摘要：
We estimated associations between ambient air pollution, home environment and asthma as well as rhinitis among adults across China. A total of 40,279 young adults from eight Chinese cities participated in a questionnaire survey (participation rate 75%). There were questions on health and home environment. Information on city level gross domestic product (GDP) per capita, ambient temperature and PM10 and NO2 were collected from registers. Two-level logistic regression models were used to study health associations. Totally 1.6% reported asthma and 6.6% reported allergic rhinitis (AR). Higher temperature was associated with more asthma but less AR. Higher GDP was associated with less asthma but more AR. Higher degree of urbanization, higher level of NO2 and living near heavily trafficked road were risk factors for asthma and AR. Participants in older buildings reported more asthma. Redecoration and buying new furniture were related to more asthma and AR (OR = 1.15-1.91). Using natural gas (OR = 1.34) and biomass (OR = 1.35) for cooking were risk factors for AR. Burning mosquito coils and incense increased the risk of asthma and AR. Cat keeping (OR = 2.88), dog keeping (OR = 2.04), cockroaches (OR = 1.54) and rats or mice (OR = 1.46) were associated with asthma. Cockroaches increased the risk of AR (OR = 1.22). Air humidifier and air cleaner were linked to asthma and AR. Frequent cleaning and exposing bedding to sunshine were protective. In conclusion, urbanization, NO2 and traffic exhaust can increase the risk of adult asthma and AR. Higher ambient temperature was related to more asthma but less AR. Indoor animals such as cats, dogs, rats/mice and presence of cockroaches were associated with asthma or AR. Indoor chemical sources such as redecoration and new furniture were other risk factors. Cooking with natural gas or biomass and burning mosquito coils and incense were associated with asthma or AR. Frequent cleaning and exposing bedding to sunshine were protective. (C) 2020 The Authors. Published by Elsevier B.V.
摘要：
Although it is well known that Bacillus thuringiensis Cry toxins kill insect pest by disrupting midgut cells of susceptible larvae through their pore formation activity, it is not clear what intracellular events are triggered after pore formation on the cell membrane of the target cells. Here we analyzed the role of Cry toxins on autophagy activation using several cell lines as models as well as in Helicoverpa armigera larvae. The selected insect cell lines (Hi5, Sl-HP and Sf9) were susceptible to activated Cry1Ca toxin, but only Sl-HP cells were also susceptible to activated Cry1Ac toxin. In contrast, the mammalian cell line 293 T was not susceptible to Cry1Ac or to Cry1Ca. Results show that Cry toxins induced autophagy only in the susceptible cell lines as shown by the analysis of the changes in the ratio of Atg8-PE to Atg8 and by formation of autophagosome dots containing Atg8-PE. The Cry1Ac enhanced autophagy in the midgut tissue of H. armigera larvae. Silencing expression of specific genes by RNAi assays confirmed that the autophagy induced by activated Cry toxins was dependent on AMPK and JNK pathways. Finally, inhibition of autophagy in the cell lines by specific inhibitors or RNAi assays resulted in delayed cell death triggered by Cry toxins, suggesting that the increased autophagy activity observed after toxin intoxication may contribute to cell death.
通讯机构：
[Linjing Deng] s;[Qihong Deng] S;School of Public Health, Zhengzhou University, Zhengzhou 450001, China<&wdkj&>school of tourism and ubran management, Jiangxi University of Finance and Economics, Nanchang 330000, China
摘要：
Circulating tumor DNA (ctDNA) as a class of liquid biopsy is a type of gene fragment that contains tumor-specific gene changes in body fluids such as human peripheral blood. More and more evidences show that ctDNA is an excellent tumor biomarker for diagnosis, prognosis, tumor heterogeneity and so on. ctDNA is a tumor code in the blood. Liquid biopsy of ctDNA is firstly summarized. Compared with the traditional detection technologies of ctDNA, the biosensor is an excellent choice for the detection of ctDNA because of its portability, sensitivity, specificity and ease of use. This review mainly evaluates various biosensors applied to the detection of ctDNA. We discuss the most commonly used bioreceptors to specifically identify and bind ctDNA, including complementary DNA (cDNA), peptide nucleic acid (PNA) and anti-5 MethylCytosines, and the biotransducers which convert biological signals to analysable signs. The review also discusses signal amplification strategies in biosensors to detect ctDNA.
