Injectable biomimetic hydrogels have great potential for use in regenerative medicine as cellular delivery vectors. However, they can suffer from issues relating to hypoxia, including poor cell survival, differentiation, and functional integration owing to the lack of an established vascular network. Here we engineer a hybrid myoglobin:peptide hydrogel that can concomitantly deliver stem cells and oxygen to the brain to support engraftment until vascularisation can occur naturally. We show that this hybrid hydrogel can modulate cell fate specification within progenitor cell grafts, resulting in a significant increase in neuronal differentiation. We find that the addition of myoglobin to the hydrogel results in more extensive innervation within the host tissue from the grafted cells, which is essential for neuronal replacement strategies to ensure functional synaptic connectivity. This approach could result in greater functional integration of stem cell-derived grafts for the treatment of neural injuries and diseases affecting the central and peripheral nervous systems.

Wound infection by multidrug-resistant bacteria seriously threatens human life. Chronic wounds, with necrosis, persistent inflammation, and covered by hypoxic tissue, seriously hinder anti-infection treatments. Herein, we have developed a multifunctional hydrogel dressing with antibacterial activity in the hypoxia environment to promote wound healing. The hydrogel comprises Cypate-conjugated antimicrobial peptides (AMP-Cypates), liposome-encapsulated perfluorodecalin, and recombinant type III collagen. AMP-Cypates exhibited outstanding antibacterial activity, jointly achieved through antimicrobial peptide (AMP) activity, photothermal therapy (PTT), and photodynamic therapy (PDT). The perfluorodecalin liposomes act as the oxygen carrier to mitigate wound hypoxia condition and enhance the efficacy of PDT. The recombinant type III collagen in the hydrogel further promoted the healing of the wounds together with the eradication of bacterial infection. Taken together, the hydrogel dressing provides a platform for integrating multiple antimicrobial mechanisms for the rapid removal of bacterial infection and the healing of chronic wounds.

This research aimed to evaluate the physicochemical and biocidal properties of chitosan films obtained through the solvent casting method using two different molecular weights, and thermally treated for an extended time (3 weeks) at 70 °C under vacuum condition (RH 0 %). The effect of storage time (for 30 and 180 days) under ambient conditions (23 °C and RH 40 %) on the properties of heat-treated cast films and their biocidal effectiveness was also assessed. FTIR-ATR, TGA and XRD of resulting films were analyzed to explore the dependency of antibacterial performance on the alteration in molecular and chemical structure. The results demonstrated that the solubility of treated films at 70 °C was proportionally reduced, resulting from the reduction of protonated amines and an increase in crystallinity. Likewise, increasing storage time led to a significant lowering in the solubilization of cast films. It was found that the solubilized fraction of chitosan cast films is the active fraction with the biocide behavior that can act against bacteria. In addition, the effectiveness of migrated chitosan was examined against the natural flora of pasteurized milk, such as Paenibacillus and Pseudomonas fluorescens. The results showed that cast films obtained from chitosan with lower molecular weight caused a reduction in the total count of viable cells without a significant effect on the properties of milk.

Craniofacial dysmorphism, skeletal anomalies, and impaired intellectual development syndrome-1 (CFSMR1; OMIM#213980) is a rare autosomal recessive disorder characterized by the clinical triad of developmental delay and/or intellectual disability, a typical facial gestalt with brachycephaly, highly-arched bushy eyebrows, synophrys, hypertelorism, wide nasal bridge, and short nose, as well as multiple vertebrae and rib malformations, such as bifid and fused ribs and abnormal vertebral segmentation and fusion. Biallelic loss-of-function variants in TMCO1 cause CFSMR1. We report on two unrelated Egyptian patients with a phenotype suggestive of CFSMR. Single whole-exome sequencing in patient 1 and Sanger sequencing of TMCO1 in patient 2 revealed the same homozygous TMCO1 nonsense variant c.187C > T/p.(Arg63*) in both affected individuals; patients' healthy parents were heterozygous carriers of the variant. Congenital hearing loss in patients 1 and 2 is an occasional finding in individuals affected by CFSMR. Camptodactyly and syndactyly, which were noted in patient 2, have not or rarely been reported in CFSMR. Review of the literature revealed a total of 30 individuals with the clinically recognizable and unique phenotype of CFSMR1, including the patients reported here, who all carried biallelic TMCO1 variants. Six different TMCO1 variants have been reported in the 30 patients from 14 families, comprising three nonsense, two 2-bp deletions, and a splice donor site variant. All disease-associated TMCO1 variants likely represent null alleles resulting in absence of the encoded protein. TMCO1 has been proposed to act as a Ca2+ channel, while other data revealed TMCO1 as a mitochondrial protein and a component of the translocon at the endoplasmic reticulum, a cellular machinery important for the biogenesis of multi-pass membrane proteins. RAB5IF/C20orf24 has recently been identified as causative gene for craniofacial dysmorphism, skeletal anomalies, and impaired intellectual development syndrome-2 (CFSMR2; OMIM#616994). Heterodimerization of RAB5IF/C20orf24 and TMCO1 and their interdependence may suggest a pathophysiological role of ER-mitochondria interaction underlying CFSMR.

