The Role of Big Data in Promoting Green Development: Based on the Quasi-Natural Experiment of the Big Data Experimental Zone.

Against the backdrop of the pressing issue of global warming, the concept of green development, which emphasizes the rational utilization of resources and energy, has emerged as a viable model for future economic growth. Despite this, the interplay between big data technology and green development has yet to receive due consideration. This study aims to shed light on the role of big data in green development from the perspective of factor configuration distortion. To this end, a panel data analysis of 284 prefecture-level cities spanning from 2007 to 2020 was conducted, utilizing the Difference-in-Differences (DID) and Propensity Score Matching-Difference-in-Differences (PSM-DID) models to assess the impact of the establishment of the National Big Data Comprehensive Experimental Zone on green total factor productivity. The findings reveal that the establishment of the National Big Data Comprehensive Experimental Zone has a positive impact on green total factor productivity, primarily through optimizing the capital and labor allocation distortions, with the effect being more pronounced in areas with high levels of human capital, financial development, and economic activity. This research provides empirical evidence to evaluate the impact of the establishment of the National Big Data Comprehensive Experimental Zone and offers valuable policy implications for the pursuit of high-quality economic development.

The Effect of Environmental Regulation on the Efficiency of the Green Economy: The Intermediary Role of the Aggregation of Innovative Elements.

Green development is the only way to realize harmonious coexistence between people and nature, so it is of great significance to create a benchmark for high-quality development. Based on the panel data of 30 provinces (except Tibet, Hong Kong, Macao, and Taiwan) in China from 2009 to 2020, the super-efficiency slacks-based measure model was used to calculate the green economic efficiency of various regions in China, and a related statistical model was used to verify the influence of different types of environmental regulation policies on green economic efficiency and the intermediary effect of innovation factor agglomeration. The results show that: (1) during the inspection period, the influence of public-participation environmental regulation on the efficiency of the green economy presents an "inverted U" trend, while command-control and market-incentive environmental regulation policies inhibit the improvement of green economic efficiency; (2) the agglomeration of innovative elements plays a significant intermediary role in the transmission path of environmental regulation affecting green economic efficiency, but the intermediary effects of different types of environmental regulation are slightly different. Finally, we discuss environmental regulation and innovative elements, and some corresponding suggestions are put forward.

Study on the Impact of Environmental Tax on Industrial Green Transformation.

Tax revenue is one of the essential means through which the government controls the macro-economy and plays a vital role in promoting environmental protection and sustainable development. This study takes Chinese panel data from 2004 to 2020 as sample observations, uses the SBM-GML index method to measure industrial green total factor productivity, and then uses econometric methods such as the two-way fixed effects model and instrumental variable method to analyze the impact of an environmental tax on industrial green transformation. It is found that the generalized environmental tax represented by vehicle and vessel tax, resource tax, and urban land use tax has a significant positive effect on industrial green transformation. After a series of robustness tests and the exclusion of endogeneity, this conclusion remains valid. The research shows that credit governance, the agglomeration of producer service, and their co-agglomeration with manufacturing are important adjustment mechanisms. Among them, credit management is special and compulsory, greatly restricting the environmental pollution behavior of industrial enterprises, and encourages enterprises to make green investments and to actively improve production processes.

Enhanced catalytic sulfamethoxazole degradation via peroxymonosulfate activation over amorphous CoSx@SiO2 nanocages derived from ZIF-67.

