Adaptation of indoor ornamental plants to various lighting levels in growth chambers simulating workplace environments.

Despite the growing interest in indoor greenery and its positive effects on occupants' well-being, there is limited knowledge on the optimal light levels for indoor plants that ensure energy efficiency and sustainable growth. This study explored the survival of ornamental plants under low-light conditions typical of indoor workplaces without daylight and investigated the impact of increased light intensity or extended day length on their growth. Three species of foliage plants (Epipremnum aureum, Pachira aquatica, and Rhaphidophora tetrasperma) were cultivated in growth chambers with three different lighting schemes. The results showed that plants sustained growth with 6.8 µmol m-2 s-1 white LED light for 9 h/day, suggesting that extra lighting might not be necessary for shade-tolerant species in offices. In this environment, plants maintained efficient photosynthesis under low illumination by increasing their specific leaf area. Elevating the light to 20.1 µmol m-2 s-1 and extending the day length to 18 h/day enhanced the plants' relative growth rate. Climbing plants allocated more biomass to stems, resulting in a lower leaf weight ratio and noticeably altering their appearance. This study demonstrates that customized lighting strategies effectively support indoor greening goals, like adjusting intensity for energy savings or adding light for greening large spaces.

Mandating indoor air quality for public buildings.

If some countries lead by example, standards may increasingly become normalized.

Coronavirus Disease 2019 and Airborne Transmission: Science Rejected, Lives Lost. Can Society Do Better?

This is an account that should be heard of an important struggle: the struggle of a large group of experts who came together at the beginning of the COVID-19 pandemic to warn the world about the risk of airborne transmission and the consequences of ignoring it. We alerted the World Health Organization about the potential significance of the airborne transmission of SARS-CoV-2 and the urgent need to control it, but our concerns were dismissed. Here we describe how this happened and the consequences. We hope that by reporting this story we can raise awareness of the importance of interdisciplinary collaboration and the need to be open to new evidence, and to prevent it from happening again. Acknowledgement of an issue, and the emergence of new evidence related to it, is the first necessary step towards finding effective mitigation solutions.

How can airborne transmission of COVID-19 indoors be minimised?

During the rapid rise in COVID-19 illnesses and deaths globally, and notwithstanding recommended precautions, questions are voiced about routes of transmission for this pandemic disease. Inhaling small airborne droplets is probable as a third route of infection, in addition to more widely recognized transmission via larger respiratory droplets and direct contact with infected people or contaminated surfaces. While uncertainties remain regarding the relative contributions of the different transmission pathways, we argue that existing evidence is sufficiently strong to warrant engineering controls targeting airborne transmission as part of an overall strategy to limit infection risk indoors. Appropriate building engineering controls include sufficient and effective ventilation, possibly enhanced by particle filtration and air disinfection, avoiding air recirculation and avoiding overcrowding. Often, such measures can be easily implemented and without much cost, but if only they are recognised as significant in contributing to infection control goals. We believe that the use of engineering controls in public buildings, including hospitals, shops, offices, schools, kindergartens, libraries, restaurants, cruise ships, elevators, conference rooms or public transport, in parallel with effective application of other controls (including isolation and quarantine, social distancing and hand hygiene), would be an additional important measure globally to reduce the likelihood of transmission and thereby protect healthcare workers, patients and the general public.

Emerging developments in the standardized chemical characterization of indoor air quality.

Despite the fact that the special characteristics of indoor air pollution make closed environments quite different from outdoor environments, the conceptual ideas for assessing air quality indoors and outdoors are similar. Therefore, the elaboration of International Standards for air quality characterization in view of controlling indoor air quality should resort to this common basis. In this short review we describe the possibilities of standardization of tools dedicated to indoor air quality characterization with a focus on the tools permitting to study the indoor air chemistry. The link between indoor exposure and health as well as the critical processes driving the indoor air quality are introduced. Available International Standards for the assessment of indoor air quality are depicted. The standards comprise requirements for the sampling on site, the analytical procedures, and the determination of material emissions. To date, these standardized procedures assure that indoor air, settled dust and material samples are analyzed in a comparable manner. However, existing International Standards exclusively specify conventional, event-driven target-screening using discontinuous measurement methods for long-lived pollutants. Therefore, this review draws a parallel between physico-chemical processes in indoor and outdoor environments. The achievements in atmospheric sciences also improve our understanding of indoor environments. The community of atmospheric scientists can be both ideal and supporter for researchers in the area of indoor air quality characterization. This short review concludes with propositions for future standardization activities for the chemical characterization of indoor air quality. Future standardization efforts should focus on: (i) the elaboration of standardized measurement methods and measurement strategies for online monitoring of long-lived and short-lived pollutants, (ii) the assessment of the potential and the limitations of non-target screening, (iii) the paradigm shift from event-driven investigations to systematic approaches to characterize indoor environments, and (iv) the development of tools for policy implementation.

