1.Progress of Epidemiology Study on Cooking Oil Fume Toxicity
Journal of Environment and Health 1992;0(02):-
In China, cooking oil fume is a kind of indoor air pollutant that is ubiquitous. With the development of catering trade, the pollution of cooking oil fume is becoming more and more severe. The results of animal experiments showed that cooking oil fume could damage the genetic substance and cause cancer. The results from the epidemiological studies indicated that cooking oil fume could induce lipid peroxidation and change the pulmonary and immunologic functions, cause chromosome damage and increase the risk of lung cancer.
2.Meta Analysis of Female Lung Cancer Associated With Cooking Oil Fume
Shuidong FENG ; Hongyan LING ; Feng CHEN
Journal of Environment and Health 1989;0(06):-
Objective To estimate quantitatively the relationship between female lung cancer and cooking oil fume (COF)?Methods Meta-analysis was employed to estimate the relationship between COF and non-smoking female lung cancer based on8relevant epidemiological articles publisked at home and abroad?Fixed Effect Model Analysis was used to calculate the incorporated odds ratio(OR c )based on homogeneity test.Results The OR c for female lung cancer associated with COF was2.94(95%CI =2.43~3.56)with statistical significance(? 2 =120.64,P
3.The Effect of Gadd Genes Expression in Surveillance of DNA Damage Induced by Nitrogen Mustard
Shuidong FENG ; Feng CHEN ; Hongyan LING
Journal of Environment and Health 1992;0(05):-
Objective To study the effect of Gadd genes expression in surveillance of DNA damage. Methods The human liver tumor cells were treated with alkylating agent(nitrogen mustard) and total RNA was extracted, the expression levels of Gadd genes were determined by RT-PCR. Results Treated with 1 ng/?l nitrogen mustard for 3 h, 24 h, 48 h respectively and with 1 ng/?l, 5 ng/?l nitrogen mustard for 24 h respectively, the expression levels of Gadd genes increased at first (P0.05). Conclusion Gadd genes expression can be used as the indexes in the surveillance of DNA damage induced by nitrogen mustard.
4.The expression of miR-221 and miR-222 in non-small cell lung cancer and their significances
Li LIAO ; Jun WANG ; Shuidong FENG ; Zhihua LAN ; Xueying LYU ; Mengyi WU ; Xin YANG
Cancer Research and Clinic 2016;28(9):590-594
Objective To explore the expression of miR-221/222 in non-small cell lung cancer (NSCLC) and its correlation with clinical pathological parameters. Methods The clinical pathological data and formalin fixed-paraffin embedded (FFPE) tissues of 55 NSCLC patients and 10 benign lesion patients who underwent surgery in the First Affiliated Hospital of Nanhua University from February 2012 to May 2014 were collected and followed. The relationship between miR-221/222 expression detected by real-time PCR and clinical pathological parameters and progression-free survival (PFS) were analyzed. The differential survival between the high expression group and the low expression group of miR-221/222 were compared. A Cox proportional hazard regression model was utilized to examine the prognostic factors of NSCLC. Results The expression level of miR-221/222 was significantly higher in tumor tissues than that in corresponding benign lesion tissues (Fold change=3.52, P=0.000;Fold change=2.01, P=0.000). There was a negative correlation between miR-221/222 expression and pathological grades (r=-0.732, P=0.000;r=-0.451, P=0.001). The relative expression of miR-221 showed a positive correlation with miR-222 (r=0.376, P=0.000). Patients with higher levels of miR-221/222 were closely associated with a shorter PFS (miR-221: 55.43 weeks vs. 81.29 weeks, P=0.028; miR-222: 45.00 weeks vs. 87.04 weeks, P=0.008). Finally, multivariate analysis demonstrated that miR-222 expression was independently associated with poor PFS (RR=2.808, P=0.033). Conclusions miR-221/222 is highly expressed in NSCLC tumor tissues with a positive correlation. A negative correlation is observed between the expression of miR-221/222 and tumor differentiation. The potential high expression of miR-221/222 is considered as tumor biomarkers for the prognosis of NSCLC patients.
5.Effects of rosiglitazone on endocrine function of endothelia in insulin resistant rats
Hongyan LING ; Shuidong FENG ; Bili HU ; Shouhong ZHOU ; Jianqin HE ; Bi HU
Chinese Journal of Endocrinology and Metabolism 1985;0(01):-
Insulin resistant rats induced by fructose were treated with rosiglitazone (RSG), and the effect of RSG on the endocrine function of vascular endothelial cells were investigated. The results showed that RSG can improve the endocrine function of endothelia by enhancing aortic NO synthase activity and the ability of anti-oxidative stress.