In this work, the amorphous CoSx@SiO2 nanocages were hydrothermally synthesized by sulfurizing ZIF-67@SiO2 in the presence of thioacetamide (TAA). The catalytic performances of CoSx@SiO2 nanocages as heterogeneous catalysts to activate peroxymonosulfate (PMS) for the sulfamethoxazole (SMX) degradation were systematically investigated. 100% SMX was degraded within 6 min in CoSx@SiO2/PMS system, indicating that the amorphous CoSx@SiO2 nanocages exhibited outstanding sulfate radical-advanced oxidation process (SR-AOP) activity toward SMX degradation due to the regeneration of Co2+ by surficial sulfur species like S2-/S22-. The effects of PMS dosages, initial pH, SMX concentrations and co-existing ions on SMX degradation efficiency were explored in detail. The SMX removal efficiency was obviously improved in the simulated wastewater containing chloride ions (Cl-) and low-concentration bicarbonate ions (HCO3-). The residual PMS and the generated sulfate radical (SO4·-) were determined quantitatively in CoSx@SiO2/PMS system. A possible mechanism in CoSx@SiO2/PMS system was proposed based on the results of quenching experiments, X-ray photoelectron spectroscopy (XPS) analysis, electrochemical tests, and electron spin resonance (ESR). The CoSx@SiO2 exhibited good stability and reusability, in which 100% SMX removal was achieved even after five consecutive cycles. This work provided a strategy for regulating the stability of cobalt-based catalyst for efficient pollutant degradation by PMS activation.

Psychological stress enhances tumor growth and diminishes radiation response in preclinical model of lung cancer.

BACKGROUND AND PURPOSE: Patients with life-threatening illnesses, such as cancer, experience emotional distress. This study was to investigate the molecular and cellular mechanisms of relevant psychological stressor on tumor growth and therapeutic resistance. MATERIALS AND METHODS: Stress was induced in C57BL/6J mice bearing LLC lung tumors by exposure to a conspecific mice receiving inescapable foot shocks. Mice were irradiated at 7 Gy for 3 consecutive days. Behaviors were monitored by open field test (OFT), elevated plus maze (EPM), sucrose preference test (SPT), and learned helplessness (LH) test. Protein expression in tissues and cultured cells were measured by Western blot. RESULTS: This study in animals showed that observing a conspecific mouse receiving foot shocks induced depression like behaviors with increased plasma corticosterone and adrenaline levels which increased tumor growth and radioresistance. Stress increased Wnt1, Drosha, and vimentin expression and decreased E-cadherin expression in tumor tissues. The combination of stress and irradiation enhanced radioresistance along with the increase in vimentin expression. The in vitro study showed that a ß2-adrenergic receptor (ß2-AR) agonist blocked irradiation-induced cell apoptosis and decreased cell viability, while silencing ß2-AR expression reduced the protective effects of ß2-AR agonist. ß2-AR agonist obviously increased Wnt1 and Drosha expression in LLC-1 cells. CONCLUSION: Psychological stress increased tumor growth and enhanced radioresistance associated with the activation of epithelial-mesenchymal transition by stress hormone-stimulated adrenergic receptors.

Divergent anomaly in mesocorticolimbic dopaminergic circuits might be associated with different depressive behaviors, an animal study.

BACKGROUND: The mesocorticolimbic dopamine system, which originates from the ventral tegmental area (VTA) and projects primarily to the prefrontal cortex (PFC), olfactory tubercle (OT), nucleus accumbens (NAc), dorsal striatum (ST), and the amygdala (AMy), plays a pivotal role in determining individual motivation and sensitivity to rewards, namely, anhedonia. Not all depressive individuals exhibited anhedonia, thus, it is natural to speculate that the heterogenous manifestations of depression might be related to the mesocorticolimbic dopamine system. Maternal deprivation (MD) and chronic unpredictable stress (CUPS) are two well-established depressogenic stressors, and they were proven to induce different depressive phenotypes. METHODS: The depressive and anxiety-like behaviors of MD and CUPS-treated rats were measured by classical behavioral tests including open field, forced swimming, and sucrose preference test. The expression of D1-5 dopamine receptors and DAT mRNA and protein in the mesocorticolimbic dopamine system of rats exposed to MD and CUPS were measured by real-time PCR and Western blot, respectively. RESULTS: Severe anhedonia was observed in MD but not CUPS rats. Divergent expression of D1 and D2 receptors and DAT mRNA and protein in the mesocorticolimbic dopamine system were found between MD and CUPS rats. Significant correlations between different depressive behaviors and D1-/D2-like receptors and DAT protein levels in the mesocorticolimbic dopamine system were observed. CONCLUSION: Different depressive behaviors of rats such as anhedonia, passive coping behavior, and declined exploratory interest might be related to divergent dopaminergic pathways. Anhedonia is associated with the dysfunction of VTA-NAc and VTA-OT dopaminergic pathways, the passive coping behavior is related to the dysregulation of VTA-PFC and VTA-AMy pathways, and individual exploratory interest is associated with abnormal activity of VTA-PFC and VTA-ST pathways.