Aldosterone affects blood flow and vascular tone regulated by endothelium-derived NO: therapeutic implications.

Aldosterone, in doses inappropriate to the salt status, plays an important role in the development of cardiovascular injury, including endothelial dysfunction, independent of its hypertensive effects. Acute non-genomic effects of aldosterone acting on mineralocorticoid receptors are inconsistent in healthy humans: vasoconstriction or forearm blood flow decrease via endothelial dysfunction, vasodilatation mediated by increased NO actions, or no effects. However, in studies with experimental animals, aldosterone mostly enhances vasodilatation mediated by endothelium-derived NO. Chronic exposure to aldosterone, which induces genomic responses, results in impairments of endothelial function through decreased NO synthesis and action in healthy individuals, experimental animals and isolated endothelial cells. Chronic aldosterone reduces NO release from isolated human endothelial cells only when extracellular sodium is raised. Oxidative stress is involved in the impairment of endothelial function by promoting NO degradation. Aldosterone liberates endothelin-1 (ET-1) from endothelial cells, which elicits ET(A) receptor-mediated vasoconstriction by inhibiting endothelial NO synthesis and action and through its own direct vasoconstrictor action. Ca(2+) flux through T-type Ca(2+) channels activates aldosterone synthesis and thus enhances unwanted effects of aldosterone on the endothelium. Mineralocorticoid receptor inhibitors, ET(A) receptor antagonists and T-type Ca(2) + channel blockers appear to diminish the pathophysiological participation of aldosterone in cardiovascular disease and exert beneficial actions on bioavailability of endothelium-derived NO, particularly in resistant hypertension and aldosteronism.

Characterization of volatile sulfur compound production by Solobacterium moorei.

OBJECTIVE: Solobacterium moorei is a Gram positive bacterium that has been specifically associated with halitosis. The aim of this study was to characterize volatile sulfur compound (VSC) production by S. moorei. METHODS: S. moorei was either grown or incubated in the presence of various supplements prior to determining VSC production with a Halimeter sulfide monitor. The effect of exogenous proteases or glycosidase inhibitors on VSC production by S. moorei was examined. RESULTS: We first showed that S. moorei can convert cysteine into hydrogen sulfide. The capacity of S. moorei to produce VSCs from serum, saliva, and mucin was dependent on the presence of an exogenous source of proteases such as pancreatic trypsin or Porphyromonas gingivalis gingipains. VSC production from mucin was inhibited by the presence of a ß-galactosidase inhibitor, thus suggesting that deglycosylation of mucin by S. moorei is critical for VSC production. CONCLUSION: Our study suggests that S. moorei can be a major source of malodorous compounds in halitosis by producing VSCs through a process involving the ß-galactosidase activity of the bacterium and an exogenous source of proteases.

Anthocyanin-rich black currant extract and cyanidin-3-O-glucoside have cytoprotective and anti-inflammatory properties.

Periodontal diseases are a group of multifactorial polymicrobial infections characterized by a progressive inflammatory destruction of the periodontium. Flavonoids, including anthocyanins, are receiving increasing attention because of their promising human health benefits. The aim of our study was to investigate the effect of anthocyanins, pure or as part of a standardized black currant extract, on nicotine-induced cytotoxicity and lipopolysaccharide (LPS)-induced inflammatory responses in human cells. Using a colorimetric assay that measures cell viability, it was found that a pretreatment with an anthocyanin-rich black currant extract or cyanidin-3-O-glucoside neutralized the cytotoxic effect of nicotine on epithelial cells and fibroblasts in a dose-dependent manner. The black currant extract and cyanidin-3-O-glucoside also inhibited the LPS-induced secretion of interleukin-6 by human macrophages. The results of the present study suggest that black currant extract and cyanidin-3-O-glucoside may be promising candidates for the development of novel therapies to prevent and/or to treat smoking-related periodontal diseases.

Reduction of bacterial volatile sulfur compound production by licoricidin and licorisoflavan A from licorice.