Chromium (Cr), a hazardous heavy metal, is toxic to human health and the environment. Severe detrimental effects of Cr on different physiological systems involve oxidative stress. In the current study, sodium dichromate di-hydrate was subcutaneously injected to male Wistar rats at a dose of 5 mg/kg b.w. and experimented up to 14 days to induce alterations in hepatic and renal tissues. Another group of rats was pre-treated with melatonin at three different doses (5, 10, and 20 mg/kg b.w.; orally) and 20 mg/kg b.w. dose was evidenced to provide maximal protection against Cr-induced alterations. The study demonstrated that melatonin efficiently preserved body weight, organ weight, intracellular antioxidant enzymes, and tissue morphology. Furthermore, melatonin was also found to protect organ damage markers, oxidative stress-biomarkers, activities of pro-oxidant enzymes, levels of reactive oxygen species (ROS), nitric oxide (NO), and collagen content through its antioxidative mechanisms. Moreover, melatonin effectively decreased tissue Cr content through its metal-chelating activity. Hence, the present study has established melatonin as a promising antioxidant for conserving the liver and kidney tissues from Cr-induced oxidative damage thereby strengthening the notion that this small indoleamine can act as a future therapeutic against Cr-induced oxidative stress-mediated tissue damage.

Currently, no effective disc reconstruction treatment strategy is clinically available for temporomandibular joint (TMJ) disc-related diseases. To address this, we developed a prosthesis construct with laser-drilled decellularized natural disc reinforced by polycaprolactone, which mimics the natural morphology, and structural, biomechanical and biological property of the TMJ disc. The construct demonstrated good biocompatibility, safety and immunological tolerance both in vitro, and in a rat subcutaneous model. During 6 months implantation in an allogeneic rabbit TMJ disc reconstruction model, the disc prosthesis maintained its integrity, collagen fiber-orientation, mechanical property, joint structural stability and prevented articular cartilage and bone from damage. Furthermore, the "upgraded" disc prosthesis obtained from decellularized porcine disc was implanted into a goat TMJ disc reconstruction model. The xenograft prosthesis, with strength and viscoelasticity similar to a natural TMJ disc, was able to restore the structure and function of TMJ up to 20 weeks. These results demonstrate the translational feasibility of an allogeneic or xenogeneic decellularized disc prosthesis for treatment of advanced TMJ disc-related diseases. STATEMENT OF SIGNIFICANCE: This study makes a significant contribution to TMJ disc disease treatment both in theory and in clinics, because: (1) it provided an innovative approach to prepare an artificial TMJ disc with decent mechanical properties and long-term condyle-protecting effect; (2) it specified an advanced decellularized method for fibrocartilage decellularization and xenograft application; (3) it developed a facile and reproducible TMJ disc reconstruction model not only for middle size animal but also for large animal study; (4) the comprehensive and unreported biomechanical tests on the natural TMJ discs would act as a valuable reference for further research in the field of artificial TMJ disc materials or TMJ disc tissue engineering; (5) it suggested a potential treatment for patients with severe TMJ diseases that were commonly met but difficult to treat in clinics.

