sensory-motor transition of the brain in response to noxious stimuli.

Mitophagy-related gene signature predicts prognosis, immune infiltration and chemotherapy sensitivity in colorectal cancer.

BACKGROUND: Mitophagy plays essential role in the development and progression of colorectal cancer (CRC). However, the effect of mitophagy-related genes in CRC remains largely unknown. AIM: To develop a mitophagy-related gene signature to predict the survival, immune infiltration and chemotherapy response of CRC patients. METHODS: Non-negative matrix factorization was used to cluster CRC patients from Gene Expression Omnibus database (GSE39582, GSE17536, and GSE37892) based on mitophagy-related gene expression. The CIBERSORT method was applied for the evaluation of the relative infiltration levels of immune cell types. The performance signature in predicting chemotherapeutic sensitivity was generated using data from the Genomics of Drug Sensitivity in Cancer database. RESULTS: Three clusters with different clinicopathological features and prognosis were identified. Higher enrichment of activated B cells and CD4+ T cells were observed in cluster III patients with the most favorable prognosis. Next, a risk model based on mitophagy-related genes was developed. Patients in training and validation sets were categorized into low-risk and high-risk subgroups. Low risk patients showed significantly better prognosis, higher enrichment of immune activating cells and greater response to chemotherapy (oxaliplatin, irinotecan, and 5-fluorouracil) compared to high-risk patients. Further experiments identified CXCL3 as novel regulator of cell proliferation and mitophagy. CONCLUSION: We revealed the biological roles of mitophagy-related genes in the immune infiltration, and its ability to predict patients' prognosis and response to chemotherapy in CRC. These interesting findings would provide new insight into the therapeutic management of CRC patients.

Targeting a vulnerable septum-hippocampus cholinergic circuit in a critical time window ameliorates tau-impaired memory consolidation.

BACKGROUND: Abnormal tau accumulation and cholinergic degeneration are hallmark pathologies in the brains of patients with Alzheimer's disease (AD). However, the sensitivity of cholinergic neurons to AD-like tau accumulation and strategies to ameliorate tau-disrupted spatial memory in terms of neural circuits still remain elusive. METHODS: To investigate the effect and mechanism of the cholinergic circuit in Alzheimer's disease-related hippocampal memory, overexpression of human wild-type Tau (hTau) in medial septum (MS)-hippocampus (HP) cholinergic was achieved by specifically injecting pAAV-EF1α-DIO-hTau-eGFP virus into the MS of ChAT-Cre mice. Immunostaining, behavioral analysis and optogenetic activation experiments were used to detect the effect of hTau accumulation on cholinergic neurons and the MS-CA1 cholinergic circuit. Patch-clamp recordings and in vivo local field potential recordings were used to analyze the influence of hTau on the electrical signals of cholinergic neurons and the activity of cholinergic neural circuit networks. Optogenetic activation combined with cholinergic receptor blocker was used to detect the role of cholinergic receptors in spatial memory. RESULTS: In the present study, we found that cholinergic neurons with an asymmetric discharge characteristic in the MS-hippocampal CA1 pathway are vulnerable to tau accumulation. In addition to an inhibitory effect on neuronal excitability, theta synchronization between the MS and CA1 subsets was significantly disrupted during memory consolidation after overexpressing hTau in the MS. Photoactivating MS-CA1 cholinergic inputs within a critical 3 h time window during memory consolidation efficiently improved tau-induced spatial memory deficits in a theta rhythm-dependent manner. CONCLUSIONS: Our study not only reveals the vulnerability of a novel MS-CA1 cholinergic circuit to AD-like tau accumulation but also provides a rhythm- and time window-dependent strategy to target the MS-CA1 cholinergic circuit, thereby rescuing tau-induced spatial cognitive functions.

The relationship between cancer-related fatigue, quality of life and pain among cancer patients.

Objectives: This study aimed to select patients with cancer-related pain to further analyze the relationship between pain severity, fatigue severity, and quality of life. Methods: A cross-sectional study was conducted. A convenience sampling method was used to select 224 patients with cancer-related pain who were undergoing chemotherapy and met the inclusion criteria in two hospitals of two provinces from May to November 2019. All participants were invited to complete a general information questionnaire, the Brief Fatigue Inventory (BFI), the Numerical Rating Scale (NRS) for pain intensity, and the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire (EORTC QLQ-C30). Results: In the 24 h before completing the scales, 85 patients (37.9%) had mild pain, 121 (54.0%) had moderate pain, and 18 (8.0%) had severe pain. In addition, 92 (41.1%) patients had mild fatigue, 72 (32.1%) had moderate fatigue, and 60 (26.8%) had severe fatigue. Most patients with mild pain only experienced mild fatigue, and their quality of life was also at a moderate level. Patients with moderate and severe pain mostly had moderate or higher levels of fatigue and a lower quality of life. There was no correlation between fatigue and quality of life in patients with mild pain (r = -0.179, P = 0.104). There was a correlation between fatigue and quality of life in patients with moderate and severe pain (r = -0.537, P < 0.01; r = -0.509, P < 0.05). Conclusions: Patients with moderate and severe pain have more fatigue symptoms and lower quality of life than those with mild pain. Nurses should pay more attention to patients with moderate and severe pain, explore the interaction mechanism between symptoms, and carry out joint symptom intervention to improve the quality of life of patients.