Halitosis affects a large proportion of the population and is, in most cases, caused by the production of volatile sulfur compounds (VSCs), particularly methyl mercaptan and hydrogen sulfide, by specific bacterial species colonizing the oral cavity. In this study, a supercritical extract of Chinese licorice (Glycyrrhiza uralensis), and its major isoflavans, licoricidin and licorisoflavan A, were investigated for their effect on growth, VSC production and protease activity of Porphyromonas gingivalis, Prevotella intermedia and Solobacterium moorei, which have been associated with halitosis. The effects of licorice extract, licoricidin, and licorisoflavan A on VSC production in a saliva model were also tested. We first showed that licoricidin and licorisoflavan A, and to a lesser extent the licorice extract, were effective in inhibiting the growth of all three bacterial species, with minimal inhibitory concentrations in the range of 2-80 µg ml(-1). The licorice extract and the two isolates licoricidin and licorisoflavan A, were able to dose-dependently reduce VSC production by P. gingivalis, Prev. intermedia, and S. moorei as well as by a human saliva model. Although the extract and isolates did not inhibit the proteolytic activity of bacteria, they blocked the conversion of cysteine into hydrogen sulfide by Prev. intermedia. Lastly, the deodorizing effects of the licorice extract, licoricidin, and licorisoflavan A were demonstrated, as they can neutralize P. gingivalis-derived VSCs. Licorisoflavan A (10 µg ml(-1)) was found to be the most effective by reducing VSC levels by 50%. Within the limitations of this study, it can be concluded that a licorice supercritical extract and its major isoflavans (licoricidin and licorisoflavan A) represent natural ingredients with a potential for reducing bacterial VSC production and therefore for controlling halitosis.

Cranberry proanthocyanidins inhibit the adherence properties of Candida albicans and cytokine secretion by oral epithelial cells.

BACKGROUND: Oral candidiasis is a common fungal disease mainly caused by Candida albicans. The aim of this study was to investigate the effects of A-type cranberry proanthocyanidins (AC-PACs) on pathogenic properties of C. albicans as well as on the inflammatory response of oral epithelial cells induced by this oral pathogen. METHODS: Microplate dilution assays were performed to determine the effect of AC-PACs on C. albicans growth as well as biofilm formation stained with crystal violet. Adhesion of FITC-labeled C. albicans to oral epithelial cells and to acrylic resin disks was monitored by fluorometry. The effects of AC-PACs on C. albicans-induced cytokine secretion, nuclear factor-kappa B (NF-κB) p65 activation and kinase phosphorylation in oral epithelial cells were determined by immunological assays. RESULTS: Although AC-PACs did not affect growth of C. albicans, it prevented biofilm formation and reduced adherence of C. albicans to oral epithelial cells and saliva-coated acrylic resin discs. In addition, AC-PACs significantly decreased the secretion of IL-8 and IL-6 by oral epithelial cells stimulated with C. albicans. This anti-inflammatory effect was associated with reduced activation of NF-κB p65 and phosphorylation of specific signal intracellular kinases. CONCLUSION: AC-PACs by affecting the adherence properties of C. albicans and attenuating the inflammatory response induced by this pathogen represent potential novel therapeutic agents for the prevention/treatment of oral candidiasis.

Transferrin as a source of iron for Campylobacter rectus.

BACKGROUND AND OBJECTIVE: Campylobacter rectus is considered as one of the bacterial species of etiological importance in periodontitis. Iron-containing proteins such as transferrin are found in periodontal sites and may serve as a source of iron for periodontopathogens. The aim of this study was to investigate the capacity of C. rectus to assimilate transferrin-bound iron to support its growth. DESIGN: Growth studies were performed in broth media pretreated with an iron-chelating resin and supplemented with various iron sources. The uptake of iron by C. rectus was monitored using (55)Fe-transferrin. Transferrin-binding activity was assessed using a microplate assay while the degradation of transferrin and iron removal was evaluated by polyacrylamide gel electrophoresis. A colorimetric assay was used to determine ferric reductase activity. RESULTS: Holotransferrin (iron-saturated form) but not apotransferrin (iron-free form) was found to support growth of C. rectus in an iron-restricted culture medium. Incubation of holotransferrin with cells of C. rectus resulted in removal of iron from the protein. A time dependent intracellular uptake of iron by C. rectus cells from (55)Fe-transferrin was demonstrated. This uptake was significantly increased when bacteria were grown under an iron-limiting condition. Cells of C. rectus did not show transferrin-binding activity or proteolytic activity toward transferrin. However, a surface-associated ferric reductase activity was demonstrated. CONCLUSION: To survive and multiply in periodontal sites, periodontopathogens must possess efficient iron-scavenging mechanisms. In this study, we showed the capacity of C. rectus to assimilate iron from transferrin to support its growth. The uptake of iron appears to be dependent on a ferric reductive pathway.

