The metallothionein gene, LSC54, shows increased expression during leaf senescence in Brassica napus and Arabidopsis thaliana. A number of abiotic and biotic stresses have been shown to induce senescence-like symptoms in plants and, to investigate this further, the promoter of the LSC54 gene was cloned and fused to the GUS gene and transformed into Arabidopsis. The promoter was highly induced during leaf senescence and also in response to wounding; histochemical analysis indicated that this induction was localised to a few cells close to the wound site. The transgenic Arabidopsis tissue was infected with compatible and incompatible isolates of both the fungal biotroph, Peronospora parasitica and the bacterial necrotroph, Pseudomonas syringae. Incompatible isolates induced rapid cell death (the hypersensitive response) at the site of infection and, with both pathogens, early, localised expression of the GUS gene was observed. In contrast, relatively slow induction of the GUS gene was seen in the compatible interaction and this was correlated with the appearance of senescence-like symptoms in the biotrophic interaction and cell death by necrosis that occurred in response to the necrotrophic pathogen. These results suggest that there are common steps in the signalling pathways that lead to cell death in the hypersensitive response, pathogen induced necrosis and senescence.

Arabidopsis↗

PubMed1998

Effect of K+ATP channel inhibition on total and regional vascular resistance in guinea pig pregnancy.

Decreased vascular resistance and vasoconstrictor response during pregnancy enables an increase in cardiac output and regional blood flow to the uterine circulation. We sought to determine whether inhibition of vascular smooth muscle ATP-sensitive potassium (K+ATP) channel activity during pregnancy increased systemic and/or regional vascular resistance and resistance response to ANG II. A total of 32 catheterized, awake, pregnant or nonpregnant guinea pigs were treated with either the K+ATP channel inhibitor glibenclamide (3.5 mg/kg) or vehicle (DMSO) (n = 8/group). In nonpregnant and pregnant animals, glibenclamide raised blood pressure and systemic, uterine, and coronary vascular resistance, diminishing cardiac output and organ blood flow. Glibenclamide produced a greater rise in coronary vascular resistance in the pregnant than nonpregnant groups and increased renal and cerebral vascular resistance in the pregnant animals only. ANG II infusion raised blood pressure and systemic and renal vascular resistance and lowered cardiac output and renal blood flow in vehicle-treated animals. Glibenclamide augmented ANG II-induced systemic vasoconstriction in the nonpregnant and pregnant groups and the rise in uteroplacental vascular resistance in the pregnant animals. We concluded that K+ATP channel activity likely modulates systemic, uterine, and coronary vascular resistance and opposes ANG II-induced systemic vasoconstriction in nonpregnant and pregnant guinea pigs. Pregnancy augments K+ATP channel activity in the uterine, coronary, renal, and cerebral vascular beds and the uteroplacental circulation during ANG II infusion. Thus increased K+ATP channel activity appears to influence regional control of vascular resistance during guinea pig pregnancy but cannot account for the characteristic decrease in systemic vascular resistance and ANG II-induced systemic vasoconstrictor response.

Angiotensin II↗

PubMed1998

A novel leucocyte-depleting filter for use in continuous venovenous haemofiltration: preliminary in vitro studies.

Multiple organ failure (MOF) secondary to circulatory shock, sepsis, or trauma was first described over 20 years ago. Despite much research effort and clinical trials of biological response modifiers, MOF continues to be the leading cause of death in both medical and surgical intensive care units (ICU). MOF is associated with widespread cellular and humoral systemic inflammatory responses which, in turn, are linked with inadequate tissue perfusion to vital organs and the inappropriate accumulation of activated neutrophils, resulting in microcirculatory injury. Much evidence suggests that such activated neutrophils cause vascular damage by adhering to the endothelium and releasing a variety of highly reactive and toxic moieties; these may subsequently produce endothelial injury and compromised organ function. We reasoned that a clinical device designed to remove such cells in a controlled fashion from the circulation of patients with MOF by means of using a continuous venovenous circuit might be beneficial. We report the leucocyte depletion performance of a novel filter medium as a first step towards the production of a clinical device, and show specific depletion of phagocytes relative to other formed elements in the blood.

Hemofiltration↗