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Luminescent solar concentrators are translucent photovoltaic modules potentially used for building window. To store the energy generated by them, a separate energy storage module and voltage regulator module are required, but it is clear that this pairing is unwieldy for application. To address this problem, we propose a “face-to-face” tandem integration of luminescent solar concentrators and electrochromic supercapacitors. In this case, the separated energy storage module and voltage regulator module are not required, since the electric energy produced by concentrators under sunlight can be directly stored by the supercapacitors with matched voltage window. The charged energy storage module can be used to supply low-power devices. Moreover, electrochromic supercapacitors exhibit adjustable average visible transmission under different energy storage state, making the integrated device interesting for self-powered electrochromic smart windows or display devices. As an example, a self-powered information instruction display is prepared, and text messages could be clearly and rapidly displayed in a controllable manner. The integrated device capable of photovoltaic conversion, energy storage, and electrochromism is a promising alternative for smart windows. Traditional luminescent solar concentrators generally require separated energy storage modules limiting applications in smart windows. Here, authors propose an integration between luminescent solar concentrators and electrochromic supercapacitors capable of photovoltaic conversion, energy storage, and electrochromism.

Cellular senescence is a major biological process related to aging. Neuronal cell senescence contributes to the pathogenesis of many aging-related neurodegenerative diseases including Alzheimer’s disease (AD). In this study, we showed that amyloid-β42 oligomers (Aβ), one of the core pathological players of AD, significantly up-regulated the expression of senescence markers, p21, plasminogen activator inhibitor-1 (PAI-1), and SA-β-gal (senescence-associated β-galactosidase) in multiple human neuronal cells, including SK-N-SH cells, SH-SY5Y cells, and neural stem cell (NSC)-derived neuronal cells. Moreover, it was consistently observed among the cells that Aβ promoted senescence-associated DNA damage as the levels of 8-OHdG staining, histone variant γH2AX phosphorylation, and genomic DNA lesion increased. Mechanism study revealed that the exposure of Aβ markedly suppressed the expression of sirtuin-1 (SIRT1), a critical regulator of aging, and the exogenous expression of SIRT1 alleviated Aβ-induced cell senescence phenotypes. To our surprise, a widely used cardiovascular drug aspirin considerably rescued Aβ-induced cellular senescence at least partially through its regulation of SIRT1. In conclusion, our findings clearly demonstrate that exposure of Aβ alone is sufficient to accelerate the senescence of human neuronal cells through the down-regulation of SIRT1.

Aiming at the problem that power load data are stochastic and that it is difficult to obtain accurate forecasting results by a single algorithm, in this paper, a combined forecasting method for short-term power load was proposed based on the Complete Ensemble Empirical Mode Decomposition with Adaptive Noise (CEEMDAN)-sample entropy (SE), the BP neural network (BPNN), and the Transformer model. Firstly, the power load data were decomposed into several power load subsequences with obvious complexity differences by using the CEEMDAN-SE. Then, BPNN and Transformer model were used to forecast the subsequences with low complexity and the subsequences with high complexity, respectively. Finally, the forecasting results of each subsequence were superimposed to obtain the final forecasting result. The simulation was taken from our proposed model and six forecasting models by using the load dataset from a certain area of Spain. The results showed that the MAPE of our proposed CEEMDAN-SE-BPNN-Transformer model was 1.1317%, while the RMSE was 304.40, which was better than the selected six forecasting models.

The apolipoprotein E4 ( APOE4 ) genotype is one of the strongest genetic risk factors for Alzheimer’s disease (AD), and is generally believed to cause widespread pathological alterations in various types of brain cells. Here, we developed a novel engineering method of creating the chimeric human cerebral organoids (chCOs) to assess the differential roles of APOE4 in neurons and astrocytes. First, the astrogenic factors NFIB and SOX9 were introduced into induced pluripotent stem cells (iPSCs) to accelerate the induction of astrocytes. Then the above induced iPSCs were mixed and cocultured with noninfected iPSCs under the standard culturing condition of cerebral organoids. As anticipated, the functional astrocytes were detected as early as 45 days, and it helped more neurons matured in chCOs in comparation of the control human cerebral organoids (hCOs). More interestingly, this method enabled us to generate chCOs containing neurons and astrocytes with different genotypes, namely APOE3 or APOE4 . Then, it was found in chCOs that astrocytic APOE4 already significantly promoted lipid droplet formation and cholesterol accumulation in neurons while both astrocytic and neuronal APOE4 contributed to the maximum effect. Most notably, we observed that the co-occurrence of astrocytic and neuronal APOE4 were required to elevate neuronal phosphorylated tau levels in chCOs while Aβ levels were increased in chCOs with neuronal APOE4 . Altogether, our results not only revealed the essence of both neuronal and astrocytic APOE4 for tau pathology, but also suggested chCOs as a valuable pathological model for AD research and drug discovery.

The characteristics of the dual-core photonic crystal fiber (PCF) sensor are studied using the finite element method (FEM), and the structure is improved according to the numerical simulation results. The results show that whether or not the four large air holes far away from the geometry center of the PCF are filled with analyte has no influence on the wavelength sensitivity of the sensor which means those holes can be replaced by small air holes. The wavelength sensitivity can be tuned by adjusting the sizes of the other large air holes which are as for liquid holes. The dynamic detection range of the refractive index (RI) is from 1.33 to 1.51. In particular, high linearity is obtained in the range of 1.44 to 1.51. The sensitivity is as high as 6021 nm/RIU when the liquid holes are the smallest. When liquid holes are tangential with the envelope of first layer air holes, the wavelength sensitivity is 4028 nm/RIU, and the coefficient of determination (R2) is 0.99822 when the RI of the analyte varies from 1.44 to 1.51 which shows that high sensitivity and good linearity are both obtained.