Hard dental tissue pathologies, such as caries, are conventionally managed through replacement by tooth-colored inert biomaterials. Tissue engineering provides novel treatment approaches to regenerate lost dental tissues based on bioactive materials and/or signalling molecules. While regeneration in the form of reparative dentin (osteo-dentin) is feasible, the recapitulation of the tubular microstructure of ortho-dentin and its special features is sidelined. This study characterized in vitro, and in vivo human EDTA-treated, freeze-dried dentin matrices (HTFD scaffolds) conditioned with calcium phosphate nanoparticles (NPs) bearing plasmids encoding dentinogenesis-inducing factors (pBMP2/NPs or pDMP1/NPs). The uptake and transfection efficiency of the synthesized NPs on dental pulp stem cells (DPSCs) increased in a concentration- and time-dependent manner, as evaluated qualitatively by confocal laser microscopy and transmission electron microscopy, and quantitatively by flow cytometry, while, in parallel, cell viability decreased. HTFD scaffolds conditioned with the optimal transfectability-to-viability concentration at 4 μg Ca/mL of each of the pBMP2/NPs or pDMP1/NPs preserved high levels of cell viability, evidenced by live/dead staining in vitro and caused no adverse reactions after implantation on C57BL6 mice in vivo. HTFD/NPs constructs induced rapid and pronounced odontogenic shift of the DPSCs, as evidenced by relevant gene expression patterns of RunX2, ALP, BGLAP, BMP-2, DMP-1, DSPP by real-time PCR, and acquirement of polarized meta-mitotic phenotype with cellular protrusions entering the dentinal tubules as visualized by scanning electron microscopy. Taken together, HTFD/NPs constitute a promising tool for customized reconstruction of the ortho-dentin/odontoblastic layer barrier and preservation of pulp vitality. STATEMENT OF SIGNIFICANCE: In clinical dentistry, the most common therapeutic approach for the reconstruction of hard dental tissue defects is the replacement by resin-based restorative materials. Even modern bioactive materials focus on reparative dentinogenesis, leading to amorphous dentin-bridge formation in proximity to the pulp. Therefore, the natural microarchitecture of tubular ortho-dentin is not recapitulated, and the sensory and defensive role of odontoblasts is sidelined. This study approaches the reconstruction at the dentin-pulp interface using a construct of human treated dentin (HTFD) scaffold and plasmid-carrying nanoparticles (NPs) encoding dentinogenic factors (DMP-1 or BMP-2) with excellent in vitro and in vivo properties. As a future perspective, the HTFD/NPs constructs could act as bio-fillings for personalized reconstruction of the dentin-pulp interface.

Urban environment (e.g. greenspaces, air pollution and traffic noise) and individuals' behaviours (e.g. physical activity) have all been associated with mental wellbeing. The large majority of studies on the influence of nature exposure on mental wellbeing assumed that multiple pathways act independently, ignoring the interactions among potential correlated pathways that engage simultaneously. The parallel mediation approach fails to explore the complex associations of combined exposure to air pollution, traffic noise and nature exposure with physical activity, which in turn affect mental wellbeing. Hence, the interest of understanding the sophisticated interactions among different pathways is warranted. We utilized structural equation modelling to simultaneously evaluate whether actual and perceived traffic-related pollution and physical activity mediate the associations between mental wellbeing and nature exposure, which was assessed by Normalized Difference Vegetation Index (NDVI), green view index (GVI), green space density and park accessibility. In summer 2022, we conducted questionnaires from 1772 adults residing in 117 neighbourhoods in Shenzhen, China. Nature exposure was positively and directly associated with mental wellbeing in the single mediator model that considered physical activity only. The indirect effects of nature exposure on mental wellbeing were observed through all pathways in all models, except through the perceived acoustic quality pathway in the serial mediation model. In addition, the percentage mediated by perceived air quality was higher than that of perceived acoustic quality. The influence of nature exposure on mental wellbeing was only for a small proportion mediated by the physical activity pathway. The associations between nature exposure and mental wellbeing were modified by individual characteristics, such as gender, age, income level and alcohol usage, but not employment status and smoking behaviour. These findings point out the importance of both objective and subjective environmental features and human behaviours on mental wellbeing, as well as the necessity of considering multiple pathways simultaneously.

