A transformer-based approach for early prediction of soybean yield using time-series images

Crop yield prediction which provides critical information for management decision-making is of significant importance in precision agriculture. Traditional manual inspection and calculation are often laborious and time-consuming. For yield prediction using high-resolution images, existing methods, e.g., convolutional neural network, are challenging to model long range multi-level dependencies across image regions. This paper proposes a transformer-based approach for yield prediction using early-stage images and seed information. First, each original image is segmented into plant and soil categories. Two vision transformer (ViT) modules are designed to extract features from each category. Then a transformer module is established to deal with the time-series features. Finally, the image features and seed features are combined to estimate the yield. A case study has been conducted using a dataset that was collected during the 2020 soybean-growing seasons in Canadian fields. Compared with other baseline models, the proposed method can reduce the prediction error by more than 40%. The impact of seed information on predictions is studied both between models and within a single model. The results show that the influence of seed information varies among different plots but it is particularly important for the prediction of low yields

Persistence and selection of an expanded B-cell clone in the setting of rituximab therapy for Sjögren's syndrome

Introduction: Subjects with primary Sjögren's syndrome (SjS) have an increased risk of developing B-cell lymphoma and may harbor monoclonal B-cell expansions in the peripheral blood. Expanded B-cell clones could be pathogenic, and their persistence could exacerbate disease or predispose toward the development of lymphoma. Therapy with anti-CD20 (rituximab) has the potential to eliminate expanded B-cell clones and thereby potentially ameliorate disease. This study was undertaken to identify and track expanded B-cell clones in the blood of subjects with primary SjS who were treated with rituximab.Methods: To determine whether circulating B-cell clones in subjects with primary SjS emerge or remain after B cell-depleting therapy with rituximab, we studied the antibody heavy-chain repertoire. We performed single-memory B-cell and plasmablast sorting and antibody heavy-chain sequencing in six rituximab-treated SjS subjects over the course of a 1-year follow-up period.Results: Expanded B-cell clones were identified in four out of the six rituximab-treated SjS subjects, based upon the independent amplification of sequences with identical or highly similar VH, DH, and JH gene segments. We identified one SjS subject with a large expanded B-cell clone that was present prior to therapy and persisted after therapy. Somatic mutations in the clone were numerous but did not increase in frequency over the course of the 1-year follow-up, suggesting that the clone had been present for a long period of time. Intriguingly, a majority of the somatic mutations in the clone were silent, suggesting that the clone was under chronic negative selection.Conclusions: For some subjects with primary SjS, these data show that (a) expanded B-cell clones are readily identified in the peripheral blood, (b) some clones are not eliminated by rituximab, and (c) persistent clones may be under chronic negative selection or may not be antigen-driven. The analysis of sequence variation among members of an expanded clone may provide a novel means of measuring the chronicity and selection of expanded B-cell populations in humans. © 2014 Hershberg et al.; licensee BioMed Central Ltd

Concave reagents: Part 40 - The copper(II) complex of a concave reagent as a selective catalyst for ester methanolysis

We have shown that the Cu-II complexes of the concave ligand 1 and its model compound 2 are efficient catalysts of ester methanolysis under conditions close to neutrality. Turnover catalysis without product inhibition was demonstrated by the clean first-order release of a greater than stoichiometric amount of product. Compared with background methanolysis, the metal catalysts give greater rate accelerations for methyl acetate methanolysis than for the p-nitrophenyl acetate methanolysis

Early stimulation and late inhibition of peroxisome proliferator-activated receptor gamma (PPARgamma) gene expression by transforming growth factor beta in human aortic smooth muscle cells: role of early growth-response factor-1 (Egr-1), activator protein 1 (AP1) and Smads

Transforming growth factor beta (TGF beta) and peroxisome proliferator-activated receptor gamma (PPAR gamma) play major roles in the development of vascular diseases. It has been documented that PPAR gamma activation inhibits the TGF beta signal pathway in vascular smooth muscle cells (VSMC). Here we examined whether TGF beta can regulate PPAR gamma expression. Northern blot analyses revealed that both TGF beta 1 and 2 exert a biphasic effect (early stimulation and late repression) on PPAR gamma gene expression in VSMC. TGF beta rapidly and transiently induced early growth-response factor-1 (Egr-1) expression through the mitogen-activated protein kinase/extracellular signal-regulated kinase kinase 1 (MEK1)/ERK-mediated pathway. Inhibition of MEK1/ERK by PD98059 not only abrogated the induction of Egr-1 but also abolished the rapid and transient induction of PPAR gamma by TGF beta. Furthermore, overexpression of NAB2, a repressor of Egr-1 activation, also blocked the induction of PPAR gamma by TGF beta in VSMC, suggesting that Egr-1 mediates the rapid and transient induction of PPAR gamma by TGF beta. With regard to the TGF beta repression of PPAR gamma expression, activator protein 1 (AP1) and Smad3/4 dramatically inhibited the PPAR gamma promoter activity in transient-transfection studies. In contrast, adenovirus-mediated overexpression of a dominant-negative form of c-Jun partially rescued the TGF beta-induced PPAR gamma repression in VSMC. Taken together, our data demonstrate that Egr-1, AP1 and Smad are part components of the TGF beta signal transduction pathway that regulates PPAR gamma expression