Accumulating evidence has shown that some hallucinogens, such as LSD, have fast and persistent effects on anxiety and depression. According to a proposed mechanism, LSD activates the TrkB and HTR2A signaling pathways, which enhance the density of neuronal dendritic spines and synaptic function, and thus promote brain function. Moreover, TrkB signaling is also known to be crucial for neural stem cell (NSC)-mediated neuroregeneration to repair dysfunctional neurons. However, the impact of LSD on neural stem cells remains to be elucidated. In this study, we observed that LSD and BDNF activated the TrkB pathway in human NSCs similarly to neurons. However, unlike BDNF, LSD did not promote NSC proliferation. These results suggest that LSD may activate an alternative mechanism to counteract the effects of BDNF-TrkB signaling on NSCs. Our findings shed light on the previously unrecognized cell type-specificity of LSD. This could be crucial for deepening our understanding of the mechanisms underlying the effects of LSD.

As a lifelong source of neurons, neural stem cells (NSCs) serve multiple crucial functions in the brain. The senescence of NSCs may be associated with the onset and progression of Alzheimer’s disease (AD). Our study reveals a noteworthy finding, indicating that the AD-associated pathogenic protein amyloid-β (Aβ) substantially enhances senescence-related characteristics of human NSCs. These characteristics encompass the enhanced expression of p16 and p21, the upregulation of genes associated with the senescence-associated secretory phenotype (SASP), increased SA-β-gal activity, and the activation of the DNA damage response. Further studies revealed that Aβ treatment significantly downregulates the SIRT1 protein which plays a crucial role in regulating the aging process and decreases downstream PGC-1α and FOXO3. Subsequently, we found that SIRT1 overexpression significantly alleviates a range of Aβ-induced senescent markers in human NSCs. Taken together, our results uncover that Aβ accelerates cellular senescence in human NSCs, making SIRT1 a highly promising therapeutic target for senescent NSCs which may contribute to age-related neurodegenerative diseases, including AD.

Neuroinflammation induced by overactivated glia cells is believed to be a major hallmark of Alzheimer's disease (AD) and a hopeful target against AD. A rhamnoside PL201 was previously reported to promote neurogenesis and ameliorate AD, and in this study, we revealed that PL201 also significantly reduced accumulation of the activated microglia and proinflammatory cytokines in APP/PS1 mice. , PL201 consistently suppressed the microglia induction of proinflammatory cytokines after stimulation with lipopolysaccharides and Aβ42. Further mechanistic studies demonstrated that PL201 considerably enhanced the expression level and the nuclear translocation of Nrf2, a key regulator of neuroinflammation. Moreover, PL201 effectively stimulated Nrf2 signaling cascade, including upregulation of HO-1 and downregulation of NF-κB pathway. Thus, our findings indicated the anti-neuroinflammatory effect by PL201 and suggested that PL201 or the like, with multiple functions such as neurogenesis, mitochondria maintenance, and anti-neuroinflammation, could be a promising candidate in AD treatment.

Summary Aberrant neural progenitor cell (NPC) proliferation and self-renewal have been linked to age-related neurodegeneration and neurodegenerative disorders including Alzheimer's disease (AD). Rhizoma Acori tatarinowii is a traditional Chinese herbal medicine against cognitive decline. In this study, we found that the extract of Rhizoma Acori tatarinowii (AT) and its active constituents, asarones, promote NPC proliferation. Oral administration of AT enhanced NPC proliferation and neurogenesis in the hippocampi of adult and aged mice as well as that of transgenic AD model mice. AT and its fractions also enhanced the proliferation of NPCs cultured in vitro. Further analysis identified [alpha]-asarone and [beta]-asarone as the two active constituents of AT in promoting neurogenesis. Our mechanistic study revealed that AT and asarones activated extracellular signal-regulated kinase (ERK) but not Akt, two critical kinase cascades for neurogenesis. Consistently, the inhibition of ERK activities effectively blocked the enhancement of NPC proliferation by AT or asarones. Our findings suggest that AT and asarones, which can be orally administrated, could serve as preventive and regenerative therapeutic agents to promote neurogenesis against age-related neurodegeneration and neurodegenerative disorders.

Alzheimer's disease (AD) is a multi-factorial neurodegenerative disorder with abnormal accumulation of amyloid-β (Aβ) plaques, neuroinflammation and impaired neurogenesis. Mounting evidences suggest that single-target drugs have limited effects on clinical treatment and alternative or multiple targets are required. In recent decades, natural compounds and their derivatives have gained increasing attention in AD drug discovery due to their inherently enormous chemical and structural diversity. In this study, we demonstrated that naringin dihydrochalcone (NDC), a widely used dietary sweetener with strong antioxidant activity, improved the cognitive function of transgenic AD mice. Pathologically, NDC attenuated Aβ deposition in AD mouse brain. Furthermore, NDC reduced periplaque activated microglia and astrocytes, indicating the inhibition of neuroinflammation. It also enhanced neurogenesis as investigated by BrdU/NeuN double labeling. Additionally, the inhibition of Aβ level and neuroinflammation by NDC treatment was also observed in an AD cell model or a microglia cell line. Taken together, our study indicated that NDC might be a potential therapeutic agent for the treatment of AD against multiple targets that include Aβ pathology, neuroinflammation and neurogenesis.