A-type cranberry proanthocyanidins inhibit the RANKL-dependent differentiation and function of human osteoclasts.

This study investigated the effect of A-type cranberry proanthocyanidins (AC-PACs) on osteoclast formation and bone resorption activity. The differentiation of human pre-osteoclastic cells was assessed by tartrate-resistant acid phosphatase (TRAP) staining, while the secretion of interleukin-8 (IL-8) and matrix metalloproteinases (MMPs) was measured by ELISA. Bone resorption activity was investigated by using a human bone plate coupled with an immunoassay that detected the release of collagen helical peptides. AC-PACs up to 100 µg/mL were atoxic for osteoclastic cells. TRAP staining evidenced a dose-dependent inhibition of osteoclastogenesis. More specifically, AC-PACs at 50 µg/mL caused a 95% inhibition of RANKL-dependent osteoclast differentiation. This concentration of AC-PACs also significantly increased the secretion of IL-8 (6-fold) and inhibited the secretion of both MMP-2 and MMP-9. Lastly, AC-PACs (10, 25, 50 and 100 µg/ml) affected bone degradation mediated by mature osteoclasts by significantly decreasing the release of collagen helical peptides. This study suggests that AC-PACs can interfere with osteoclastic cell maturation and physiology as well as prevent bone resorption. These compounds may be considered as therapeutic agents for the prevention and treatment of periodontitis.

Nitric oxide-mediated coronary flow regulation in patients with coronary artery disease: recent advances.

Nitric oxide (NO) formed via endothelial NO synthase (eNOS) plays crucial roles in the regulation of coronary blood flow through vasodilatation and decreased vascular resistance, and in inhibition of platelet aggregation and adhesion, leading to the prevention of coronary circulatory failure, thrombosis, and atherosclerosis. Endothelial function is impaired by several pathogenic factors including smoking, chronic alcohol intake, hypercholesterolemia, obesity, hyperglycemia, and hypertension. The mechanisms underlying endothelial dysfunction include reduced NO synthase (NOS) expression and activity, decreased NO bioavailability, and increased production of oxygen radicals and endogenous NOS inhibitors. Atrial fibrillation appears to be a risk factor for endothelial dysfunction. Endothelial dysfunction is an important predictor of coronary artery disease (CAD) in humans. Penile erectile dysfunction, associated with impaired bioavailability of NO produced by eNOS and neuronal NOS, is also considered to be highly predictive of ischemic heart disease. There is evidence suggesting an important role of nitrergic innervation in coronary blood flow regulation. Prophylactic and therapeutic measures to eliminate pathogenic factors inducing endothelial and nitrergic nerve dysfunction would be quite important in preventing the genesis and development of CAD.

Modulation of matrix metalloproteinase and cytokine production by licorice isolates licoricidin and licorisoflavan A: potential therapeutic approach for periodontitis.

BACKGROUND: Inflammatory cytokines and matrix metalloproteinases (MMPs) produced by resident and inflammatory cells in response to periodontopathogens play a major role in the tissue destruction observed in periodontitis, which is a disease that affects tooth-supporting structures. In the present study, we investigate the effects of licorice-derived licoricidin (LC) and licorisoflavan A (LIA) on the secretion of various cytokines and MMPs by human monocyte-derived macrophages stimulated with Aggregatibacter actinomycetemcomitans (previously Actinobacillus actinomycetemcomitans) lipopolysaccharide (LPS). METHODS: Macrophages were treated with non-toxic concentrations of LC or LIA before being stimulated with A. actinomycetemcomitans LPS. The secretion of cytokines and MMPs and the activation of nuclear factor-kappa B (NF-κB) p65 and activator protein (AP)-1 were assessed by enzyme-linked immunosorbent assays. RESULTS: LC and LIA inhibited the secretion of interleukin (IL)-6 and chemokine (C-C motif) ligand 5 in a concentration-dependent manner but did not affect the secretion of IL-8 by LPS-stimulated macrophages. LC and LIA also inhibited the secretion of MMP-7, -8, and -9 by macrophages. The suppression of cytokine and MMP secretion by LC and LIA was associated with the reduced activation of NF-κB p65 but not that of AP-1. CONCLUSION: The present study suggests that LC and LIA have potential for the development of novel host-modulating strategies for the treatment of cytokine and/or MMP-mediated disorders such as periodontitis.