Effects of electroacupuncture on rats with cognitive impairment: An iTRAQ-based proteomics analysis.

OBJECTIVE: The study explores the effects of electroacupuncture (EA) at the governing vessel (GV) on proteomic changes in the hippocampus of rats with cognitive impairment. METHODS: Healthy male rats were randomly divided into 3 groups: sham, model and EA. Cognitive impairment was induced by left middle cerebral artery occlusion in the model and EA groups. Rats in the EA group were treated with EA at Shenting (GV24) and Baihui (GV20) for 7 d. Neurological deficit was scored using the Longa scale, the learning and memory ability was detected using the Morris water maze (MWM) test, and the proteomic profiling in the hippocampus was analyzed using protein-labeling technology based on the isobaric tag for relative and absolute quantitation (iTRAQ). The Western blot (WB) analysis was used to detect the proteins and validate the results of iTRAQ. RESULTS: Compared with the model group, the neurological deficit score was significantly reduced, and the escape latency in the MWM test was significantly shortened, while the number of platform crossings increased in the EA group. A total of 2872 proteins were identified by iTRAQ. Differentially expressed proteins (DEPs) were identified between different groups: 92 proteins were upregulated and 103 were downregulated in the model group compared with the sham group, while 142 proteins were upregulated and 126 were downregulated in the EA group compared with the model group. Most of the DEPs were involved in oxidative phosphorylation, glycolipid metabolism and synaptic transmission. Furthermore, we also verified 4 DEPs using WB technology. Although the WB results were not exactly the same as the iTRAQ results, the expression trends of the DEPs were consistent. The upregulation of heat-shock protein ß1 (Hspb1) was the highest in the EA group compared to the model group. CONCLUSION: EA can effect proteomic changes in the hippocampus of rats with cognitive impairment. Hspb1 may be involved in the molecular mechanism by which acupuncture improves cognitive impairment.

Comprehensive transcriptomic profiling and mutational landscape of primary gastric linitis plastica.

BACKGROUND: Primary gastric linitis plastica (GLP) is a distinct phenotype of gastric cancer with poor survival. Comprehensive molecular profiles and putative therapeutic targets of GLP remain undetermined. METHODS: We subjected 10 tumor-normal tissue pairs to whole exome sequencing (WES) and whole transcriptome sequencing (WTS). 10 tumor samples were all GLP which involves 100% of the gastric wall macroscopically. TCGA data were compared to generate the top mutated genes and the overexpressed genes in GLP. RESULTS: Our results reveal that GLP has distinctive genomic and transcriptomic features, dysfunction in the Hippo pathway is likely to be a key step during GLP development. 6 genes were identified as significantly highly mutated genes in GLP, including AOX1, ANKRD36C, CPXM1, PTPN14, RPAP1, and DCDC1). MUC6, as a previously identified gastric cancer driver gene, has a high mutation rate (20%) in GLP. 20% of patients in our GLP cohort had CDH1 mutations, while none had RHOA mutations. GLP exhibits high immunodeficiency and low AMPK pathway activity. Our WTS results showed that 3 PI3K-AKT pathway-related genes (PIK3R2, AKT3, and IGF1) were significantly up-regulated in GLP. Two genes were identified using immunohistochemistry (IHC), IGF2BP3 and MUC16, which specifically expressed in diffuse-type-related gastric cancer cell lines, and its knockdown inhibits PI3K-AKT pathway activity. CONCLUSIONS: We provide the first integrative genomic and transcriptomic profiles of GLP, which may facilitate its diagnosis, prognosis, and treatment.

Proposal of an automated tumor-stromal ratio assessment algorithm and a nomogram for prognosis in early-stage invasive breast cancer.

