|1.||Bonner, James C: 6 articles (03/2014 - 05/2003)|
|2.||MacGregor, Judith A: 4 articles (10/2015 - 08/2014)|
|3.||Antao-Menezes, Aurita: 4 articles (01/2010 - 01/2006)|
|4.||Turpin, Elizabeth A: 4 articles (01/2010 - 01/2006)|
|5.||Walters, Dianne M: 3 articles (03/2014 - 01/2010)|
|6.||Mangum, James B: 3 articles (01/2010 - 01/2006)|
|7.||Bonner, J C: 3 articles (02/2001 - 01/2000)|
|8.||Gollapudi, B Bhaskar: 2 articles (10/2015 - 08/2015)|
|9.||Li, Junhua: 2 articles (08/2015 - 10/2013)|
|10.||Hao, Jiming: 2 articles (08/2015 - 10/2013)|
01/01/2007 - "The induction of genes that mediate inflammation and immune responses, as well as suppression of genes involved in growth arrest appear to be important to the lung fibrotic reaction to V2O5."
01/01/2010 - "In the current investigation we examined the influence of genetic background on susceptibility to V2O5-induced inflammation and evaluated whether V2O5 functions as a tumor promoter using a 2-stage (initiation-promotion) model of pulmonary neoplasia in mice. "
01/01/2010 - "Mice were pre-exposed by intranasal aspiration to RSV or media vehicle prior to intranasal aspiration of V2O5 or saline vehicle at day 1 or day 7. A parallel group of mice were treated first with V2O5 or saline vehicle at day 1 and day 7 then post-exposed to RSV or media vehicle at day 8. V2O5-induced airway inflammation and fibrosis were decreased by RSV pre- or post-exposure. "
03/01/2014 - "Pulmonary responses to V2O5, including dose-dependent increases in lung permeability, inflammation, collagen content, and dysfunction, were significantly greater in DBA/2J mice compared to C57BL/6J mice. "
01/01/2007 - "We evaluated gene expression profiles in cultured human lung fibroblasts exposed to V2O5 in vitro in order to identify candidate genes that could play a role in inflammation, fibrosis, and repair during the pathogenesis of V2O5-induced bronchitis. "
08/01/2014 - "These results confirm the absence of any significant dose-related effect on mouse lung tumor incidence in the study groups exposed to V2O5. "
01/01/2010 - "In this study we demonstrate that V2O5, an occupational and environmentally relevant metal oxide, functions as an in vivo lung tumor promoter among different inbred strains of mice. "
12/01/2002 - "Under the conditions of this 2-year inhalation study, there was some evidence of carcinogenic activity of vanadium pentoxide in male F344/N rats and equivocal evidence of carcinogenic activity of vanadium pentoxide in female F344/Nrats based on the occurrence of alveolar/bronchiolar neoplasms. "
10/01/2015 - "V2O5 was identified as a lung carcinogen in this assay, leading to its IARC (International Agency for Research on Cancer) classification as group 2b or a "possible" human carcinogen. "
08/01/2015 - "Previously, K-ras mutations have been detected in the lung tumors in mice exposed to V2O5. "
01/01/2010 - "Mice sensitive to tumor promotion by V2O5 were also found to be more susceptible to V2O5-induced pulmonary inflammation and hyperpermeability (A/J>BALB>B6). "
01/01/2010 - "Vanadium pentoxide induces pulmonary inflammation and tumor promotion in a strain-dependent manner."
01/01/2010 - "Respiratory syncytial virus infection reduces lung inflammation and fibrosis in mice exposed to vanadium pentoxide."
12/01/1985 - "An experimental study was conducted to investigate the hypothesis that changes in pulmonary function induced by vanadium pentoxide (V2O5) inhalation would be accompanied by evidence of pulmonary inflammation. "
05/01/1996 - "NaVO3 and VOSO4, both very soluble forms of vanadium, tended to induce pulmonary inflammation and inflammatory cytokine mRNA expression more rapidly and more intensely than the less soluble form, V2O5. "
|4.||Asthma (Bronchial Asthma)
02/20/1982 - "Four workers from a recently established vanadium pentoxide refinery in Western Australia presented with green discoloration of the tongue, upper respiratory symptoms, and asthma. "
04/01/1999 - "This study provides strong supporting evidence that inhaled V2O5 induces BHR and asthma in subjects previously free of lung disease; the abnormality may persist for up to 23 months following exposure; routine spirometry will not detect affected subjects."
05/01/2000 - "Vanadium pentoxide (V(2)O(5)) is a cause of occupational asthma and chronic bronchitis, yet the molecular mechanisms through which V(2)O(5) exerts its effects on cell function are unclear. "
01/01/2000 - "Vanadium pentoxide (V(2)O(5)) is a cause of occupational asthma and bronchitis. "
07/01/2011 - "Vanadium pentoxide (V(2)O(5)) is the most common commercial source of vanadium, and it has been associated with occupational chronic bronchitis and asthma, both of which are MO diseases. "
|5.||Body Weight (Weight, Body)
08/01/2003 - "The survival and body weights of rats were minimally affected by exposure to V2O5. "
01/01/2001 - "To clarify acute toxicity and histopathological changes in the lung after exposure to V2O5 powder, rats (SD, male, n=66) were observed for 4 weeks after an intratracheal administration of V2O5 powder (geometric mean diameter 0.31 microm, geomertic standard deviation sigmag=2.19) at three doses (0.88, 3.0, 13.0 mg/kg body weight). "
02/01/2006 - "In 7-d single oral dose trials with mallard drakes (Anas platyrhynchos), the estimated median lethal dose (LD50) for vanadium pentoxide was 113 mg/kg body weight, while the LD50 for sodium metavanadate was 75.5 mg/kg. Sodium metavanadate was found to be even more potent (LD50 = 37.2 mg/kg) in male Canada geese. "
06/01/1991 - "This is a report on developmental toxicity in NIH mice following injection of vanadium pentoxide (V2O5, 5 mg/kg body weight, i.p.) at different times of gestation (on days 1-5, 6-15, 7, 8, 9, 10, 11, 14-17 of gestation). "