Application of Rice-Straw Biochar and Microorganisms in Nonylphenol Remediation: Adsorption-Biodegradation Coupling Relationship and Mechanism

Biochar adsorption presents a potential remediation method for the control of hydrophobic organic compounds (HOCs) pollution in the environment. It has been found that HOCs bound on biochar become less bioavailable, so speculations have been proposed that HOCs will persist for longer half-life periods in biochar-amended soil/sediment. To investigate how biochar application affects coupled adsorption-biodegradation, nonylphenol was selected as the target contaminant, and biochar derived from rice straw was applied as the adsorbent. The results showed that there was an optimal dosage of biochar in the presence of both adsorption and biodegradation for a given nonylphenol concentration, thus allowing the transformation of nonylphenol to be optimized. Approximately 47.6% of the nonylphenol was biodegraded in two days when 0.005 g biochar was added to 50 mg/L of nonylphenol, which was 125% higher than the relative quantity biodegraded without biochar, though the resistant desorption component of nonylphenol reached 87.1%. All adsorptive forms of nonylphenol (f _rap, f _slow, f _r) decreased gradually during the biodegradation experiment, and the resistant desorption fraction of nonylphenol (f _r) on biochar could also be biodegraded. It was concluded that an appropriate amount of biochar could stimulate biodegradation, not only illustrating that the dosage of biochar had an enormous influence on the half-life periods of HOCs but also alleviating concerns that enhanced HOCs binding by biochar may cause secondary pollution in biochar-modified environment.     

The Effects of Mobile Phone Radiofrequency Radiation on Cochlear Stria Marginal Cells in Sprague–Dawley Rats

To investigate the possible mechanisms for biological effects of 1,800 MHz mobile radiofrequency radiation (RFR), the radiation-specific absorption rate was applied at 2 and 4 W/kg, and the exposure mode was 5 min on and 10 min off (conversation mode). Exposure time was 24 h short-term exposure. Following exposure, to detect cell DNA damage, cell apoptosis, and reactive oxygen species (ROS) generation, the Comet assay test, flow cytometry, DAPI (4′,6-diamidino-2-phenylindole dihydrochloride) staining, and a fluorescent probe were used, respectively. Our experiments revealed that mobile phone RFR did not cause DNA damage in marginal cells, and the rate of cell apoptosis did not increase (P > 0.05). However, the production of ROS in the 4 W/kg exposure group was greater than that in the control group (P < 0.05). In conclusion, these results suggest that mobile phone energy was insufficient to cause cell DNA damage and cell apoptosis following short-term exposure, but the cumulative effect of mobile phone radiation still requires further confirmation. Activation of the ROS system plays a significant role in the biological effects of RFR. Bioelectromagnetics. © 2020 The Authors. Bioelectromagnetics published by Wiley Periodicals, Inc.     

Spectral composition of shade light in coastal-zone oak forests in SE Bulgaria,and relationships with leaf area index: a first overview

Major knowledge gaps exist with respect to light-quality regimes in the coastal-zone Strandzha Quercus frainetto (Q.f.) forest region adjoining the southern Bulgarian Black Sea. This paper presents preliminary results that help narrow these gaps. In conjunction with leaf area index (LAI) field campaigns we undertook measurements with an array of 7 broad-band (ca 40 nm) sensors covering the range 0.40–0.94 μm, plus 1 sensor for UVB (0.297 μm peak) and 1 for photosynthetically active radiation (PAR). Measurements focused on inside-forest shade conditions at sites 0 to ca 15 km from the Black Sea and at altitudes up to ca 120 m above sea level. Some of the sites were also studied using a high-resolution spectroradiometer. A sequential measuring strategy was necessary. This involves potentially large uncertainties, here addressed through estimations of the variability around the sinusoidal course of daylight. Light-quality regimes were found to be in general support of earlier studies of deciduous forests. Our data from the broad-band sensors and from the spectroradiometer are mutually supportive. They indicate a stronger red-shift below Q.f. canopies than below canopies in enclaves dominated by Fagus orientalis and Pinus sylvestris. Transmission in the range 0.50–0.55 μm increases beneath the three types of canopies, most pronounced in the Q.f. case. Analysis of relationships between the inside-forest to open-field irradiance ratio and LAI supports the use of Beer’s Law. We found a fairly strong relationship between the red (0.66 μm) to far-red (0.73 μm) irradiance ratios (R/FR) and LAI for the Q.f. forest. In quantitative terms, the result is new for this Q.f. region, and suggests further research to explore whether a two-sensor approach (0.66 and 0.73 μm) might offer possibilities for further low-cost mapping of the spatio-temporal patterns of R/FR and LAI in Strandzha. Such mapping would assist in further studies of the region’s forest biogeochemistry and vitality.     

