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The increasing consumption of cleaning products deteriorates water resources due to harmful components such as phosphorus (P) and nitrogen (N) compounds, oils, bleach, and acids, typical compounds in traditional detergents. The use of biodegradable detergents as an environmentally friendly alternative has been proposed in different regions. In Colombia, resolution 1770/2018 sets a minimum biodegradability rate of 60% for the surfactants present in liquid detergents, which would reduce to a similar extent the impacts on water after their use. However, the environmental impacts of the supply chain of these detergents and their raw materials have not been evaluated so far. This study presents an environmental life cycle assessment of petroleum-based liquid detergents and a comparison to traditional solid detergents, based on the ISO 14040 standard and the ReCiPe-2016 impacts assessment method. A novel bio-detergent containing anionic plant-based surfactants was proposed in this analysis. The impacts of packaging and the distribution of the product to consumers were also considered. Raw materials contributed to 91% of the total of 314 g of CO 2 eq generated per liter of liquid detergent, where the production of fatty alcohol sulfate and PET packaging shared 78.8% and 12.2% of the total impact, respectively. It was also determined that 5.4 L of water are consumed and 0.09 g of P eq and 0.1 g of N eq are emitted per liter of detergent. This liquid detergent presented better environmental performance than traditional detergents in all the impact categories, except for the fossil resource scarcity category. The evaluated detergent would significantly mitigate the generation of negative effects on ecosystems. Moreover, the substitution of PET for HDPE packaging could reduce the impacts on freshwater eutrophication by 10%, although the carbon footprint can slightly increase, which could be compensated due to its higher recyclability rate. In contrast, the proposed bio-detergent would not have significant benefits and would negatively affect water consumption and land use in its supply chain.

Many targets of plant microRNAs (miRNAs) are thought to play important roles in plant physiology and development. However, because plant miRNAs are typically encoded by medium-size gene families, it has often been difficult to assess their precise function. We report the generation of a large-scale collection of knockdowns for Arabidopsis thaliana miRNA families; this has been achieved using artificial miRNA target mimics, a recently developed technique fashioned on an endogenous mechanism of miRNA regulation. Morphological defects in the aerial part were observed for approximately 20% of analyzed families, all of which are deeply conserved in land plants. In addition, we find that non-cleavable mimic sites can confer translational regulation in cis. Phenotypes of plants expressing target mimics directed against miRNAs involved in development were in several cases consistent with previous reports on plants expressing miRNA-resistant forms of individual target genes, indicating that a limited number of targets mediates most effects of these miRNAs. That less conserved miRNAs rarely had obvious effects on plant morphology suggests that most of them do not affect fundamental aspects of development. In addition to insight into modes of miRNA action, this study provides an important resource for the study of miRNA function in plants.

Plants live in biogeochemically diverse soils with diverse microbiota. Plant organs associate intimately with a subset of these microbes, and the structure of the microbial community can be altered by soil nutrient content. Plant-associated microbes can compete with the plant and with each other for nutrients, but may also carry traits that increase the productivity of the plant. It is unknown how the plant immune system coordinates microbial recognition with nutritional cues during microbiome assembly. Here we establish that a genetic network controlling the phosphate stress response influences the structure of the root microbiome community, even under non-stress phosphate conditions. We define a molecular mechanism regulating coordination between nutrition and defence in the presence of a synthetic bacterial community. We further demonstrate that the master transcriptional regulators of phosphate stress response in Arabidopsis thaliana also directly repress defence, consistent with plant prioritization of nutritional stress over defence. Our work will further efforts to define and deploy useful microbes to enhance plant performance. In Arabidopsis thaliana , a genetic network that controls the phosphate stress response also influences the structure of the root microbiome community, even under non-stress phosphate conditions. Root microbiota coordinate plant nutrition and immunity Plants live among a community of soil bacteria, the composition of which can be altered by changes in the soil nutrients. Therefore, even beneficial soil microbes can compete with plants for nutrients. Jeff Dangl and colleagues ask how, in the presence of a microbial community, plants coordinate their immune responses to nutrient shortages. They find that, even with sufficient phosphate present, the genetic network that regulates phosphate stress response affects the composition of the local microbial community. The mechanistic logic for this observation is that the transcriptional regulators of the phosphate stress response can directly repress plant defence. The findings also suggest that plants prioritize responses to nutrient shortages over defence.