摘要：
The mechanisms of cadmium toxicity to cyanobacterial photosynthesis have been extensively studied, but the response mechanisms to combinations of different cadmium concentrations and different light intensities are not yet well understood. The two principal objectives of the present work were to: 1) study the short term (5 h) toxic effects of cadmium on Synechocystis PCC6803 under three different culturing light intensity conditions; and, 2) investigate the effects of light history on Cd toxicity to Synechocystis. The maximal (capital EF, CyrillicM) and operational (capital EF, Cyrillic'M) photosystem II quantum yields, photosystem I quantum yield [Y (I)], cyclic electron flow, relative photochemical quenching (qPrel), relative non-photochemical quenching (qNrel), relative unquenched fluorescence (UQFrel), pigment contents, and cadmium uptake were evaluated when Synechocystis cells were treated with cadmium for 5 h under three different light conditions. We demonstrated that cadmium toxicity was enhanced with increasing growth light intensities due to increased cadmium uptake under higher light exposures, and the photoprotective mechanisms could not cope with cadmium and light stress under high light conditions. We also investigated Cd toxicity to Synechocystis adapted to three growth light intensities and subsequently shifted to different light intensity conditions to compare the effects of light regime shift on cadmium toxicity. We observed increased cadmium toxicity when the cells were transferred from low light to high light conditions. Interestingly, Synechocystis cells grown at high light intensities were more tolerant to cadmium than cells grown at low light intensities after the same light regime shift, due to the development of photoprotective mechanisms.
摘要：
Around the globe, worsening air pollution is spawning major public health and environmental concerns, especially in the poorest and most populous cities. As a major secondary air pollutant, ozone is a potential risk factor for exacerbated asthma, although the underlying mechanisms remain uncertain. In this study, we aim to investigate the role of ozone on asthma exacerbation using a classic asthmatic model with allergic airway inflammation by treating Balb/c mice with ovalbumin (OVA). Our study shows ozone exposure significantly exacerbated OVA-induced asthmatic phenotypes, including serum immunoglobulin, Th cytokines, inflammatory cell counts, mucus production, airway remodeling, and airway hyper responsiveness (AHR). Interestingly, expression of transient receptor potential cation channel subfamily V memberl (TRPV1) was also significantly elevated in ozone-exacerbated asthmatic mice and that treatment with TRPVI antagonist effectively suppressed AHR, airway inflammation and remodeling. The underlying mechanisms of these effects may be associated with suppression of neuropeptide calcitonin gene-related peptide (CGRP) and thymic stromal lymphopoietin (TSLP), an epithelial cell-derived cytokine. Base on the role of TRPV1 in allergic asthma, this study further revealed that inhibition of TRPVI by TRPV1 antagonist has significant anti-inflammatory effects on ozone-induced asthma exacerbation in this study. Induction of TRPVI expression may be an important mechanism underlying the increased risks for asthma after exposure to environmental pollutants. (C) 2019 Elsevier Ltd. All rights reserved.
摘要：
Recent epidemiological studies have found that diisononyl phthalate (DINP) is associated with an increase in blood pressure. However, this correlation had not been clarified, nor has the underlying mechanism been characterized. In this study, C57/BL6 mice were exposed to DINP doses of 0.15 mg/kg/day, 1.5 mg/kg/day or 15 mg/kg/day for 6 weeks. Dexamethasone (DEXA) was used to build the hypertension model. After DINP exposure and 1 mg/kg/day DEXA treatment, the levels of systolic blood pressure (SBP), diastolic blood pressure (DBP), mean blood pressure (MBP) and heart rate (HR) were determined, and any histopathological changes in hypertension targeted organs of the mice were investigated. The results suggest that DINP exposure and DEXA treatment induced marked increases in SBP, DBP, and MBP, and that 15 mg/kg/day DINP exposure could also increase the HR level. Along with the blood pressure increase, DINP exposure induced pathological changes to the heart, aorta, and kidney. To explore the underlying mechanism, we measured the expression of angiotensin converting enzyme (ACE), angiotensin-II type 1 receptor (AT1R) and endothelial nitric oxide synthase (eNOS) in the aorta, as well as the nitric oxide (NO) concentration in serum. The data suggest that DINP exposure and DEXA treatment enhance the expression of ACE and AT1R, and inhibit eNOS expression and NO production. Interestingly, treatment with 5 mg/kg/day ACE inhibitor (ACEI) alleviated the increase in blood pressure induced by DINP exposure and DEXA treatment. These findings expand our understanding of how DINP exposure impacts the development of hypertension, and elucidates the underlying mechanisms.
