Heavy metal soil contamination detection using combined geochemistry and field spectroradiometry in the United Kingdom

Technological advances in hyperspectral remote sensing have been widely applied in heavy metal soil contamination studies, as they are able to provide assessments in a rapid and cost-effective way. The present work investigates the potential role of combining field and laboratory spectroradiometry with geochemical data of lead (Pb), zinc (Zn), copper (Cu) and cadmium (Cd) in quantifying and modelling heavy metal soil contamination (HMSC) for a floodplain site located in Wales, United Kingdom. The study objectives were to: (i) collect field- and lab-based spectra from contaminated soils by using ASD FieldSpec® 3, where the spectrum varies between 350 and 2500 nm; (ii) build field- and lab-based spectral libraries; (iii) conduct geochemical analyses of Pb, Zn, Cu and Cd using atomic absorption spectrometer; (iv) identify the specific spectral regions associated to the modelling of HMSC; and (v) develop and validate heavy metal prediction models (HMPM) for the aforementioned contaminants, by considering their spectral features and concentrations in the soil. Herein, the field- and lab-based spectral features derived from 85 soil samples were used successfully to develop two spectral libraries, which along with the concentrations of Pb, Zn, Cu and Cd were combined to build eight HMPMs using stepwise multiple linear regression. The results showed, for the first time, the feasibility to predict HMSC in a highly contaminated floodplain site by combining soil geochemistry analyses and field spectroradiometry. The generated models help for mapping heavy metal concentrations over a huge area by using space-borne hyperspectral sensors. The results further demonstrated the feasibility of combining geochemistry analyses with filed spectroradiometric data to generate models that can predict heavy metal concentrations

Synchronization of cytoplasmic and transferred mitochondrial ribosomal protein gene expression in land plants is linked to Telo-box motif enrichment

<p>Abstract</p> <p>Background</p> <p>Chloroplasts and mitochondria evolved from the endosymbionts of once free-living eubacteria, and they transferred most of their genes to the host nuclear genome during evolution. The mechanisms used by plants to coordinate the expression of such transferred genes, as well as other genes in the host nuclear genome, are still poorly understood.</p> <p>Results</p> <p>In this paper, we use nuclear-encoded chloroplast (cpRPGs), as well as mitochondrial (mtRPGs) and cytoplasmic (euRPGs) ribosomal protein genes to study the coordination of gene expression between organelles and the host. Results show that the mtRPGs, but not the cpRPGs, exhibit strongly synchronized expression with euRPGs in all investigated land plants and that this phenomenon is linked to the presence of a <it>telo</it>-box DNA motif in the promoter regions of mtRPGs and euRPGs. This motif is also enriched in the promoter regions of genes involved in DNA replication. Sequence analysis further indicates that mtRPGs, in contrast to cpRPGs, acquired <it>telo</it>-box from the host nuclear genome.</p> <p>Conclusions</p> <p>Based on our results, we propose a model of plant nuclear genome evolution where coordination of activities in mitochondria and chloroplast and other cellular functions, including cell cycle, might have served as a strong selection pressure for the differential acquisition of <it>telo</it>-box between mtRPGs and cpRPGs. This research also highlights the significance of physiological needs in shaping transcriptional regulatory evolution.</p

Long Noncoding Transcriptome in Chronic Obstructive Pulmonary Disease

Chronic airway inflammation from recurring exposures to noxious environmental stimuli results in a progressive and irreversible airflow limitation and the lung parenchymal damage that characterizes chronic obstructive pulmonary disease (COPD). The large variability observed in the onset and progression of COPD is primarily driven by complex gene-environment interactions. The transcriptomic and epigenetic memory potential of lung epithelial and innate immune cells drive responses, such as mucus hyperreactivity and airway remodeling, that are tightly regulated by various molecular mechanisms, for which several candidate susceptibility genes have been described. However, the recently described noncoding RNA species, in particular the long noncoding RNAs, may also have an important role in modulating pulmonary responses to chronic inhalation of toxic substances and the development of COPD. This review outlines the features of long noncoding RNAs that have been implicated in regulating the airway inflammatory responses to cigarette smoke exposure and their possible association with COPD pathogenesis. As COPD continues to debilitate the increasingly aging population and contribute to higher morbidity and mortality rates worldwide, the search for better biomarkers and alternative therapeutic options is pivotal

HIV-1 Productively Infects and Integrates in Bronchial Epithelial Cells

The role of lung epithelial cells in HIV-1-related lung comorbidities remains unclear, and the major hurdle in curing HIV is the persistence of latent HIV reservoirs in people living with HIV (PLWH). The advent of combined antiretroviral therapy has considerably increased the life span; however, the incidence of chronic lung diseases is significantly higher among PLWH. Lung epithelial cells orchestrate the respiratory immune responses and whether these cells are productively infected by HIV-1 is debatable. Normal human bronchial epithelial cells (NHBEs) grown on air-liquid interface were infected with X4-tropic HIV-1 and examined for latency using latency-reversing agents (LRAs). The role of CD4 and CXCR4 HIV coreceptors in NHBEs were tested, and DNA sequencing analysis was used to analyze the genomic integration of HIV proviral genes, Alu-HIVgag-pol, HIV-nef, and HIV-LTR. Lung epithelial sections from HIV-infected humans and SHIV-infected macaques were analyzed by FISH for HIV-gag-pol RNA and epithelial cell-specific immunostaining. NHBEs express CD4 and CXCR4 at higher levels than A549 cells. NHBEs are infected with HIV-1 basolaterally, but not apically, by X4-tropic HIV-1 in a CXCR4/CD4-dependent manner leading to HIV-p24 antigen production; however, NHBEs are induced to express CCR5 by IL-13 treatment. In the presence of cART, HIV-1 induces latency and integration of HIV provirus in the cellular DNA, which is rescued by the LRAs (endotoxin/vorinostat). Furthermore, lung epithelial cells from HIV-infected humans and SHIV-infected macaques contain HIV-specific RNA transcripts. Thus, lung epithelial cells are targeted by HIV-1 and could serve as potential HIV reservoirs that may contribute to the respiratory comorbidities in PLWH