Biomedical subjects

Julia Zaias

Publications and source records attributed to Julia Zaias.

6 recordsLinked to original sources

PubMed2004

Inhalation toxicity of brevetoxin 3 in rats exposed for 5 days.

Brevetoxins are potent neurotoxins produced by the marine dinoflagellate Karenia brevis. Exposure to brevetoxins may occur during a K. brevis red tide when the compounds become aerosolized by wind and surf. This study assesses possible adverse health effects associated with short-term inhalation exposure to brevetoxin 3. Male F344/Crl/Br rats were exposed to 500 microg brevetoxin 3/m3 by nose-only inhalation for 0.5 or 2 h/d for 5 consecutive days. Control rats were sham exposed for 2 h to vehicle. Calculated deposited brevetoxin doses were 8.3 and 33 microg/kg/d for the low- and high-dose groups, respectively. At the termination of exposures, only body weights of the high-dose group (Group B) were significantly below control values. By immunohistochemistry (IHC), small numbers of splenic and peribronchiolar lymphoid tissue macrophages stained positive for brevetoxin, while nasal mucosa, liver, and brain were IHC negative for brevetoxin. No gross or microscopic lesions were observed in any tissue examined. There was no biochemical evidence of cytotoxicity or inflammation in bronchoalveolar lavage fluid. Alveolar macrophages showed some evidence of activation following brevetoxin exposure. Humoral-mediated immunity was suppressed in brevetoxin-exposed rats as indicated by a >70% reduction in splenic plaque-forming cells in brevetoxin-exposed animals compared to controls. Results suggest that the immune system may be a target of toxicity following brevetoxin inhalation. Future studies will focus on identification of a no-effect level and mechanisms underlying brevetoxin-induced immune suppression.

Administration, Inhalation↗

PubMed2004

Laboratory procedures.

The main foundation to veterinary medicine is the availability of laboratory tests. These tests may be performed in-clinic or at diagnostic laboratories. In-clinic testing is advantageous in producing quick results, but demands sound technical ability, basic equipment,and access to some routine and special reagents. Laboratory-based testing can back up those routine techniques that mayor may not be available at the clinic level as well as provide specialized testing. The knowledge of commercially available diagnostic services is important as well as preparation and proper shipping of samples for accurate determinations.

Animal Diseases↗

PubMed2003

Toxicogenomic effects of marine brevetoxins in liver and brain of mouse.

Although the polyether brevetoxins (PbTx's) produced by Karenia brevis (the organism responsible for blooms of the Florida red tide) are known to exert their acute toxic effects through ion-channel mediated pathways in neural tissue, prior studies have also demonstrated that at least one form of the toxin (PbTx-6) is bound avidly by the aryl hydrocarbon receptor (AhR). Since AhR binding of a prototypical ligand such as dioxin is the first step in a cascade pathway producing major changes in gene expression, we reasoned that PbTx-6 might produce similar genomic-wide changes in expression. Mice were injected i.p. with sub-lethal doses of PbTx's (either 1.5 or 3 mg/g body weight of PbTx-6; or 0.15 mg/g body weight of PbTx-2, a toxin not avidly bound by the AhR), and liver and brain tissues were sampled at 8, 24 and 72 h and RNA was isolated. Changes in gene-specific RNA levels were assessed using commercially available mouse cDNA arrays (Incyte) containing >9600 array elements, including many elements from AhR-mediated genes. Histopathology of the two organs was also assessed. We observed minor histopathological effects and a total of only 29 significant (>2.0-fold) changes in gene expression, most of which occurred in the liver, and most of which could be attributable to an 'acute phase' inflammatory response. These results argue against the hypothesis that PbTx-6 acts via a classic AhR-mediated mechanism to evoke gene expression changes. However, given the avidity with which PbTx-6 binds to the AhR, these findings have important implications for how PbTx's may act in concert with other toxicants that are sensed by the AhR.

Animals↗

PubMed2002

Social environment influences the progression of atherosclerosis in the watanabe heritable hyperlipidemic rabbit.

