The Effect of Preozonation on the Anaerobic Biodegradability of Resistant Phenolic Compounds

Ozone pretreatment studies of four model phenolic compounds were conducted to evaluate the effects of ozonation on the anaerobic biodegradability and toxicity of these compounds. Two types of batch studies, the Biochemical Methane Potential (BMP) and the Anaerobic Toxicity Assay (ATA), were performed on samples ozonated upon phenol, o-cresol, 2,5-dichlorophenol, and 2,4-dinitrophenol. Experimental results showed that toxic and refractory phenolic compounds were converted to methane gas by means of preozonation. In general, the biodegradable fraction of the oxidation products increased as the ozone dose was increased. However, ozonation to achieve at least 60% COD reduction was necessary to faciliate methane production. Ozonation reduced the toxicity of 2,5-DCP and 2,4-DNP on both acetate utilization and phenol degradation. The early ozonation products of o-cresol and phenol, however, were more toxic than the initial compounds. The rates of COD and DOC reduction through ozonation were faster and products formed were less inhibitory in the basic pH range than in the acid pH range

Effects of Aromatic Concentration on Methane Fermentation

The anaerobic biodegradability and toxicity of fourteen aromatic compounds were evaluated over a wide range of concentrations using a serum bottle technique. Benzene, toluene, and all three isomers of xylene were not significantly degraded to methane in a phenol-enriched culture. Complete degradation of 1000 mg/L phenol, 800 mg/L catechol, 100 mg/L 2-NP, 100 mg/L 3- NP, and 100 mg/L 4-NP was observed within two months while depletion of 100 mg/L resorcinol and 1000 mg/L hydroquinone required more than six and eight months incubation, respectively. None of the three isomers of chlorophenol were degraded in the phenol-enriched culture. Batch toxicity assay revealed that the phenol-enriched culture was more susceptible to inhibition caused by substituted phenols than the acetate-enriched culture. In general, the inhibitory effects on both phenol degradation and acetate utilization did not vary significantly with the isomer but rather with the substituted group. The degree of inhibition was in the order of nitrophenols \u3e chlorophenols \u3e hydroxyphenols. The Haldane inhibition model was used to fit experimental data from phenol and catechol. The inhibition of phenol degradation by chlorophenols, resorcinol, and hydroquinone was described rather well by a Monod-type, noncompetitive model

Asian Primate Species Richness Correlates with Rainfall

Previous studies of meta-analyses found significantly positive correlations between primate species richness and rainfall for Africa, Madagascar and the Neotropics, with the exception of Asia, leaving the open question whether that anomaly is the result of sampling bias, biogeography, or some other factor. This study re-examines the question using modelled data, with primate species richness data from the Southeast Asian Mammals Databank and rainfall data from the Climatic Research Unit. Data processing with Geographical Information Systems resulted in 390 sample points. Reduced major axis and ordinary least squares regressions were employed to examine the relationship for six regions, including the whole study area of Southeast Asia, and the subareas of Huxley West, Huxley East, Mainland Southeast Asia, Borneo, and Sumatra. The results showed a significant positive relationship between primate species richness and mean annual rainfall for Southeast Asia (r = 0.26, P,0.001). Comparing the results for the large islands and Mainland Southeast Asia showed that Sumatra had the highest correlation (r = 0.58; P,0.05). After controlling for the major biogeographic effect associated with Huxley’s Line, our results showed that primate species richness is positively associated with mean annual rainfall in Southeast Asia. Our findings contrast to prior studies of meta-analyses that showed no relationship between rainfall and primate species richness in Asia, and thereby bring Asia into agreement with results showing significant positive correlations between rainfall and primate species richness everywhere else in the world. The inference is that previous anomalous results for Asia were result of sampling bias in the meta-analysis

Insights into information contained in multiplicative scatter correction parameters and the potential for estimating particle size from these parameters

This paper investigates the nature of information contained in scatter correction parameters. The study had two objectives. The first objective was to examine the nature and extent of information contained in scatter correction parameters. The second objective is to examine whether this information can be effectively extracted by proposing a method to obtain particularly the mean particle diameter from the scatter correction parameters. By using a combination of experimental data and simulated data generated using fundamental light propagation theory, a deeper and more fundamental insight of what information is removed by the multiplicative scatter correction (MSC) method is obtained. It was found that the MSC parameters are strongly influenced not only by particle size but also by particle concentration as well as refractive index of the medium. The possibility of extracting particle size information in addition to particle concentration was considered by proposing a two-step method which was tested using a 2-component and 4-component data set. This method can in principle, be used in conjunction with any scatter correction technique provided that the scatter correction parameters exhibit a systematic dependence with respect to particle size and concentration. It was found that the approach which uses the MSC parameters gave a better estimate of the particle diameter compared to using partial least squares (PLS) regression for the 2-component data. For the 4 component data it was found that PLS regression gave better results but further examination indicated this was due to chance correlations of the particle diameter with the two of the absorbing species in the mixture

Co-delivery of salinomycin and curcumin for cancer stem cell treatment by inhibition of cell proliferation, cell cycle arrest, and epithelial-mesenchymal transition