Marine plastic contamination is currently considered ubiquitous in aquatic environments. These particles present a resistant and hydrophobic substrate known to promote microbial colonisation and biofilm formation in aquatic ecosystems, the so-called "Plastisphere", raising concerns about its potential ecological risks. The novelty of this topic translates into a relatively low number of studies, including for transitional coastal ecosystems, such as sandy beaches or estuarine habitats. Therefore, a sampling campaign was conducted in two transitional coastal ecosystems - the Mondego estuary (Portugal) - and adjacent sandy beaches (winter 2020). After visual sorting and filtering of suspected particles under sterile conditions DNA extraction and 16S rRNA amplicon high throughput sequencing was used to profile the bacterial communities on the surface of plastic particles and from those found on the water and sediments from the sampled transitional coastal ecosystems. All particles were characterised according to type, colour and size, and the chemical nature of the particles was determined by FTIR-ATR or μ-FTIR spectroscopy after DNA extraction. All samples contained plastics in several sizes (micro and mesoplastics), shapes (higher abundances of fragments on beaches and fibres in the estuarine waters), colours and polymers. Although no significant differences were detected in the α-diversity indexes of the bacterial communities between plastics and their surrounding environments, data showed the occurrence of unique key bacterial groups on plastics from both environments, such as pathogens (e.g., Lactococcus, Staphylococcus and Streptococcus) and groups commonly associated with wastewater treatment plants (e.g., members of the phylum Firmicutes). This highlights the concerns for plastics to act as vectors of transmission and spread of these bacterial groups in transitional coastal ecosystems. Furthermore, it raises the possibility that (micro)plastics entering the estuary from the sea play a substantial contribution to overall dynamics of microplastics and their microbial assemblages in the estuarine system.

Periodontal regenerative techniques are performed to accomplish the restitution of soft and hard teeth-supporting tissues that have been lost due to trauma or inflammatory disease. Periodontal membranes are used for these techniques to provide support and a framework for cell growth and tissue regeneration. They act as a temporary and selective barrier to cell proliferation. Easy clinical handling, biomechanical specifications, high biocompatibility, cell-occlusivity, and satisfactory bioresorption rate are essential properties a membrane needs to be effective. The creation and maintenance of a secluded space is also a fundamental rule in periodontal regenerative techniques. The use of barrier membranes in the field of restorative dentistry has progressed toward the use of minimally invasive approaches optimizing wound closure and limiting patient morbidity. This review intends to provide an overview of the major cellular events in the surgical wound and membrane surface. It was also performed to assess, from literature data, the pertinence of using non-resorbable and resorbable membranes for this regenerative purpose. Special attention will be given to collagen membranes.

The AgingPLUS program targets motivational barriers, including negative views of aging, as mechanisms to increase adult physical activity. A pilot study was conducted to test the efficacy of this new program against a generic successful aging program. Fifty-six participants were randomly assigned to the AgingPLUS group, and 60 participants were assigned to the active control group. Repeated-measures multivariate analyses of variance assessed changes in views of aging, physical activity, blood pressure, and hand-grip strength from pretest (Week 0) to delayed posttest (Week 8). The Condition × Occasion interactions were nonsignificant; however, significant main effects for condition and occasion were found. Follow-up tests showed that views of aging were more positive, and physical activity had significantly increased at Week 8 for all participants. In addition, in the treatment group, elevated blood pressure had significantly decreased and hand-grip strength had significantly increased at Week 8. Despite the nonsignificant multivariate findings, the main effect findings provided partial support for the efficacy of the AgingPLUS program.

