ABSTRACT
@#The aim of this study was to investigate the effect of transmembrane 9 superfamily protein member 2 (TM9SF2) in proliferation and migration of triple negative breast cancer cell line MDA-MB-231.The expression of TM9SF2 in triple negative breast cancer cell line MDA-MB-231 and nontumorigenic mammary epithelial cell line MCF-10A were measured by Western blot. MDA-MB-231 cells were treated with siRNA-TM9SF2 to knock-down the expression of TM9SF2. The effect of silencing TM9SF2 was measured with Western blot.The proliferation of cells was tested by MTS,and the migration was measured with Transwell and wound-healing assay.Proteins related to proliferation (PI3K,AKT,SRC and ERK) and migration (Snail,Slug and N-cadherin) were measured with Western blot.Protein expressions of TM9SF2 was better improved in triple negative breast cancer MDA-MB-231 cell line than MCF-10A.Compared with the control group, the siRNA-TM9SF2 infected group had lower expressions of PI3K, Snail, Slug and N-cadherin, and at the same time phosphorylation of AKT was decreased. The results suggest TM9SF2 can promote the proliferation and metastasis of triple negative breast cancer MDA-MB-231 cell line.
ABSTRACT
Objective To investigate tentatively the role of angiotensionⅡ( AngⅡ) in perfluoroisobutylene ( PFIB)-in-duced acute lung injury ( ALI) in rats.Methods Twenty-eight male Wistar rats were randomly divided into one control group(0 h) and six PFIB-exposed groups which were executed at 1, 2, 4, 8, 16 and 24 h after PFIB exposure (n=4). The PFIB-exposed groups inhaled PFIB at a concentration of 145 mg/m3 for 8 min in a flow-past header while the control group was exposed to the filtered air in a similar manner .After execution at the corresponding time-point, the samples of the lung, serum and brochoalveolar lavage fluid (BALF) were harvested.The measurement of the lung wet-to-dry weight ratio ( W/D) and total protein content in BALF , and the histopathological examination of the lung were carried out to evalu -ate the degree of lung injury .The over-time changes in the content of AngⅡin the lung homogenates and blood plasma and the activity of angiotensin converting enzyme ( ACE) in the lung tissue were observed .Results The lung W/D and total protein content in BALF were increased significantly at 16 h after PFIB exposure with severe acute lung edema and abun-dant neutrophil exudation to the alveoli , which were alleviated dramatically at 24 h after PFIB exposure .The content of AngⅡin the lung homogenate showed a tendency of increase during the first 8 hours with significant decrease at 16 and 24 h after exposure.However, the content of AngⅡin the plasma and the activity of ACE in the lung experienced of fluctuations , but without significant difference compared to the control group .Conclusion There is no obvious correlation between the extent of lung injury and that of AngⅡin the lung.The pathological significance of AngⅡin PFIB-induced ALI needs to be further clarified.
ABSTRACT
Different antiepileptic drugs (AEDs) may cause similar adverse effects, one of which is diplopia. However, the AEDs causing diplopia and the dose-response effect of each drug remains uncertain. In this study, we compared several second-generation AEDs to find out whether they would contribute to the risk of diplopia and their effect-causing dose. A meta-analysis was performed on 19 studies in agreement with our inclusion criteria. The results showed that eight commonly used second-generation AEDs (gabapentin, levetiracetam, oxcarbazepine, lamotrigine, pregabalin, topiramate, vigabatrin and zonisamide) could cause diplopia. The reported odds ratios (ORs) ranged from 1.406 to 7.996. Ranking risks from the highest to the lowest ORs of the eight AEDs of any dose resulted in the following order: use of oxcarbazepine (7.996), levetiracetam (7.472), lamotrigine (5.258), vigabatrin (3.562), pregabalin (3.048), topiramate (2.660), gabapentin (1.966), zonisamide (1.406). Taking into account the ORs above, we can conclude that second-generation AEDs of any dose may cause diplopia. However, the levetiracetam-caused diplopia needs to be further studied according to the data (OR, 7.472; 95% confidence interval, 0.375-148.772). These findings ask for better concerns about patients' quality of life when giving antiepileptic treatments.
ABSTRACT
Different antiepileptic drugs (AEDs) may cause similar adverse effects, one of which is diplopia. However, the AEDs causing diplopia and the dose-response effect of each drug remains uncertain. In this study, we compared several second-generation AEDs to find out whether they would contribute to the risk of diplopia and their effect-causing dose. A meta-analysis was performed on 19 studies in agreement with our inclusion criteria. The results showed that eight commonly used second-generation AEDs (gabapentin, levetiracetam, oxcarbazepine, lamotrigine, pregabalin, topiramate, vigabatrin and zonisamide) could cause diplopia. The reported odds ratios (ORs) ranged from 1.406 to 7.996. Ranking risks from the highest to the lowest ORs of the eight AEDs of any dose resulted in the following order: use of oxcarbazepine (7.996), levetiracetam (7.472), lamotrigine (5.258), vigabatrin (3.562), pregabalin (3.048), topiramate (2.660), gabapentin (1.966), zonisamide (1.406). Taking into account the ORs above, we can conclude that second-generation AEDs of any dose may cause diplopia. However, the levetiracetam-caused diplopia needs to be further studied according to the data (OR, 7.472; 95% confidence interval, 0.375-148.772). These findings ask for better concerns about patients' quality of life when giving antiepileptic treatments.
Subject(s)
Adolescent , Adult , Aged , Aged, 80 and over , Child , Humans , Middle Aged , Young Adult , Anticonvulsants , Therapeutic Uses , Diplopia , Drug Therapy , Placebo EffectABSTRACT
Objective To ascertain the role of NF?B and relationship among TGF?1,caspase-3 and apoptosis in CsA-induced nephrotoxicity.Methods Sixty-four wistar male rats were randomly divided into 4 groups:Vehicle,PDTC,CsA and CsA + PDTC group.The animals were daily subcutaneously injected either with CsA(15 mg/kg)or vehicle/PDTC(100 mg/kg).Four weeks later,BUN,serum creatinine,NAG and urine routine were examined.The kidneys were processed for light microscopy,immunohistochemistry and TENUL.Results A rat model of CsA-induced nephrotoxicity was established.CsA group showed significant increase in BUN,SCr and urine NAG compared with the controls,whereas CsA + PDTC group did not.Apoptosis is observered by TUNEL and the expressions of NF-?B,TGF-?1,caspase-3 increased significantly in CsA group compared with conrtol group.Whereas,both the apoptosis and the expressions of these proteins significantly decreased in rats treated with PDTC.Conclusion Apoptosis is induced in the CsA-induced chronic nephrotoxicity.Inhibition of NF-?B activation blockaded apoptosis and ameliorated CsA-induced chronic nephrotoxicity.The results suggest that NF-?B plays important roles in the progression of chronic CsA nephrotoxicity.