Hypo-CpG methylation controls PTEN expression and cell apoptosis in irradiated lung.

PURPOSE: The current study was designed to address our hypothesis that oxidative stress secondary to the ionizing event upregulates phosphatase and tensin homolog (PTEN) mRNA and protein in the lungs of C57BL/6J mice through oxidative DNA damage resulting in CpG hypomethylation in the PTEN promoter. METHODS: Fibrosis-prone C57BL/6J mice were exposed to 0 or 15 Gy of 320 kVp X-rays to the whole thorax. Lung tissue was serially harvested at time points between one day and six months postirradiation. Tissue levels of PTEN mRNA, total protein, and phosphorylated PTEN, as well as CpG methylation of the PTEN promoter, expression of DNA methyltransferases 1 (Dnmt1) and 3a (Dnmt3a), NADPH oxidase 4 (Nox4) protein expression, and DNA damage levels were measured. The induction of DNA damage and global methylation changes were also examined in hydrogen peroxide (H2O2)-treated human umbilical vein endothelial cells (HUVECs) and human bronchial epithelial cells in vitro. RESULTS: These experiments demonstrate that PTEN mRNA and protein, Nox4 protein, and DNA damage levels increase continuously from one day to six months following radiation exposure. Elevated PTEN transcription and translation are likely the result of the observed decrease in CpG methylation of the PTEN promoter region. This finding is not consistent with the observed increase in Dnmt1 and Dnmt3a protein expression, implicating an alternative mechanism as the driving force behind hypomethylation. In vitro results provide evidence that H2O2 can induce DNA damage and affect DNA methylation status. The Mn porphyrin-based superoxide dismutase (SOD) mimic MnTnHEx-2-PyP(5+ )exhibited partial rescue from radiation-induced hypomethylation. CONCLUSIONS: Taken together, these data suggest that reactive oxygen species (ROS)-induced DNA damage results in hypomethylation of the PTEN promoter, upregulation of PTEN mRNA and protein, and a subsequent increase in apoptosis in irradiated lung tissue.

Molecular changes in the medial prefrontal cortex and nucleus accumbens are associated with blocking the behavioral sensitization to cocaine.

Previous studies have demonstrated that cocaine-induced behavioral sensitization is associated with persistent functional and structural alterations in the medial prefrontal cortex (mPFC) and nucleus accumbens (NAc); however, the molecular mechanisms underlying these changes have not been elucidated. In this study, the behavioral sensitization to cocaine was established in Sprague Dawley rats and was measured by locomotion and behavioral rating. The brain tissue homogenization was used for measuring the level of brain-derived neurotrophic factor (BDNF), the expression and activity of integrin-linked kinase (ILK), level of protein kinase B (Akt) phosphorylation at serine 473 and threonine 308, and the expression of p75(NTR), TrkA, and TrkB protein. The Results showed that cocaine sensitization was associated with increased BDNF, ILK activity, phospho-Akt Ser(473), p75(NTR), and TrkB protein levels in the mPFC and NAc core. The combination of pergolide and ondansetron normalized not only behavioral sensitization, but also the increases in these molecular markers. Dual immunofluoresence staining showed that ILK expression is co-distributed with p75(NTR) and TrkA expression in both the mPFC and NAc core. Results suggested that the BDNF-TrkA/p75(NTR)-ILK-Akt signaling pathway may be active in cocaine sensitization and associated neural plasticity in the mPFC and NAc core.

