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Summary: Grain size and weight determine rice yield. Although numerous genes and pathways involved in regulating grain size have been identified, our knowledge of post‐transcriptional control of grain size remains elusive. In this study, we characterize a rice mutant, decreased grain width and weight 1 (dgw1), which produces small grains. We show that DGW1 encodes a member of the heterogeneous nuclear ribonucleoprotein (hnRNP) family protein and preferentially expresses in developing panicles, positively regulating grain size by promoting cell expansion in spikelet hulls. Overexpression of DGW1 increases grain weight and grain numbers, leading to a significant rise in rice grain yield. We further demonstrate that DGW1 functions in grain size regulation by directly binding to the mRNA of Grain Width 6 (GW6), a critical grain size regulator in rice. Overexpression of GW6 restored the grain size phenotype of DGW1‐knockout plants. DGW1 interacts with two oligouridylate binding proteins (OsUBP1a and OsUBP1b), which also bind the GW6 mRNA. In addition, the second RRM domain of DGW1 is indispensable for its mediated protein‐RNA and protein–protein interactions. In summary, our findings identify a new regulatory module of DGW1‐GW6 that regulates rice grain size and weight, providing important insights into the function of hnRNP‐like proteins in the regulation of grain size. [ABSTRACT FROM AUTHOR]

With the prevalence of mental health problems among college students, perceptual recovery and the sensory dimensions of perception (PSD) have emerged as crucial environment-related factors for psychological well-being. However, there has been relatively limited research on how these factors directly and indirectly impact the restoration experience of college students in green spaces on campuses. Therefore, the aim of this study was to determine the influence of college students' intrinsic motivation on their psychological well-being when exposed to campus green spaces. Special attention was given to the role of solitude and perceptual recovery in this process. Research Methodology: Based on a literature review and field research, we classified campus green spaces into eight types based on perceptual dimensions. We collected 550 questionnaires on campus, and the data processing involved structural equation modeling (SEM) and mediation analysis. Findings: A positive correlation was found between perceived sensory dimensions and the recovery experience. College students' perceptual recovery and ability to be alone emerged as mediating variables in this process. In essence, this study sheds light on the mechanism through which intrinsic motivation impacts the mental health of college students when they engage with campus green spaces. [ABSTRACT FROM AUTHOR]

Background: Progressive spreading of α‐synuclein via gut‐brain axis has been hypothesized in the pathogenesis of Parkinson's disease (PD). However, the source of seeding‐capable α‐synuclein in the gastrointestinal tract (GIT) has not been fully investigated. Additionally, the mechanism by which the GIT microbiome contributes to PD pathogenesis remains to be characterized. Objectives: We aimed to investigate whether blood‐derived α‐synuclein might contribute to PD pathology via a gut‐driven pathway and involve GIT microbiota. Methods: The GIT expression of α‐synuclein and the transmission of extracellular vesicles (EVs) derived from erythrocytes/red blood cells (RBCs), with their cargo α‐synuclein, to the GIT were explored with various methods, including radioactive labeling of RBC‐EVs and direct analysis of the transfer of α‐synuclein protein. The potential role of microbiota on the EVs transmission was further investigated by administering butyrate, the short‐chain fatty acids produced by gut microbiota and studying mice with different α‐synuclein genotypes. Results: This study demonstrated that RBC‐EVs can effectively transport α‐synuclein to the GIT in a region‐dependent manner, along with variations closely associated with regional differences in the expression of gut‐vascular barrier markers. The investigation further revealed that the infiltration of α‐synuclein into the GIT was influenced significantly by butyrate and α‐synuclein genotypes, which may also affect the GIT microbiome directly. Conclusion: By demonstrating the transportation of α‐synuclein through RBC‐EVs to the GIT, and its potential association with gut‐vascular barrier markers and gut microbiome, this work highlights a potential mechanism by which RBC α‐synuclein may impact PD initiation and/or progression. © 2023 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society. [ABSTRACT FROM AUTHOR]

