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3,648 results for “induction”
Data from: Pharmacological HIF-1 activation upregulates extracellular vesicle production synergistically with adiponectin through transcriptional induction and protein stabilization of T-cadherin
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Chemical defense strategies, induction timing, growth, and tradeoffs in Pinus aristata and Pinus flexilis
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Inductive biases of neural network modularity in spatial navigation
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Nuclear induction lineshape: Non-Markovian diffusion with boundaries
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Reproductive activity and diapause induction in Ips typographus
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Data from: Genotypic variation in the induction and persistence of transgenerational responses to seasonal cues
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Mesocosm experiments validate induction of Daphnia vertical migration by the fish-derived kairomone 5α-cyprinol sulfate
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Data from: Diet-dependent induction of life-history changes in Daphnia: 5α-cyprinol sulfate is not the kairomone
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Data from: Age-specific induction of mutant p53 drives clonal hematopoiesis and acute myeloid leukemia in adult mice
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IL1b induction of endothelial surface IL15 by let7c3p downregulation
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Larval development and diapause induction under climate change: an experimental test with the Wall Brown butterfly
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Gene induction by natural toxins in Drosophila melanogaster
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A sensitive method for atmospheric sulfur dioxide determination by reaction cell inductively coupled plasma mass spectrometer
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Low-dose alemtuzumab induction in a tailored immunosuppression protocol for sensitized kidney transplant recipients
<p class="BodyText31"><u>Background:</u> Induction therapy is crucial in kidney transplantation and constitutes an important cornerstone for long-term allograft survival. Alemtuzumab is a depleting CD52-specific antibody with T and B cell activity, leading to prolonged lymphocyte depletion for up to 12 months, with profound immunosuppression and an associated risk of serious infections. Current concepts aim to optimize dosing strategies to reduce side effects. Here we present data from an ongoing centre protocol consisting of low-dose alemtuzumab induction and tailored immunosuppression in sensitized patients undergoing kidney transplantation.</p> <p><u>Methods:</u> 10-year results of the protocol were analysed. Low-dose alemtuzumab induction consisted of a single dose of 20mg intraoperatively, followed by tacrolimus and corticosteroids for initial immunosuppression, with mycophenolate mofetil suspended until a total lymphocyte count >5% or 200/µl was reached.</p> <p><u>Results:</u> Between 01/2007 and 04/2017, 46 patients were treated in accordance with the protocol in 48 kidney transplantations. Median PRA<sub>max</sub> was 43 [22-76; IQR] %; all patients had negative CDC-crossmatch prior to transplantation. Low-dose alemtuzumab was well tolerated. Median time to TLC recovery was 77 [62-127; IQR] d. Within a median follow-up of 3.3 [1.5-5.6; IQR] years, 12 (25%) patients developed BPAR, 10 of which were antibody-mediated (3 acute, 7 chronic ABMR). Death-censored 5-year allograft survival was 79.2%, with an excellent allograft function at the end of follow-up. There was no increased rate of infections, in particular viral infections.</p> <p><u>Conclusions</u>: Our protocol, comprising low-dose alemtuzumab induction, initial suspension of mycophenolate mofetil and triple maintenance immunosuppression, provides excellent patient and allograft outcome in sensitized renal allograft recipients.</p>
Single-cell data on lac operon induction by lactose in E. coli
<p>Raw data from experiments presented in https://doi.org/10.1101/2020.01.04.894766. </p> <p>Escherichia coli cells are exposed alternatively to glucose and lactose as carbon source, while their growth and lac operon expression are monitored using phase contrast and epifluorescence microscopy.</p> <p>Data from 36 independent experiments are provided: details about conditions are given in Julou_2020_lacInduction_assays.xlsx, and the list of data files in Julou_2020_lacInduction_GL_Preproc_fileList.txt</p>
Data from: Leptin increases sympathetic nerve activity via induction of its own receptor in the paraventricular nucleus
Whether leptin acts in the paraventricular nucleus (PVN) to increase sympathetic nerve activity (SNA) is unclear, since PVN leptin receptors (LepR) are sparse. We show in rats that PVN leptin slowly increases SNA to muscle and brown adipose tissue, because it induces the expression of its own receptor and synergizes with local glutamatergic neurons. PVN LepR are not expressed in astroglia and rarely in microglia; instead, glutamatergic neurons express LepR, some of which project to a key presympathetic hub, the rostral ventrolateral medulla (RVLM). In PVN slices from mice expressing GCaMP6, leptin excites glutamatergic neurons. LepR are expressed mainly in thyrotropin-releasing hormone (TRH) neurons, some of which project to the RVLM. Injections of TRH into the RVLM and dorsomedial hypothalamus increase SNA, highlighting these nuclei as likely targets. We suggest that this neuropathway becomes important in obesity, in which elevated leptin maintains the hypothalamic pituitary thyroid axis, despite leptin resistance.
