Ultra-high-resolution UAV-imaging and supervised deep learning for accurate detection of Alternaria solani in potato fields.

Alternaria solani is the second most devastating foliar pathogen of potato crops worldwide, causing premature defoliation of the plants. This disease is currently prevented through the regular application of detrimental crop protection products and is guided by early warnings based on weather predictions and visual observations by farmers. To reduce the use of crop protection products, without additional production losses, it would be beneficial to be able to automatically detect Alternaria solani in potato fields. In recent years, the potential of deep learning in precision agriculture is receiving increasing research attention. Convolutional Neural Networks (CNNs) are currently the state of the art, but also come with challenges, especially regarding in-field robustness. This stems from the fact that they are often trained on datasets that are limited in size or have been recorded in controlled environments, not necessarily representative of real-world settings. We collected a dataset consisting of ultra-high-resolution modified RGB UAV-imagery of both symptomatic and non-symptomatic potato crops in the field during various years and disease stages to cover the great variability in agricultural data. We developed a convolutional neural network to perform in-field detection of Alternaria, defined as a binary classification problem. Our model achieves a similar accuracy as several state-of-the-art models for disease detection, but has a much lower inference time, which enhances its practical applicability. By using training data of three consecutive growing seasons (2019, 2020 and 2021) and test data of an independent fourth year (2022), an F1 score of 0.93 is achieved. Furthermore, we evaluate how different properties of the dataset such as its size and class imbalance impact the obtained accuracy.

SpectroFood dataset: A comprehensive fruit and vegetable hyperspectral meta-dataset for dry matter estimation.

In the dataset presented in this article, samples belonging to one of the following crops, apple, broccoli, leek, and mushroom, were measured by hyperspectral cameras in the visible/near-infrared spectral domain (430-900 nm). The dataset was compiled by putting together measurements from different calibrated hyperspectral imaging cameras and crops to facilitate the training of artificial intelligence models, helping to overcome the generalization problem of hyperspectral models. In particular, this dataset focuses on estimating dry matter content across various crops by a single model in a non-destructive way using hyperspectral measurements. This dataset contains extracted mean reflectance spectra for each sample (n=1028) and their respective dry matter content (%).

The induction of CCN2 by TGFbeta1 involves Ets-1.

CCN2 is encoded by an immediate-early gene induced in mesenchymal cells during the formation of blood vessels, bone and connective tissue. It plays key roles in cell adhesion and migration, as well as matrix remodeling. CCN2 is overexpressed in fibrosis, arthritis and cancer; thus, an understanding of how to control CCN2 expression is likely to have importance in developing therapies to combat these pathologies. Previously, we found that the promoter sequence GAGGAATG is important for Ccn2 gene regulation in NIH 3T3 fibroblasts. In this report, we show that this sequence mediates activation of the CCN2 promoter by the ETS family of transcription factors. Endogenous Ets-1 binds this element of the CCN2 promoter, and dominant negative Ets-1 and specific Ets-1 small interfering RNA block induction of CCN2 expression by TGFbeta. In the absence of added TGFbeta1, Ets-1, but not the related fli-1, synergizes with Smad 3 to activate the CCN2 promoter. Whereas the ability of transfected Ets-1 to activate the CCN2 promoter is dependent on protein kinase C (PKC), Ets-1 in the presence of co-transfected Smad3 does not require PKC, suggesting that the presence of Smad3 bypasses the requirement of Ets-1 for PKC to activate target promoter activity. Our results are consistent with the notion that Smad3 and Ets-1 cooperate in the induction of the CCN2 promoter by TGFbeta1. Antagonizing Ets-1 might be of benefit in attenuating CCN2 expression in fibrosis, arthritis and cancer, and may be useful in modulating the outcome of these disorders.

Matrix contraction by dermal fibroblasts requires transforming growth factor-beta/activin-linked kinase 5, heparan sulfate-containing proteoglycans, and MEK/ERK: insights into pathological scarring in chronic fibrotic disease.

Scarring is characterized by excessive synthesis and contraction of extracellular matrix. Here, we show that fibroblasts from scarred (lesional) areas of patients with the chronic fibrotic disorder diffuse scleroderma [diffuse systemic sclerosis (dSSc)] show an enhanced ability to adhere to and contract extracellular matrix, relative to fibroblasts from unscarred (nonlesional) areas of dSSc patients and dermal fibroblasts from normal, healthy individuals. The contractile abilities of normal and dSSc dermal fibroblasts were suppressed by blocking heparin sulfate-containing proteoglycan biosynthesis or antagonizing transforming growth factor-beta receptor type I [activin-linked kinase (ALK5)] or ras/mitogen-activated protein kinase (MEK)/extracellular signal-regulated kinase (ERK). Compared with both normal and nonlesional fibroblasts, lesional dSSc fibroblasts overexpressed the heparin sulfate-containing proteoglycan syndecan 4. We also found that the procontractile signals from transforming growth factor (TGF)-beta were integrated through syndecan 4 and MEK/ERK because the ability of TGFbeta to induce contraction of dermal fibroblasts was prevented by MEK antagonism. TGFbeta could not induce a contractile phenotype or phosphorylate ERK in syndecan 4(-/-) dermal fibroblasts. These results suggest that integrating TGFbeta and ERK signals via syndecan 4 is essential for the contractile ability of dermal fibroblasts. We conclude that antagonizing MEK/ERK, TGFbeta1/ALK5, or syndecan 4 may alleviate scarring in chronic fibrotic disease.

