The integration of unmanned aerial vehicle (UAV)-assisted remote sensing with the Internet of Things (IoT) and Internet of Everything (IoE) offers a robust platform for optimizing precision agriculture by capturing spatiotemporal variability in crop growth. In this context, the present study aimed to predict the bulb yield of rainy-season onion crops across four staggered planting dates using UAV-based multispectral imagery. Canopy reflectance mosaics acquired at key growth stages, along with vegetation indices (VIs), viz. NDVI, NDRE, SAVI, LAI, NORM2, and GNDVI, were extracted for yield modeling. Yield prediction models at three onion growth stages were developed and assessed using five machine learning algorithms: linear regression (lm), random forest (rf), support vector machine with radial kernel (svmRadial), gradient boosting (gbm), and elastic net regression (glmnet), with model training and evaluation performed using 10-fold cross-validation. Among these, random forest consistently outperformed the other models at all growth stages, showing promising results at the bulb development stage, with a training R 2 = 0.944, RMSE = 1.919 t ha -1 , MAE = 1.523 t ha −1 , and a validation R² = 0.755, RMSE = 3.824 t ha −1 , and MAE = 3.11 t ha −1 . The support vector machine also demonstrated strong generalization (training R² = 0.787; validation R 2 = 0.716), highlighting its predictive capability. Year-wise evaluation revealed notable interannual variability in model performance, with models trained on data from 2024 outperforming those from 2023. Overall, these results demonstrate the efficacy of UAV-derived multispectral sensing, combined with machine learning, as an effective, scalable, and timely approach for reliable onion yield prediction and decision support in rainy-season onion crops under varying agronomic conditions.

Transforming growth factor-β1 (TGF-β1) is a pleiotropic factor sensed by most cells. It regulates a broad spectrum of cellular responses including hematopoiesis. In order to process TGF-β1-responses in time and space in an appropriate manner, there is a tight regulation of its signaling at diverse steps. The downstream signaling is mediated by type I and type II receptors and modulated by the 'accessory' receptor Endoglin also termed cluster of differentiation 105 (CD105). Endoglin was initially identified on pre-B leukemia cells but has received most attention due to its high expression on activated endothelial cells. In turn, Endoglin has been figured out as the causative factor for diseases associated with vascular dysfunction like hereditary hemorrhagic telangiectasia-1 (HHT-1), pre-eclampsia, and intrauterine growth restriction (IUPR). Because HHT patients often show signs of inflammation at vascular lesions, and loss of Endoglin in the myeloid lineage leads to spontaneous inflammation, it is speculated that Endoglin impacts inflammatory processes. In line, Endoglin is expressed on progenitor/precursor cells during hematopoiesis as well as on mature, differentiated cells of the innate and adaptive immune system. However, so far only pro-monocytes and macrophages have been in the focus of research, although Endoglin has been identified in many other immune system cell subsets. These findings imply a functional role of Endoglin in the maturation and function of immune cells. Aside the functional relevance of Endoglin in endothelial cells, CD105 is differentially expressed during hematopoiesis, arguing for a role of this receptor in the development of individual cell lineages. In addition, Endoglin expression is present on mature immune cells of the innate (i.e., macrophages and mast cells) and the adaptive (i.e., T-cells) immune system, further suggesting Endoglin as a factor that shapes immune responses. In this review, we summarize current knowledge on Endoglin expression and function in hematopoietic precursors and mature hematopoietic cells of different lineages.

CD62L (L-Selectin) dependent lymphocyte infiltration is known to induce inflammatory bowel disease (IBD), while its function in the liver, especially in non-alcoholic steatohepatitis (NASH), remains unclear. We here investigated the functional role of CD62L in NASH in humans as well as in two mouse models of steatohepatitis. Hepatic expression of a soluble form of CD62L (sCD62L) was measured in patients with steatosis and NASH. Furthermore, CD62L−/− mice were fed with a methionine and choline deficient (MCD) diet for 4 weeks or with a high fat diet (HFD) for 24 weeks. Patients with NASH displayed increased serum levels of sCD62L. Hepatic CD62L expression was higher in patients with steatosis and increased dramatically in NASH patients. Interestingly, compared to wild type (WT) mice, MCD and HFD-treated CD62L−/− mice were protected from diet-induced steatohepatitis. This was reflected by less fat accumulation in hepatocytes and a dampened manifestation of the metabolic syndrome with an improved insulin resistance and decreased cholesterol and triglyceride levels. Consistent with ameliorated disease, CD62L−/− animals exhibited an enhanced hepatic infiltration of Treg cells and a strong activation of an anti-oxidative stress response. Those changes finally resulted in less fibrosis in CD62L−/− mice. Additionally, this effect could be reproduced in a therapeutic setting by administrating an anti-CD62L blocking antibody. CD62L expression in humans and mice correlates with disease activity of steatohepatitis. CD62L knockout and anti-CD62L-treated mice are protected from diet-induced steatohepatitis suggesting that CD62L is a promising target for therapeutic interventions in NASH.

