摘要：
Epidemiological studies have shown that there is a link between asthma and brain damage, but toxicological studies have not fully confirmed yet, especially the effects of asthma on the brain. In this sωdy， at first， we explore the effects of asthma on the brain through the establishment of an allergic asthma model. Then PM_(2.5), a typical outdoor air pollutant and formaldehyde, a typical indoor air pollutant were selected to be closer to the true environment and find whether there is any synergism between them. In this study, an ovalbumin (OVA)-sensitized mice asthma model was established. 30 male Balb/c mice were randomly divided into 5 groups: (1) saline control group, (2) OVA-sensitized group, (3) OVA-combined with formaldehyde exposure group, (4) OVA-combined with PM_(2.5) exposure group， (5) Combination of OVA, formaldehyde and PM_(2.5) exposure group. The mice were inhaled with formaldehyde or/and instilled with PM_(2.5) from day 1 to 18. The mice asthma model was developed by OVA sensitization and challenge. The mice were sensitized with OVA+Al(OH)_3(5 mg OVA and 175 mg Al(OH)_3 in 30 mL saline each time) or saline (30 mL saline each time) by intraperitoneal injection on day 1, 7 and 14. This was then followed by an aerosol challenge in 1% OVA (30 min. d~(-1) from day 19 to 25 (7 times) using an ultrasonic nebulizer. On the 26th day, the organ coefficient of mice brain was counted, then the contents of oxidative stress of mice brain were measured, including reactive oxygen species' (ROS), glutathione (GSH) and malondialdehyde (MDA), and the concentrations of NF-kB and interleukin-1? (IL-1β) were detected by using ELISA kits. Detection of interleukin-6 (IL-6) was made with immunohistochemical method. Histological assay for brain was also conducted. In our results, all the OVA treated groups showed a significant increase of ROS and a significant decrease of GSH contents when compared with the control group. Except OVA-sensitized group, other OVA treated groups also showed a significant increase of MDA contents when compared with the control group, and MDA contents of OVA-sensitized group showed significant change when compared to the combined exposure group. In ROS and GSH， combined exposure showed some joint effect compared with single exposure. When OVA was applied in combination with formaldehyde and PM_(2.5), NF-kB was activated. And all the OVA treated groups showed increased levels of IL-l ? and IL-6 compared with the control group. And the combined exposure showed an aggravated effect when compared with OVA-sensitized group. Histopathological observation of the hippocampus in mice brain clearly showed the difference of eosin (EO) stained neurons in the combined exposure group compared with the control group and OVA-sensitized group. The pyramidal neurons of the mice with allergic asthma exposed to formaldehyde and/or PM_(2.5) had been reduced in number, the cells were swollen and the dendrites had disappeared. Allergic asthma can cause damage to the brain through oxidative stress. Exposure to formaldehyde and PM_(2.5) will increase the damage caused by allergic asthma to the brain, which may be mediated by oxidative stress and NF-kB activation. This promotes the release of the inflammatory factors, resulting in increased inflammation.
摘要：
A multi-functional anti-pathogen coating with “release-killing”, “contact-killing” and “anti-adhesion” properties was prepared from biocompatible polymer encapsulated chlorine dioxide (ClO2) which protected the active ingredient from the outside environment. A slow sustained-release of ClO2 from micelles over fifteen days was detected for long-term release-killing. Micelles only release ClO2 on demand in minimum inhibitory concentrations. We prepared nanoparticles which were covalently clustered on micelle surfaces to improve contact-killing as well as to improve the stability of the micelle. Copper nanoparticles were generated using the biosynthesis method including L-vitamin C, which avoids the toxicity and allows for the preparation of copper nanoparticles in a green environment. Synergistic anti-pathogen activity could be generated by a combination of micelle released ClO2 and ascorbic acid. In addition to release-killing and contact-killing, a pluronic polymer coated surface also provides an additional “anti-adhesion” property through its protein-repelling ability. In this research, the designed coating demonstrated a broad-spectrum of activity to kill drug-resistant bacteria, viruses and spores in short period of time. Based on scanning electron microscopy (SEM), transmission electron microscopy (TEM) and anti-oxidase assays, we found that the designed coatings killed the pathogens via bio-oxidation. We also carried out acute respiratory toxicity tests in this research. Analysis of blood samples, lung function and histopathological slices indicated that the synthesized micelles allowed a controlled and sustained release of ClO2 to kill pathogens while maintaining an overall ClO2 concentration in the air within a safe range.
