Phytoplankton abundance and size-fractionated structure in three contrasting periods in the Pear River Estuary

Phytoplankton abundance, composition and size-fractionated chlorophyll a (micro-, nano- and pico-chl. a) in the Pearl River Estuary (PRE), South China were assessed in three surveys (Aug. 2010, Jan. 2011 and Aug. 2011) to identify key environmental indicators that shape their distribution patterns. Non-metric multidimensional scaling (MDS) showed that the PRE formed three regional clusters that were characterized by a transition from dominant freshwater species to estuarine diatoms in normal summer flow conditions (Aug. 2010). With a reduced river flow in winter (Jan. 2011), the inner estuary was categorized as one group marked by the predominance of the nanoflagellate, Plagioselmis prolonga. This small-sized cryptophyte was first recorded in the PRE and was likely to outcompete other phytoplankton species in turbid or well-mixed waters. During the extreme drought of summer of 2011 (Aug. 2011), the estuarine plume was limited and regional division by MDS was similar to winter patterns, as some marine species were observed in the upper estuary. We considered that the higher phytoplankton density in the summer of 2011 was presumably a combined effect of longer residence time and higher phosphate concentration. With respect to the size-fractionated phytoplankton composition, our results showed that almost half of the chl. a in the estuary was contained in microplankton particles, while the proportion of pico-chl. a increased from the upstream of the PRE towards the estuary boundary (Wanshan Islands). Furthermore, phytoplankton abundance, three size classes of chl. a and environmental factors were explored by principal component regression (PCR) analysis. In three surveys, pico-chl. a was negatively correlated with the first principal component (PCL, positively loaded with salinity and inversely with inorganic nutrients), which indicated a negative influence of the riverine and coastal waters on picophytoplankton and the specific oligotrophic niche of picophytoplankton. Similarly, PC1 was also considered as the key environmental variable basis controlling micro-chl. a in summer of 2010, while in the summer of 2011, zooplankton and copepods were positively associated with phytoplankton abundance, suggesting a resource effect of phytoplankton on zooplankton development

Tetraodon nigroviridis as a nonlethal model of infectious spleen and kidney necrosis virus (ISKNV) infection

AbstractInfectious spleen and kidney necrosis virus (ISKNV) is the type species of the genus Megalocytivirus, family Iridoviridae. We have previously established a high mortality ISKNV infection model of zebrafish (Danio rerio). In this study, a nonlethal Tetraodon nigroviridis model of ISKNV infection was established. ISKNV infection did not cause lethal disease in Tetraodon but could infect almost all the organs of this species. Electron microscopy showed ISKNV particles were present in infected tissues. Immunofluorescence and quantitative real-time PCR analysis showed that nearly all the virions and infected cells were cleared at 14d postinfection. The expression profiles of interferon-γ and tumor necrosis factor-α gene in response to ISKNV infection were significantly different in Tetraodon and zebrafish. The establishment of the nonlethal Tetraodon model of ISKNV infection can offer a valuable tool complementary to the zebrafish infection model for studying megalocytivirus disease, fish immune systems, and viral tropism

DiDang Tang Inhibits Endoplasmic Reticulum Stress-Mediated Apoptosis Induced by Oxygen Glucose Deprivation and Intracerebral Hemorrhage Through Blockade of the GRP78-IRE1/PERK Pathways

DiDang Tang (DDT), a Chinese traditional medicine formula, contains 4 Chinese traditional medicine substances, has been widely used to treat intracerebral hemorrhage (ICH) patients. However, the molecular mechanisms of DDT for protecting neurons from oxygen and glucose deprivation (OGD)-induced endoplasmic reticulum (ER) stress and apoptosis after ICH still remains elusive. In this study, high-performance liquid chromatography fingerprint analysis was performed to learn the features of the chemical compositions of DDT. OGD-induced ER stress, Ca2+ overload, and mitochondrial apoptosis were investigated in nerve growth factor -induced PC12, primary neuronal cells, and ICH rats to evaluate the protective effect of DDT. We found that DDT treatment protected neurons against OGD-induced damage and apoptosis by increasing cell viability and reducing the release of lactate dehydrogenase. DDT decreased OGD-induced Ca2+ overload and ER stress through the blockade of the glucose-regulated protein 78 (GRP78)- inositol-requiring protein 1α (IRE1)/ protein kinase RNA-like ER kinase (PERK) pathways and also inhibited apoptosis by decreasing mitochondrial damage. Moreover, we observed similar findings when we studied DDT for inhibition of ER stress in a rat model of ICH. In addition, our experiments further confirmed the neuroprotective potential of DDT against tunicamycin (TM)-induced neural damage. Our in vitro and in vivo results indicated that the neuroprotective effect of DDT against ER stress damage and apoptosis occurred mainly by blocking the GPR78-IRE1/PERK pathways. Taken together, it provides reliable experimental evidence and explains the molecular mechanism of DDT for the treatment of patients with ICH