Journal Article Inheritance of rudimentary corolla in red clover Get access N. L. Taylor, N. L. Taylor The authors are, respectively, professor of agronomy, and student assistant, University of Kentucky, Lexington, KY 40546. The investigation reported in this paper (85-3-154) was in connection with a project of the Kentucky Agricultural Experiment Station and is published with the approval of the director. Search for other works by this author on: Oxford Academic PubMed Google Scholar L. D. Snead L. D. Snead The authors are, respectively, professor of agronomy, and student assistant, University of Kentucky, Lexington, KY 40546. The investigation reported in this paper (85-3-154) was in connection with a project of the Kentucky Agricultural Experiment Station and is published with the approval of the director. Search for other works by this author on: Oxford Academic PubMed Google Scholar Journal of Heredity, Volume 77, Issue 5, September 1986, Pages 371–372, https://doi.org/10.1093/oxfordjournals.jhered.a110263 Published: 01 September 1986

Supplementary Figure from Colorectal Cancer Is Associated with the Presence of Cancer Driver Mutations in Normal Colon

BACKGROUND AND AIMS: Mid-regional pro atrial natriuretic peptide (MR-proANP) is an established biomarker for heart failure, based on its key role in regulating homeostasis of water balance and blood pressure. The aim of the study was to determine the value of MR-proANP as a clinical biomarker in critical illness and/or sepsis. Upon admission to the medical intensive care unit (ICU), we investigated MR-proANP plasma concentrations in 217 critically ill patients (144 with sepsis, 73 without sepsis). Results were compared with 65 healthy controls. RESULTS: MR-proANP plasma levels were significantly elevated in critically ill patients, when compared to healthy controls. Notably, MR-proANP levels were significantly higher in ICU patients with sepsis. MR-proANP levels were not associated with metabolic comorbidities like diabetes or obesity. In critically ill patients, MR-proANP plasma concentrations correlated with inflammatory cytokines, markers of organ dysfunction and several adipocytokines, such as resistin, retinol-binding protein 4 (RBP4) and adiponectin. Importantly, high MR-proANP plasma levels were associated with mortality, as MR-proANP levels above 227.0 pmol/l indicated a particularly increased mortality risk in ICU patients. The association between MR-proANP and mortality was independent of single organ failure and inflammation markers. CONCLUSION: Our study emphasizes the role of circulating MR-proANP as a biomarker in critically ill patients, in which high MR-proANP indicates organ dysfunction, sepsis and mortality risk. The association between high MR-proANP and inflammatory as well as adipose tissue-derived endocrine mediators warrants further pathophysiological investigations.

Injury of the liver involves a wound healing partial reaction governed by hepatic stellate cells and portal fibroblasts. Individual members of the transforming growth factor-β (TGF-β) superfamily including TGF-β itself and bone morphogenetic proteins (BMP) exert diverse and partially opposing effects on pro-fibrogenic responses. Signaling by these ligands is mediated through binding to membrane integral receptors type I/type II. Binding and the outcome of signaling is critically modulated by Endoglin (Eng), a type III co-receptor. In order to learn more about trafficking of Eng in liver cells, we investigated the membranal subdomain localization of full-length (FL)-Eng. We could show that FL-Eng is enriched in Caveolin-1-containing sucrose gradient fractions. Since lipid rafts contribute to the pool of exosomes, we could consequently demonstrate for the first time that exosomes isolated from cultured primary hepatic stellate cells and its derivatives contain Eng. Moreover, via adenoviral overexpression, we demonstrate that all liver cells have the capacity to direct Eng to exosomes, irrespectively whether they express endogenous Eng or not. Finally, we demonstrate that block of N-glycosylation does not interfere with dimerization of the receptor, but abrogates the secretion of soluble Eng (sol-Eng) and prevents exosomal targeting of FL-Eng.