The Mitogen-activated Protein (MAP) Kinases p38 and Extracellular Signal-regulated Kinase (ERK) Are Involved in Hepatocyte-mediated Phenotypic Switching in Prostate Cancer Cells

The greatest challenge for the seeding of cancer in metastatic sites is integration into the ectopic microenvironment despite the lack of an orthotopic supportive environment and presence of pro-death signals concomitant with a localized “foreign-body” inflammatory response. In this metastatic location, many carcinoma cells display a reversion of the epithelial-to-mesenchymal transition that marks dissemination in the primary tumor mass. This mesenchymal to epithelial reverting transition (MErT) is thought to help seeding and colonization by protecting against cell death. We have previously shown that hepatocyte coculture induces the re-expression of E-cadherin via abrogation of autocrine EGFR signaling pathway in prostate cancer (PCa) cells and that this confers a survival advantage. Herein, we show that hepatocytes educate PCa to undergo MErT by modulating the activity of p38 and ERK1/2. Hepatocytes inhibited p38 and ERK1/2 activity in prostate cancer cells, which allowed E-cadherin re-expression. Introduction of constitutively active MEK6 and MEK1 to DU145 cells cocultured with hepatocytes abrogated E-cadherin re-expression. At least a partial phenotypic reversion can be achieved by suppression of p38 and ERK1/2 activation in DU145 cells even in the absence of hepatocytes. Interestingly, these mitogen-activated protein kinase activities were also triggered by re-expressed E-cadherin leading to p38 and ERK1/2 activity in PCa cells; these signals provide protection to PCa cells upon challenge with chemotherapy and cell death-inducing cytokines. We propose that distinct p38/ERK pathways are related to E-cadherin levels and function downstream of E-cadherin allowing, respectively, for hepatocyte-mediated MErT and tumor cell survival in the face of death signals.     

Impact of Conditional miRNA126 Overexpression on Apoptosis-Resistant Endothelial Cell Production

The activation of endothelial cells is essential to repair damage caused by atherosclerosis via endothelial cell proliferation and migration. Overexpression of VEGF (vascular endothelial growth factor) and the downstream gene, B-cell lymphoma-2 (BCL-2) could result in apoptosis-resistant endothelial cells, which are responsible for aggravated hyperplasia and instable plaques generation. Previous studies have shown that miRNA126 could regulate the expression of VEGF. Here, we verified the existence of a miRNA126 binding site in VEGF’s 3’UTR. Additionally, VEGF regulated BCL-2 expression via AP1 (Activator Protein 1) binding site in BCL-2’s promoter. Next, we established an apoptosis-resistant endothelial cell line and constructed a lentiviral vector to express miRNA126 under the control of the BCL-2 promoter to investigate whether conditional expression of miRNA126 could modulate VEGF and BCL-2 expression in apoptosis-resistant endothelial cells. This lentiviral system specifically expressed miRNA126 in cells with high BCL-2 levels, downregulated VEGF expression, inhibited MAPK pathway activation and downregulated BCL-2 expression via suppression of AP1, and as a whole, reduced apoptosis-resistant endothelial cells, while the effects of miRNA126 on normal endothelial cells were relatively small. Our results demonstrate that conditional miRNA126 overexpression under the control of the downstream BCL-2 promoter provides a flexible regulatory strategy for reducing the apoptosis-resistant endothelial cells without having a significant impact on normal endothelial cells.     

Heterogeneity of Regional Brain Atrophy Patterns Associated with Distinct Progression Rates in Alzheimer’s Disease

We aimed to identify and characterize subtypes of Alzheimer’s disease (AD) exhibiting different patterns of regional brain atrophy on MRI using age- and gender-specific norms of regional brain volumes. AD subjects included in the Alzheimer''s Disease Neuroimaging Initiative study were classified into subtypes based on standardized values (Z-scores) of hippocampal and regional cortical volumes on MRI with reference to age- and gender-specific norms obtained from 222 cognitively normal (CN) subjects. Baseline and longitudinal changes of clinical characteristics over 2 years were compared across subtypes. Whole-brain-level gray matter (GM) atrophy pattern using voxel-based morphometry (VBM) and cerebrospinal fluid (CSF) biomarkers of the subtypes were also investigated. Of 163 AD subjects, 58.9% were classified as the “both impaired” subtype with the typical hippocampal and cortical atrophy pattern, whereas 41.1% were classified as the subtypes with atypical atrophy patterns: “hippocampal atrophy only” (19.0%), “cortical atrophy only” (11.7%), and “both spared” (10.4%). Voxel-based morphometric analysis demonstrated whole-brain-level differences in overall GM atrophy across the subtypes. These subtypes showed different progression rates over 2 years; and all subtypes had significantly lower CSF amyloid-β_1–42 levels compared to CN. In conclusion, we identified four AD subtypes exhibiting heterogeneous atrophy patterns on MRI with different progression rates after controlling the effects of aging and gender on atrophy with normative information. CSF biomarker analysis suggests the presence of Aβ neuropathology irrespective of subtypes. Such heterogeneity of MRI-based neuronal injury biomarker and related heterogeneous progression patterns should be considered in clinical trials and practice with AD patients.