Compound K Inhibits Autophagy-Mediated Apoptosis Through Activation of the PI3K-Akt Signaling Pathway Thus Protecting Against Ischemia/Reperfusion Injury

Background/Aims: A series of reports revealed that autophagy and apoptosis exerted detrimental effects on the pathology of cardiac ischemia/reperfusion (I/R) injury. Ginsenoside compound K (CK), a major intestinal metabolite underlying the pharmacological actions of orally administered ginseng, has a protective effect against myocardial I/R injury. However, the molecular mechanisms by which CK protects against I/R injury remain unclear. In this study, we hypothesized that the cardioprotective effects of CK against I/R injury are mediated by inhibiting autophagy/apoptosis-related signaling pathways in H9c2 cardiomyocyte cells. Methods: H9c2 cells were incubated with CK and exposed to I/R. Cell viability and damage was analyzed by MTT and lactate dehydrogenase assays. Reactive oxygen species (ROS) generation, mitochondrial damage, and cell apoptosis were analyzed by flow cytometry and TUNEL staining. The expression of autophagy, apoptosis, and related signaling proteins was analyzed by Western blotting and immunofluorescence staining. Results: CK pretreatment promoted cell viability and attenuated ROS accumulation and intracellular mitochondrial damage induced by I/R injury Moreover, CK reduced autophagy by regulating the formation of phagocytic precursors to autophagosomes and also inhibited apoptosis through a mitochondrial-mediated pathway. Additionally the cardioprotective effect of CK against I/R injury was mainly through the activation of the PI3K-Akt signaling pathway. Conclusions: CK pretreatment inhibits autophagy-mediated apoptosis induced by I/R injury through the activation of the PI3K-Akt signaling pathway, which reveals that CK may be one of the key bioactive ingredients of ginseng for the treatment of myocardial I/R injury

Anisotropic Polymer Adsorption on Molybdenite Basal and Edge Surfaces and Interaction Mechanism With Air Bubbles

The anisotropic surface characteristics and interaction mechanisms of molybdenite (MoS2) basal and edge planes have attracted much research interest in many interfacial processes such as froth flotation. In this work, the adsorption of a polymer depressant [i.e., carboxymethyl cellulose (CMC)] on both MoS2 basal and edge surfaces as well as their interaction mechanisms with air bubbles have been characterized by atomic force microscope (AFM) imaging and quantitative force measurements. AFM imaging showed that the polymer coverage on the basal plane increased with elevating polymer concentration, with the formation of a compact polymer layer at 100 ppm CMC; however, the polymer adsorption was much weaker on the edge plane. The anisotropy in polymer adsorption on MoS2 basal and edge surfaces coincided with water contact angle results. Direct force measurements using CMC functionalized AFM tips revealed that the adhesion on the basal plane was about an order of magnitude higher than that on the edge plane, supporting the anisotropic CMC adsorption behaviors. Such adhesion difference could be attributed to their difference in surface hydrophobicity and surface charge, with weakened hydrophobic attraction and strengthened electrostatic repulsion between the polymers and edge plane. Force measurements using a bubble probe AFM showed that air bubble could attach to the basal plane during approach, which could be effectively inhibited after polymer adsorption. The edge surface, due to the negligible polymer adsorption, showed similar interaction behaviors with air bubbles before and after polymer treatment. This work provides useful information on the adsorption of polymers on MoS2 basal/edge surfaces as well as their interaction mechanism with air bubbles at the nanoscale, with implications for the design and development of effective polymer additives to mediate the bubble attachment on solid particles with anisotropic surface properties in mineral flotation and other engineering processes

Outdoor particulate matter exposure affects metabolome in chronic obstructive pulmonary disease: Preliminary study

IntroductionThe metabolomic changes caused by airborne fine particulate matter (PM2.5) exposure in patients with chronic obstructive pulmonary disease (COPD) remain unclear. The aim of this study was to determine whether it is possible to predict PM2.5-induced acute exacerbation of COPD (AECOPD) using metabolic markers.MethodsThirty-eight patients with COPD diagnosed by the 2018 Global Initiative for Obstructive Lung Disease were selected and divided into high exposure and low exposure groups. Questionnaire data, clinical data, and peripheral blood data were collected from the patients. Targeted metabolomics using liquid chromatography-tandem mass spectrometry was performed on the plasma samples to investigate the metabolic differences between the two groups and its correlation with the risk of acute exacerbation.ResultsMetabolomic analysis identified 311 metabolites in the plasma of patients with COPD, among which 21 metabolites showed significant changes between the two groups, involving seven pathways, including glycerophospholipid, alanine, aspartate, and glutamate metabolism. Among the 21 metabolites, arginine and glycochenodeoxycholic acid were positively associated with AECOPD during the three months of follow-up, with an area under the curve of 72.50% and 67.14%, respectively.DiscussionPM2.5 exposure can lead to changes in multiple metabolic pathways that contribute to the development of AECOPD, and arginine is a bridge between PM2.5 exposure and AECOPD