Dopamine Receptor D2 and Associated microRNAs Are Involved in Stress Susceptibility and Resistance to Escitalopram Treatment.

BACKGROUND: Early life stress has been demonstrated to increase the risk of developing depression in adulthood. However, the roles and associated molecular mechanisms of stresses in the onset and relapse of depression have yet to be fully elucidated. METHODS: Depression-like behaviors were induced in rats by maternal deprivation and chronic unpredictable stress. Depression- and anxiety-like behaviors of rats, dopamine receptor D2 level, and microRNAs expression in rats' brain tissues were measured. RESULTS: Chronic unpredictable stress alone induced depression-like behaviors in rats, but maternal deprivation enhanced the effect of chronic unpredictable stress. Escitalopram significantly decreased depression-like behaviors in chronic unpredictable stress rats but was less effective in maternal deprivation with chronic unpredictable stress rats. Maternal deprivation increased dopamine receptor D2 messenger RNA expression and decreased microRNA-9 expression in the striatum. Chronic unpredictable stress increased dopamine receptor D2 mRNA and protein levels and decreased microRNA-9 expression in the nucleus accumbens. Furthermore, maternal deprivation enhanced the effect of chronic unpredictable stress on dopamine receptor D2 gene and microRNA-9 expression. Chronic unpredictable stress increased the expression of microRNA-326 in the nucleus accumbens but decreased it in the striatum, whereas maternal deprivation elevated microRNA-326 expression in the striatum. Escitalopram normalized microRNA-326 expression but had no effect on the expression of microRNA-9, dopamine receptor D2 mRNA, and dopamine receptor D2 protein in both the nucleus accumbens and striatum. The in vitro study showed that only microRNA-9 directly targeted the 3' untranslated region of dopamine receptor D2 mRNA and inhibited dopamine receptor D2 protein expression. CONCLUSION: Early life stress enhanced the susceptibility to late life stress and resistance to escitalopram treatment through decreasing microRNA-9 expression and subsequently upregulating dopamine receptor D2 expression in the nucleus accumbens. microRNA-326 may be a novel target of escitalopram.

Anhedonia was associated with the dysregulation of hippocampal HTR4 and microRNA Let-7a in rats.

OBJECTIVE: Depression is a serious mental illness. However, the molecular mechanisms responsible for the development of depression remain unknown. METHODS: In this study, animal models of depression were established using maternal deprivation (MD) and chronic unpredictable stress (CUPS). Behavioral performance of rats was monitored by open field test, forced swim test, and sucrose consumption test. The expression of serotonin receptor-4 (Htr4) mRNA and Let-7a microRNA was detected by real-time PCR, while Htr4 protein level was measured by Western blot. RESULTS: In the open field test, rats subjected to MD and CUPS exhibited significant decreases in vertical activity. CUPS rats spent less time in the central area and excreted more fecal pellets than MD and control rats. In the forced swim and sucrose consumption tests, CUPS and MD rats exhibited significantly longer floating time and consumed less sucrose than control rats. MD rats exhibited significantly shorter floating time and consumed less sucrose than CUPS rats. MD rats showed significantly lower Htr4 mRNA and protein expression and significantly higher Let-7a level in the hippocampus than control rats. Htr4 mRNA and protein expression negatively correlated with Let-7a expression. Htr4 mRNA expression positively correlated with sucrose preference rate, while Let-7a expression negatively correlated with the sucrose preference rate. CONCLUSION: Anhedonia, not despair or a decline in exploratory interest, may be associated with upregulation of Let-7a and downregulation of Htr4 expression in the hippocampus. The hippocampal Htr4 level may be regulated by Let-7a in rats.

Concentrations of asbestos fibers and metals in drinking water caused by natural crocidolite asbestos in the soil from a rural area.

