ABSTRACT
Coking wastewater is a typical industrial wastewater with high toxicity. Its treatment with biological processes is often challenging because it contains constituents inhibiting microbial activity. To study the inhibitory effect and possible acclimation of microbes in coking wastewater treatment, municipal sludge was inoculated into coking wastewater. Time-dependent concentrations of COD, phenol, ammonia nitrogen, and thiocyanide in coking wastewater were analyzed. The microbial community structure was investigated by the Illumina high-throughput sequencing technology during inoculation. The results showed that COD began to decrease after 16 h and 97.1% of phenol disappeared after 40 h. Thiocyanide began to degrade at 72 h and was undetectable after 96 h. Accordingly, the concentration of ammonia increased as the thiocyanide concentrations decreased. High-throughput pyrosequencing analysis showed that the microbial community structure and species richness varied at different culture stages. In the stage of phenol degradation, the abundance of Acinetobacter and Pseudomonas increased rapidly; the species richness was 13.04% of the community at 48 h. In the stage of thiocyanate degradation, Sphingobacterium,Brevundimonas,Lysobacter, and Chryseobacterium were the dominant bacteria and were 16.13% of the community at 96 h. At 144 h, Fluviicola,Stenotrophomonas, and Thiobacillus became the dominant species and were 22.45% of the community abundance. The results showed that municipal sludge can rapidly overcome the toxicity of coking wastewater because the pollutants are degraded rapidly. The microbial community structure changed as wastewater components were degraded. Environmental factors and the competition among bacteria played a key role in microbial community succession.
Subject(s)
Bacteria/classification , Bioreactors , Coke , Sewage/microbiology , Waste Disposal, Fluid , Wastewater , PhenolABSTRACT
The pathophysiology of ventilator-induced lung injury (VILI) involves multiple mechanisms including inflammation. Histone deacetylase inhibitors have been shown to exert anti-inflammation activity. The purpose of this study was to examine the protecting roles and mechanisms of the histone deacetylase inhibitors trichostatin A (TSA) and suberoylanilide hydroxamic acid (SAHA) in ventilator-induced lung injury in normal rat lung. Male Sprague-Dawley rats were divided into four groups: lung-protective ventilation (LV), injurious ventilation (HV), HV+TSA and HV+ SAHA groups. Mechanical ventilation (MV) settings were 7 ml/kg VT and 3cm H2O positive end-expiratorypressure [PEEP], 40 breaths/min for LV group and 42 ml/kg VT, zero end-expiratoryvolume [ZEEP], 40 breaths/min for the HV, HV+TSA and HV+ SAHA groups. After 2 h of MV, acute lung injury (ALI) score, wet-to-dry (W/D) weight ratio and the activity of myeloperoxidase (MPO) were determined. The concentration of tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta) and interleukin-10 (IL-6) in the homogenized lung were measured by ELISA. The expression ICAM-1 was measured by both realtime PCR and Western blot assays. In addition, survival of each group was also assessed. Our results indicated that administration of TSA or SAHA alleviated ventilator-induced lung injury. This was accompanied by reduced neutrophil infiltration, reduced MPO activity, decreased intercellular adhesion molecule-1 (ICAM-1) expression in lung tissue, and lower TNF-alpha, IL-1beta and IL-6 levels. In addition, treatment with HDAC inhibitors significantly prolonged the survival time of ventilator-induced lung injury rats. Our data suggested that TSA and SAHA could significantly alleviate ventilator-induced rat lung injury and prolong the survival time of those rats by attenuate intrapulmonary inflammatory response.
Subject(s)
Histone Deacetylase Inhibitors/therapeutic use , Hydroxamic Acids/therapeutic use , Ventilator-Induced Lung Injury/drug therapy , Animals , Blotting, Western , Capillary Leak Syndrome/drug therapy , Capillary Leak Syndrome/pathology , Down-Regulation/drug effects , Enzyme-Linked Immunosorbent Assay , Intercellular Adhesion Molecule-1/biosynthesis , Interleukin-1beta/metabolism , Interleukin-6/metabolism , Lung/pathology , Male , Neutrophil Infiltration/drug effects , Peroxidase/metabolism , Pulmonary Edema/drug therapy , Pulmonary Edema/pathology , Pulmonary Edema/prevention & control , Rats , Rats, Sprague-Dawley , Real-Time Polymerase Chain Reaction , Tumor Necrosis Factor-alpha/metabolism , Ventilator-Induced Lung Injury/mortality , Ventilator-Induced Lung Injury/pathology , VorinostatABSTRACT
A kind of new ionization source, atmospheric pressure matrix-assisted laser desorption/ionization (AP-MALDI), is introduced in the present paper. This ionization source was studied and developed on the basis of vacuum MALDI. It has been applied widely in the field of biomacromolecule. This ionization source has softer analyte ionization and produces fewer fragmentations compared with conventional vacuum MALDI. It works at atmospheric pressure, therefore eases to be coupled to mass spectrometers, acting as an external ion source, and greatly extends the application fields of MALDI. The principle, configuration and technical development of AP-MALDI are described detailedly. Moreover, the current applications and prospect of the device in analyzing biopolymers are summarized.
