Autophagy: a key player in the recovery of plants from heat stress.

Plants can be primed to withstand otherwise lethal heat stress (HS) through exposure to a preceding temporary and mild HS, commonly known as the 'thermopriming stimulus'. Plants have also evolved mechanisms to establish 'memories' of a previous stress encounter, or to reset their physiology to the original cellular state once the stress has ended. The priming stimulus triggers a widespread change of transcripts, proteins, and metabolites, which is crucial for maintaining the memory state but may not be required for growth and development under optimal conditions or may even be harmful. In such a scenario, recycling mechanisms such as autophagy are crucial for re-establishing cellular homeostasis and optimizing resource use for post-stress growth. While pivotal for eliminating heat-induced protein aggregates and protecting plants from the harmful impact of HS, recent evidence implies that autophagy also breaks down heat-induced protective macromolecules, including heat shock proteins, functioning as a resetting mechanism during the recovery from mild HS. This review provides an overview of the latest advances in understanding the multifaceted functions of autophagy in HS responses, with a specific emphasis on its roles in recovery from mild HS, and the modulation of HS memory.

Associations between infant amygdala functional connectivity and social engagement following a stressor: A preliminary investigation.

Functional architecture of the infant brain, especially functional connectivity (FC) within the amygdala network and between the amygdala and other networks (i.e., default-mode [DMN] and salience [SAL] networks), provides a neural basis for infant socioemotional functioning. Yet, little is known about the extent to which early within- and between-network amygdala FC are related to infant stress recovery across the first year of life. In this study, we examined associations between amygdala FC (i.e., within-network amygdala connectivity, and between-network amygdala connectivity with the DMN and SAL) at 3 months and infant recovery from a mild social stressor at 3, 6 and 9 months. At 3 months, thirty-five infants (13 girls) underwent resting-state functional magnetic resonance imaging during natural sleep. Infants and their mothers completed the still-face paradigm at 3, 6, and 9 months, and infant stress recovery was assessed at each time point as the proportion of infant social engagement during the reunion episode. Bivariate correlations indicated that greater positive within-network amygdala FC and greater positive amygdala-SAL FC, but not amygdala-DMN FC, at 3 months predicted lower levels of stress recovery at 3 and 6 months, but were nonsignificant at 9 months. These findings provide preliminary evidence that early functional synchronization within the amygdala network, as well as segregation between the amygdala and the SAL, may contribute to infant stress recovery in the context of infant-mother interaction.

The role of therapist support on the efficacy of an internet-delivered stress recovery intervention for healthcare workers: a randomized control trial.

Internet-delivered CBT interventions effectively improve different aspects of mental health, although the therapist's role remains unclear. The aim of this trial was to evaluate the efficacy of a therapist-supported 6-week internet-delivered intervention in improving stress recovery among healthcare workers compared to a group with optional therapist support. A total of 196 participants were recruited and randomly allocated to regular therapists' support or optional therapists' support groups. The primary outcome measure was the Recovery Experiences Questionnaire (REQ), developed to assess four components of stress recovery: psychological detachment, relaxation, mastery, and control. Secondary outcomes measured perceived stress (PSS-10), anxiety (GAD-7), depression (PHQ-9), and psychological well-being (WHO-5). All four stress recovery skills improved significantly after participating in the intervention at a 3-month follow-up, with small to medium effects (0.27-0.65) in both groups. At follow-up, we also found a significant reduction in perceived stress, depression, and anxiety in both groups, as well as an improvement in psychological well-being. The results indicate that ICBT can be effective in improving stress recovery skills among healthcare workers with optional support from the therapist, provided at the participants' request. This RCT suggests that optional therapist support could meet participants' needs and reduce resources needed in routine care.

Exploring the association between self-reported and objective measures in search of the restorative quality of natural environments: a systematic review.