SUMMARY: Brassinosteroids (BRs) are a class of steroid phytohormones that control various aspects of plant growth and development. Several transcriptional factors (TFs) have been suggested to play roles in BR signaling. However, their possible relationship remains largely unknown. Here, we identified a rice mutant dwarf and low‐tillering 2 (dlt2) with altered plant architecture, increased grain width, and reduced BR sensitivity. DLT2 encodes a GIBBERELLIN INSENSITIVE (GAI)‐REPRESSOR OF GAI (RGA)‐SCARECROW (GRAS) TF that is mainly localized in the nucleus and has weak transcriptional activity. Our further genetic and biochemical analyses indicate that DLT2 interacts with two BR‐signaling‐related TFs, DLT and BRASSINAZOLE‐RESISTANT 1, and probably modulates their transcriptional activity. These findings imply that DLT2 is implicated in a potentially transcriptional complex that mediates BR signaling and rice development and suggests that DLT2 could be a potential target for improving rice architecture and grain morphology. This work also sheds light on the role of rice GRAS members in regulating numerous developmental processes. [ABSTRACT FROM AUTHOR]

We study the effect of imperfect channel estimation (ICE) on the error probability performance of M-level quadrature amplitude modulation (M-QAM) with maximal-ratio combining and equal-gain combining diversity formats in Nakagami fading channels. We provide a novel formulation of the biterror rate (BER) of M-QAM with ICE in terms of the signal constellation-dependent effective signal-to-noise ratios (SNRs) or amplitudes, which allows us to derive the general, accurate, and easy-to-evaluate BER formulas for square and rectangular diversity M-QAM with channel estimation errors. Our result shows that the performance loss caused by ICE may be manifested by the signal decision space distortion and a scaling of the effective SNR. Using our analytical result, we evaluate the performance of M-QAM with pilot-symbol assisted modulation and present some insightful findings. Index Terms--Error rate analysis, imperfect channel estimation (ICE), Nakagami fading channels, pilot symbol assisted modulation (PSAM), quadrature amplitude modulation (QAM).

Maximum-likelihood (ML) method for estimating the parameters of composite gamma-lognormal fading channels is proposed. Newton-Raphson and expectation-maximization (EM) algorithms are developed to compute the ML estimates of the mean and variance of shadowing component and the Nakagami-m parameter of the fading component.

Abstract Background Many studies have shown that mitochondrial dysfunction, complex I inhibition in particular, is involved in the pathogenesis of Parkinson's disease (PD). Rotenone, a specific inhibitor of mitochondrial complex I, has been shown to produce neurodegeneration in rats as well as in many cellular models that closely resemble PD. However, the mechanisms through which complex I dysfunction might produce neurotoxicity are as yet unknown. A comprehensive analysis of the mitochondrial protein expression profile affected by rotenone can provide important insight into the role of mitochondrial dysfunction in PD. Results Here, we present our findings using a recently developed proteomic technology called SILAC (stable isotope labeling by amino acids in cell culture) combined with polyacrylamide gel electrophoresis and liquid chromatography-tandem mass spectrometry to compare the mitochondrial protein profiles of MES cells (a dopaminergic cell line) exposed to rotenone versus control. We identified 1722 proteins, 950 of which are already designated as mitochondrial proteins based on database search. Among these 950 mitochondrial proteins, 110 displayed significant changes in relative abundance after rotenone treatment. Five of these selected proteins were further validated for their cellular location and/or treatment effect of rotenone. Among them, two were confirmed by confocal microscopy for mitochondrial localization and three were confirmed by Western blotting (WB) for their regulation by rotenone. Conclusion Our findings represent the first report of these mitochondrial proteins affected by rotenone; further characterization of these proteins may shed more light on PD pathogenesis.

Abstract Background The pathogenesis of idiopathic Parkinson's disease (PD) remains elusive, although evidence has suggested that neuroinflammation characterized by activation of resident microglia in the brain may contribute significantly to neurodegeneration in PD. It has been demonstrated that aggregated α-synuclein potently activates microglia and causes neurotoxicity. However, the mechanisms by which aggregated α-synuclein activates microglia are not understood fully. Methods We investigated the role of prostaglandin E2 receptor subtype 2 (EP2) in α-synuclein aggregation-induced microglial activation using ex vivo, in vivo and in vitro experimental systems. Results Results demonstrated that ablation of EP2(EP2-/-) significantly enhanced microglia-mediated ex vivo clearance of α-synuclein aggregates (from mesocortex of Lewy body disease patients) while significantly attenuating neurotoxicity and extent of α-synuclein aggregation in mice treated with a parkinsonian toxicant 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. Furthermore, we report that reduced neurotoxicity by EP2-/- microglia could be attributed to suppressed translocation of a critical cytoplasmic subunit (p47-phox) of NADPH oxidase (PHOX) to the membranous compartment after exposure to aggregated α-synuclein. Conclusion Thus, it appears that microglial EP2 plays a critical role in α-synuclein-mediated neurotoxicity.