Organisms adapt to seasonal changes in photoperiod and temperature to survive; however, the mechanisms by which these signals are integrated in the brain to alter seasonal biology are poorly understood. We previously reported that EYES ABSENT (EYA) shows higher levels in cold temperature or short photoperiod and promotes winter physiology in Drosophila. Nevertheless, how EYA senses seasonal cues is unclear. Pigment-dispersing factor (PDF) is a neuropeptide important for regulating circadian output rhythms. Interestingly, PDF has also been shown to regulate seasonality, suggesting that it may mediate the function of the circadian clock in modulating seasonal physiology. In this study, we investigated the role of EYA in mediating the function of PDF on seasonal biology. We observed that PDF abundance is lower on cold and short days as compared with warm and long days, contrary to what was previously observed for EYA. We observed that manipulating PDF signaling in eya+ fly brain neurons, where EYA and PDF receptor are co-expressed, modulates seasonal adaptations in daily activity rhythm and ovary development via EYA-dependent and EYA-independent mechanisms. At the molecular level, altering PDF signaling impacted EYA protein abundance. Specifically, we showed that protein kinase A (PKA), an effector of PDF signaling, phosphorylates EYA promoting its degradation, thus explaining the opposite responses of PDF and EYA abundance to changes in seasonal cues. In summary, our results support a model in which PDF signaling negatively modulates EYA levels to regulate seasonal physiology, linking the circadian clock to the modulation of seasonal adaptations.

The appearance in 2008 in western Cambodia of Plasmodium falciparum tolerant to artemisinin, defined by longer parasite clearance time following drug administration and in vitro by a slightly higher survival rate of the ring stage after a 3-h treatment with 700 nM artemisinin (or analogues, collectively termed ART), has raised concerns of the possible loss of this frontline antimalarial [used in the form of an artemisinin combination therapy (ACT)], with its low IC50 value against the ring stage and pleiotropic pro-drug/poison property. The key genetic marker of ART tolerance phenotype is a number of non-synonymous mutations in Pfkelch13 propeller domain. This results in defective assembly at the ring stage of a cytostome structure located at cytoplasmic side of the parasite membrane required for invagination of a double-membrane endosome carrying host cytosol haemoglobin to the digestive vacuole. The consequential deprivation of amino acids initiates ring stage parasites bearing the causal mutations in PfK13 (or other key cytostome components) entry into a dormant state ("Sleeping Beauty"), which, after a duration longer than that the short-lived ART, "Sleeping Beauty" ring parasite resumes its normal, but accelerated, development to maintain the 48-h intra-erythrocytic life-cycle. We posit that when ART-tolerant P. falciparum has acquired under ART stress the causative PfK13 mutation (not obligatory if mutations occur in other critical cytostome components), together with other necessary mutations to adjust to the new normalcy and to provide survival competitiveness, ART-tolerant parasite has now evolved into a genetically programmed "Sleeping Beauty". The onus of preventing the spread of ART-tolerant P. falciparum lies with the efficacy of ACT partner drug, hence the recommendation of a triple ACT (TACT). Nevertheless, attention should also be focussed on understanding the mechanisms of dormancy, such as induction, maintenance and recovery, to enable discovery and development of novel antimalarials targeting this unique parasite stage.

Breast cancer is the frequently diagnosed cancer and the leading cancer death among women. The growing tumour of the breast is composed of both normoxic and hypoxic cells, and the heterogeneity of tumour affects the targeted treatment strategies against breast cancer. The functional and therapeutic status of the Warburg effect is mostly recognized, and the genes involved in glycolysis have become a target for anticancer therapeutic strategies. Glut-1 is essential for basal glucose uptake among the glucose transporters and could act as a potential target for anticancer therapy. In the present study, we explored the alteration in the metabolic phenotype of SKBR-3 cells, representing HER-2 overexpressed breast cancer cell line, with Glut-1 inhibition by a synthetic small molecule inhibitor WZB117 in the presence or absence of cobalt chloride (CoCl2) induced biochemical hypoxia in vitro. We found that WZB117 and CoCl2 in combination could inhibit metabolic phenotype characteristics such as glucose uptake, cell migration, lactate and ATP production in SKBR-3 cells. Also, Glut-1 inhibition induced apoptosis and cell cycle arrest at the G0-G1 phase even under CoCl2-induced mimic hypoxia. Our findings suggest that Glut-1 inhibition by WZB117 could overcome the protective effect of CoCl2 mimic hypoxia by regulating glycolysis and altering the metabolic phenotype of breast cancer cells. The considering excellent efficacy and minimal toxicity suggest that WZB117 may be a promising anticancer drug to the current therapies.