Data from: Exposure effects beyond the epithelial barrier: trans-epithelial induction of oxidative stress by diesel exhaust particulates in lung fibroblasts in an organotypic human airway model
<p><i>In vitro</i> bronchial epithelial monoculture models have been pivotal in defining the adverse effects of inhaled toxicant exposures; however, they are only representative of one cellular compartment and may not accurately reflect the effects of exposures on other cell types. Lung fibroblasts exist immediately beneath the bronchial epithelial barrier and play a central role in lung structure and function, as well as disease development and progression. We tested the hypothesis that <i>in vitro</i> exposure of a human bronchial epithelial cell barrier to the model oxidant diesel exhaust particulates caused trans-epithelial oxidative stress in the underlying lung fibroblasts using a human bronchial epithelial cell and lung fibroblast co-culture model. We observed that diesel exhaust particulates caused trans-epithelial oxidative stress in underlying lung fibroblasts as indicated by intracellular accumulation of the reactive oxygen species hydrogen peroxide, oxidation of the cellular antioxidant glutathione, activation of NRF2, and induction of oxidative stress responsive genes. Further, targeted antioxidant treatment of lung fibroblasts partially mitigated the oxidative stress response gene expression in adjacent human bronchial epithelial cells during diesel exhaust particulate exposure. This indicates that exposure induced oxidative stress in the airway extends beyond the bronchial epithelial barrier and that lung fibroblasts are both a target and a mediator of the adverse effects of inhaled chemical exposures despite a lack of direct exposure to the inhaled material. These findings illustrate the value of co-culture models and suggest that trans-epithelial exposure effects should be considered in inhalation toxicology research and testing.</p>
Data from: Distribution of the specialist aphid Uroleucon nigrotuberculatum (Homoptera: Aphididae) in response to host plant semiochemical induction by the gall fly Eurosta solidaginis (Diptera: Tephritidae)
Many plants use terpenoids and other volatile compounds as semiochemicals. Reception of plant volatiles by conspecifics may trigger a defensive phytochemical response. These same compounds can also function as host recognition signals for phytophagous insects. In this experiment we find that when the specialist gall-forming fly Eurosta solidaginis attacks its tall goldenrod (Solidago altissima) host plant, the fly indirectly induces a phytochemical response in nearby tall goldenrod plants. This phytochemical response may, in turn, act as a positive signal attracting the goldenrod specialist aphid Uroleucon nigrotuberculatum. Laboratory based experiments exposing ungalled tall goldenrod plants to the volatiles released by E. solidaginis galls demonstrated a consistent increase in foliar terpenoid concentrations in ungalled plants. Analysis of tall goldenrod stem and gall tissue chemistry revealed induction of terpenoids in gall tissue, with a simultaneous decrease in green leaf volatile concentrations. Field experiments demonstrated a consistent spatial relationship in tall goldenrod foliar terpenoid concentrations with distance from an E. solidaginis gall. Both laboratory and field experiments establish consistent induction of the terpene β-farnesene, and that this compound is a strong positive predictor of U. nigrotuberculatum aphid presence on goldenrod plants along with plant biomass and several other foliar terpenoids. These findings suggest E. solidaginis induced phytochemistry, especially β-farnesene, may be acting as a kairomone, driving aphid distribution in the field.
Data from the study: Effect of experimental DNA demethylation on phytohormones production and palatability of a clonal plant after induction via jasmonic acid
<p>Many plant species protect themselves against herbivores through mechanical or chemical so-called inducible defences (ID). These are regulated via a hormonal cascade which may be under epigenetic control and in which jasmonic acid (JA) plays a prominent role.</p> <p>In this study, we indirectly tested the role of DNA methylation in the production of ID and the synthesis of hormones involved in the ID signalling cascade. Using different intensities of 5-azacytidine application, we aimed to produce plants of <i>Trifolium repens</i> with different levels of DNA methylation alteration. We then elicited the plants together with controls, i.e. plants with natural DNA methylation status, with JA and then indirectly recorded ID production in herbivore-choice trials in which the leaves of plants with different DNA methylation statuses were provided to caterpillars of a generalist herbivore, <i>Spodoptera littoralis.</i></p> <p>We also analysed the balance of several key defence hormones such as jasmonates, abscisic acid (ABA), indole-3-acetic acid (IAA) and salicylic acid in the plants. We found that the <i>Spodoptera littoralis</i> preferred demethylated plants over non-demethylated controls. Demethylation also reduced production of JA, ABA and IAA. We conclude that DNA methylation modulates expression of ID likely via regulation of signalling hormones involved in the establishment of defence.</p>
Data from: Morphological, cellular and molecular evidences of chromosome random elimination in vivo upon haploid induction in maize
The mechanism of maternal in vivo haploid induction is not fully understood. In this study, the young embryos were identified by morphology, cytology and simple sequence repeat (SSR) markers at different developmental stages in the cross HZ514 (sweet corn) × HZI1 (inducer). The results indicated that the low seed setting rate was determined by the inducer pollen during the process of fertilization. The mosaic endosperm kernels and the different percentages of aneuploidy, mixploidy, lagged chromosome, micronuclei, chromosomal bridge and ring chromosome were found in the cross; 7.37% of the haploid embryos carried chromosome segments from HZI1. About 1% twin seedlings resulted from the cross and were analyzed by cytology and SSR markers. Four pairs of twin seedlings had different chromosome numbers (2n = 20 and 2n = 10–20) and there were some chromosome fragments from HZI1. Aneuploidy, mixploidy and the abnormal chromosomes occurred in the in vivo haploid induction by HZI1, which is the cytological basis for haploid induction and indicates that the inducer's chromosomes are prone to be lost during mitotic and meiotic divisions. Morphological, cellular and molecular evidences reveal that complete or partial chromosome elimination from inducer HZI1 controls the maize in vivo haploid induction.
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Allen Brain Atlas
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Annotated Behaviour and Observability Dataset (ABODe)
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The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
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