With an incidence of 1:20,000-1:30,000, Wilson's disease is regarded as a rare disease. Yet rarer, however, is the co-occurrence of two unrelated orphan diseases in the same patient. By means of two case reports, we would like to illustrate the necessity of an appropriate differential diagnostic evaluation and treatment of these disorders.

Six cycles of phenotypic recurrent selection for stem length were conducted in a 91-cm-spaced planted population of red clover (Trifolium pratense L.) as a means of increasing herbage yield. The objectives of this investigation were (1) to compare the effectiveness of selection for stem length tested in transplants at wide (91 cm) and narrow (7 cm) spacings, and in row seedings and (2) to determine the effect of selection for stem length on herbage yield. Response to selection for stem length was obtained under all plantings; however, greater gains were observed at the wide transplant spacing (3.3 cm∙cycle −1 ) compared to the narrow transplant spacing (0.7 cm∙cycle −1 ) and row seeding (0.8 cm∙cycle −1 ). Densely spaced transplants gave performance similar to row seedings and may be of value to forage crop breeders in situations where yield or quality assessment is desired but seed supplies are insufficient for the establishment of seeded plots, such as in the early stages of breeding programs. Selection for stem length was effective in increasing herbage yield at first harvest but was associated with reduced persistance, decreased regrowth yields, and increased partitioning of dry matter towards the shoot rather than the root during seedling development. Selection for stem length in the regrowth or in the second year, rather than in the primary (seedling) growth, might have avoided the declines in persistence and regrowth yields.Key words: Trifolium pratense L., red clover, recurrent selection, stem length, density, herbage yield

<div>Abstract<p>Although somatic mutations in colorectal cancer are well characterized, little is known about the accumulation of cancer mutations in the normal colon before cancer. Here, we have developed and applied an ultrasensitive, single-molecule mutational test based on CRISPR-DS technology, which enables mutation detection at extremely low frequency (<0.001) in normal colon from patients with and without colorectal cancer. This testing platform revealed that normal colon from patients with and without colorectal cancer carries mutations in common colorectal cancer genes, but these mutations are more abundant in patients with cancer. Oncogenic <i>KRAS</i> mutations were observed in the normal colon of about one third of patients with colorectal cancer but in none of the patients without colorectal cancer. Patients with colorectal cancer also carried more <i>TP53</i> mutations than patients without cancer and these mutations were more pathogenic and formed larger clones, especially in patients with early-onset colorectal cancer. Most mutations in the normal colon were different from the driver mutations in tumors, suggesting that the occurrence of independent clones with pathogenic <i>KRAS</i> and <i>TP53</i> mutations is a common event in the colon of individuals who develop colorectal cancer. These results indicate that somatic evolution contributes to clonal expansions in the normal colon and that this process is enhanced in individuals with cancer, particularly in those with early-onset colorectal cancer.</p>Significance:<p>This work suggests prevalent somatic evolution in the normal colon of patients with colorectal cancer, highlighting the potential of using ultrasensitive gene sequencing to predict disease risk.</p></div>

Mast cells (MCs) are immune cells of the myeloid lineage that are present in the connective tissue throughout the body and in mucosa tissue. They originate from hematopoietic stem cells in the bone marrow and circulate as MC progenitors in the blood. After migration to various tissues, they differentiate into their mature form, which is characterized by a phenotype containing large granules enriched in a variety of bioactive compounds, including histamine and heparin. These cells can be activated in a receptor-dependent and -independent manner. Particularly, the activation of the high-affinity immunoglobulin E (IgE) receptor, also known as FcεRI, that is expressed on the surface of MCs provoke specific signaling cascades that leads to intracellular calcium influx, activation of different transcription factors, degranulation, and cytokine production. Therefore, MCs modulate many aspects in physiological and pathological conditions, including wound healing, defense against pathogens, immune tolerance, allergy, anaphylaxis, autoimmune defects, inflammation, and infectious and other disorders. In the liver, MCs are mainly associated with connective tissue located in the surrounding of the hepatic arteries, veins, and bile ducts. Recent work has demonstrated a significant increase in MC number during hepatic injury, suggesting an important role of these cells in liver disease and progression. In the present review, we summarize aspects of MC function and mediators in experimental liver injury, their interaction with other hepatic cell types, and their contribution to the pathogenesis of fibrosis.