6.Pollution characteristics and health risk assessment of metals in farmland soil around the largest realgar mining area in Asia
Shuidong FENG ; Mengyue CAO ; Jun LIU ; Yan TANG ; Yuke ZENG ; Minxue SHEN ; Fei YANG
Journal of Environmental and Occupational Medicine 2023;40(8):923-930
Background Heavy metal emissions from mining and smelting areas are a global problem, and health risks associated with heavy metal contamination of soils are of great concern. The long-term mining of the largest realgar mine in Asia has caused severe arsenic and other metal pollution to the surrounding rivers and soils. Objective To understand the levels of metal contamination and health risks in agricultural soils of villages surrounding the largest realgar mine in Asia, and to lay a good foundation for further necessary pollution control actions and decisions. Methods A field survey was conducted to collect soil samples according to the Technical rules for monitoring of environmental quality of farmland soil (NY/T 395-2012), and then inductively coupled plasma mass spectrometry was used to determine the contents of 28 heavy metals [cadmium (Cd), arsenic (As), lead (Pb), mercury (Hg), chromium (Cr), nickel (Ni), copper (Cu), zinc (Zn), beryllium (Be), selenium (Se), cobalt (Co), antimony (Sb), molybdenum (Mo), vanadium (V), barium (Ba), thallium (Tl), boron (B) , bismuth (Bi), lithium (Li), manganese (Mn), strontium (Sr), calcium (Ca), rubidium (Rb), iron (Fe), magnesium (Mg), aluminum (Al), kalium (K), and titanium (Ti)]. Geoaccumulation index, single factor pollution index, and Nemerow comprehensive index were used to evaluate the degree and characteristics of single metal pollution and combined pollution in soil, respectively. A health risk assessment model was used to evaluate the risks of metals in soil to human health. Results The results of geoaccumulation index calculation revealed that 22 heavy metals were enriched in the soil, and the indexes of target heavy metals from high to low were Cd > Se > Pb >Hg > As > Co> Ni > Cu > Zn > Bi > Sb > Mo > Be> Cr > Ba >V > Li > Sr> Mn> Rb > Ca> Tl . The single factor pollution indexes of 17 heavy metals from high to low were Be > Cd > B > Mo > V > As > Ni > Cu > Pb > Zn > Co > Se > Tl > Ba > Cr > Hg > Sb. The Nemerow comprehensive index indicated all sampling points were graded as severe pollution. The mean of total non-carcinogenic health risk values and the mean of carcinogenic health risk values for the target heavy metals in the area were higher than the threshold (1) and the maximum acceptable risk (1.0×10–4), respectively. The total carcinogenic health risks for adults and children reached 1.1×10–3 and 1.67×10–3, respectively. The mean non-carcinogenic health risk values of As, Co, Cr, and Pb pollution were greater than 1, and the maximum non-cancer risk value of Sb for children was greater than 1. The mean carcinogenic risk values of Ni, As, and Cu exceeded 1.0×10–4 for both adults and children, and the maximum carcinogenic risk values of Be and Cr for children were more than 1.0×10–4. Conclusion The farmland soil around the hugest realgar mine in Asia is contaminated by multiple metals. The study soil is seriously polluted by Cd, Se, Pb, As, Hg, Be, B, Mo, V, Ni, Cu, Pb, Zn, Co, and Ba. The pollution of Ni, As, Cu, Cr, and Be is considered as carcinogenic hazards to health, while the pollution of As, Co, Cr, Pb, and Sb poses non-carcinogenic health risks. Our study findings show that the soil is polluted by Co and Group 1 carcinogen Be, which could cause health risks; although Cr and Sb have not reached severe pollution levels, there are certain health risks and also need attention.
7.Dihydromyricetin improves Parkinson's disease-like lesions in T2DM rats by activating AMPK/ULK1 pathway.
Qi LI ; Nian CHEN ; Jin-Ding LUO ; Hui-Lin WU ; Zi-Han WANG ; Meng-Wei LI ; Shui-Dong FENG ; Hong-Yan LING
Acta Physiologica Sinica 2023;75(1):59-68
The purpose of this study was to explore the effect and mechanism of dihydromyricetin (DHM) on Parkinson's disease (PD)-like lesions in type 2 diabetes mellitus (T2DM) rats. The T2DM model was established by feeding Sprague Dawley (SD) rats with high-fat diet and intraperitoneal injection of streptozocin (STZ). The rats were intragastrically administered with DHM (125 or 250 mg/kg per day) for 24 weeks. The motor ability of the rats was measured by balance beam experiment, the changes of dopaminergic (DA) neurons and the expression of autophagy initiation related protein ULK1 in the midbrains of the rats were detected by immunohistochemistry, and the protein expression levels of α-synuclein (α-syn), tyrosine hydroxylase (TH), as well as AMPK activation level, in the midbrains of the rats were detected by Western blot. The results showed that, compared with normal control, the rats with long-term T2DM exhibited motor dysfunction, increased α-syn aggregation, down-regulated TH protein expression, decreased number of DA neurons, declined activation level of AMPK, and significantly down-regulated ULK1 expression in the midbrain. DHM (250 mg/kg per day) treatment for 24 weeks significantly improved the above PD-like lesions, increased AMPK activity, and up-regulated ULK1 protein expression in T2DM rats. These results suggest that DHM may improve PD-like lesions in T2DM rats by activating AMPK/ULK1 pathway.
Rats
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Animals
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Parkinson Disease
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Rats, Sprague-Dawley
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AMP-Activated Protein Kinases
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Diabetes Mellitus, Type 2
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Autophagy-Related Protein-1 Homolog