Metastable ferrihydrite is omnipresent in environments and can influence the fate of Pb(II) during ferrihydrite transformation. Ferrihydrite is rarely pure and often coexists with impurities, which may influence the mineralogical changes of ferrihydrite and Pb(II) behavior. In this work, we investigated the effect of malic acid or phosphate on Pb(II)-ferrihydrite coprecipitates (Fh-Pb) transformation and the subsequent fate of Pb(II) during the 10-day aging of Fh-Pb. Results showed that both malic acid and phosphate retarded Fh-Pb transformation and prevented the release of Pb(II) from Fh-Pb back into solutions. Pb(II) was beneficial to goethite formation by inhibiting hematite formation while both malic acid and phosphate inhibited goethite formation since they could act as templates of nucleation. Besides, malic acid and phosphate improved the proportion of non-extracted Pb(II) during Fh-Pb transformation, indicating that Pb(II) was incorporated into secondary minerals. Pb(II) could not replace Fe(III) within the crystal lattice due to its large radius but was occluded into pores and defect structures within the secondary mineral lattices. This work can advance our understanding of the influences of malic acid and phosphate on Pb(II) immobility during Fh-Pb aging.

Oxygen is critical for the high output of energy (adenosine triphosphate) generated by oxidative phosphorylation in the mitochondria, and when oxygen delivery is impaired due to systemic hypoxia, impaired or reduced delivery of red blood cells, or from local ischemia, survival processes are activated.

Exosomes have previously been isolated from Chinese hamster ovary (CHO) cells and their anti-apoptotic properties reported. However, to further facilitate the study of CHO cell derived exosomes and allow their comparison across studies, it is necessary to characterise and define such exosomes using at least three criteria that can act as a reference for the generation of CHO cell produced exosomes. Here we report on the isolation of exosomes from CHO cells, an industrially relevant and widely used cell host for biopharmaceutical protein production, during the exponential and stationary phase of growth during batch culture using a Total Exosome Isolation (TEI) method. The resulting vesicles were characterized and visualized using a diverse range of techniques including Dynamic Light Scattering (DLS), Zeta potential, Electron Microscopy and immunoblotting, and their protein and RNA content determined. We also generated the lipid fingerprint of isolated exosomes using MALDI-ToF mass spectroscopy. We confirmed the presence of nano sized extracellular vesicles from CHO cells and their subsequent characterization revealed details of their size, homogeneity, surface charge, protein and RNA content. The lipid content of exosomes was also found to differ between exosomes isolated on different days of batch culture. This analysis provides a profile and characterisation of CHO cell exosomes to aid future studies on exosomes from CHO cells and improving the manufacturing of exosomes for biotherapeutic application.

Synthetic cannabinoid receptor agonists (SCRAs) are one of the fastest growing classes of recreational drugs. Despite their growth in use, their vast chemical diversity and rapidly changing landscape of structures makes understanding their effects challenging. In particular, the side effects for SCRA use are extremely diverse, but notably include severe outcomes such as cardiac arrest. These side effects appear at odds with the main putative mode of action, as full agonists of cannabinoid receptors. We have hypothesised that SCRAs may act as MAO inhibitors, owing to their structural similarity to known monoamine oxidase inhibitors (MAOI's) as well as matching clinical outcomes (hypertensive crisis) of 'monoaminergic toxicity' for users of MAOIs and some SCRA use. We have studied the potential for SCRA mediated inhibition of MAO-A and MAO-B via a range of SCRAs used commonly in the UK, as well as structural analogues to prove the atomistic determinants of inhibition. By combining in silico and experimental kinetic studies we demonstrate that SCRAs are MAO-A specific inhibitors and their affinity can vary significantly between SCRAs, most notably affected by the nature of the SCRA 'head' group. Our data allow us to posit a putative mechanism of inhibition. Crucially our data demonstrate that SCRA activity is not limited to just cannabinoid receptor agonism and that alternative interactions might account for some of the diversity of the observed side effects and that these effects can be SCRA-specific.