Malignant cancer is a devastating disease often associated with a poor clinical prognosis. For decades, modern drug discoveries have attempted to identify potential modulators that can impede tumor growth. Cancer stem cells however are more resistant to therapeutic intervention, which often leads to treatment failure and subsequent disease recurrence. Here in this study, we have developed a specific multi-target drug delivery nanoparticle system against breast cancer stem cells (BCSCs). Therapeutic agents curcumin and salinomycin have complementary functions of limiting therapeutic resistance and eliciting cellular death, respectively. By conjugation of CD44 cell-surface glycoprotein with poly(lactic-co-glycolic acid) (PLGA) nanoparticles that are loaded with curcumin and salinomycin, we investigated the cellular uptake of BCSCs, drug release, and therapeutic efficacy against BCSCs. We determined CD44-targeting co-delivery nanoparticles are highly efficacious against BCSCs by inducing G1 cell cycle arrest and limiting epithelial–mesenchymal transition. This curcumin and salinomycin co-delivery system can be an efficient treatment approach to target malignant cancer without the repercussion of disease recurrence

An overview of epigenetics and chemoprevention

AbstractIt is now appreciated that both genetic alteration, e.g. mutations, and aberrant epigenetic changes, e.g. DNA methylation, cause cancer. Epigenetic dysregulation is potentially reversible which makes it attractive as targets for cancer prevention. Synthetic drugs targeting enzymes, e.g. DNA methyltransferase and histone deacetylase, that regulate epigenetic patterns are active in clinical settings. In addition, dietary factors have been suggested to have potential to reverse aberrant epigenetic patterns. Uncovering the human epigenome can lead us to better understand the dynamics of DNA methylation in disease progression which can further assist in cancer prevention

Acute necrotizing eosinophilic myocarditis in a young woman

Abstract Eosinophilic myocarditis is recognized by severe heart failure and marked eosinophilia infiltration resulting from different etiologies. Acute necrotizing eosinophilic myocarditis, the initial presentation of the disease, is rare and often fatal, with unique echocardiographic pictures, and followed by endocardial thrombosis and chronic endomyocardial fibrosis. We report a young female with acute lymphoblastic leukemia who presented fever and acute heart failure syndrome. The echocardiography showed severe left ventricle diastolic dysfunction with preserved ejection fraction. Systemic eosinophilia and the unique echocardiographic images made the diagnosis of acute necrotizing eosinophilic myocarditis. The patient survived after intensive cytotoxic chemotherapy including high-dose steroid

Overweight worsens apoptosis, neuroinflammation and blood-brain barrier damage after hypoxic ischemia in neonatal brain through JNK hyperactivation

<p>Abstract</p> <p>Background</p> <p>Apoptosis, neuroinflammation and blood-brain barrier (BBB) damage affect the susceptibility of the developing brain to hypoxic-ischemic (HI) insults. c-Jun N-terminal kinase (JNK) is an important mediator of insulin resistance in obesity. We hypothesized that neonatal overweight aggravates HI brain damage through JNK hyperactivation-mediated upregulation of neuronal apoptosis, neuroinflammation and BBB leakage in rat pups.</p> <p>Methods</p> <p>Overweight (OF) pups were established by reducing the litter size to 6, and control (NF) pups by keeping the litter size at 12 from postnatal (P) day 1 before HI on P7. Immunohistochemistry and immunoblotting were used to determine the TUNEL-(+) cells and BBB damage, cleaved caspase-3 and poly (ADP-ribose) polymerase (PARP), and phospho-JNK and phospho-Bim_ELlevels. Immunofluorescence was performed to determine the cellular distribution of phospho-JNK.</p> <p>Results</p> <p>Compared with NF pups, OF pups had a significantly heavier body-weight and greater fat deposition on P7. Compared with the NF-HI group, the OF-HI group showed significant increases of TUNEL-(+) cells, cleaved levels of caspase-3 and PARP, and ED1-(+) activated microglia and BBB damage in the cortex 24 hours post-HI. Immunofluorescence of the OF-HI pups showed that activated-caspase 3 expression was found mainly in NeuN-(+) neurons and RECA1-(+) vascular endothelial cells 24 hours post-HI. The OF-HI group also had prolonged escape latency in the Morris water maze test and greater brain-volume loss compared with the NF-HI group when assessed at adulthood. Phospho-JNK and phospho-Bim_ELlevels were higher in OF-HI pups than in NF-HI pups immediately post-HI. JNK activation in OF-HI pups was mainly expressed in neurons, microglia and vascular endothelial cells. Inhibiting JNK activity by AS601245 caused more attenuation of cleaved caspase-3 and PARP, a greater reduction of microglial activation and BBB damage post-HI, and significantly reduced brain damage in OF-HI than in NF-HI pups.</p> <p>Conclusions</p> <p>Neonatal overweight increased HI-induced neuronal apoptosis, microglial activation and BBB damage, and aggravated HI brain damage in rat pups through JNK hyperactivation.</p