BACKGROUND: Although there is evidence that emotionally stressful behavior can accelerate the progression of atherosclerosis, there is less data to support the notion that affiliative social behavior can slow disease progression. The present study examines the influence of social environment on the progression of atherosclerosis in the Watanabe Heritable Hyperlipidemic (WHHL) rabbit, a model that spontaneously develops lesions because of a genetic defect in lipoprotein clearance. METHODS AND RESULTS: WHHL rabbits were assigned to 1 of 3 social or behavioral groups: an unstable group, in which unfamiliar rabbits were paired daily, with the pairing switched each week; a stable group, in which littermates were paired daily for the entire study; and an individually caged group. The stable group exhibited more affiliative social behavior and less agonistic behavior than the unstable group and significantly less aortic atherosclerosis than each of the other 2 groups. Although the unstable and individually caged groups had comparable aortic lesion areas, the severity of the disease progressed faster in the unstable group, as indexed by a larger area of calcification and increased fibrous cap thickness in complex lesions. The unstable group showed increased agonistic behavior and signs of chronic adrenocortical and gonadal activation, whereas the individually caged group was relatively sedentary, had low glucocorticoid levels, and was hyperinsulinemic compared with the other groups. CONCLUSIONS: The present study demonstrates that social environment can slow, as well as accelerate, the progression of atherosclerosis. It also emphasizes the importance of behavioral factors in atherogenesis, even in a model of disease with strong genetic determinants.

Adrenal Glands↗

PubMed2002

Early injection of high-dose recombinant factor VIIa decreases blood loss and prolongs time from injury to death in experimental liver injury.

BACKGROUND: Recombinant factor VIIa (rFVIIa) is used for treatment of bleeding episodes in hemophilia patients who develop inhibitors to factors VIII and IX. We tested the hypothesis that administration of rFVIIa early after injury would decrease bleeding and prolong the time from injury to death after experimental hepatic trauma. METHODS: Anesthetized swine were cannulated for blood sampling and hemodynamic monitoring. Avulsion of the left median lobe of the liver induced uncontrolled hemorrhage. After a 10% reduction in mean arterial pressure, animals (n = 8 per group) were blindly randomized to receive intravenous rFVIIa 180 microg/kg, rFVIIa 720 microg/kg, or placebo. Pathologic examination of brain, lung, kidney, heart, and small bowel was performed to assess intravascular thrombosis. RESULTS Mortality during the first hour was 50% (four of eight) in controls versus 0% with rFVIIa 720 microg/kg (p = 0.02, chi2). Blood loss was decreased in the rFVIIa 720 microg/kg group versus the placebo group (13.2 +/- 5.5 mL/kg vs. 21.9 +/- 7.7 mL/kg;p = 0.0223). Time from injury to death was significantly prolonged in the rFVIIa 720 microg/kg group compared with placebo (116 minutes vs. 8.5 +/- 3.5 minutes; p= 0.02). No macro- or microthrombi in vital organs were identified on pathologic examination. CONCLUSION: Intravenous administration of high-dose rFVIIa early after induction of hemorrhage decreased bleeding and prolonged survival. No evidence of thrombosis in vital organs was observed.

Analysis of Variance↗

PubMed2002

Prevalence of Sarcocystis sp. in stranded Atlantic white-sided dolphins (Lagenorhynchus acutus).

In January 1998 and 1999, two mass strandings of dolphins occurred in Wellfleet, Massachusetts. The strandings were composed of 97 and 53 animals, respectively. Tissues from 35 Atlantic white-sided dolphins (Lagenorhynchus acutus) from the 1998 stranding and 52 from the 1999 stranding were examined histologically. In the 1998 stranding, unidentified protozoal tissue cysts were seen in skeletal muscle from 11 of 28 (39%) dolphins. In addition, two dolphins had a protozoal tissue cyst in cardiac muscle. In the 1999 stranding, nine of 23 (39%) dolphins had the same protozoal tissue cysts in skeletal muscle. The identification of these protozoal tissue cysts as Sarcocystis sp. was confirmed by light and transmission electron microscopy. The high prevalence of sarcocysts in these dolphins suggests that they are likely intermediate hosts for previously undescribed Sarcocystis spp. The ultrastructure of the sarcocyst walls suggests that more than one species of Sarcocystis are present in dolphins.

Animals↗