Arsenic is a common environmental toxin,but also a carcinogen.Long-term exposure to inorganic arsenic can cause multi-system and multi-organ damage in the body,including cancerous and non-cancerous lesions.As one of the main target organs of arsenic exposure,skin damage is of great significance for the diagnosis and health assessment of arsenic poisoning in population threatened by the disease.From the perspective of arsenic exposure and skin cancer,the aim of this article is to summarize the epidemiology,pathogenesis and medical intervention of arsenic-induced skin cancer,and to provide reference for the pathogenesis and prevention of endemic arsenic poisoning related skin diseases.

Aim To investigate the protective effect of RTP1,one of the polysaccharide isolated from Rheum tanguticum,on H2O2 induced apoptosis in IEC-6 cells and its possible mechanism.Methods H2O2(100 mmol?L~-1)was used to induce IEC-6 cell apoptosis.Different doses(10,30,100 mg?L~-1)of RTP1 were administrated before H2O2 was added into IEC-6 cell culture.Cell viability was observed by MTT assay.Reactive oxygen species were measured with laser scanning confocal microscopy(LSCM).DNA content and percentage of apoptosis were assayed by DNA agarose gel electrophoresis,acridine orange staining and flow cytometry.The activation of Caspase-3 was detected with Western blot analysis.Results Following treatment with H2O2 for 2 h,H2O2 induced a significant decrease in cell viability,while DNA ladder was observed and apoptosis percentage was as high as 31.3%.Accumulation of intracellular ROS and increase in Caspase-3 activity were also detected.Pretreatment with RTP1 for 24 h exhibited cytoprotective effects in a dose-dependent manner.RTP1 obviously enhanced cell viability,reduced formation of DNA ladder and significantly reduced the number of cells labeled with Annexin V.The percentage of apoptosis/necrosis cells was markedly decreased to 24.4% and 21.5%,respectively.LSCM showed that RTP1 attenuated the accumulation of ROS.The significant decrease in Caspase-3 activity was detected.Conclusion RTP1 has cytoprotective capacity to antagonize H2O2-induced IEC-6 cell apoptosis and injury,and this effect may be related to decrease ROS and inhibit Caspase-3 activity

AIM To study whether nitric oxide preconditioning induce early protection of neonatal rat cardiomyocytes. METHODS Cultured neonatal rat cardiomyocytes were divided into 6 groups. ①Normal group;②NO group: SNAP(500 ?mol?L -1 ) was added to cell medium 1 h before lethal hypoxia/reoxygenation (HR) injury (6 h hypoxia and 3 h reoxygenation); ③HP group: Cells were cultured for 60min hypoxia followed by 30 min reoxygenation to form hypoxia preconditioning before lethal HR injury;④ L NAME+HP group: Nitric oxide synthase antagonist L NAME was added during HP stage;⑤ L Arg group: L arginine was added to cell medium 1h before lethal HR injury;⑥ L NAME+ L Arg group: Both L NAME and L Arg were added to cell medium 1 h before lethal HR injury;⑦H/R group: Cells underwent lethal HR injury without any treatment. Cardiomyocytes injury was detected by lactate dehydrogenase(LDH) activity and cell viability. RESULTS Nitric oxide preconditioning can protect cardiomyocytes by reducing LDH activity and improving cell viability ( P

OBJECTIVE:To estabilish a HPLC-MS method for determining enalapril in human plasma METHODS:Alprozalam was added into plasma sample as an internal standard,then supernate of the sample was extracted through solid-phase extration column,washed with methanol and detected by HPLC-MS method:column,ODS C18;mobile phase,methanol-0 01% formic acid(45∶55);flow rate,0 8ml/min;capillary voltage,3 81kV;cone voltage,39 0V The selected ion was determined by EST RESULTS:The calibration curve was linear within the range of 2 5～400ng/ml r=0 9 996,the recovery was 102 2%,RSDs of intra -day and inter-day were 4 0% and 5 4%,respectively CONCLUSION:The method is accurate and sensitive with no endogenous interference It can be applied to studying the pharmacokinetics and bioavailability of enalapril tablets in humans

OBJECTIVE:To investigate the measures and roles of pharmaceutical care in improving the safety of chemotherapy by clinical pharmacists. METHODS:Chemotherapy drug-induced ADR medical records were collected from oncology department of our hospital during Jan.-Dec. 2013 (before intervention) and Apr. 2014-Mar. 2015 (after intervention),and then analyzed and compared in respects of chemotherapy plan,patient’age and gender,route of administration,involved organs and systems,severe ADR,etc. RESULTS:After the formulation and implementation of pharmaceutical care for improving safe use of chemotherapy drugs,the incidence of chemotherapy drugs-induced ADR decreased from 88.48%to 72.14%;the incidence of ADR of involved di-gestive system,skin and its appendants decreased from 67.28% and 7.37% to 42.29% and 1.99%,respectively;the incidence of severe nausea and vomiting decreased from 27.65%to 18.91%;the constituent ratio of single agent chemotherapy and oral adminis-tration route increased from 31.80%(69/217) and 14.29%(31/217) to 44.28%(89/201) and 22.39%(45/201),respectively (P<0.05). CONCLUSIONS:Pharmaceutical care intervention measures formulated by clinical pharmacists can significantly lower the incidence of ADR,promote safe use of chemotherapy drugs and guarantee the safety of drug use.