BACKGROUND: The tumor-stromal ratio (TSR) has been verified to be a prognostic factor in many solid tumors. In most studies, it was manually assessed on routinely stained H&E slides. This study aimed to assess the TSR using image analysis algorithms developed by the Qupath software, and integrate the TSR into a nomogram for prediction of the survival in invasive breast cancer (BC) patients. METHODS: A modified TSR assessment algorithm based on the recognition of tumor and stroma tissues was developed using the Qupath software. The TSR of 234 invasive BC specimens in H&E-stained tissue microarrays (TMAs) were assessed with the algorithm and categorized as stroma-low or stroma-high. The consistency of TSR estimation between Qupath prediction and pathologist annotation was analyzed. Univariable and multivariable analyses were applied to select potential risk factors and a nomogram for predicting survival in invasive BC patients was constructed and validated. An extra TMA containing 110 specimens was obtained to validate the conclusion as an independent cohort. RESULTS: In the discovery cohort, stroma-low and stroma-high were identified in 43.6% and 56.4% cases, respectively. Good concordance was observed between the pathologist annotated and Qupath predicted TSR. The Kaplan-Meier curve showed that stroma-high patients were associated with worse 5-DFS compared to stroma-low patients (p = 0.007). Multivariable analysis identified age, T stage, N status, histological grade, ER status, HER-2 gene, and TSR as potential risk predictors, which were included in the nomogram. The nomogram was well calibrated and showed a favorable predictive value for the recurrence of BC. Kaplan-Meier curves showed that the nomogram had a better risk stratification capability than the TNM staging system. In the external validation of the nomogram, the results were further validated. CONCLUSIONS: Based on H&E-stained TMAs, this study successfully developed image analysis algorithms for TSR assessment and constructed a nomogram for predicting survival in invasive BC.

Effects of electroacupuncture on rats with cognitive impairment: An iTRAQ-based proteomics analysis / 中西医结合学报

OBJECTIVE@#The study explores the effects of electroacupuncture (EA) at the governing vessel (GV) on proteomic changes in the hippocampus of rats with cognitive impairment.@*METHODS@#Healthy male rats were randomly divided into 3 groups: sham, model and EA. Cognitive impairment was induced by left middle cerebral artery occlusion in the model and EA groups. Rats in the EA group were treated with EA at Shenting (GV24) and Baihui (GV20) for 7 d. Neurological deficit was scored using the Longa scale, the learning and memory ability was detected using the Morris water maze (MWM) test, and the proteomic profiling in the hippocampus was analyzed using protein-labeling technology based on the isobaric tag for relative and absolute quantitation (iTRAQ). The Western blot (WB) analysis was used to detect the proteins and validate the results of iTRAQ.@*RESULTS@#Compared with the model group, the neurological deficit score was significantly reduced, and the escape latency in the MWM test was significantly shortened, while the number of platform crossings increased in the EA group. A total of 2872 proteins were identified by iTRAQ. Differentially expressed proteins (DEPs) were identified between different groups: 92 proteins were upregulated and 103 were downregulated in the model group compared with the sham group, while 142 proteins were upregulated and 126 were downregulated in the EA group compared with the model group. Most of the DEPs were involved in oxidative phosphorylation, glycolipid metabolism and synaptic transmission. Furthermore, we also verified 4 DEPs using WB technology. Although the WB results were not exactly the same as the iTRAQ results, the expression trends of the DEPs were consistent. The upregulation of heat-shock protein β1 (Hspb1) was the highest in the EA group compared to the model group.@*CONCLUSION@#EA can effect proteomic changes in the hippocampus of rats with cognitive impairment. Hspb1 may be involved in the molecular mechanism by which acupuncture improves cognitive impairment.

Surface modification of ZnIn2S4 layers to realize energy-transfer-mediated photocatalysis.

Photocatalytic selective aerobic oxidation reactions are crucial in designing advanced organic intermediates, but suffer from low conversion efficiency. Hence, activating O2 to create suitable reactive oxygen species, such as singlet oxygen (1O2), can significantly increase the yield of desired products. Herein, using ZnIn2S4 nanosheets as a model system, we build a surface-modified theoretical structure, where a surface-covered non-conductive macromolecular chain, polyvinyl pyrrolidone (PVP), is bound to ZnIn2S4 and influences the O2 adsorption process. PVP on the surface significantly changes the electronic structure and suppresses electron conduction of ZnIn2S4 nanosheets. Therefore, abundantly photogenerated and long-lived species transfer their energy to physically absorbed O2 to efficiently generate 1O2, which can oxidize sulphides into their corresponding sulphoxides. For sulphoxidation of different sulphides, surface modification brings a 3-9-fold increase in conversion efficiency and high selectivities ≥98%. This study provides a feasible way of boosting 1O2-generation-related photocatalytic reactions.

Spatial Band Separation in a Surface Doped Heterolayered Structure for Realizing Efficient Singlet Oxygen Generation.

