Microplastics are present throughout the marine environment and ingestion of these plastic particles (<1 mm) has been demonstrated in a laboratory setting for a wide array of marine organisms. Here, we investigate the presence of microplastics in two species of commercially grown bivalves: and . Microplastics were recovered from the soft tissues of both species. At time of human consumption, contains on average 0.36 ± 0.07 particles g (wet weight), while a plastic load of 0.47 ± 0.16 particles g ww was detected in . As a result, the annual dietary exposure for European shellfish consumers can amount to 11,000 microplastics per year. The presence of marine microplastics in seafood could pose a threat to food safety, however, due to the complexity of estimating microplastic toxicity, estimations of the potential risks for human health posed by microplastics in food stuffs is not (yet) possible. Microplastics were detected in two commercially grown bivalve species ( and ), enabling us to estimate a preliminary human dietary exposure.
(AC), a highly valued polypore mushroom native only to Taiwan, has been traditionally used as a medicine for the treatment of food and drug intoxication, diarrhea, abdominal pain, hypertension, skin itching, and cancer. In this study, both of solid-state-cultured AC (S-AC) and wood-cultured AC (W-AC) were evaluated the anti-inflammatory effects on hyperoxia-induced lung injury in NF-κB-luciferase transgenic mice. The homozygous transgenic mice (NF-κB-luciferase ) were randomly assigned to four groups for treatment ( = 6) including Normoxia/DMSO group, Hyperoxia/DMSO group, Hyperoxia/S-AC group, and Hyperoxia/W-AC group. After 72 h of hyperoxia, we examined the bioluminescence images, reactive oxygen species (ROS), the mRNA and protein expression levels of inflammation factors, and histopathological analyses of the lung tissues. Hyperoxia-induced lung injury significantly increased the generation of ROS, the mRNA levels of , , and , and the protein expression levels of IKKα/β, iNOS and IL-6. Pulmonary edema and alveolar infiltration of neutrophils was also observed in the hyperoxia-induced lung tissue. However, treatment with either S-AC or W-AC obviously decreased hyperoxia-induced generation of ROS and the expression of IL-6, TNF-α, IL-1β, IL-8, IKKα/β and iNOS compared to hyperoxia treatment alone. Lung histopathology also showed that treatment with either S-AC or W-AC significantly reduced neutrophil infiltration and lung edema compared to treatment with hyperoxia treated alone. To find out their major compounds, eburicoic acid and dehydroeburicoic acid were both isolated and identified from S-AC and W-AC by using HPLC, MS, and NMR spectrometry. These results demonstrated that methanolic extracts both of S-AC and W-AC have excellent anti-inflammatory activities and thus have great potential as a source for natural health products.
Alternative sources of animal proteins are needed that can be produced efficiently, thereby providing food security with diminished ecological burden. It is feasible to culture beef from bovine skeletal muscle stem cells, but the technology is still under development. The aim is to create a beef mimic with equivalent taste, texture, and appearance and with the same nutritional value as livestock‐produced beef. More specifically, there is a need for optimization of protein content and fat content. In addition, scalability of production requires modification of current small‐scale bioreactors to the largest possible scale. The necessary steps and current progress suggest that this aim is achievable, but formal evidence is still required. Similarly, we can be optimistic about consumer acceptance based on initial data, but detailed studies are needed to gain more insight into potential psychological obstacles that could lead to rejection. These challenges are formidable but likely surmountable. The severity of upcoming food‐security threats warrants serious research and development efforts to address the challenges that come with bringing cultured beef to the market.