The benefits of nature contact for psychophysiological restoration have sparked a surge of scientific attention in recent years. The diverse psychophysiological mechanisms of stress recovery make assessment with a single marker impractical. The majority of restoration research employs a holistic approach, including subjective psychological and objective physiological measures concurrently. However, this association has not been decisively supported by empirical studies. The purpose of this systematic review is to determine the degree to which subjectively experienced restoration, as measured by self-reported scales, is associated with actual physiological changes. Searches for peer-reviewed primary research articles were conducted in SCOPUS and PubMed, returning 216 papers; the final synthesis includes 21 empirical studies published between 2008 and 2022. Findings show that there is a strong association between subjective and objective measures of restoration. Further analysis verified that using concurrently self-reported and objective measures in measuring restoration, notably the associations of Profile of Mood States (POMS), Perceived Restorativeness Scale (PRS), and Positive and Negative Affect Scale (PANAS) with Blood Pressure (BP) and Heart Rate (HR), resulted in the highest degree of consistency. However, there were negligible inconsistent associations, which were mainly reported by Restoration Outcome Scale (ROS) in psychological indicators and Salivary Cortisol (SC) and Electroencephalography (EEG) in physiological indicators. This suggests that the results of research that uses these measures simultaneously should be interpreted with caution.

Histone H3K4 methyltransferases SDG25 and ATX1 maintain heat-stress gene expression during recovery in Arabidopsis.

Plants have short-term stress memory that enables them to maintain the expression state of a substantial subset of heat-inducible genes during stress recovery after heat stress. Little is known about the molecular mechanisms controlling stress-responsive gene expression at the recovery stage in plants, however. In this article, we demonstrate that histone H3K4 methyltransferases SDG25 and ATX1 are required for heat-stress tolerance in Arabidopsis. SDG25 and ATX1 are not only important for stress-responsive gene expression during heat stress, but also for maintaining stress-responsive gene expression during stress recovery. A combination of whole-genome bisulfite sequencing, RNA-sequencing and ChIP-qPCR demonstrated that mutations of SDG25 and ATX1 decrease histone H3K4me3 levels, increase DNA cytosine methylation and inhibit the expression of a subset of heat stress-responsive genes during stress recovery in Arabidopsis. ChIP-qPCR results confirm that ATX1 binds to chromatins associated with these target genes. Our results reveal that histone H3K4me3 affects DNA methylation at regions in the loci associated with heat stress-responsive gene expression during stress recovery, providing insights into heat-stress transcriptional memory in plants.

Impaired Restoration of Global Protein Synthesis Contributes to Increased Vulnerability to Acute ER Stress Recovery in Huntington's Disease.

Neurons are susceptible to different cellular stresses and this vulnerability has been implicated in the pathogenesis of Huntington's disease (HD). Accumulating evidence suggest that acute or chronic stress, depending on its duration and severity, can cause irreversible cellular damages to HD neurons, which contributes to neurodegeneration. In contrast, how normal and HD neurons respond during the resolution of a cellular stress remain less explored. In this study, we challenged normal and HD cells with a low-level acute ER stress and examined the molecular and cellular responses after stress removal. Using both striatal cell lines and primary neurons, we first showed the temporal activation of p-eIF2α-ATF4-GADD34 pathway in response to the acute ER stress and during recovery between normal and HD cells. HD cells were more vulnerable to cell death during stress recovery and were associated with increased number of apoptotic/necrotic cells and decreased cell proliferation. This is also supported by the Gene Ontology analysis from the RNA-seq data which indicated that "apoptosis-related Biological Processes" were more enriched in HD cells during stress recovery. We further showed that HD cells were defective in restoring global protein synthesis during stress recovery and promoting protein synthesis by an integrated stress response inhibitor, ISRIB, could attenuate cell death in HD cells. Together, these data suggest that normal and HD cells undergo distinct mechanisms of transcriptional reprogramming, leading to different cell fate decisions during the stress recovery.

CCR2 monocytes repair cerebrovascular damage caused by chronic social defeat stress.

Immune surveillance of the brain plays an important role in health and disease. Peripheral leukocytes patrol blood-brain barrier interfaces, and after injury, monocytes cross the cerebrovasculature and follow a pattern of pro- and anti-inflammatory activity leading to tissue repair. We have shown that chronic social defeat (CSD) causes scattered vasculature disruptions. Here, we assessed CCR2+ monocyte trafficking to the vascular injury sites in Ccr2wt/rfp reporter mice both during CSD and one week following CSD cessation. We found that CSD for 14 days induced microhemorrhages where plasma fibrinogen leaked into perivascular spaces, but it did not affect the distribution or density of CCR2rfp+ monocytes in the brain. However, after recovery from CSD, many vascularly adhered CCR2+ cells were detected, and gene expression of the CCR2 chemokine receptor ligands CCL7 and CCL12, but not CCL2, was elevated in endothelial cells. Adhered CCR2+ cells were mostly the non-classical, anti-inflammatory Ly6Clo type, and they phagocytosed fibrinogen in perivascular spaces. In CCR2-deficient Ccr2rfp/rfp mice, fibrinogen levels remained elevated in recovery. Fibrinogen infused intracerebroventricularly induced CCR2+ cells to adhere to the vasculature and phagocytose perivascular fibrinogen in Ccr2wt/rfp but not Ccr2rfp/rfp mice. Depletion of monocytes with clodronate liposomes during CSD recovery prevented fibrinogen clearance and blocked behavioral recovery. We hypothesize that peripheral CCR2+ monocytes are not elevated in the brain on day 14 at the end of CSD and do not contribute to its behavioral effects at that time, but in recovery following cessation of stress, they enter the brain and exert restorative functions mediating vascular repair and normalization of behavior.