通讯机构：
[El-Hashash, Ahmed] C;Care of Yang A, Edinburgh Med Sch, UoE ZJU Inst, Univ Edinburgh, Off 429,Zhejiang Int Campus,Arts & Sci Bldg, Haining 314400, Zhejiang, Peoples R China.
关键词：
lung;regeneration;stem cells;tissue repair
摘要：
Lung diseases are major cause of morbidity and mortality worldwide. The progress in regenerative medicine and stem cell research in the lung are currently a fast-growing research topic that can provide solutions to these major health problems. Under normal conditions, the rate of cellular proliferation is relatively low in the lung in vivo, compared to other major organ systems. Lung injury leads to the activation of stem/progenitor cell populations that re-enter the cell cycle. Yet, little is known about stem cells in the lung, despite common thoughts that these cells could play a critical role in the repair of lung injuries. Nor do we fully understand the cellular and architectural complexity of the respiratory tract, and the diverse stem/progenitor cells that are involved in the lung repair and regeneration. In this review, we discuss the conceptual framework of lung stem/progenitor cell biology, and describe lung diseases, in which stem cell manipulations may be physiologically significant. In addition, we highlight the challenges of lung stem cell-based therapy.
作者机构：
[Rao, Yan; Huang, Xiaoxiao] Wuhan Sports Univ, Coll Art, Wuhan, Hubei, Peoples R China.;[Yang, Xu; Ma, Ping] Hubei Univ Sci & Technol, Xianning, Peoples R China.;[Zhao, Wei; Yang, Xu] Cent China Normal Univ, Sch Life Sci, Wuhan, Hubei, Peoples R China.
通讯机构：
[Yang, Xu] H;[Yang, Xu] C;Hubei Univ Sci & Technol, Xianning, Peoples R China.;Cent China Normal Univ, Sch Life Sci, Wuhan, Hubei, Peoples R China.
会议名称：
Joint Symposium of the 8th International Conference of th Chinese-Society-of-Micro-Nano-Technology (CSMNT) / Microsystems and Nanoengineering Summit (MAN) / Symposium of Materials Science and Technology (SOMST)
会议时间：
OCT 13-16, 2017
会议地点：
Tianjin, PEOPLES R CHINA
会议主办单位：
[Huang, Xiaoxiao;Rao, Yan] Wuhan Sports Univ, Coll Art, Wuhan, Hubei, Peoples R China.^[Ma, Ping;Yang, Xu] Hubei Univ Sci & Technol, Xianning, Peoples R China.^[Zhao, Wei;Yang, Xu] Cent China Normal Univ, Sch Life Sci, Wuhan, Hubei, Peoples R China.
摘要：
Several epidemiological and experimental studies indicate a positive association between exposure to formaldehyde or phthalates and allergic asthma. However, nothing is yet known about the effects of exposure to for-maldehyde and phthalates together, nor the role of each on allergic asthma. Here, we investigated the effects of a combined exposure to formaldehyde and diisononyl phthalate (DINP) on asthma-like pathology in mice, and determined the underlying mechanisms implicated in NF-kappa B and ROS. Mice were exposed to formaldehyde and/or DINP and sensitization with OVA. The results showed that exposure to 1.0 mg/m(3) formaldehyde or 20 mg/kg.d DINP slightly aggravated the airway wall remodeling, promoted the production of IgE and IgG1, and induced the occurrence of airway hyperresponsiveness (AHR). However, these pathological responses and AHR were greatly exacerbated by the combined exposure to formaldehyde and DINP. Administering melatonin to block oxidative stress, alleviated the pathological responses and AHR induced by formaldehyde and DINP, and inhibited the activation of the NF-kappa B and the secretion of TSLP. Blocking NF-kappa B with Dehydroxymethylepoxyquinimicin, inhibited the elevation of TSLP expression and Th2/Th17 cytokine secretion, and effectively alleviated the allergic asthma-like symptoms. The results suggested that exposure to both formaldehyde and DINP aggravated hypersensitivity asthma symptoms by promoting oxidative stress and activating NF-kappa B. These findings expand our understanding of how formaldehyde and DINP exposure affect the development of allergic asthma.