Autophagic (type II) cell death, characterized by the massive accumulation of autophagic vacuoles in the cytoplasm of cells, has been suggested to play pathogenetic roles in cerebral ischemia, brain trauma, and neurodegenerative disorders. 3,4-Methylenedioxymethamphetamine (MDMA or ecstasy) is an illicit drug causing long-term neurotoxicity in the brain. Apoptotic (type I) and necrotic (type III) cell death have been implicated in MDMA-induced neurotoxicity, while the role of autophagy in MDMA-elicited neurotoxicity has not been investigated. The present study aimed to evaluate the occurrence and contribution of autophagy to neurotoxicity in cultured rat cortical neurons challenged with MDMA. Autophagy activation was monitored by expression of microtubule-associated protein 1 light chain 3 (LC3; an autophagic marker) using immunofluorescence and western blot analysis. Here, we demonstrate that MDMA exposure induced monodansylcadaverine (MDC)- and LC3B-densely stained autophagosome formation and increased conversion of LC3B-I to LC3B-II, coinciding with the neurodegenerative phase of MDMA challenge. Autophagy inhibitor 3-methyladenine (3-MA) pretreatment significantly attenuated MDMA-induced autophagosome accumulation, LC3B-II expression, and ameliorated MDMA-triggered neurite damage and neuronal death. In contrast, enhanced autophagy flux by rapamycin or impaired autophagosome clearance by bafilomycin A1 led to more autophagosome accumulation in neurons and aggravated neurite degeneration, indicating that excessive autophagosome accumulation contributes to MDMA-induced neurotoxicity. Furthermore, MDMA induced phosphorylation of AMP-activated protein kinase (AMPK) and its downstream unc-51-like kinase 1 (ULK1), suggesting the AMPK/ULK1 signaling pathway might be involved in MDMA-induced autophagy activation.
ATP is an important regulator of microglia and its effects on microglial cytokine release are currently discussed as important contributors in a variety of brain diseases. We here analyzed the effects of ATP on the production of six inflammatory mediators (IL-6, IL-10, CCL2, IFN-gamma, TNF-alpha, and IL-12p70) in cultured mouse primary microglia. Stimulation of P2X7 receptor by ATP (1 mM) or BzATP (500 mu M) evoked the mRNA expression and release of proinflammatory cytokines IL-6, TNF-alpha, and the chemokine CCL2 in WT cells but not in P2X7(-/-) cells. The effects of ATP and BzATP were inhibited by the nonselective P2 receptor antagonists PPADs and suramin. Various selective P2X7 receptor antagonists blocked the P2X7-dependent release of IL-6 and CCL2, but, surprisingly, had no effect on BzATP-induced release of TNF-alpha in microglia. Calcium measurements confirmed that P2X7 is the main purine receptor activated by BzATP in microglia and showed that all P2X7 antagonists were functional. It is also presented that pannexin-1 hemichannel function and potential P2X4/P2X7 heterodimers are not involved in P2X7-dependent release of IL-6, CCL2, and TNF-alpha in microglia. How P2X7-specific antagonists only affect P2X7-dependent IL-6 and CCL2 release, but not TNF-alpha release is at the moment unclear, but indicates that the P2X7-dependent release of cytokines in microglia is differentially regulated. GLIA 2014;62:592-607
Publicly available sequence databases of the small subunit ribosomal RNA gene, also known as 16S rRNA in bacteria and archaea, are growing rapidly, and the number of entries currently exceeds 4 million. However, a unified classification and nomenclature framework for all bacteria and archaea does not yet exist. In this Analysis article, we propose rational taxonomic boundaries for high taxa of bacteria and archaea on the basis of 16S rRNA gene sequence identities and suggest a rationale for the circumscription of uncultured taxa that is compatible with the taxonomy of cultured bacteria and archaea. Our analyses show that only nearly complete 16S rRNA sequences give accurate measures of taxonomic diversity. In addition, our analyses suggest that most of the 16S rRNA sequences of the high taxa will be discovered in environmental surveys by the end of the current decade.
Abstract Background Cell therapy for cardiovascular disease has been limited by low engraftment of administered cells and modest therapeutic effects. Bone marrow (BM) -derived CD31+ cells are a promising cell source owing to their high angiovasculogenic and paracrine activities. Objectives This study sought to identify culture conditions that could augment the cell adhesion, angiogenic, and anti-inflammatory activities of BM-derived CD31+ cells, and to determine whether these cultured CD31+ cells are effective for cardiac and vascular repair. Methods CD31+ cells were isolated from human BM by magnetic-activated cell sorting and cultured for 10 days under hematopoietic stem cell, mesenchymal stem cell, or endothelial cell culture conditions. These cells were characterized by adhesion, angiogenesis, and inflammatory assays. The best of the cultured cells were implanted into myocardial infarction (MI) and hindlimb ischemia (HLI) models to determine therapeutic effects and underlying mechanisms. Results The CD31+ cells cultured in endothelial cell medium (EC-CD31+ cells) showed the highest adhesion and angiogenic activities and lowest inflammatory properties in vitro compared with uncultured or other cultured CD31+ cells. When implanted into mouse MI or HLI models, EC-CD31+ cells improved cardiac function and repaired limb ischemia to a greater extent than uncultured CD31+ cells. Histologically, injected EC-CD31+ cells exhibited higher retention, neovascularization, and cardiomyocyte proliferation. Importantly, cell retention and endothelial transdifferentiation was sustained up to 1 year. Conclusions Short-term cultured EC-CD31+ cells have higher cell engraftment, vessel-formation, cardiomyocyte proliferation, and anti-inflammatory potential, are highly effective for both cardiac and peripheral vascular repair, and enhance survival of mice with heart failure. These cultured CD31+ cells may be a promising source for treating ischemic cardiovascular diseases.