The soil contributes to the main pool of essential mineral nutrients for plants. These mineral nutrients are critical elements for the building blocks of plant biomolecules, play fundamental roles in cell processes, and act in various enzymatic reactions. The roots are the main entry point for mineral nutrients used within the plant to grow, develop, and produce seeds In this regard, a suite of plant nutrient transport systems, sensors, and signaling proteins function in acquiring mineral nutrients through the roots. Mineral nutrients from chemical fertilizers, composed mainly of nitrogen, phosphorous, and potassium (NPK), are added to agricultural land to maximize crop yields, worldwide. However, improving nutrient uptake and use within crops is critical for economically and environmentally sustainable agriculture. Therefore, we review the molecular basis for N, P, and K nutrient uptake into the roots. Remarkably, plants are responsive to heterogeneous nutrient distribution and align root growth and nutrient uptake with nutrient-rich patches. We highlight the relationship between nutrient distribution in the growth environment and root system architecture. We discuss the exchange of information between the root and shoot systems through the xylem and phloem, which coordinates nutrient uptake with photosynthesis. The size and structure of the root system, along with the abundance and activity of nutrient transporters, largely determine the nutrient acquisition rate. Lastly, we discuss connections between N, P, and K uptake and signaling.

Understanding the mechanisms by which the geomorphic structures affect habitat invasibility by mediating various abiotic and biotic factors is essential for predicting whether these geomorphic structures may provide spatial windows of opportunity to facilitate range-expansion of invasive species in salt marshes. Many studies have linked geomorphic landscape features such as tidal channels to invasion by exotic plants, but the role of tidal channel meanders (i.e., convex and concave sides) in regulating the Spartina alterniflora invasion remains unclear. Here, we examined the combined effects of tidal channel meander-mediated hydrodynamic variables, soil abiotic stresses and propagule pressure on the colonization of Spartina in the Yellow River Delta, China, by conducting field observations and experiments. The results showed that lower hydrodynamic disturbance, bed shear stress, and higher propagule pressure triggered by eddies due to the convex structure of channel meanders facilitated Spartina seedling establishment and growth, whereas the concave side considerably inhibited the Spartina invasion. Lower soil abiotic stresses also significantly promoted the invasibility of the channel meanders by Spartina. Based on these findings, we propose a conceptual framework to illustrate the effects of the meandering geomorphology of tidal channels on the mechanisms that might allow the landward spread of Spartina and related processes. Our results demonstrate that the meandering geomorphic structures of tidal channels could act as stepping-stones to significantly facilitate the landward invasion of Spartina along tidal channels. This implies that geomorphic characteristics of tidal channels should be integrated into invasive species control and salt marsh management strategies.

Psoriasis is a chronic immune-mediated condition that affects the skin and joints, with current treatments still unable to offer a cure and long-term use of treatments posing health risks. Understanding the pathogenesis of the disease has helped identify new targets that have allowed for the expansion of the therapeutic arsenal. Extracellular vesicles (EVs) have recently emerged as pathophysiological mediators of psoriasis, and there have been increasing reports of EVs as potential biomarkers and therapeutics. Given their innate role as natural vehicles for cell-to-cell communication, EVs have vast potential in their ability to determine disease status based on EV-specific cargo as well as act as therapeutics because of their anti-inflammatory properties and potential for enhancement. In this review we summarize the role of EVs in the pathogenesis of psoriasis and discuss EVs as both diagnostic and therapeutic agents.

This 5-year study evaluated a virtual visitation implementation initiative in a neonatal intensive care unit. Our objectives were to (1) use the Plan-Do-Study-Act methodological framework to implement a virtual visitation program, (2) investigate whether implementation of virtual visitation could be done with no patient harm and minimal workflow disruption, (3) foster a top-down participatory structure for decision making, and (4) evaluate parent use and satisfaction. The study involved a qualitative and quantitative description of cycles and results. Routine collection of outcome data allowed problems that arose as a result of changing practices to be quickly and efficiently addressed. The study results suggested that the virtual visitation implementation initiative in a neonatal intensive care unit using Plan-Do-Study-Act cycles helped create an environment of trust and provided benefits. A steady increase in the use of virtual visitation by parents and their extended families indicated utilization. During the COVID-19 pandemic, virtual visitation helped families feel connected with each other and their neonate, despite being in separate locations.