Lottery Action, January 6-26, 2003, Vol. 10, no. 1

Newsletter for Iowa Lottery

Lottery Action, January 27-February 9 2003, Vol. 10, no. 2

Newsletter for Iowa Lottery

Lottery Action, November 17-30, 2003, Vol. 10, no. 23

Newsletter for Iowa Lottery

Lottery Action, December 1-14 2003, Vol.10, no.24

Newsletter for Iowa Lottery

On the cellular site of two-pore channel TPC1 action in the Poaceae.

The slow vacuolar (SV) channel has been characterized in different dicots by patch-clamp recordings. This channel represents the major cation conductance of the largest organelle in most plant cells. Studies with the tpc1-2 mutant of the model dicot plant Arabidopsis thaliana identified the SV channel as the product of the TPC1 gene. By contrast, research on rice and wheat TPC1 suggested that the monocot gene encodes a plasma membrane calcium-permeable channel. To explore the site of action of grass TPC1 channels, we expressed OsTPC1 from rice (Oryza sativa) and TaTPC1 from wheat (Triticum aestivum) in the background of the Arabidopsis tpc1-2 mutant. Cross-species tpc1 complementation and patch-clamping of vacuoles using Arabidopsis and rice tpc1 null mutants documented that both monocot TPC1 genes were capable of rescuing the SV channel deficit. Vacuoles from wild-type rice but not the tpc1 loss-of-function mutant harbor SV channels exhibiting the hallmark properties of dicot TPC1/SV channels. When expressed in human embryonic kidney (HEK293) cells OsTPC1 was targeted to Lysotracker-Red-positive organelles. The finding that the rice TPC1, just like those from the model plant Arabidopsis and even animal cells, is localized and active in lyso-vacuolar membranes associates this cation channel species with endomembrane function.

Interference of pollutants with PPARs: endocrine disruption meets metabolism.

The concept of endocrine disruption emerged over a decade ago with the observation that several natural or industrial compounds can interfere with estrogen and androgen signaling, and thereby affect both male and female reproductive functions. Since then, many endocrine-disrupting chemicals (EDCs) have been identified and the concept has been broadened to receptors regulating other aspects of endocrine pathways. In that context, interference of EDCs with receptors regulating metabolism has been proposed as a factor that could contribute to metabolic diseases such as obesity and diabetes. We review recent studies showing that several pollutants, including phthalates and organotins, interfere with PPAR (peroxisome proliferator-activated receptors) nuclear receptors and may thereby affect metabolic homeostasis. Particular emphasis is given on the mechanisms of action of these compounds. However, unlike what has been suspected, we provide evidence from mouse models suggesting that in utero exposure to the phthalate ester di-ethyl-hexyl-phthalate most likely does not predispose to obesity. Collectively, these studies define a subclass of EDCs that perturb metabolic signaling and that we propose to define as metabolic disruptors.

Lottery Action, January 5-25, 2004, Vol. 11, no. 1

Iowa Lottery Authority Retailer Information Newsletter

Lottery Action, February 9-22, 2004, Vol. 11, no. 3

Iowa Lottery Authority Retailer Information Newsletter

Lottery Action, March 8-21, 2004, Vol. 11, no. 5

Iowa Lottery Authority Retailer Information Newsletter

Lottery Action, March 22 - April 4, 2004, Vol. 11, no. 6

Iowa Lottery Authority Retailer Information Newsletter

Lottery Action, April 19-22, 2004, Vol. 11, no. 8

Iowa Lottery Authority Retailer Information Newsletter

Lottery Action, May 17-June 6, 2004, Vol. 11, no. 10

Iowa Lottery Authority Retailer Information Newsletter

Lottery Action, June 21-July 11, 2004, Vol. 11, no. 12

Iowa Lottery Authority Retailer Information Newsletter

Lottery Action, October 6-19, 2003, Vol. 10, no. 20

Iowa Lottery Authority Retailer Information Newsletter