期刊：
PROTEIN JOURNAL,2018年37(6):531-538 ISSN：1572-3887
通讯作者：
Liu, Yanli
作者机构：
[Liu, Jinlin; Liang, Xiao; Yang, Xiajie; Gong, Siying; Li, Fangzhou; Qi, Chao; Lei, Ming; Liu, Ke; Li, Bing; Liu, Yanli; Zhou, Mengqi] Cent China Normal Univ, Hubei Key Lab Genet Regulat & Integrat Biol, Sch Life Sci, Wuhan 430079, Hubei, Peoples R China.;[Cao, Yu] Cent China Normal Univ, Key Lab Pesticide & Chem Biol, Minist Educ, Coll Chem, Wuhan 430079, Hubei, Peoples R China.
通讯机构：
[Liu, Yanli] C;Cent China Normal Univ, Hubei Key Lab Genet Regulat & Integrat Biol, Sch Life Sci, Wuhan 430079, Hubei, Peoples R China.
关键词：
AL protein;PHD domain;Histone binding
摘要：
Alfin1-like (AL) is a family of proteins homologous to the alfalfa Alfin1 in plant and bears an Alfin domain and a PHD domain at their N- and C-terminus, respectively. There are 7 AL proteins in Arabidopsis, and the PHD domains of most AL proteins are reported to bind to histone H3K4me3. Here we reported gene cloning, protein expression and purification of the PHD domains of all the AL family proteins in Arabidopsis. We then systematically characterized their histone binding abilities by quantitative isothermal titration calorimetry and fluorescence polarization binding assays. Our binding results indicate that all the PHD domains of the AL proteins bind to the histone H3K4me3 peptide with varying methylation state preference and binding affinities. Our study presented here provides the foundation for further studies of the peptide state-specific recognition by PHD domains of AL proteins.
作者机构：
[Tong, Zhiqian; Tan, Tao] Capital Med Univ, Beijing Inst Brain Disorders, Alzheimers Dis Ctr, Beijing 100069, Peoples R China.;[Tan, Tao] Sichuan Prov Hosp Women & Children, Chengdu, Sichuan, Peoples R China.;[Song, Weihong; Zhang, Yun] Univ British Columbia, Dept Psychiat, Townsend Family Labs, Vancouver, BC, Canada.;[Luo, Hongjun; Li, Hui; Luo, Wenhong] Shantou Univ, Cent Lab, Med Coll, Shantou, Guangdong, Peoples R China.;[Lv, Jihui] Beijing Geriatr Hosp, Beijing, Peoples R China.
通讯机构：
[Tong, Zhiqian] C;[Song, Weihong] U;Capital Med Univ, Beijing Inst Brain Disorders, Alzheimers Dis Ctr, Beijing 100069, Peoples R China.;Univ British Columbia, 2255 Wesbrook Mall, Vancouver, BC V6T 1Z3, Canada.
