Organic Photocathode Supported by Copper Nanosheets Array for Overall Water Splitting.

The Z-scheme overall solar water splitting is a mimic of natural photosynthesis to convert solar energy into chemical energy. Since the energy levels of most organic semiconductors match well with the hydrogen evolution potential, they have great application prospects as photocathodes in Z-scheme photoelectrochemical systems. However, due to the weak light absorption and difficult carrier separation, the photocurrent density and onset potential of organic photocathodes are still low. To solve these problems, we introduced a copper nanosheets array (Cu NSA) framework under organic layers to increase the surface reaction sites, improve the light absorption and enhance the distribution range of built-in electric field simultaneously. As a result, the photocurrent density and onset potential of poly(3-hexylthiophene) : [6,6]-phenyl-C61 -butyric acid (P3HT : PCBM) photocathode were enhanced significantly. The onset potential increased by 50 mV to 0.65 V vs. RHE, and the photocurrent density reached -1 mA cm-2 at 0 V vs. RHE, which was 18 times that of the sample without Cu NSA. The optimized photocathode was connected with titanium dioxide nanorods array photoanode in a tandem manner to realize the spontaneous overall water splitting. Without bias and co-catalyst, the photocurrent density was maintained at 110 µA cm-2 and the solar-to-fuel conversion efficiency was 0.14 % in neutral solution. These results provide a feasible method for optimizing the performance of organic photocathodes.

Deletion of Dcf1 Reduces Amyloid-ß Aggregation and Mitigates Memory Deficits.

BACKGROUND: Alzheimer's disease (AD) is a progressive neurodegenerative disease. One of the pathologies of AD is the accumulation of amyloid-ß (Aß) to form senile plaques, leading to a decline in cognitive ability and a lack of learning and memory. However, the cause leading to Aß aggregation is not well understood. Dendritic cell factor 1 (Dcf1) shows a high expression in the entorhinal cortex neurons and neurofibrillary tangles in AD patients. OBJECTIVE: Our goal is to investigate the effect of Dcf1 on Aß aggregation and memory deficits in AD development. METHODS: The mouse and Drosophila AD model were used to test the expression and aggregation of Aß, senile plaque formation, and pathological changes in cognitive behavior during dcf1 knockout and expression. We finally explored possible drug target effects through intracerebroventricular delivery of Dcf1 antibodies. RESULTS: Deletion of Dcf1 resulted in decreased Aß42 level and deposition, and rescued AMPA Receptor (GluA2) levels in the hippocampus of APP-PS1-AD mice. In Aß42 AD Drosophila, the expression of Dcf1 in Aß42 AD flies aggravated the formation and accumulation of senile plaques, significantly reduced its climbing ability and learning-memory. Data analysis from all 20 donors with and without AD patients aged between 80 and 90 indicated a high-level expression of Dcf1 in the temporal neocortex. Dcf1 contributed to Aß aggregation by UV spectroscopy assay. Intracerebroventricular delivery of Dcf1 antibodies in the hippocampus reduced the area of senile plaques and reversed learning and memory deficits in APP-PS1-AD mice. CONCLUSION: Dcf1 causes Aß-plaque accumulation, inhibiting dcf1 expression could potentially offer therapeutic avenues.

Dcf1 deletion presents alterations in gut microbiota of mice similar to Parkinson's disease.

The gut-brain communication is increasingly being recognized as a profound effector on Parkinson's disease (PD). Gut microbiota changes have become the focus of attention. However, the mechanism leading to changes in the gut microbiota is not clear. In the present study, we found that knockout of Dcf1 (Dcf1-/-) caused changes in the gut microbiota in mice. Results indicated that the increased Proteobacteria (phylum-level) and decreased Prevotellaceae (family-level) in the microbiota composition of Dcf1-/- (KO) mice, which is consistent with the situation of PD patients. On species-level, Prevotellaceae_UCG-001 and Helicobacter_ganmani were significantly different between KO and WT mice, suggesting glycolipid metabolism disorders and inflammatory lesions in KO mice. In the behavior of Y-maze and Open field test, KO mice showed typical PD symptoms such as memory deficits, slowness of movement and anxiety. Further Nissl staining of brain tissue sections confirmed that the deletion of Dcf1 caused damage to amygdala neurons. These results provide a new mechanism for understanding gut microbiota changes, and provide a new basis for PD treatment from a new perspective of Gut-brain axis.

Proteomics and molecular network analyses reveal that the interaction between the TAT-DCF1 peptide and TAF6 induces an antitumor effect in glioma cells.

