|1.||Wu, Yijie: 2 articles (08/2015 - 03/2008)|
|2.||Pei, Fengkui: 2 articles (08/2015 - 03/2008)|
|3.||Wei, Lai: 2 articles (08/2015 - 03/2008)|
|4.||Li, Xiaojing: 2 articles (08/2015 - 03/2008)|
|5.||Huang, Chun-Fa: 2 articles (01/2012 - 05/2008)|
|6.||Hsu, Chuan-Jen: 2 articles (01/2012 - 05/2008)|
|7.||Lin-Shiau, Shoei-Yn: 2 articles (01/2012 - 05/2008)|
|8.||Liu, Shing-Hwa: 2 articles (01/2012 - 05/2008)|
|9.||Tang, Yi-shan: 2 articles (05/2006 - 05/2005)|
|10.||Lin, Pu-yue: 2 articles (05/2006 - 05/2005)|
|1.||Body Weight (Weight, Body)
08/01/2015 - "In this study, (1)H NMR-based metabolomics, combined with multivariate pattern recognition, were applied to investigate the neurotoxic effects of cinnabar after intragastrical administration (dosed at 2 and 5 g/kg body weight) on male Wistar rats. "
03/15/2008 - "In this study, an NMR-based metabolomics approach has been applied to investigate the toxicological effects of cinnabar after intragastrical administration (dosed at 0.5, 2 and 5 g/kg body weight) on male Wistar rats. "
02/01/2009 - "Thus, for safe use of cinnabar, the acceptable daily intake (ADI) of cinnabar was 0.0009-0.0017 g x kg(-1) x d(-1), namely daily dose 0.05-0.1 g for an adult with body weight about 60 kg. Considering the difference of drug sensitivity and lifecircle between human and rats, we suggest that cinnabar which contains absoluble Hg < or = 21 microg x g(-1) should be used for no longer than 2 weeks at daily dose 0.05-0.1 g. "
04/01/2001 - "The results obtained showed that MeHg and cinnabar prominently and irreversibly caused a decrease in body weight, prolongation of latency for escape from electric shock, a decrease in the percentage for the conditioned avoidance response (CAR) to electric shock, impairment of spontaneous locomotion and inhibition of Na+/K+-ATPase activity of the cerebral cortex. "
|2.||Wounds and Injuries (Trauma)
01/01/2012 - "In conclusion, this study demonstrates that exposure to low-dose of cinnabar during the perinatal and developmental stages results in irreversible and severe injuries of the neurotoxicity in offspring, and NO(x) and Na(+)/K(+)-ATPase activities may exist potential and useful biomarkers for neurotoxicity-induced by low-doses of mercuric compounds."
01/15/2011 - "Histopathology showed moderate liver and kidney injuries after arsenite and HgCl₂, but injuries were mild or absent after AGNH, realgar, and cinnabar. "
01/01/2015 - "Cinnabar induces renal inflammation and fibrogenesis in rats."
01/01/2015 - "The purpose of this study was to investigate whether cinnabar causes renal inflammation and fibrosis in rats. "
01/01/2015 - "In conclusion, cinnabar may cause kidney damage due to the accumulation of mercury, and renal inflammation and slight fibrogenesis may occur in rats. "
|5.||Brain Ischemia (Cerebral Ischemia)
07/01/2003 - "[Absorption and distribution of mercury and arsenic from realgar and cinnabar of angong niuhuang pill in normal rats and rats with cerebral ischemia]."
07/01/2003 - "To study comparatively the characteristics of absorption and distribution of mercury and arsenic from realgar and cinnabar of Angong Niuhuang Pill in normal rats and the rats with cerebral ischemia after oral administration. "
|2.||arsenic disulfide (realgar)
|3.||Adenosine Triphosphatases (ATPase)
|4.||Biological Markers (Surrogate Marker)
|6.||cinnabar (mercuric sulfide)
|7.||Kynurenine 3-Monooxygenase (Kynurenine 3 Monooxygenase)
|8.||Nitric Oxide Synthase (NO Synthase)
|3.||First Aid (Aids, First)