Healthy versus unhealthy comfort eating for psychophysiological stress recovery in low-income Black and Latinx adults.

Low-income Black and Latinx individuals are disproportionately vulnerable to chronic stress and metabolic disease. Evidence suggests that these populations engage in elevated levels of comfort eating (i.e., eating comforting food to alleviate stress), which can harm diet quality. For this reason, many interventions discourage comfort eating. However, if comfort eating does indeed buffer stress, it may be a protective health behavior, particularly if healthy foods (e.g., strawberries) buffer stress as effectively as traditional unhealthy comfort foods (e.g., brownies). By choosing healthy foods, people may be able to simultaneously improve their nutrition and reduce their stress levels, both of which have the potential to reduce health disparities among chronically stressed populations. The present study tested the efficacy of healthy and unhealthy comfort eating for improving psychophysiological stress recovery. A sample of low-income Black and Latinx individuals (N = 129) were randomly assigned to consume a healthy food (e.g., grapes), unhealthy comfort food (e.g., chips), or no food after exposure to a laboratory stressor. Throughout, we measured participants' psychophysiological stress responses, including self-reported stress, rumination, autonomic nervous system activation (i.e., electrodermal activity (EDA), heart rate variability (HRV)) and neuroendocrine responses (i.e., salivary cortisol). We compared participants' stress recovery trajectories by condition and found no significant group differences (p = 0.12 for self-reported stress; p = 0.92 for EDA; p = 0.22 for HRV, p = 1.00 for cortisol). Participants in all conditions showed decreases in self-reported stress and in cortisol post-stressor (ps < 0.01), but rates of decline did not differ by condition (i.e., healthy or unhealthy comfort food, brief no-food waiting period). Although null, these results are important because they challenge the widely-held assumption that comfort foods help people decrease stress.

High-pressure processing-induced transcriptome response during recovery of Listeria monocytogenes.

BACKGROUND: High-pressure processing (HPP) is a commonly used technique in the food industry to inactivate pathogens, including L. monocytogenes. It has been shown that L. monocytogenes is able to recover from HPP injuries and can start to grow again during long-term cold storage. To date, the gene expression profiling of L. monocytogenes during HPP damage recovery at cooling temperature has not been studied. In order identify key genes that play a role in recovery of the damage caused by HPP treatment, we performed RNA-sequencing (RNA-seq) for two L. monocytogenes strains (barotolerant RO15 and barosensitive ScottA) at nine selected time points (up to 48 h) after treatment with two pressure levels (200 and 400 MPa). RESULTS: The results showed that a general stress response was activated by SigB after HPP treatment. In addition, the phosphotransferase system (PTS; mostly fructose-, mannose-, galactitol-, cellobiose-, and ascorbate-specific PTS systems), protein folding, and cobalamin biosynthesis were the most upregulated genes during HPP damage recovery. We observed that cell-division-related genes (divIC, dicIVA, ftsE, and ftsX) were downregulated. By contrast, peptidoglycan-synthesis genes (murG, murC, and pbp2A) were upregulated. This indicates that cell-wall repair occurs as a part of HPP damage recovery. We also observed that prophage genes, including anti-CRISPR genes, were induced by HPP. Interestingly, a large amount of RNA-seq data (up to 85%) was mapped to Rli47, which is a non-coding RNA that is upregulated after HPP. Thus, we predicted that Rli47 plays a role in HPP damage recovery in L. monocytogenes. Moreover, gene-deletion experiments showed that amongst peptidoglycan biosynthesis genes, pbp2A mutants are more sensitive to HPP. CONCLUSIONS: We identified several genes and mechanisms that may play a role in recovery from HPP damage of L. monocytogenes. Our study contributes to new information on pathogen inactivation by HPP.

