Ash-laden runoff samples collected near Ground Zero soon after the September 11, 2001 attack on the World Trade Center (WTC) and subsequent fire demonstrate the release of polychlorinated biphenyls (PCBs), polybrominated dipheyl ethers (PBDEs), polybrominated dibenzo-p-dioxins and polybrominated dibenzofurans (PBDD/Fs), polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans (PCDD/Fs), and tetra- and pentachlorinated biphenylenes (PCBPs) from the incident. Relative abundances of PCDD/F congeners in the runoff water and post-disaster lower Manhattan dust samples were different from those seen in pre-disaster NYC combined sewer outfall (CSO) samples. The WTC-related samples showed a greater relative abundance of 2,3,4,7,8-PeCDF than usually seen in CSOs, sludges, and treated wastewaters. This congener may be associated with certain types of incineration. Comparison of sediment and water samples collected in the lower Hudson River before and shortly after September 11, 2001 (9/11) showed no changes in PCB or PCDD/F concentrations or homologue profiles determined down to the parts per quadrillion range. Comparisons of ambient water samples collected post-9/11 with archived samples suggest that the WTC disaster did not significantly impact ambient concentrations of the target chemicals. Ambient concentrations of PBDD/Fs in New York Harbor are similar to those of PCDD/Fs, suggesting that these contaminants deserve increased scrutiny with respect to toxicity, sources, and fate in the environment.

The expression of receptors for cholecystokinin (CCK) and other similar acting Ca2 -mobilizing hormones was studied in Xenopus laevis oocytes. Poly(A)+ RNA was prepared from pancreatic AR42J cells, which normally express receptors for CCK and bombesin and the RNA injected into oocytes. The presence of these pancreatic receptors on the oocytes was then demonstrated by hormone-induced mobilization of &5Ca2 CCK receptors were present 1 day (maxnum, 2 days) after injection of RNA and were generally proportional to the amount of poly(A)+ RNA injected (1-50 ng Cholecystokinin (CCK) is a gastrointestinal hormone that acts to regulate secretion of the exocrine and endocrine pancreas, gallbladder contraction, and gastric emptying (1,2). Moreover, it is also present in brain and other neural tissue where it appears to function as a neurotransmitter or neuromodulator (3-6). The actions of CCK on peripheral target cells are mediated by enhanced inositol phospholipid turnover, diacylglycerol formation, and mobilization of intracellular Ca2" (7). These actions are initiated by specific membrane receptors, which have been characterized as to number, specificity, size, and subunit composition (8)(9)(10)(11)(12)

SUMMARY1. In isolated mouse pancreatic acini, vasoactive intestinal polypeptide (VIP) and secretin potentiated amylase release stimulated by cholecystokinin (CCK). VIP (1-100 nM) or secretin (100-1000 nM) alone elicited a negligible secretary response, whereas in combination with CCK, these agents induced a significantly larger response.2. VIP increased maximal amylase release elicited by CCK without affecting the potency with which CCK stimulated secretion.3. The phosphodiesterase inhibitor, 3-isobutyl-1-methyl xanthine (IBMX), from 0-03-1-0 mM had effects on secretion similar to those of VIP. VIP, IBMX and 8-Br-cyclic AMP, all of which act through or mimic the action of cyclic AMP, potentiated the secretary response to maximal concentrations of CCK, carbamylcholine and the ionophore A23187, all of which act via intracellular calcium.4. In contrast to amylase release, stimulation of acinar glucose transport by CCK or carbamylcholine was not augmented by VIP, secretin, IBMX or 8-Br-cyclic AMP.5. The results indicate that for amylase release from mouse pancreas, secretagogues acting via cyclic AMP potentiate those acting via calcium. However, potentiation does not apply to all biological responses of the pancreatic acinus and each response must be studied individually.

No abstract

No abstract