Seasonal distribution, abundance, and growth of young-of-the-year Atlantic croaker (Micropogonias undulatus) in Delaware Bay and adjacent marshes

We examined the spatial and temporal distribution, abundance, and growth of young-of-the-year (YOY) Atlantic croaker (Micropogonias undulatus) in Delaware Bay, one of the northernmost estuaries in which they consistently occur along the east coast of the United States. Sampling in Delaware Bay and in tidal creeks in salt marshes adjacent to the bay with otter trawls, plankton nets and weirs, between April and November 1996–99, collected approximately 85,000 YOY. Ingress of each year class into the bay and tidal creeks consistently occurred in the fall, and the first few YOY appeared in August. Larvae as small as 2–3 mm TL were collected in September and October 1996. Epibenthic individuals <25 mm TL were present each fall and again during spring of each year, but not in 1996 when low water temperatures in January and February apparently caused widespread mortality, resulting in their absence the following spring and summer. In 1998 and 1999, a second size class of smaller YOY entered the bay and tidal creeks in June. When YOY survived the winter, there was no evidence of growth until after April. Then the YOY grew rapidly through the summer in all habitats (0.8–1.4 mm/d from May through August). In the bay, they were most abundant from June to August over mud sediments in oligohaline waters. They were present in both subtidal and intertidal creeks in the marshes where they were most abundant from April to June in the mesohaline portion of the lower bay. The larger YOY began egressing out of the marshes in late summer, and the entire year class left the tidal creeks at lengths of 100–200 mm TL by October or November when the next year class was ingressing. These patterns of seasonal distribution and abundance in Delaware Bay and the adjacent marshes are similar to those observed in more southern estuaries along the east coast; however, growth is faster—in keeping with that in other northern estuaries

The significance of measuring monocyte tissue factor activity in patients with breast and colorectal cancer

Monocytes express tissue factor (mTF) in several conditions including cancer where levels may be valuable in assessing tumour presence and progression. Using a two-stage kinetic chromogenic assay (KCA), mTF levels were measured in controls [normal subjects (n = 60) and patients undergoing hernia repair or cholecystectomy (n = 60)], in patients with benign and malignant disease of the breast (n = 83) and of the large bowel (n = 62). This was performed under fresh (resting) conditions and after incubation for 6 h without (unstimulated) and with (stimulated) Escherichia coli endotoxin. The malignant groups showed higher mTF levels than each of the three controls for resting (P &lt; 0.05 breast, P &lt; 0.05 colorectal) unstimulated (P &lt; 0.05 breast, P &lt; 0.05 colorectal) and stimulated cells (P &lt; 0.001 breast, P &lt; 0.01 colorectal). Similarly, the benign inflammatory groups had higher mTF levels than controls for resting (P &lt; 0.05 colorectal), unstimulated (P &lt; 0.05 colorectal) and stimulated cells (P &lt; 0.01 breast, P &lt; 0.01 colorectal). There was no significant difference between malignant and benign inflammatory groups in each organ. mTF levels showed an increase corresponding to that of histological tumour progression and were higher in non-surviving patients. In conclusion, mTF levels are raised in malignant and inflammatory disease compared to controls and patients with non-inflammatory conditions. Stimulated cells give better discrimination between the groups and may be of value in identifying high risk individuals. mTF levels showed an association with tumour grade or stage and the patients' survival time

Up-regulation of Tissue Factor in Human Pulmonary Artery Endothelial Cells after Ultrafine Particle Exposure

BACKGROUND: Epidemiology studies have linked exposure to pollutant particles to increased cardiovascular mortality and morbidity, but the mechanisms remain unknown. OBJECTIVES: We tested the hypothesis that the ultrafine fraction of ambient pollutant particles would cause endothelial cell dysfunction. METHODS: We profiled gene expression of human pulmonary artery endothelial cells (HPAEC) exposed to ultrafine particles (UFPs; 100 μg/mL) from Chapel Hill, North Carolina, or vehicle for 4 hr with Affymetrix HG U133 Plus 2.0 chips (n = 4 each). RESULTS: We found 320 up-regulated genes and 106 down-regulated genes (p < 0.01, 5% false discovery rate). We noted up-regulation of genes related to coagulation [tissue factor (F3) and coagulation factor II receptor-like 2 (F2RL2)] and differential regulation of genes related to F3 signaling (FOS, JUN, and NFKBIA). Results of quantitative polymerase chain reaction show a significant up-regulation of F3 after 10 and 100 μg/mL UFP exposures. Additionally, the water-soluble fractions of UFPs were sufficient to induce the expression of F3, F2RL2, and heme oxygenase 1 (HMOX1). Treatment of HPAEC with UFPs for 16 hr increased the release of interleukin (IL)-6 and IL-8. Pretreatment of HPAEC with a blocking antibody against F3 attenuated IL-6 and IL-8 release by 30 and 70%, respectively. CONCLUSIONS: Using gene profiling, we discovered that UFPs may induce vascular endothelial cells to express genes related to clotting. These results indicate that PM may cause adverse cardiovascular health effects by activating coagulation-inflammation circuitry