Plant heat stress: Concepts directing future research.

Predicted increases in future global temperatures require us to better understand the dimensions of heat stress experienced by plants. Here we highlight four key areas for improving our approach towards understanding plant heat stress responses. First, although the term 'heat stress' is broadly used, that term encompasses heat shock, heat wave and warming experiments, which vary in the duration and magnitude of temperature increase imposed. A greater integration of results and tools across these approaches is needed to better understand how heat stress associated with global warming will affect plants. Secondly, there is a growing need to associate plant responses to tissue temperatures. We review how plant energy budgets determine tissue temperature and discuss the implications of using leaf versus air temperature for heat stress studies. Third, we need to better understand how heat stress affects reproduction, particularly understudied stages such as floral meristem initiation and development. Fourth, we emphasise the need to integrate heat stress recovery into breeding programs to complement recent progress in improving plant heat stress tolerance. Taken together, we provide insights into key research gaps in plant heat stress and provide suggestions on addressing these gaps to enhance heat stress resilience in plants.

Autophagy complements metalloprotease FtsH6 in degrading plastid heat shock protein HSP21 during heat stress recovery.

Moderate and temporary heat stresses (HS) prime plants to tolerate, and survive, a subsequent severe HS. Such acquired thermotolerance can be maintained for several days under normal growth conditions, and create a HS memory. We recently demonstrated that plastid-localized small heat shock protein HSP21 is a key component of HS memory in Arabidopsis thaliana. A sustained high abundance of HSP21 during the HS recovery phase extends HS memory. The level of HSP21 is negatively controlled by plastid-localized metalloprotease FtsH6 during HS recovery. Here, we demonstrate that autophagy, a cellular recycling mechanism, exerts additional control over HSP21 degradation. Genetic and chemical disruption of both, metalloprotease activity and autophagy trigger superior HSP21 accumulation, thereby improving memory. Furthermore, we provide evidence that autophagy cargo receptor ATG8-INTERACTING PROTEIN1 (ATI1) is associated with HS memory. ATI1 bodies colocalize with both autophagosomes and HSP21, and their abundance and transport to the vacuole increase during HS recovery. Together, our results provide new insights into the control module for the regulation of HS memory, in which two distinct protein degradation pathways act in concert to degrade HSP21, thereby enabling cells to recover from the HS effect at the cost of reducing the HS memory.

Brief Resilience Scale (BRS) Portuguese Version: validity and metrics for the older adult population.

OBJECTIVE: This study aims to analyze the psychometric properties of the new Brazilian-Portuguese version of the Brief Resilience Scale (B-BRS) in older adults. METHOD: A sample of 1251 participants (54.20% women; M = 68.02 years, SD = 6.52) completed the B-BRS and seven scales on successful aging and mental health. Confirmatory factor analysis was used to study the B-BRS dimensionality. Convergent and divergent validity was analyzed by means of examining the relationships of B-BRS with scales on successful aging and mental health. RESULTS: The results supported the unidimensionality of the B-BRS after controlling for wording method, as well as satisfactory reliability (ω = .79). B-BRS structure remained invariant across education level and income groups. B-BRS scores positively correlated with successful aging factors and negatively with psychopathology symptoms. CONCLUSION: To conclude, our findings provide some evidence on the reliability and validity of the B-BRS, as well as its validation for use in the senior population.

Recent increases in drought frequency cause observed multi-year drought legacies in the tree rings of semi-arid forests.

Recent analyses on the length of drought recovery in forests have shown multi-year legacies, particularly in semi-arid, coniferous ecosystems. Such legacies are usually attributed to ecophysiological memory, although drought frequency itself, and its effect on overlapping recovery times, could also contribute. Here, we describe a multi-decadal study of drought legacies using tree-ring carbon-isotope ratios (δ13C) and ring-width index (RWI) in Pinus ponderosa at 13 montane sites traversing a winter-summer precipitation gradient in the Southwestern U.S. Sites and trees were selected to avoid collection biases that exist in archived tree-ring databanks. The spatial hydroclimate gradient and winter-summer seasonal patterns were well predicted by seasonal and inter-annual correlations between δ13C and atmospheric vapor pressure deficit (VPD). Using VPD, we found that the probability of extreme drought has increased up to 70% in this region during the past two decades. When the recent increase in drought frequency was not considered, multi-year legacies in both δ13C and RWI were observed at most sites. When the increase in drought frequency was detrended from tree-ring chronologies, some sites exhibited short legacies (1-2 years) in both δ13C and RWI, and there was a sight trend for longer legacies in RWI. However, when considered broadly across the region and multiple decades, no significant legacies were observed, which contrasts with past studies. Our results reveal that a contribution to observed multi-year legacies is related to shifts in the climate system itself, an exogenous factor, that must be considered along with physiological memory.

