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Biomedical subjects

A M Lacombe

Publications and source records attributed to A M Lacombe.

8 recordsLinked to original sources
PubMed2000

Arabidopsis SGS2 and SGS3 genes are required for posttranscriptional gene silencing and natural virus resistance.

Posttranscriptional gene silencing (PTGS) in plants resuits from the degradation of mRNAs and shows phenomenological similarities with quelling in fungi and RNAi in animals. Here, we report the isolation of sgs2 and sgs3 Arabidopsis mutants impaired in PTGS. We establish a mechanistic link between PTGS, quelling, and RNAi since the Arabidopsis SGS2 protein is similar to an RNA-dependent RNA polymerase like N. crassa QDE-1, controlling quelling, and C. elegans EGO-1, controlling RNAi. In contrast, SGS3 shows no significant similarity with any known or putative protein, thus defining a specific step of PTGS in plants. Both sgs2 and sgs3 mutants show enhanced susceptibility to virus, definitively proving that PTGS is an antiviral defense mechanism that can also target transgene RNA for degradation.

Amino Acid Sequence↗
PubMed1991

Role of adrenal catecholamines during forced submergence in ducks.

Maximum underwater tolerance (UTmax) of chronically adrenalectomized ducks (ADX, 5.3 +/- 0.3 min) and chronically adrenal-denervated ducks (DNX, 7.2 +/- 0.2 min) was significantly lower than sham-operated controls (SH-ADX, 10 +/- 0.8 min; SH-DNX, 12.2 +/- 0.5 min). After 4 min forced submergence, heart rates of ADX (62 +/- 16 beats/min) and DNX (31 +/- 2 beats/min) ducks were significantly higher than in their respective sham-operated controls (23 +/- 3 and 17 +/- 2 beats/min), although their blood pressure was significantly lower. Arterial partial pressure of O2, arterial O2 content, arterial pH, and lactate levels in DNX ducks (42 +/- 2 mmHg, 4.5 +/- 0.8 ml O2/100 ml blood, 7.233 +/- 0.016, 3.1 +/- 0.3 mM, respectively) were significantly lower than in SH-DNX ducks after 5 min forced submergence (53 +/- 1 mmHg, 6.8 +/- 0.4 ml O2/100 ml blood, 7.301 +/- 0.007, 4.8 +/- 0.4 mM, respectively). Venous infusion of catecholamines in ADX and DNX ducks during forced submergence significantly increased UTmax. It is suggested that adrenal catecholamines increase tolerance to underwater submersion by enhancing peripheral vasoconstriction, thus preserving the O2 stores for the heart and brain. Other adrenal products could also be involved.

Adrenal Glands↗
PubMed1991

Neural and humoral effects on hindlimb vascular resistance of ducks during forced submergence.

Circulating catecholamines increase by three orders of magnitude in forced submerged ducks; their role in promoting vascular resistance was studied using vascular perfusion of hindlimbs. Perfusion pressure and blood flow were recorded simultaneously in hindlimbs of ducks during forced submergence. One leg was perfused with blood mixtures devoid of catecholamines (test leg) and compared with the other autoperfused leg. Perfusion pressures in test legs perfused with hyperoxic and hypocapnic blood or with hypoxic and hypocapnic blood were not significantly different from those in the matching autoperfused legs. However, when test legs were perfused with hypercapnic blood, regardless of whether blood was hypoxic or hyperoxic, perfusion pressures were significantly lower than in autoperfused legs. Adding catecholamines to test legs perfused with hypoxic and hypercapnic blood, after 3 min submergence, significantly enhanced vasoconstriction. Hypercapnia acts directly on the peripheral vascular beds and impairs the neurally mediated vasoconstriction during submergence, while circulating catecholamines restore peripheral vasoconstriction. Thus circulating catecholamines are needed to compensate for the depressant action of hypercapnia on neurally mediated vasoconstriction.

Animals↗
PubMed1990

The source of circulating catecholamines in forced dived ducks.

Plasma catecholamines have been measured in chronically adrenalectomized (ADX) ducks, in chronically adrenal-denervated ducks (DNX), and in their respective shamoperated controls (SH-adx, SH-dnx) after 3 min forced submergence. The results showed that 100% of the plasma epinephrine (EP) and 70 to 80% of plasma norepinephrine (NE) released during the dive came from the adrenal glands. Only 20 to 30% of plasma NE came from the endings of the autonomic vascular sympathetic nerves which are strongly stimulated during diving. Adrenal catecholamines were released by nerve activation only; nonneural mechanisms did not play any role in their release. The action of adrenal catecholamines on the cardiovascular system during dives was investigated by measuring heart rate and arterial blood pressure in operated and sham-operated ducks. Cardiovascular adjustments, associated with 3 min of forced diving, were not affected by any differences in the levels of plasma catecholamines.

Adrenal Glands↗
PubMed1987

Adrenal gland denervation and diving in ducks.

The extreme elevation in plasma levels of free norepinephrine (NE) and free epinephrine (EP), which occurs during forced diving of ducks (Anas platyrhynchos), was studied before and after denervation of the adrenal glands. In intact animals both NE and EP concentration increased by up to two orders of magnitude in a 4-min dive but by a significantly lesser amount if the duck breathed O2 before the dive. Denervating the adrenal glands reduced the amounts of both catecholamines (CA) released during dives, plasma EP decreased to 10%, and NE to 50% of values obtained before denervation. Breathing O2 before a dive virtually eliminated CA release in denervates, indicating that hypoxia was the important non-neural releasing agent. Hypoxia was also the most important neural releasing agent compared with hypercapnia, acidosis, or hypoglycemia. Adrenal denervation did not cause significant changes in heart rate, blood pressure, arterial blood gas tensions, pH, or plasma glucose during dives, although denervation caused increased variation in some of these variables. In ducks CA release in dives is largely due to decreasing arterial O2 partial pressure, and full expression of the response is dependent on intact innervation of the adrenal gland.

Adrenal Glands↗