Antibacterial and anti-inflammatory activities of 4-hydroxycordoin: potential therapeutic benefits.

4-Hydroxycordoin (1), a natural isopentenyloxychalcone, is a plant secondary metabolite that is relatively rare. Since there are very few reports about the biological activities of 1, its potential benefits for periodontal disease were investigated. A marked and dose-dependent antibacterial activity of 1 was observed against the three major periodontal pathogens, Porphyromonas gingivalis, Fusobacterium nucleatum, and Prevotella intermedia. Moreover, compound 1 showed an antiadhesion effect, since it inhibited attachment of P. gingivalis to oral epithelial cells. Finally, using a macrophage model, the ability of 1 to inhibit the secretion of inflammatory mediators induced by Aggregatibacter actinomycetemcomitans lipopolysaccharide was demonstrated. The anti-inflammatory effect observed was associated with reduced activation of the nuclear factor-κB (NF-κB) p65 and activator protein-1 (AP-1) pathways.

Pleiotropic effects of polysaccharide capsule loss on selected biological properties of Streptococcus suis.

In this study, an unencapsulated Streptococcus suis mutant was used to investigate the pleiotropic effects resulting from capsule loss. The capsule deficient mutant of S. suis acquired a biofilm-positive phenotype, which was associated with significantly increased cell surface hydrophobicity. Cell-associated fibrinogen-binding and chymotrypsin-like activities were decreased in the unencapsulated mutant. The mutant did not differ significantly from the encapsulated parent strain for minimal inhibitory concentrations to penicillin G, ampicillin, and tetracycline. However, while the encapsulated strain was highly resistant to the bactericidal action of penicillin G and ampicillin, the unencapsulated mutant was approximately 60-fold more sensitive. Compared with the parent strain, the unencapsulated mutant induced a much higher inflammatory response in monocyte-derived macrophages resulting in an increased secretion of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6, and IL-8. The capsule appears to hinder important adhesins or hydrophobic molecules that mediate biofilm formation, as well as cell wall components capable of stimulating immune cells.

Porphyromonas gingivalis gingipains trigger a proinflammatory response in human monocyte-derived macrophages through the p38α mitogen-activated protein kinase signal transduction pathway.

Porphyromonas gingivalis, the major etiologic agent of chronic periodontitis, produces a broad spectrum of virulence factors, including Arg- and Lys-gingipain cysteine proteinases. In this study, we investigated the capacity of P. gingivalis gingipains to trigger a proinflammatory response in human monocyte-derived macrophages. Both Arg- and Lys-gingipain preparations induced the secretion of TNF-α and IL-8 by macrophages. Stimulation of macrophages with Arg-gingipain A/B preparation at the highest concentration was associated with lower amounts of cytokines detected, a phenomenon likely related to proteolytic degradation. The inflammatory response induced by gingipains was not dependent of their catalytic activity since heat-inactivated preparations were still effective. Stimulating macrophages with gingipain preparations was associated with increased levels of phosphorylated p38α MAPK suggesting its involvement in cell activation. In conclusion, our study brought clear evidence that P. gingivalis Arg- and Lys-gingipains may contribute to the host inflammatory response, a critical factor in periodontitis-associated tissue destruction.

Left ventricular free wall rupture associated with a combination of acute myocardial infarction and stress-provoked cardiomyopathy: An autopsy case.

A 74-year-old female was admitted to our hospital due to prolonged chest pain that had lasted about 2 h. An electrocardiogram revealed ST-elevation in leads I, aVL, and V3-6, with an increase in myocardial necrosis markers. Emergency coronary angiography was performed, and left ventriculography showed the typical features of apical ballooning, and so a diagnosis of Takotsubo cardiomyopathy (TC) was made. On the 10th day after admission, the patient suddenly went into cardiopulmonary arrest because of a blow-out type left ventricular (LV) free wall rupture. Despite extensive cardiopulmonary resuscitation, the patient died. The autopsy revealed hemopericardium and a perforating wound located in the anterior wall of the LV. It was revealed that the diagonal branch of the coronary artery was occluded, and so a diagnosis of TC coexisting with acute myocardial infarction (AMI) was made. No previous case of TC accompanied by AMI has been reported. We present its clinical course during hospitalization and the result of a histopathologic examination.