Asbestos fibers and metals in drinking water are of significant importance to the field of asbestos toxicology. However, little is known about asbestos fibers and metals in drinking water caused by naturally occurring asbestos. Therefore, concentrations of asbestos fibers and metals in well and surface waters from asbestos and control areas were measured by scanning electron microscopy (SEM), inductively coupled plasma (ICP) optical emission spectrometer, and ICP-mass spectrometry in this study. The results indicated that the mean concentration of asbestos fibers was 42.34 millions of fibers per liter by SEM, which was much higher than the permission exposure level. The main compositions of both asbestos fibers in crocidolite mineral and in drinking water were Na, Mg, Fe, and Si based on energy dispersive X-ray analysis. This revealed that the drinking water has been contaminated by asbestos fibers from crocidolite mineral in soil and rock. Except for Cr, Pb, Zn, and Mn, the mean concentrations of Ni, Na, Mg, K, Fe, Ca, and SiO2 were much higher in both surface water and well waters from the asbestos area than in well water from the control area. The results of principal component and cluster analyses indicated that the metals in surface and well waters from the asbestos area were significantly influenced by crocidolite mineral in soil and rock. In the asbestos area, the mean concentrations of asbestos fibers and Ni, Na, Mg, K, Fe, Ca, and SiO2 were higher in surface and well waters, indicating that asbestos fibers and the metals were significantly influenced by crocidolite in soil and rock.

Abnormal hippocampal BDNF and miR-16 expression is associated with depression-like behaviors induced by stress during early life.

Some environmental stressors lead to the onset of depression via inhibiting hippocampal BDNF expression, but other environmental stressors-induced depression exhibits no change in BDNF expression. The underlying mechanisms behind the divergence remain unknown. In this study, depression-like behaviors were induced in rats by maternal deprivation (MD) and chronic unpredictable stress (CUPS). Depression-like behaviors were tested by open field test, forced swimming test, and sucrose consumption test. BDNF and miR-16 expressions in the hippocampus were examined by real-time PCR. MD and CUPS rats crawled less distance, exhibited decreased vertical activity, and produced more fecal pellets than control rats in the open field test. However, MD rats crawled less distance and produced significantly less fecal pellets than CUPS rats. In the forced swimming and sucrose consumption tests, CUPS and MD rats exhibited longer floating time and consumed less sucrose than control rats, but MD rats exhibited shorter floating time and consumed less sucrose than CUPS rats. MD but not CUPS rats showed lower BDNF mRNA and higher miR-16 expression than control rats. In MD rats, BDNF mRNA expression negatively correlated with the expression of miR-16. BDNF expression positively correlated with the total distance rats crawled and vertical activity in the open field test while miR-16 expression negatively correlated the two behaviors. BDNF positively correlated with sucrose preference rate while miR-16 negatively correlated with sucrose preference rate of the sucrose consumption test. Our study suggests that MD and CUPS induced different depression-like behaviors in rats. Depression induced by MD but not CUPS was significantly associated with upregulation of miR-16 and possibly subsequent downregulation of BDNF in hippocampus.

Oncolytic virus-mediated tumor radiosensitization in mice through DNA-PKcs-specific shRNA.

One of the key issues in cancer radiotherapy research is to sensitize tumor cells to the cell killing effects of ionizing radiation while leaving normal tissues intact. One potential approach to achieve this is through tumor-specific targeting of DNA repair genes. In this study, we engineered a replication-deficient adenovirus encoding a mini shRNA gene targeted to the DNA-PKcs gene, which is involved in double strand break DNA repair, and evaluated its anti-tumor efficacy in combination with radiotherapy. Our shRNA-encoding adenovirus showed significant efficacy in down-regulating the levels of the DNA-PKcs protein that was accompanied by increased radiation sensitivity in the human HCT116 colon cancer cells. However, when delivered intratumorally to xenograft human tumors, minimal anti-tumor effects of the virus were seen either alone or in combination with radiation therapy, suggesting an inefficiency of the non-replicative adenovirus in delivering shRNA genes to the tumor mass. When a conditionally replicative adenovirus targeted to telomerase-positive tumor cells was used in conjunction with the DNA-PKcs-targeted shRNA-encoding non-replicative adenovirus, the efficiency of tumor-specific anti-DNA-PKcs shRNA gene expression was enhanced significantly. Most importantly, this enhanced shRNA expression led to significant anti-tumor efficacy of concurrently delivered radiation therapy. Our results suggest our shRNA-based DNA-PKcs- targeting approach in combination with tumor-targeting replicative adenovirus is a promising method to sensitize solid tumors to radiation therapy.