Glioblastoma is the most lethal brain cancer in adults. Despite advances in surgical techniques, radiotherapy, and chemotherapy, their therapeutic effect is far from significant, since the detailed underlying pathological mechanism of this cancer is unclear. The establishment of molecular interaction networks has laid the foundation for the exploration of these mechanisms with a view to improving therapy for glioblastoma. In the present study, to further explore the cellular role of DCF1 (dendritic cell-derived factor 1), the proteins bound to TAT-DCF1 (transactivator of transcription-dendritic cell-derived factor 1) were identified, and biosystem analysis was employed. Functional enrichment analyses indicate that TAT-DCF1 induced important biological changes in U251 cells. Furthermore, the established molecular interaction networks indicated that TAT-DCF1 directly interacted with TAF6 in glioma cells and with UBC in HEK293T (human embryonic kidney 293T) cells. In addition, further biological experiments demonstrate that TAT-DCF1 induced the activation of the RPS27A/TOP2A/HMGB2/BCL-2 signaling pathway via interaction with TAF6 in U251 cells. Taken together, these findings suggest that the TAT-DCF1 peptide possesses great potential for the development of glioblastoma therapy through the interaction with TAF6-related pathways and provides further theoretic evidence for the mechanisms underlying the antitumor effects of TAT-DCF1.

Progress in Target Drug Molecules for Alzheimer's Disease.

Alzheimer's disease (AD) is a chronic neurodegenerative disease that 4 widespread in the elderly. The etiology of AD is complicated, and its pathogenesis is still unclear. Although there are many researches on anti-AD drugs, they are limited to reverse relief symptoms and cannot treat diseases. Therefore, the development of high-efficiency anti-AD drugs with no side effects has become an urgent need. Based on the published literature, this paper summarizes the main targets of AD and their drugs, and focuses on the research and development progress of these drugs in recent years.

Dcf1 Affects Memory and Anxiety by Regulating NMDA and AMPA Receptors.

The hippocampus is critical for memory and emotion and both N-methyl-D-aspartate (NMDA) and α-amino-3-hydroxy-5-methyl- 4-isoxazolepropionic acid (AMPA) receptors are known to contribute for those processes. However, the underlying molecular mechanisms remain poorly understood. We have previously found that mice undergo memory decline upon dcf1 deletion through ES gene knockout. In the present study, a nervous system-specific dcf1 knockout (NKO) mouse was constructed, which was found to present severely damaged neuronal morphology. The damaged neurons caused structural abnormalities in dendritic spines and decreased synaptic density. Decreases in hippocampal NMDA and AMPA receptors of NKO mice lead to abnormal long term potentiation (LTP) at DG, with significantly decreased performance in the water maze, elevated- plus maze, open field and light and dark test. Investigation into the underlying molecular mechanisms revealed that dendritic cell factor 1 (Dcf1) contributes for memory and emotion by regulating NMDA and AMPA receptors. Our results broaden the understanding of synaptic plasticity's role in cognitive function, thereby expanding its known list of functions.

ATP11B deficiency leads to impairment of hippocampal synaptic plasticity.

Synaptic plasticity is known to regulate and support signal transduction between neurons, while synaptic dysfunction contributes to multiple neurological and other brain disorders; however, the specific mechanism underlying this process remains unclear. In the present study, abnormal neural and dendritic morphology was observed in the hippocampus following knockout of Atp11b both in vitro and in vivo. Moreover, ATP11B modified synaptic ultrastructure and promoted spine remodeling via the asymmetrical distribution of phosphatidylserine and enhancement of glutamate release, glutamate receptor expression, and intracellular Ca2+ concentration. Furthermore, experimental results also indicate that ATP11B regulated synaptic plasticity in hippocampal neurons through the MAPK14 signaling pathway. In conclusion, our data shed light on the possible mechanisms underlying the regulation of synaptic plasticity and lay the foundation for the exploration of proteins involved in signal transduction during this process.

Dendritic cell factor 1 inhibits proliferation and migration and induces apoptosis of neuroblastoma cells by inhibiting the ERK signaling pathway.

Neuroblastoma (NB) is the most common extracranial solid tumor that affects mainly children and has extremely high mortality and recurrence rates. A previous study revealed that dendritic cell factor 1 (DCF1), also called transmembrane protein 59, could activate apoptosis in glioma cells. In the present study, we applied immunofluorescence, western blot analysis, flow cytometry and cell tumorigenicity to investigate the DCF1 mechanisms involved in NB apoptosis. DCF1 was overexpressed in Neuro-2a and SK-N-SH cells through instantaneous transfection. The data revealed that overexpression of DCF1 could inhibit cell proliferation, migration, invasion and promote cell apoptosis in vitro, and suppress NB growth in vivo. The ERK1/2 signaling pathway, which promotes cell survival, was the target of DCF1 in neuroblastoma cells. All the results indicated that DCF1 could be a potential therapeutic target for the understanding and treatment of NB.