Accumulating evidences indicate that pulmonary exposure to carbon nanotubes (CNTs) is associated with increased risk of lung diseases, whereas the effect on the vascular system is less studied. We investigated vascular effects of 2 types of multiwalled CNTs (MWCNTs) in apolipoprotein E-/ mice, wild-type mice, and cultured cells. The ApoE(/) mice had accelerated plaque progression in aorta after 5 intracheal instillations of MWCNT (25.6 g/mouse weekly for 5 weeks). The exposure was associated with pulmonary inflammation, lipid peroxidation, and increased expression of inflammatory, oxidative stress, DNA repair, and vascular activation response genes. The level of oxidatively damaged DNA in lung tissue was unaltered, probably due to increased DNA repair capacities. Despite upregulation of inflammatory genes in the liver, effects on systemic cytokines and lipid peroxidation were minimal. The exposure to MWCNTs in cultured human endothelial cells increased the expression of cell adhesion molecules (ICAM1 and VCAM1). In cocultures, there was increased adhesion of monocytes to endothelial cells after exposure to MWCNT. The exposure to both types of MWCNT was also associated with increased lipid accumulation in monocytic-derived foam cells, which was dependent on concomitant oxidative stress because the antioxidant N-acetylcysteine inhibited the lipid accumulation. Collectively, our results indicate that exposure to MWCNT is associated with accelerated progression of atherosclerosis, which could be related to both increased adherence of monocytes onto the endothelium and oxidative stress-mediated transformation of monocytes to foam cells.
The morphology of astrocytes, likely regulated by cAMP, determines the structural association between astrocytes and the synapse, consequently modulating synaptic function. β‐Adrenergic receptors (β‐AR), which increase cytosolic cAMP concentration ([cAMP] i ), may affect cell morphology. However, the real‐time dynamics of β‐AR‐mediated cAMP signaling in single live astrocytes and its effect on cell morphology have not been studied. We used the fluorescence resonance energy transfer (FRET)‐based cAMP biosensor Epac1‐camps to study time‐dependent changes in [cAMP] i ; morphological changes in primary rat astrocytes were monitored by real‐time confocal microscopy. Stimulation of β‐AR by adrenaline, noradrenaline, and isoprenaline, a specific agonist of β‐AR, rapidly increased [cAMP] i (∼15 s). The FRET signal response, mediated via β‐AR, was faster than in the presence of forskolin (twofold) and dibutyryl‐cAMP (>35‐fold), which directly activate adenylyl cyclase and Epac1‐camps, respectively, likely due to slow entry of these agents into the cytosol. Oscillations in [cAMP] i have not been recorded, indicating that cAMP‐dependent processes operate in a slow time domain. Most Epac1‐camps expressing astrocytes revealed a morphological change upon β‐AR activation and attained a stellate morphology within 1 h. The morphological changes exhibited a bell‐shaped dependency on [cAMP] i . The 5–10% decrease in cell cross‐sectional area and the 30–50% increase in cell perimeter are likely due to withdrawal of the cytoplasm to the perinuclear region and the appearance of protrusions on the surface of astrocytes. Because astrocyte processes ensheath neurons, β‐AR/cAMP‐mediated morphological changes can modify the geometry of the extracellular space, affecting synaptic, neuronal, and astrocyte functions in health and disease. GLIA 2014;62:566–579 The results show the first β‐Adrenergic receptor evoked time‐dependent changes in cytosolic cAMP in astrocytes measured by FRET nanosensor and subsequent changes in astrocyte morphology that exhibited bell‐shaped dependency on cytosolic cAMP levels.