Impacts of land use on spatial distribution of mortality rates of cancers caused by naturally occurring asbestos.

This study investigated the spatial distributions of mortality rates of six cancers: mesothelioma, lung cancer, intestinal cancer, nasopharyngeal and laryngeal cancer, liver cancer, and stomach cancer in Dayao using Geographic Information Systems. Relationships between the mortality rates of the six cancers and land use patterns were investigated by Pearson Correlation Coefficients. The results indicated that the mortality rates of nasopharyngeal and laryngeal cancer, lung cancer, intestinal cancer, and mesothelioma were significantly associated with outcropped asbestos. Both the proportions of farmland and urban area were positively related to the mortality rates of nasopharyngeal and laryngeal cancer, lung cancer, intestinal cancer, and mesothelioma, and significant negative correlations were found between the proportion of forestland and nasopharyngeal and laryngeal cancer and intestinal cancer. It can be concluded that naturally occurring asbestos may significantly elevate the mortality rates of nasopharyngeal and laryngeal cancer, intestinal cancer, lung cancer, and mesothelioma. Moreover, higher proportions of farmland, urban area, and lower proportions of forested land may elevate the mortality rate of the four cancers.

Temporal expression of hypoxia-regulated genes is associated with early changes in redox status in irradiated lung.

The development of normal lung tissue toxicity after radiation exposure results from multiple changes in cell signaling and communication initiated at the time of the ionizing event. The onset of gross pulmonary injury is preceded by tissue hypoxia and chronic oxidative stress. We have previously shown that development of debilitating lung injury can be mitigated or prevented by administration of AEOL10150, a potent catalytic antioxidant, 24h after radiation. This suggests that hypoxia-mediated signaling pathways may play a role in late radiation injury, but the exact mechanism remains unclear. The purpose of this study was to evaluate changes in the temporal expression of hypoxia-associated genes in irradiated mouse lung and determine whether AEOL10150 alters expression of these genes. A focused oligo array was used to establish a hypoxia-associated gene expression signature for lung tissue from sham-irradiated or irradiated mice treated with or without AEOL10150. Results were further verified by RT-PCR. Forty-four genes associated with metabolism, cell growth, apoptosis, inflammation, oxidative stress, and extracellular matrix synthesis were upregulated after radiation. Elevated expression of 31 of these genes was attenuated in animals treated with AEOL10150, suggesting that expression of a number of hypoxia-associated genes is regulated by early development of oxidative stress after radiation. Genes identified herein could provide insight into the role of hypoxic signaling in radiation lung injury, suggesting novel therapeutic targets, as well as clues to the mechanism by which AEOL10150 confers pulmonary radioprotection.

Levels of Cd, Pb, As, Hg, and Se in hair of residents living in villages around Fenghuang polymetallic mine, southwestern China.

Heavy metal levels in hair of residents living in villages around Fenghuang mine were investigated. Samples belonging to mine areas showed the highest values, with mean concentrations (mg kg(-1)) of 0.17 for Cd, 8.67 for Pb, 0.11 for As, 2.19 for Hg, and 0.64 for Se. Significant correlations (p < 0.01) were found between Cd-Pb, Cd-As, Pb-As, and Se-Hg. There is no significant difference in any of the elements among age groups. However, significant differences in Cd and Pb levels were found between genders. Results revealed that children and females were more susceptible to Cd and Pb exposure.