To cope with growth in low-phosphate (Pi) soils, plants have evolved adaptive responses that involve both developmental and metabolic changes. PHOSPHATE STARVATION RESPONSE 1 (PHR1) and related transcription factors play a central role in the control of Pi starvation responses (PSRs). How Pi levels control PHR1 activity, and thus PSRs, remains to be elucidated. Here, we identify a direct Pi-dependent inhibitor of PHR1 in Arabidopsis , SPX1, a nuclear protein that shares the SPX domain with yeast Pi sensors and with several Pi starvation signaling proteins from plants. Double mutation of SPX1 and of a related gene, SPX2, resulted in molecular and physiological changes indicative of increased PHR1 activity in plants grown in Pi-sufficient conditions or after Pi refeeding of Pi-starved plants but had only a limited effect on PHR1 activity in Pi-starved plants. These data indicate that SPX1 and SPX2 have a cellular Pi-dependent inhibitory effect on PHR1. Coimmunoprecipitation assays showed that the SPX1/PHR1 interaction in planta is highly Pi-dependent. DNA-binding and pull-down assays with bacterially expressed, affinity-purified tagged SPX1 and ΔPHR1 proteins showed that SPX1 is a competitive inhibitor of PHR1 binding to its recognition sequence, and that its efficiency is highly dependent on the presence of Pi or phosphite, a nonmetabolizable Pi analog that can repress PSRs. The relative strength of the SPX1/PHR1 interaction is thus directly influenced by Pi, providing a link between Pi perception and signaling. Significance When P levels are low, plants activate an array of adaptive responses to increase efficient acquisition and use of phosphate (Pi), the form in which P is preferentially absorbed, and to protect themselves from Pi starvation stress. Considerable progress has been made recently in dissecting the plant Pi starvation signaling pathway. Nonetheless, little is known as to how Pi levels are perceived by plants. Here, we identify the nuclear protein SPX1 as a Pi-dependent inhibitor of DNA binding by PHOSPHATE STARVATION RESPONSE 1 (PHR1), a master regulator of Pi starvation responses. We show that the Pi dependence of SPX1 inhibition of PHR1 activity can be recreated in vitro using purified proteins, which indicates that the SPX1/PHR1 module links Pi sensing and signaling.

Takotsubo syndrome (TTS) is an acute cardiac condition characterized by transient regional left ventricular systolic dysfunction. Traditionally, it has been associated with physical or psychological stressors. Clinically, the onset of TTS is similar to acute coronary syndrome, requiring appropriate differential diagnosis to distinguish between the two clinical entities. Its treatment is usually conservative, and the prognosis is generally favorable. We report the case of a 57-year-old woman who was referred to the Department of Rehabilitation after suffering a non-ST-segment elevation myocardial infarction. During her eighth physical rehabilitation session, she developed palpitations and hypertension. Initial telemetry monitoring showed ventricular bigeminy with extrasystoles, tachycardia episodes, and ST-segment elevation. She was admitted to the Department of Cardiology, and cardiac catheterization and subsequent coronary angiography were performed, revealing no incidence of coronary lesions. However, ventriculography demonstrated severe left ventricular dysfunction in the systolic phase, characterized by akinesia of the mid-apical segments. These findings were suggestive of Takotsubo syndrome, which was subsequently confirmed by cardiac magnetic resonance imaging.

Plants respond to different stresses by inducing or repressing transcription of partially overlapping sets of genes. In Arabidopsis, the PHR1 transcription factor (TF) has an important role in the control of phosphate (Pi) starvation stress responses. Using transcriptomic analysis of Pi starvation in phr1, and phr1 phr1-like (phl1) mutants and in wild type plants, we show that PHR1 in conjunction with PHL1 controls most transcriptional activation and repression responses to phosphate starvation, regardless of the Pi starvation specificity of these responses. Induced genes are enriched in PHR1 binding sequences (P1BS) in their promoters, whereas repressed genes do not show such enrichment, suggesting that PHR1(-like) control of transcriptional repression responses is indirect. In agreement with this, transcriptomic analysis of a transgenic plant expressing PHR1 fused to the hormone ligand domain of the glucocorticoid receptor showed that PHR1 direct targets (i.e., displaying altered expression after GR:PHR1 activation by dexamethasone in the presence of cycloheximide) corresponded largely to Pi starvation-induced genes that are highly enriched in P1BS. A minimal promoter containing a multimerised P1BS recapitulates Pi starvation-specific responsiveness. Likewise, mutation of P1BS in the promoter of two Pi starvation-responsive genes impaired their responsiveness to Pi starvation, but not to other stress types. Phylogenetic footprinting confirmed the importance of P1BS and PHR1 in Pi starvation responsiveness and indicated that P1BS acts in concert with other cis motifs. All together, our data show that PHR1 and PHL1 are partially redundant TF acting as central integrators of Pi starvation responses, both specific and generic. In addition, they indicate that transcriptional repression responses are an integral part of adaptive responses to stress.

