Ink and cleaner waste reduction evaluation for flexographic printers /

"HWRIC TR-012."

Performing well surveys.

"May 2003."

Recycling nickel electroplating rinse waters by low temperature evaporation and reverse osmosis /

"Contract no. CR-815829."

U.S. EPA regulations have changed the focus of lead and copper monitoring.

Caption title.

The National cancer program [microform] : hearing before a subcommittee of the Committee on Government Operations, House of Representatives, Ninety-fifth Congress, first session.

Reuse of record except for individual research requires license from Congressional Information Service, Inc.

Urinary arsenic speciation and porphyrins in C57B1/6J mice chronically exposed to low doses of sodium arsenate

Arsenic has been classified as a human carcinogen based on epidemiological data however the mechanism of its carcinogenicity is still unclear. Urinary biomarkers for chronic arsenic exposure would be valuable as an early warning indicator for timely interventions. In this study, young female C57BI/6J mice were given drinking water containing 0, 100, 250 and 500 mug As-v/L as sodium arsenate ad libitum for 12 months. Urine was collected bimonthly for urinary arsenic methylation assay and porphyrin analysis. All detectable arsenic species showed strong linear correlation with administered dosage and the arsenic methylation patterns were similar in all three treatment groups. No significant changes of methylation patterns were observed over time for either the control or test groups. Urinary coproporphyrin III was significantly increased in the 8th month in 250 and 500 mug/L groups and remained significantly dose-related after 10 and 12 months. Coproporphyrin I also showed a significant dose-response relationship after 12 months. Our results confirm that urinary arsenic is a useful biomarker for internal dose. The alteration of porphyrin profile suggests that arsenic can affect the heme metabolism and this may occur prior to the onset of arsenic induced carcinogenesis. (C) 2004 Elsevier Ireland Ltd. All rights reserved.

L-arginine attenuates cardiovascular impairment in DOCA-salt hypertensive rats

Nitric oxide (NO) is essential for normal function of the cardiovascular system. This study has determined whether chronic administration of L-arginine, the biological precursor of NO, attenuates the development of structural and functional changes in hearts and blood vessels of deoxycorticosterone acetate (DOCA)-salt hypertensive rats. Uninephrectomized rats treated with DOCA (25 mg every 4th day sc) and 1% NaCl in the drinking water for 4 wk were treated with L-arginine (5% in food, 3.4 +/- 0.3 g.kg body wt(-1).day(-1)). Changes in cardiovascular structure and function were determined by echocardiography, microelectrode studies, histology, and studies in isolated hearts and thoracic aortic rings. DOCA-salt hypertensive rats developed hypertension, left ventricular hypertrophy with increased left ventricular wall thickness and decreased ventricular internal diameter, increased inflammatory cell infiltration, increased ventricular interstitial and perivascular collagen deposition, increased passive diastolic stiffness, prolonged action potential duration, increased oxidative stress, and inability to increase purine efflux in response to an increased workload. L-Arginine markedly attenuated or prevented these changes and also normalized the reduced efficacy of norepinephrine and acetylcholine in isolated thoracic aortic rings of DOCA-salt hypertensive rats. This study suggests that a functional NO deficit in blood vessels and heart due to decreased NO synthase activity or increased release of reactive oxygen species such as superoxide may be a key change initiating many aspects of the cardiovascular impairment observed in DOCA-salt hypertensive rats. These changes can be prevented or attenuated by administration of L-arginine.

Reversal of cardiac dysfunction by selective ET-A receptor antagonism

1 The effectiveness of a selective endothelin receptor- A ( ET- A) antagonist, A- 127722 ( approximately 10 mg kg(-1) day(-1) as 200 mg kg(-1) powdered food), to reverse existing cardiac remodelling and prevent further remodelling was tested in deoxycorticosterone acetate ( DOCA)- salt hypertensive rats. 2 Uninephrectomised rats ( UNX) administered DOCA ( 25 mg every fourth day s. c.) and 1% NaCl in drinking water for 28 days developed hypertension ( systolic blood pressure ( BP): UNX 128 +/- 6 mmHg, DOCA- salt 182 +/- 5* mmHg; *P