Infusion of BDNF into the nucleus accumbens of aged rats improves cognition and structural synaptic plasticity through PI3K-ILK-Akt signaling.

To investigate the involvement of the nucleus accumbens (NAc) in cognitive impairment and the therapeutic effects of brain-derived neurotrophic factor (BDNF) in an animal model of cognitive deficit, we infused BDNF into the NAc of cognitively impaired aged rats. Cognition was evaluated by Morris water maze test. Structural synaptic plasticity was measured by Golgi staining. Brain tissue homogenization was used to measure the changes in signal molecules. Cultured PC-12 cells expressing tyrosine kinase receptor (Trk) B/p75 neurotrophin receptor (p75(NTR)), p75(NTR) or TrkA/p75(NTR) receptors were used for BDNF stimulation assays. Significant decreases in the levels of BDNF, phosphatidylinositol-3-kinase (PI3K) and integrin-linked kinase (ILK) activity, protein kinase B (Akt) Ser47³ phosphorylation, dendritic branching, and density of dendritic spines on medium spiny neurons were observed in the NAc. Importantly, infusion of BDNF restored cognition, synaptic plasticity, and cell signaling. In cultured PC-12 cells, BDNF activated PI3K/Akt signaling through the TrkB receptor, whereas stimulation of ILK/Akt occurred through TrkA/p75(NTR) heteroreceptor. Our study suggested that the decreased BDNF level and its downstream signaling as well as loss of synaptic plasticity in the NAc are associated with cognitive impairments in aged rats. The BDNF-activated PI3K-Akt and ILK-Akt signaling play a key role in structural synaptic plasticity. Our study also suggested that BDNF could be a mechanism-based treatment for dementia.

Oxidative stress mediates radiation lung injury by inducing apoptosis.

PURPOSE: Apoptosis in irradiated normal lung tissue has been observed several weeks after radiation. However, the signaling pathway propagating cell death after radiation remains unknown. METHODS AND MATERIALS: C57BL/6J mice were irradiated with 15 Gy to the whole thorax. Pro-apoptotic signaling was evaluated 6 weeks after radiation with or without administration of AEOL10150, a potent catalytic scavenger of reactive oxygen and nitrogen species. RESULTS: Apoptosis was observed primarily in type I and type II pneumocytes and endothelium. Apoptosis correlated with increased PTEN expression, inhibition of downstream PI3K/AKT signaling, and increased p53 and Bax protein levels. Transforming growth factor-ß1, Nox4, and oxidative stress were also increased 6 weeks after radiation. Therapeutic administration of AEOL10150 suppressed pro-apoptotic signaling and dramatically reduced the number of apoptotic cells. CONCLUSION: Increased PTEN signaling after radiation results in apoptosis of lung parenchymal cells. We hypothesize that upregulation of PTEN is influenced by Nox4-derived oxidative stress. To our knowledge, this is the first study to highlight the role of PTEN in radiation-induced pulmonary toxicity.

Bioaccessibility and risk assessment of cadmium from uncooked rice using an in vitro digestion model.

Cadmium (Cd)-contaminated rice is one of the most important sources of cadmium exposure in the general population from some Asian countries. This study was conducted to assess cadmium exposure from uncooked rice in rural mining areas based on the bioaccessible fraction of cadmium using an in vitro digestion model. The biotoxic effects of cadmium in uncooked rice from mining areas were much higher than those in the control area, based not only on their higher total concentration (52.49 vs. 7.93 µg kg(-1)), but also on their higher bioaccessibility (16.94% vs. 2.38%). In the mining areas, the bioaccessible fraction of cadmium in uncooked rice has a significant positive correlation with the total concentration of cadmium in rice and there was quarterly unsafe rice to the public in the mining areas. The results indicated that the in vitro digestion model could be a useful and economical tool for providing the solubilization or bioaccessibility of uncooked rice in the mining area. The results could be helpful in conducting future experiments of cooked rice in the vitro model.