作者机构：
[Zhang, Yuzhe; Bristow, Robert G.; van der Kwast, Theo; Xu, Xin; Hua, Junjie Tony; He, Housheng Hansen; Tsao, Ming-Sound; Liang, Yi; Ahmed, Musaddeque; Berlin, Alejandro; Haibe-Kains, Benjamin; Soares, Fraser; Guo, Haiyang; Tran Nguyen; Wouters, Bradly G.; Koritzinsky, Marianne; Xu, Jing; Su, Peiran; Chen, Sujun; Mahamud, Osman; Vellanki, Ravi N.; Ba-Alawi, Wail] Univ Hlth Network, Princess Margaret Canc Ctr, Toronto, ON M5G 1L7, Canada.;[Gleave, Martin; Fazli, Ladan; Ci, Xinpei; Lin, Dong; Li, Estelle; Zoubeidi, Amina; Xue, Hui; Wang, Yuzhuo] Univ British Columbia, Vancouver Gen Hosp, Vancouver Prostate Ctr, Vancouver, BC V6H 3Z6, Canada.;[Gleave, Martin; Fazli, Ladan; Ci, Xinpei; Lin, Dong; Li, Estelle; Zoubeidi, Amina; Xue, Hui; Wang, Yuzhuo] Univ British Columbia, Dept Urol Sci, Vancouver, BC V6H 3Z6, Canada.;[Zhang, Si; Ci, Xinpei; Lin, Dong; Xue, Hui; Wang, Yuzhuo] BC Canc Res Ctr, Dept Expt Therapeut, Vancouver, BC V5Z 1L3, Canada.;[Bristow, Robert G.; Boutros, Paul C.; Hua, Junjie Tony; He, Housheng Hansen; Haibe-Kains, Benjamin; Wouters, Bradly G.; Su, Peiran; Chen, Sujun; Mahamud, Osman; Ba-Alawi, Wail] Univ Toronto, Dept Med Biophys, Toronto, ON M5G 2M9, Canada.
通讯机构：
[Guo, HY; He, HH; Wang, Yuzhuo; He, Housheng Hansen] U;[Wang, Yuzhuo] B;Univ Hlth Network, Princess Margaret Canc Ctr, Toronto, ON M5G 1L7, Canada.;Univ British Columbia, Vancouver Gen Hosp, Vancouver Prostate Ctr, Vancouver, BC V6H 3Z6, Canada.;Univ British Columbia, Dept Urol Sci, Vancouver, BC V6H 3Z6, Canada.
摘要：
Neuroendocrine prostate cancer (NEPC), a lethal form of the disease, is characterized by loss of androgen receptor (AR) signaling during neuroendocrine transdifferentiation, which results in resistance to AR-targeted therapy. Clinically, genomically and epigenetically, NEPC resembles other types of poorly differentiated neuroendocrine tumors (NETs). Through pan-NET analyses, we identified ONECUT2 as a candidate master transcriptional regulator of poorly differentiated NETs. ONECUT2 ectopic expression in prostate adenocarcinoma synergizes with hypoxia to suppress androgen signaling and induce neuroendocrine plasticity. ONEUCT2 drives tumor aggressiveness in NEPC, partially through regulating hypoxia signaling and tumor hypoxia. Specifically, ONECUT2 activates SMAD3, which regulates hypoxia signaling through modulating HIF1alpha chromatin-binding, leading NEPC to exhibit higher degrees of hypoxia compared to prostate adenocarcinomas. Treatment with hypoxia-activated prodrug TH-302 potently reduces NEPC tumor growth. Collectively, these results highlight the synergy between ONECUT2 and hypoxia in driving NEPC, and emphasize the potential of hypoxia-directed therapy for NEPC patients.