Adipose tissue gene expression profiling reveals distinct molecular pathways that define visceral adiposity in offspring of maternal protein-restricted rats.

There is increasing evidence that poor early growth confers an increased risk of type 2 diabetes, hypertension, and other features of the metabolic syndrome in later life. We hypothesized that this may result from poor nutrition during early life exerting permanent effects on the structure and function of key metabolic organ systems. To study the long-term impact of early-life undernutrition on susceptibility to visceral adiposity, we used a rat model of maternal protein restriction (MPR) in which dams were fed a low-protein diet (containing 8% instead of 20% protein in control diet) throughout pregnancy and lactation. MPR offspring were born smaller than controls (offspring of dams on control diet) and in adulthood developed visceral adiposity. We compared the pattern of gene expression in visceral adipose tissue (VAT) between MPR offspring and controls with Affymetrix rat expression arrays. Of the total number of genes and expressed sequence tags analyzed (15,923 probe sets), 9,790 (61.5%) were expressed in VAT. We identified 650 transcripts as differentially expressed > or =1.5-fold in the VAT of MPR offspring. Gene ontology analysis revealed a global upregulation of genes involved in carbohydrate, lipid, and protein metabolism. A number of genes involved in adipocyte differentiation, angiogenesis, and extracellular matrix remodeling were also upregulated. However, in marked contrast to other rodent models of obesity, the expression of a large number of genes associated with inflammation was reduced in this rat model. Thus visceral adiposity in this early-life programmed rat model is marked by dynamic changes in the transcriptional profile of VAT. Our data provide new insights into the molecular mechanisms that underlie the early-life programming of visceral adiposity.

Peroxisome proliferator-activated receptor delta suppresses 11beta-hydroxysteroid dehydrogenase type 2 gene expression in human placental trophoblast cells.

Accumulating evidence suggests that the human placental enzyme 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2) plays a key role in fetal development by controlling fetal exposure to maternal glucocorticoids. Recently, the nuclear peroxisome proliferator-activated receptor delta (PPAR delta) has been found to be the most abundantly expressed PPAR subtype in the human placenta, but its function in this organ is unknown. Given that PPAR delta-null mice exhibited placental defects and consequent intrauterine growth restriction, the present study was undertaken to examine the hypothesis that PPAR delta regulates human placental function in part by targeting 11beta-HSD2. Using cultured human trophoblast cells as a model system, we demonstrated that 1) the putative PPAR delta agonist carbaprostacyclin (cPGI2) reduced 11beta-HSD2 activity as well as 11beta-HSD2 expression at both protein and mRNA levels; 2) GW610742 (a selective PPAR delta agonist) mimicked the effect of cPGI2, whereas indomethacin (a known ligand for PPARalpha and PPAR gamma) had no effect; 3) the cPGI2-induced down-regulation of 11beta-HSD2 mRNA did not require de novo protein synthesis; 4) cPGI2 suppressed HSD11B2 promoter activity, but did not alter the half-life of 11beta-HSD2 mRNA; and 5) the inhibitory effect of cPGI2 on HSD11B2 promoter activity was abrogated in trophoblast cells cotransfected with a dominant negative PPAR delta mutant. Taken together, these findings suggest that activation of PPAR delta down-regulates HSD11B2 gene expression in human trophoblast cells, and that this effect is mediated primarily at the transcriptional level. Thus, the present study reveals 11beta-HSD2 as an additional target for PPAR delta and identifies a molecular mechanism by which this nuclear receptor may regulate human placental function.

Glucocorticoids stimulate the expression of 11beta-hydroxysteroid dehydrogenase type 2 in cultured human placental trophoblast cells.

Proper glucocorticoid exposure in utero is vital for normal fetal organ growth and maturation. The placental enzyme, 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2), plays a pivotal role in controlling fetal exposure to high levels of maternal glucocorticoid by converting cortisol into its inactive metabolite, cortisone. The present study was designed to determine whether glucocorticoids auto-regulate 11beta-HSD2 in the human placenta using cultured trophoblast cells as a model system. Trophoblasts were isolated from uncomplicated term placentas and treated with glucocorticoids. The synthetic glucocorticoid dexamethasone increased 11beta-HSD2 activity in a time- and concentration-dependent manner; this effect was accompanied by a corresponding increase in 11beta-HSD2 mRNA. Furthermore, the glucocorticoid receptor antagonist, RU-486, abrogated the dexamethasone-induced increase in 11beta-HSD2 activity, suggesting that the effect of dexamethasone is mediated through the glucocorticoid receptor. Results from transient transfection and mRNA decay experiments indicate that the glucocorticoid-induced increase in 11beta-HSD2 expression is mediated at both the transcriptional and posttranscriptional levels. In conclusion, the present study demonstrates that in cultured human trophoblasts, 11beta-HSD2 is subject to auto-regulation by glucocorticoids. If this occurs in the human placenta in vivo, the glucocorticoid-induced up-regulation of placental 11beta-HSD2 would represent an important safeguard mechanism by which the fetus may be protected from detrimental exposure to elevated levels of maternal glucocorticoids.