Background/Objectives: Suprascapular nerve block (SSNB) is a useful therapeutic option for chronic shoulder pain, although the synergistic use of corticosteroids with anesthetics to prolong its effect is a controversial topic. The primary objective of this study was to compare the evolution of pain and functionality using the visual analog scale (VAS) and the Disabilities of the Arm, Shoulder and Hand (DASH) questionnaire between patients treated with SSNB with corticosteroids (cSSNB) and without them (sSSNB). Methods: A retrospective, observational, longitudinal, analytical cohort study was conducted in 28 patients (14 n per group) aged 50–80 years who had undergone SSNB with 4 mL of 0.25% bupivacaine and 40 mg/mL triamcinolone during 2024 for chronic shoulder pain lasting more than 6 months. The variables to be collected were VAS, DASH, range of motion (ROM) and Lattinen Index (LI) at baseline, the first and the third month. Patients were grouped according to the type of SSNB (cSSNB vs. sSSNB) and analyzed longitudinally and cross-sectionally using IBM-SPSS Statistics version 28.0.0. Results: Regarding pain, the cSSNB obtained a significant reduction in the median VAS of 4 points in the first month (p = 0.001) and in the third month (p = 0.002). In addition, significantly lower evaluations in VAS were obtained in the third month of 3 points (p = 0.04) in favor of the cSSNB. Regarding functionality, a reduction in evaluations with respect to the initial DASH were observed only in the cSSNB, with a difference in the first month of 21.80 points (p = 0.001) and 21.35 points (p = 0.003) in the third month. In addition, differences between groups were found, in favor of the cSSNB, of 19.20 points (p = 0.017) in the first month and 12.55 points (p = 0.012) in the third month. Conclusions: The combined use of corticosteroids in SSNB appears to be associated with better short-to medium-term outcomes in terms of pain and function, compared to the use of SSNB without corticosteroids in chronic rotator cuff pathologies.

MicroRNAs (miRNA) regulate key aspects of development and physiology in animals and plants. These regulatory RNAs act as guides of effector complexes to recognize specific mRNA sequences based on sequence complementarity, resulting in translational repression or site-specific cleavage 1 , 2 . In plants, most miRNA targets are cleaved and show almost perfect complementarity with the miRNAs around the cleavage site 3 , 4 , 5 , 6 , 7 , 8 . Here, we examined the non–protein coding gene IPS1 ( INDUCED BY PHOSPHATE STARVATION1 ) from Arabidopsis thaliana . IPS1 contains a motif with sequence complementarity to the phosphate (P i ) starvation–induced miRNA miR-399, but the pairing is interrupted by a mismatched loop at the expected miRNA cleavage site. We show that IPS1 RNA is not cleaved but instead sequesters miR-399. Thus, IPS1 overexpression results in increased accumulation of the miR-399 target PHO2 mRNA and, concomitantly, in reduced shoot P i content 5 , 6 , 7 , 8 . Engineering of IPS1 to be cleavable abolishes its inhibitory activity on miR-399. We coin the term 'target mimicry' to define this mechanism of inhibition of miRNA activity. Target mimicry can be generalized beyond the control of P i homeostasis, as demonstrated using artificial target mimics.

Phosphate transporters (PTs) mediate phosphorus uptake and are regulated at the transcriptional and posttranslational levels. In one key mechanism of posttranslational regulation, phosphorylation of PTs affects their trafficking from the endoplasmic reticulum (ER) to the plasma membrane. However, the kinase(s) mediating PT phosphorylation and the mechanism leading to ER retention of phosphorylated PTs remain unclear. In this study, we identified a rice (Oryza sativa) kinase subunit, CK2β3, which interacts with PT2 and PT8 in a yeast two-hybrid screen. Also, the CK2α3/β3 holoenzyme phosphorylates PT8 under phosphate-sufficient conditions. This phosphorylation inhibited the interaction of PT8 with PHOSPHATE TRANSPORTER TRAFFIC FACILITATOR1, a key cofactor regulating the exit of PTs from the ER to the plasma membrane. Additionally, phosphorus starvation promoted CK2β3 degradation, relieving the negative regulation of PT phosphorus-insufficient conditions. In accordance, transgenic expression of a nonphosphorylatable version of OsPT8 resulted in elevated levels of that protein at the plasma membrane and enhanced phosphorus accumulation and plant growth under various phosphorus regimes. Taken together, these results indicate that CK2α3/β3 negatively regulates PTs and phosphorus status regulates CK2α3/β3.