Singlet oxygen (1 O2 ) with electrical neutrality and long lifetime holds great promise in producing high-added-value chemicals via a selective oxidation reaction. However, photocatalytic 1 O2 generation via the charge-transfer mechanism still suffers from low efficiency due to the mismatched redox capacities and low concentration of photogenerated carriers in confined systems. Herein, by taking bismuth oxysilicate (Bi2 O2 SiO3 ) with alternating heterogeneous layered structure as a model, it is shown that iodine doping can facilitate the spatial redistributions of bands on alternated [Bi2 O2 ] and [SiO3 ] layers, which can promote the separation and transfer of photogenerated charge carriers. Meanwhile, the band positions of Bi2 O2 SiO3 are optimized to match the redox potential of 1 O2 generation. Benefiting from these features, iodine-doped Bi2 O2 SiO3 exhibits efficient 1 O2 generation with respect to its pristine counterpart, leading to promoted performance in the selective sulfide oxidation reaction. A new strategy is offered here for optimizing charge-transfer-mediated 1 O2 generation.

Anatomical Evidence for the Neural Connection from the Emotional Brain to Autonomic Innervation in the Anterior Chamber Structures of the Eye.

OBJECTIVE: Previous studies have shown that the autonomic nervous system (ANS), which can be affected by emotions, is important in the occurrence or progression of glaucoma. The autonomic innervation distributed in the anterior chamber (AC) structures might play an efferent role in the neural regulation of intraocular pressure (IOP). This study aimed to investigate the anatomic neural connection from the emotional brain to autonomic innervation in the AC. METHODS: A retrograde trans-multisynaptic pseudorabies virus encoded with an enhanced green fluorescent protein (PRV531) and non-trans-synaptic tracer FAST Dil were injected into the right eye of mice, respectively. Fluorescent localization in the emotional brain and preganglionic nuclei was studied. Five and a half days after PRV531 injection into the right AC, fluorescent signals were observed in several emotional brain regions, including the amygdala, agranular insular cortex, lateral septal nuclei, periaqueductal gray, and hypothalamus. Autonomic preganglionic nuclei, including Edinger-Westphal nucleus, superior salivatory nucleus, and intermediolateral nucleus, were labeled using PRV531. RESULTS: The sensory trigeminal nuclei were not labeled using PRV531. The fluorescence signals in the nuclei mentioned above showed bilateral distribution, primarily on the ipsilateral side. Seven days after injecting FAST Dil into the AC, we observed no FAST Dil-labeled neurons in the central nervous system. CONCLUSION: Our results indicate a neural connection from the emotional brain to autonomic innervation in the AC, which provides anatomical support for the emotional influence of IOP via the ANS.

Construction of a mouse model of Posner-Schlossman syndrome by anterior chamber infection with cytomegalovirus.

Accumulated clinical evidence has shown that Posner-Schlossman syndrome (PSS) is most likely the result of recurrent human cytomegalovirus (HCMV) infection in the anterior chamber (AC). Establishing an animal model is necessary to investigate the pathogenesis of PSS. In this study, we constructed a mouse model of (PSS) by injecting murine cytomegalovirus (MCMV) into the AC of BALB/c mice. Twenty-five BALB/c mice were divided into 5 groups. Smith strain MCMV expressing enhanced green fluorescent protein (EGFP) was passaged with mouse embryonic fibroblast (MEF). Right eyes in the 4 experiment groups received AC injection of 1 µL of virus solution with concentrations of 103,104,105,106 pfu/mL respectively, and the control group received only PBS. PSS-like signs (mutton-fat keratic precipitates (KP), pupil dilation, IOP elevation and corneal edema) were recorded 0-28 days post-injection (DPI). Sections of eyeballs from another 9 mice harvested on 0,10 and 28 DPI were examined to locate KP and the fluorescence signal of the virus. Reversible PSS-like signs except KP were observed in 20% and 60% mice of 104 and 105 groups while no PSS-like signs in the control and 103 group; 80% in the 106 group with partially unreversible signs till 28DPI. Much More fluorescent signals of virus in the iris and KP were found on 10DPI than 28 DPI, while no fluorescent signals and KP on 0DPI. The extent of PSS-like signs (pupil dilation, IOP elevation and corneal edema) was virus concentration-dependent (Spearman correlation coefficient, r = 0.830, = 0.475, = 0.662, p < 0.0001, <0.05, <0.001, respectively, n = 25). Success rate of PSS model (mice with PSS-like signs) was also virus concentration-dependent (Chi-square trend test, χ2 = 6.828, df = 1, p < 0.01, n = 25). Our results indicate that AC injection of 1 µL MEF passaged MCMV (Smith strain) of 104-106 pfu/mL in BALB/c mice can be used to construct a mouse model of PSS. MCMV can infect iris tissue and replicate in it and then establish latency. This might account for the recurrent and self-limited nature of PSS.