摘要：
Anther/pollen development is a highly programmed process in flowering plants. However, the molecular mechanism of regulating anther/pollen development is still largely unclear so far. Here, we report a cotton WRKY transcription factor (GhWRKY22) that functions in anther/pollen development. Quantitative RT-PCR and GUS activity analyses revealed that GhWRKY22 is predominantly expressed in the late developing anther/pollen of cotton. The transgenic Arabidopsis plants expressing GhWRKY22 displayed the male fertility defect with the fewer viable pollen grains. Expression of the genes involved in jasmonate (JA) biosynthesis was up-regulated, whereas expression of the JA-repressors (JAZ1 and JAZ8) was down-regulated in the transgenic Arabidopsis plants expressing GhWRKY22, compared with those in wild type. Yeast one-hybrid and ChIP-qPCR assays demonstrated that GhWRKY22 modulated the expression of JAZ genes by directly binding to their promoters for regulating anther/pollen development. Yeast two-hybrid assay indicated that GhMYB24 could interact with GhJAZ8-A and GhJAZ13-A. Furthermore, expression of AtMYB24, AtPAL2 and AtANS2 was enhanced in the transgenic Arabidopsis plants, owing to GhWRKY22 overexpression. Taking the data together, our results suggest that GhWRKY22 acts as a transcriptional repressor to regulate anther/pollen development possibly by modulating the expression of the JAZ genes.
摘要：
The toxicity of formaldehyde (FA) has always been of great concern, particularly since its use is unavoidable. On the other hand, epigallocatechin-3-gallate (EGCG), an active substance in tea polyphenols, has been shown to demonstrate physiological protective functions by in both epidemiological and zoological studies, particularly in the nervous system. The study described here, aims to explore whether EGCG can alleviate the neurotoxic effects induced by formaldehyde. After 14 days of exposure to 3 mg/m(3) formaldehyde, mice exhibited significant cognitive impairment. In the FA group, a significant increase in iNOS level compared with the control group was observed. The reduced GSH level was significantly decreased. The levels of IL-1beta, TNF-alpha and Caspase-3 were obviously raised, while H&E and Nissl staining illustrated significant neuronal damage. After administering EGCG as a protective agent, all the above observed changes were reversed, and the protective effect of EGCG became gradually evident in the 20-500 mg/kg range. Immunohistochemistry results showed that EGCG could activate the Nrf2 signaling pathway, thus alleviating the oxidative damage caused by formaldehyde.
期刊：
Human Genetics,2019年138(2):151-166 ISSN：0340-6717
通讯作者：
Huang, Qingyang
作者机构：
[Zhang, Manling; Zhou, Qian; Huang, Qingyang; Mei, Bing; Wang, Ya; Ye, Weiyuan; Huang, Han; Chen, Yuanyuan; Niu, Yajing] Cent China Normal Univ, Sch Life Sci, Hubei Key Lab Genet Regulat & Integrat Biol, Wuhan 430079, Hubei, Peoples R China.
通讯机构：
[Huang, Qingyang] C;Cent China Normal Univ, Sch Life Sci, Hubei Key Lab Genet Regulat & Integrat Biol, Wuhan 430079, Hubei, Peoples R China.
摘要：
Previous genome-wide linkage and association studies have identified an osteoporosis-associated locus at 1p36 that harbors SNPs rs34920465 and rs6426749. The 1p36 locus also comprises the WNT4 gene with known role in bone metabolism and functionally unknown ZBTB40/lncRNA ZBTB40-IT1 genes. How these might interact to contribute to osteoporosis susceptibility is not known. In this study, we show that lncRNA ZBTB40-IT1 is able to suppress osteogenesis and promote osteoclastogenesis by regulating the expression of WNT4, RUNX2, OSX, ALP, COL1A1, OPG and RANKL in U-2OS and hFOB1.19 cell lines, whereas ZBTB40 plays an opposite role in bone metabolism. Treatment with parathyroid hormone significantly downregulates the expression of ZBTB40-IT1 in U-2OS cell lines. ZBTB40 can suppress ZBTB40-IT1 expression but has no response to parathyroid hormone treatment. Dual-luciferase assay and biotin pull-down assay demonstrate that osteoporosis GWAS lead SNPs rs34920465-G and rs6426749-C alleles can respectively bind transcription factors JUN::FOS and CREB1, and upregulate ZBTB40 and ZBTB40-IT1 expression. Our study discovers the critical role of ZBTB40 and lncRNA ZBTB40-IT1 in bone metabolism, and provides a mechanistic basis for osteoporosis GWAS lead SNPs rs34920465 and rs6426749.