Estimation of Stresses in Concrete by Using Coda Wave Interferometry to Establish an Acoustoelastic Modulus Database.

This article presents an experimental study of estimating stresses in concrete by applications of coda wave interferometry to establish an acoustoelastic modulus database. Under well-controlled laboratory conditions, uniaxial load cycles were performed on three groups of 15 × 15 × 35-cm concrete prisms, with ultrasonic signals being collected continuously. Then, the coda wave interferometry technique, together with acoustoelastic and Kaiser theories, are utilized to analyze the stress-velocity relations for the distinct ranges before and after historical maximum loads, forming an acoustoelastic modulus database. When applied to different concrete samples, their stresses are estimated with a high degree of accuracy. This study could be used to promote the development of novel nondestructive techniques that aid in structural stress monitoring.

Urocortin 3 signalling in the auditory brainstem aids recovery of hearing after reversible noise-induced threshold shift.

KEY POINTS: Ongoing, moderate noise exposure does not instantly damage the auditory system but may cause lasting deficits, such as elevated thresholds and accelerated ageing of the auditory system. The neuromodulatory peptide urocortin-3 (UCN3) is involved in the body's recovery from a stress response, and is also expressed in the cochlea and the auditory brainstem. Lack of UCN3 facilitates age-induced hearing loss and causes permanently elevated auditory thresholds following a single 2 h noise exposure at moderate intensities. Outer hair cell function in mice lacking UCN3 is unaffected, so that the observed auditory deficits are most likely due to inner hair cell function or central mechanisms. Highly specific, rather than ubiquitous, expression of UCN3 in the brain renders it a promising candidate for designing drugs to ameliorate stress-related auditory deficits, including recovery from acoustic trauma. ABSTRACT: Environmental acoustic noise is omnipresent in our modern society, with sound levels that are considered non-damaging still causing long-lasting or permanent changes in the auditory system. The small neuromodulatory peptide urocortin-3 (UCN3) is the endogenous ligand for corticotropin-releasing factor receptor type 2 and together they are known to play an important role in stress recovery. UCN3 expression has been observed in the auditory brainstem, but its role remains unclear. Here we describe the detailed distribution of UCN3 expression in the murine auditory brainstem and provide evidence that UCN3 is expressed in the synaptic region of inner hair cells in the cochlea. We also show that mice with deficient UCN3 signalling experience premature ageing of the auditory system starting at an age of 4.7 months with significantly elevated thresholds of auditory brainstem responses (ABRs) compared to age-matched wild-type mice. Following a single, 2 h exposure to moderate (84 or 94 dB SPL) noise, UCN3-deficient mice exhibited significantly larger shifts in ABR thresholds combined with maladaptive recovery. In wild-type mice, the same noise exposure did not cause lasting changes to auditory thresholds. The presence of UCN3-expressing neurons throughout the auditory brainstem and the predisposition to hearing loss caused by preventing its normal expression suggests UCN3 as an important neuromodulatory peptide in the auditory system's response to loud sounds.

Co-activation of SAM and HPA responses to acute stress: A review of the literature and test of differential associations with preadolescents' internalizing and externalizing.

Understanding co-activation patterns of the hypothalamic-pituitary-adrenal axis (HPA) and sympathetic adrenal medullary (SAM) during early adolescence may illuminate risk for development of internalizing and externalizing problems. The present study advances empirical work on the topic by examining SAM-HPA co-activation during both the reactivity and recovery phases of the stress response following acute stress exposure. Fourth and fifth grade boys and girls (N = 149) provided cortisol and alpha-amylase via saliva at seven times throughout a 95-min assessment in which they were administered the modified Trier Social Stress Test. Parents reported on adolescents' life stress, pubertal development, medication use, and externalizing problems. Adolescents reported their own internalizing symptoms. Multiple linear regressions tested both direct and interactive effects of SAM and HPA reactivity and recovery on internalizing and externalizing problems. Results from these analyses showed that whereas SAM and HPA reactivity interacted to predict internalizing symptoms, it was their interaction during the recovery phase that predicted externalizing. Concurrent high SAM and HPA reactivity scores predicted high levels of internalizing and concurrently low SAM and HPA recovery scores predicted high levels of externalizing. Implications of the findings for further study and clinical application are discussed.