Serum Protein-Based Profiles as Novel Biomarkers for the Diagnosis of Alzheimer's Disease.

As a multi-stage disorder, Alzheimer's disease (AD) is quickly becoming one of the most prevalent neurodegenerative diseases worldwide. Thus, a non-invasive, serum-based diagnostic platform is eagerly awaited. The goal of this study was to identify a serum-based biomarker panel using a predictive protein-based algorithm that is able to confidently distinguish AD patients from control subjects. One hundred and fifty-six patients with AD and the same number of gender- and age-matched control participants with standardized clinical assessments and neuroimaging measures were evaluated. Serum proteins of interest were quantified using a magnetic bead-based immunofluorescent assay, and a total of 33 analytes were examined. All of the subjects were then randomized into a training set containing 70% of the total samples and a validation set containing 30%, with each containing an equal number of AD and normal samples. Logistic regression and random forest analyses were then applied to develop a desirable algorithm for AD detection. The random forest method was found to generate a more robust predictive model than the logistic regression analysis. Furthermore, an eight-protein-based algorithm was found to be the most robust with a sensitivity of 97.7%, specificity of 88.6%, and AUC of 99%. Our study developed a novel eight-protein biomarker panel that can be used to distinguish AD and control multi-source candidates regardless of age. It is hoped that these results provide further insight into the applicability of serum-based screening methods and contribute to the development of lower-cost, less invasive methods for diagnosing AD and monitoring progression.

DCF1 subcellular localization and its function in mitochondria.

Dendritic cell factor 1 (DCF1) is a transmembrane protein that plays important roles in regulating neural stem cell differentiation and dendritic spine formation. Apart from its cytoplasmic functions, DCF1 plays a role in autophagy during the regulation of amyloid precursor proteins. However, the subcellular localization of DCF1 remains unknown. Therefore, in this study, DCF1 tagged with green fluorescent protein was transiently expression in HelaS3 and HEK293T cells. The results showed that DCF1 was widely expressed in different organelles, including the mitochondria, Golgi apparatus, endoplasmic reticulum, endosomes and lysosomes. An iodixanol step gradient further confirmed that DCF1 is localized to the mitochondria, endosomes, lysosomes, endoplasmic reticulum, and proteasome. Finally, functional analysis of the mitochondria revealed that DCF1 affected the expression and localization of MGST1. This study presents a comprehensive evaluation of the subcellular localization of DCF1, which provides important information on complex functions mediated by DCF1.

[Response of yield, quality and nitrogen use efficiency to nitrogen fertilizer from mechanical transplanting super japonica rice].

Five super japonica rice cultivars were grown by mechanical transplanting in field and seven N treatments with total N application rate of 0, 150, 187.5, 225, 262.5, 300 and 337.5 kg x hm(-2) respectively were adopted to study the effects of N rate on rice yield, quality and N use efficiency. The differences between N requirement for obtaining the highest yield and for achieving the best economic benefit were compared. With the increase of N fertilizer rate, the yields of five super japonica rice cultivars increased firstly and then descended, achieving the highest yield at the N level of 300 kg x hm(-2) ranging from 10.33-10.60 kg x hm(-2). Yield increase mainly attributed to the large number of spikelet, for the total spikelet number of each rice cultivar reached the maximum value at the 300 kg x hm(-2) N level. With the increase of N application, the rates of brown rice, milled rice, head milled rice and the protein content of the five super japonica rice cultivars were all increased, and the rates of brown rice, milled rice, head milled rice and the protein con- tent were higher at 337.5 kg x hm(-2) N level than at 0 kg x hm(-2) N level by 3.3%-4.2%, 2.9%-6.0%, 4.4%-33.7% and 23.8%-44.3%, respectively. While the amylose content, gel consistency and taste value of the five rice cultivars were all decreased, and the amylose content, gel consistency and taste value were lower at 337.5 kg x hm(-2) N level than at 0 kg x hm(-2) N level by 12.4%-38.9%, 10.3%-28.5% and 20.3%-29.7%, respectively. The chalkiness increased firstly and then decreased while the change of chalky rate varied with the cultivars. With the increase of N application, the N use efficiency, agronomic N use efficiency and physiological N use efficiency decreased while the N uptake of grain increased significantly. If the cost of N fertilizer was taken into account, the N fertilizer amount to obtain the optimal economic benefits would be 275.68 kg x hm(-2) with the corresponding yield of 9.97 t x hm(-2). Therefore, in the existing super rice production, classified management of N fertilizer would be required to meet differentiated demands of high yield, good quality, high efficiency, low N fertilizer input and so on.