AIM: To investigate the pharmacological effects and mechanism of ethyl ferulate (EF). METHODS: The platelet congregate rate was observed by congregater TYXN-91 and the platelet intracellular calcium oscillation was observed by laser scanning. The acute liver injury model of mice was made by using the CCl 4 156 mg?kg -1, ip. Then the levels of ALT and AST were determined in serum and the levels of MDA and SOD in the liver. RESULTS: The inhibition rate of the platelet congregate were 26.3%? 3.3%, 33.4%? 2.4%, 73.4%? 3.1%, and 94.9%? 2.7% (n=8) in different concentration( 0.1, 0.5, 1.5, and 3.0 mmol?L -1)of ethyl ferulate,respectively. It was higher than those in the same concentrations of ferulic acid. The change of the fluctuation of calcium (?FI 4.6? 1.7) in EF group was much lower than the rest level ( 10.3? 2.6) (n=8,P

AIM: To evaluate the protection of Mn~(2+) on injury of human kidney tubular epithelial cell line induced by gentamicin, and investigate its principals. METHODS: Gentamicin was used to injury human kidney tubular epithelial cell line (HK-2) to produce model of kidney injury. MTT method was used to measure effect of Mn~(2+) on proliferation of cells after they were injured by gentamicin. The spectrophotometry method was used to observe the change of LDH,NAG and SOD effected by Mn~(2+). Ultrastructure was examined by electron microscopy. RESULTS: Although HK-2 cells were injured, Mn~(2+) promoted cells proliferation, decreased LDH activity and NAG content, increased SOD activity, and alleviated dilation of the mitochondria and crushing of lysosomes. CONCLUSION: Mn~(2+) can protect human kidney tubular epithelial cell line from injury induced by gentamicin. It may be in relation to inhibiting the oxidative injury, lightening dilation of the mitochondria, protecting the integrity of lysosomes and decrease the leakage of enzyme.

AIM: To explore the effects of rheum tanguticum polysaccharides(RTP) on TNBS-induced colitis in mice and its probable mechanisms.METHODS: Mice colitis model was induced by 2,4,6-trinitrobenzene sulfonic acid(TNBS).The mice were randomly divided into 5 groups,normal group,model group,RTP-100,200 and 400 group.The macroscopical and histological changes of the colon were evaluated and the cytokines IL-8,IL-10,TNF-?and IL-4 produced by splenocyts were analyzed with ELISA.RESULTS: Compared with the model group,both symptoms and the lesions of colonic mucosa of RTP-200 and 400 group were slighter on ulcerative colitis induced by TNBS in mice. Furthermore,the expressions of TNF-?and IL-8 in colon tissue of mice with TNBS-induced colitis were higher and the IL-10 and IL-4 were lower than that of normal control(P

AIM To get an insight into intracellular signaling steps, a very early step in the signaling cascade, the biphasic Ca 2+ elicited by 5 HT in rat stomach fundus smooth muscle cells was investigated. METHODS Cells were cultured and loaded with Fluo 3 AM. [Ca 2+ ] i was measured by fluorescent intensity (FI) in each cell with confocal microscopy. RESULTS The resting FI level of SFSMC was 264?15. Stimulation of SFSMCs by 5 HT produced an elevation of [Ca 2+ ] i; Depletion of external Ca 2+ by addition of EGTA led to a significant attenuation of [Ca 2+ ] i change induced by 5 HT; Pre treatment of SFSMCs with ryanodine (10 ?mol?L -1 , 5 min) in D Hanks, the effect of 5 HT was completely inhibited; The stimulation of SFSMCs by 5 HT was partly attenuated by miaserin(10 ?mol?L -1 ), however, L type Ca 2+ channel antagonist lacidipine and G protein inhibitor NEM completely abolished the increase of [Ca 2+ ] i mediated by 5 HT; 5 HT mediated Ca 2+ release was reduced by phospholipase C specific inhibitor compound 48/80(1 2 ?g?ml -1 ); When protein kinase C was activated by phorbol 12 myristate 13 acetate (PMA 0 1 ?mol?L -1 , 5 min) the effect of 5 HT was inhibited, and the inhibitory effect of PMA was reversed by D sphingosine, a PKC inhibitor. CONCLUSION Our data suggest that G protein coupled 5 HT 2B receptor in the rat stomach fundus modulates 5 HT stimulated Ca 2+ increase, and it is coupled to calcium influx through L type calcium channels, and also intracellular calcium release by the opening of ryanodine receptor. The 5 HT 2B receptor mediated signal of 5 HT is transduced by PLC and PKC.