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Light-emitting transistors (LETs) uniquely combine the electroluminescent features of LEDs with the switching capabilities of field-effect transistors, offering promising applications in advanced display technology, lighting, electrically pumped lasers, and optical communication systems. This study reports on the fabrication and performance of perovskite light-emitting transistors (PeLETs) using solution-processed CsPbBr3 thin films, enhanced with phenethylammonium bromide (PEABr) and polyethylene oxide (PEO) to create a multi-dimensional mixed phase with a quantum well structure, characterized by a reduced presence of low-dimensional phases and an increased proportion of high-dimensional phases, thereby enhancing exciton recombination efficiency. The incorporation of high-mobility zinc tin oxide (ZTO) films as channel and electron transport layers is investigated. Direct contact between the perovskite and ZTO layers initially leads to an increased off-state current and degraded electrical characteristics of ZTO field-effect transistors (FETs). However, introducing polyvinylpyrrolidone (PVP) as a modification layer significantly improves these characteristics, resulting in a more uniform electric field distribution and consistent surface emission under coplanar electrodes. The optimized PeLET demonstrates mobility of 0.73 cm2 V−1 s−1 and an on–off ratio exceeding 105. High-purity green light emission at 514 nm with a narrow full-width at half-maximum (FWHM) of 19.97 nm is achieved, showcasing the potential of PeLETs in various optoelectronic applications. [ABSTRACT FROM AUTHOR]

The quality of perovskite films plays a fundamental role in determining the performance of perovskite solar cells (PSCs). It is widely recognized that achieving high crystalline quality and minimizing defect density in perovskite films are essential. In this study, the utilization of the multifunctional additive 5‐ammonium acid (5‐AVA) to improve the morphology of perovskite films is proposed. The ‐NH2 and ‐COOH groups in 5‐AVA enable effective coordination with Pb ions and organic ions in perovskite, resulting in the suppression of defect formation and the reduction of non‐radiative recombination losses. Furthermore, the addition of 5‐AVA facilitates a more favorable energy level alignment, thereby enhancing the transfer of carriers between the perovskite layer and transport layers. Consequently, this process contributes to the improvement of the open circuit voltage (VOC) in PSCs. Attributing to the addition of 5‐AVA, the optimized PSCs achieve significantly enhanced performance with a maximum photoelectric conversion efficiency (PCE) of 24.74% and excellent long‐term stability. This work presents a straightforward and effective approach to enhance the performance and long‐term stability of PSCs. [ABSTRACT FROM AUTHOR]

Background Cognitive decline is among the most common non-motor symptoms in Parkinson's disease (PD), while its physiological mechanisms remain poorly understood. Genetic factors constituted a fundamental determinant in the heterogeneity of cognitive decline among PD patients. However, the underlying genetic background was still less studied. Methods To explore the genetic determinants contributing to cognitive decline in PD, we performed genome-wide survival analysis using a Cox proportional hazards model in a longitudinal cohort of 450 Chinese patients with PD, and further explored the functional effect of the target variant. Additionally, we built a clinical-genetic model by incorporating clinical characteristics and polygenic risk score (PRS) to predict cognitive decline in PD. Results The cohort was followed up for an average of 5.25 (SE  = 2.46) years, with 95 incidents of cognitive impairment. We identified significant association between locus rs75819919 (DPP6) and accelerated cognitive decline (p  = 8.63E-09, beta = 1.74, SE  = 0.30). Dual-luciferase reporter assay suggested this locus might be involved in the regulation of DPP6 expression. Using data set from the UK Biobank, we identified rs75819919 was associated with cognitive performance in the general population. Incorporation of PRS increased the model's predictability, achieving an average AUC of 75.6% through fivefold cross-validation in 1 000 iterations. Conclusions These findings improve the current understanding of the genetic etiology of cognitive impairment in PD, and provide a novel target DPP6 to explore therapeutic options. Our results also demonstrate the potential to develop clinical-genetic model to identify patients susceptible to cognitive impairment and thus provide personalized clinical guidance. [ABSTRACT FROM AUTHOR]

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease. Abnormalities in the peripheral immune system in ALS have been paid attention; however, the results of changes in peripheral immune parameters were inconsistent. A total of 1109 ALS patients were enrolled in the study. All patients received clinical evaluation and peripheral immune parameters measurement. The outcomes were analyzed by correlation analysis, multiple linear regression and cox survival analysis. We found that ALS patients had significantly higher percentage of CD4+ T cells (39.3 vs. 37.1%, p < 0.001) and CD4+/CD8+ ratio (1.88 vs. 1.72, p = 0.011), significantly lower IgG (11.73 vs.12.82, p < 0.001) and IgA (2130.70 vs. 2284.8, p = 0.013) compared with the health controls. In the multivariate linear model, we found that each increase of 1.262, 0.278, and 4.44E-4 in ALSFRS-R scores were significantly associated with each increment of lymphocyte count, IgG, and IgA, respectively. However, each decrease of 0.341, 0.068, and 0.682 in ALSFRS-R score was associated with each increment in neutrophils, CD4+ T cells, and CD4+/CD8+ ratio, respectively. Cox survival regression analysis showed that the death risk of ALS patients was related to the levels of C3 (HR 0.592, 95% CI 0.361–0.973). We found that there were differences in peripheral immune parameters of ALS patients with the severity of the disease, especially neutrophil, lymphocyte, CD4+ T, and IgG; C3 is an independent predictor of survival in ALS patients. More studies are needed to elucidate the mechanisms associated with altered immune parameters in ALS. [ABSTRACT FROM AUTHOR]

Background Excessive daytime sleepiness (EDS) is one of the most frequent nonmotor symptoms in Parkinson's disease (PD); however, the pathogenesis of EDS is unclear, and there is a lack of information on plasma biomarkers for EDS in PD. We aimed to investigate the plasma biomarkers of EDS in a large PD cohort. Methods A total of 159 PD patients were included in the prospective cohort study and followed up annually for 3 years. Plasma biomarkers including glial fibrillary acidic protein, amyloid-beta, p-tau181, and neurofilament light chain (NfL), were measured using an ultrasensitive single-molecule array (Simoa) technology at each visit. EDS was evaluated using the Epworth Sleepiness Scale (ESS). Results The frequency of EDS in PD increased from 15.1% at baseline to 25.0% after 3 years. The mean ESS scores increased from 5.1 (standard deviation [ SD ]: 4.8) at baseline to 6.1 (SD : 5.5) at the third year of follow-up. At baseline, compared with patients with PD without EDS, those with EDS were more likely to be male, had poorer cognitive performance, and more severe motor and nonmotor symptoms. The adjusted generalized estimating equations models showed that higher plasma NfL levels (OR: 1.047 [1.002–1.094], p  = .042) were associated with EDS during follow-ups. The adjusted linear mixed-effects model showed that higher plasma NfL levels (β 0.097 [0.012–0.183], p  = .026) were associated with ESS scores during follow-ups. Conclusions Higher plasma NfL levels were associated with EDS in PD, indicating an association between neuro-axonal degeneration and EDS in PD. [ABSTRACT FROM AUTHOR]