Prophylactic Ketamine Treatment Promotes Resilience to Chronic Stress and Accelerates Recovery: Correlation with Changes in Synaptic Plasticity in the CA3 Subregion of the Hippocampus.

Ketamine is an N-methyl-d-aspartate receptor antagonist that has gained wide attention as a potent antidepressant. It has also been recently reported to have prophylactic effects in animal models of depression and anxiety. Alterations of neuroplasticity in different brain regions; such as the hippocampus; prefrontal cortex; and amygdala; are a hallmark of stress-related disorders; and such changes may endure beyond the treatment of symptoms. The present study investigated whether a prophylactic injection of ketamine has effects on structural plasticity in the brain in mice that are subjected to chronic unpredictable stress followed by an 8-day recovery period. Ketamine administration (3 mg/kg body weight) 1 h before stress exposure increased the number of resilient animals immediately after the cessation of stress exposure and positively influenced the recovery of susceptible animals to hedonic deficits. At the end of the recovery period; ketamine-treated animals exhibited significant differences in dendritic spine density and dendritic spine morphology in brain regions associated with depression compared with saline-treated animals. These results confirm previous findings of the prophylactic effects of ketamine and provide further evidence of an association between the antidepressant-like effect of ketamine and alterations of structural plasticity in the brain.

Decentering mediates the relationship between vmPFC activation during a stressor and positive emotion during stress recovery.

The stress response has profound implications on health and behavior and stress is considered a risk factor for the development of psychopathologies including depression. The neural mechanisms supporting successful stress recovery are not fully understood; however, a novel study by Yang et al. (Yang X, Garcia KM, Jung Y, Whitlow CT, McRae K, Waugh CE. Soc Cogn Affect Neurosci 13: 256-268, 2018) demonstrates that ventromedial prefrontal cortex (vmPFC) activation during a stressor is related to improved stress recovery, and that decentering is able to mediate this relationship, suggesting a role during stress recovery. It was also revealed that vmPFC activation at different time points during the stressor predicts altering aspects of stress recovery, an observation that was only possible due to the adoption of change-point analysis.

Changes in photosynthetic rate and stress volatile emissions through desiccation-rehydration cycles in desiccation-tolerant epiphytic filmy ferns (Hymenophyllaceae).

Exposure to recurrent desiccation cycles carries a risk of accumulation of reactive oxygen species that can impair leaf physiological activity upon rehydration, but changes in filmy fern stress status through desiccation and rewatering cycles have been poorly studied. We studied foliage photosynthetic rate and volatile marker compounds characterizing cell wall modifications (methanol) and stress development (lipoxygenase [LOX] pathway volatiles and methanol) through desiccation-rewatering cycles in lower-canopy species Hymenoglossum cruentum and Hymenophyllum caudiculatum, lower- to upper-canopy species Hymenophyllum plicatum and upper-canopy species Hymenophyllum dentatum sampled from a common environment and hypothesized that lower canopy species respond more strongly to desiccation and rewatering. In all species, rates of photosynthesis and LOX volatile emission decreased with progression of desiccation, but LOX emission decreased with a slower rate than photosynthesis. Rewatering first led to an emission burst of LOX volatiles followed by methanol, indicating that the oxidative burst was elicited in the symplast and further propagated to cell walls. Changes in LOX emissions were more pronounced in the upper-canopy species that had a greater photosynthetic activity and likely a greater rate of production of photooxidants. We conclude that rewatering induces the most severe stress in filmy ferns, especially in the upper canopy species.

Physical Polyurethane Hydrogels via Charge Shielding through Acids or Salts.

Physical hydrogels with tunable stress-relaxation and excellent stress recovery are formed from anionic polyurethanes via addition of acids, monovalent salts, or divalent salts. Gel properties can be widely adjusted through pH, salt valence, salt concentration, and monomer composition. We propose and investigate a novel gelation mechanism based on a colloidal system interacting through charge repulsion and chrage shielding, allowing a broad use of the material, from acidic (pH 4-5.5) to pH-neutral hydrogels with Young's moduli ranging from 10 to 140 kPa.