关键词：
ALDH2;hyperglycemia;dementia;Alzheimer
摘要：
Patients with type 2 diabetes mellitus (T2DM) often develop cognitive impairments and have an increased risk of developing Alzheimer's disease. Hyperglycemia is a major characteristic of T2DM, but how elevated glucose levels lead to cognitive decline remains elusive. Here, we report that patients with T2DM and mutations in the formaldehyde (FA)-degrading enzyme aldehyde dehydrogenase 2 (ALDH2) gene had higher levels of FA and more severe dementia. Injection of FA induced hyperglycemia and cognitive deficits in rats. Ablation of gene expression of ALDH2, the main enzyme to oxidize FA, resulted in abnormally high levels of hippocampal FA, leading to hyperglycemia and cognitive impairments as well as potentiating streptozotocin-induced diabetes development in ALDH2 knockout mice. We found that FA interacts with insulin to form FA-insulin adducts, and these FA-insulin adducts caused insulin deficiency, contributing to memory decline in diabetic rodent models. Reduction of FA by transgenic overexpression of human ALDH2 attenuates hyperglycemia and alleviates cognitive deficits in diabetic mouse models. These findings suggest that excess FA plays a critical role in mediating diabetes-related dementia. Targeting FA and its metabolizing enzyme ALDH2 may be a valid approach for preventing and treating dementia in diabetes mellitus.Tan, T., Zhang, Y., Luo, W., Lv, J., Han, C., Hamlin, J. N. R., Luo, H., Li, H., Wan, Y., Yang, X., Song, W., Tong, Z. Formaldehyde induces diabetes-associated cognitive impairments.
作者机构：
[Huang, Xiaoxiao] Wuhan Sports Univ, Coll Art, Wuhan, Hubei, Peoples R China.;[Zhao, Wei; Yang, Xu; Peng, Mei] Cent China Normal Univ, Sch Life Sci, Wuhan, Hubei, Peoples R China.;[Zhao, Xiaoyan] Hubei Univ Med, Clin Coll 3, Shiyan, Hubei, Peoples R China.
通讯机构：
[Yang, Xu] C;Cent China Normal Univ, Sch Life Sci, Wuhan, Hubei, Peoples R China.
会议名称：
Joint Symposium of the 8th International Conference of th Chinese-Society-of-Micro-Nano-Technology (CSMNT) / Microsystems and Nanoengineering Summit (MAN) / Symposium of Materials Science and Technology (SOMST)
会议时间：
OCT 13-16, 2017
会议地点：
Tianjin, PEOPLES R CHINA
会议主办单位：
[Huang, Xiaoxiao] Wuhan Sports Univ, Coll Art, Wuhan, Hubei, Peoples R China.^[Peng, Mei;Zhao, Wei;Yang, Xu] Cent China Normal Univ, Sch Life Sci, Wuhan, Hubei, Peoples R China.^[Zhao, Xiaoyan] Hubei Univ Med, Clin Coll 3, Shiyan, Hubei, Peoples R China.
关键词：
SWCNTs;nerve cells;protection effect;viability;vitamin C
摘要：
Autoimmune thyroid disease (AITD) is the most common autoimmune disease that causes hypothyroidism. High iodine is a well-known factor that can induce thyroid disorders, including Hashimoto’s thyroiditis, one of the main types of AITD. Recent epidemiological studies have indicated that phthalates, especially di-n-butyl phthalate (DBP) may induce thyroid disease. In this study, we aim to determine the effects and underlying mechanisms of high iodine and/or DBP exposure on AITD. Female Wistar rats were modeled with thyroglobulin and exposed to high iodine and/or DBP. We investigated histopathological changes in the thyroid and measured thyroid hormone levels in serum to assess thyroid function. In the thyroid and liver, we detected oxidative stress, proinflammatory factors (IL-1β, IL-6, and IL-17) and the activation of activator protein 1 (AP-1), a transcription factor that is related to the synthesis of the thyroxine-binding globulin (TBG) and the activation of Th17. After blocking AP-1 with SP600125, we detected TBG and the Th17 related cytokines (IL-6 and IL-17). The data showed that thyroid damage and the alteration of thyroid hormones were greater when the rats were exposed to both high iodine and DBP. Coexposure to DBP and high iodine enhanced the activation of AP-1 in the liver and thyroid, and induced an increase in the levels of TBG in serum and IL-17 in the thyroid. Blocking AP-1 activation prevented the increase of TBG and IL-17. The results indicate that high iodine and/or DBP exposure exacerbated AITD through altering TBG levels in serum and aggravating IL-17 in the thyroid.
