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Biomedical subjects

P Etienne

Publications and source records attributed to P Etienne.

At least 19 recordsLinked to original sources
PubMed2001

Cryptogein affects expression of alpha3, alpha6 and beta1 20S proteasome subunits encoding genes in tobacco.

Twelve alpha and beta 20S proteasome subunits cDNAs showing 70-82% identity with the corresponding genes in Arabidopsis or rice, and features of eukaryotic proteasome subunits were cloned in tobacco. Only beta1-tcI 7, alpha3 and alpha6, 20S proteasome subunits encoding genes were up-regulated by cryptogein, a proteinaceous elicitor of plant defence reactions. These results led to the hypothesis that the activation of beta1-tcI 7, alpha3 and alpha6 could induce a specific proteolysis involved in the hypersensitive response and systemic acquired resistance monitored by cryptogein.

Algal Proteins↗
PubMed2001

Hydrogen peroxide induces programmed cell death features in cultured tobacco BY-2 cells, in a dose-dependent manner.

Active oxygen species (AOS), especially hydrogen peroxide, play a critical role in the defence of plants against invading pathogens and in the hypersensitive response (HR). This is characterized by the induction of a massive production of AOS and the rapid appearance of necrotic lesions is considered as a programmed cell death (PCD) process during which a limited number of cells die at the site of infection. This work was aimed at investigating the mode of cell death observed in cultures of BY-2 tobacco cells exposed to H(2)O(2). It was shown that H(2)O(2) is able to induce various morphological cell death features in cultured tobacco BY-2 cells. The hallmarks of cell death observed with fluorescent and electron microscopy differed greatly with the amount of H(2)O(2) added to the cell culture. The appearance of nuclear fragmentation similar to 'apoptotic bodies' associated with a fragmentation of the nuclear DNA into small fragments appear for almost 18% of the cells treated with 12.5 mM H(2)O(2). The early stages of the induction of this PCD process consisted in cell shrinkage and chromatin condensation at the periphery of the nucleus. Above 50 mM, H(2)O(2) induces high necrotic cell death. These data suggest that H(2)O(2)-induced cell damage is associated with the induction of various cell death processes that could be involved differently in plant defence reactions.

Apoptosis↗
PubMed2000

Induction of tcI 7, a gene encoding a beta-subunit of proteasome, in tobacco plants treated with elicitins, salicylic acid or hydrogen peroxide.

We previously isolated, by differential display and 5' RACE (rapid amplification of cDNA ends), cDNAs corresponding to genes activated following cryptogein treatment of tobacco cell suspensions, among them tcI 7 (tcI for tobacco cryptogein Induced), a gene encoding a beta-subunit of proteasome. Here, we report that tcl 7 was up-regulated in tobacco plants treated with elicitins (cryptogein and parasiticein) that have been shown to induce a systemic acquired resistance (SAR). Moreover, subsequent inoculation of tobacco with the pathogen Phytophthora parasitica var. nicotianae (Ppn) was shown to induce an additional activation of tcI 7 in tobacco plants pretreated with cryptogein. We also showed an up-regulation of tcI 7 by salicylic acid (SA). Moreover, accumulation of tcI 7 transcripts after treatment with cryptogein or with SA only occurred in NahG 9-tobacco plants that do not express the salicylate hydroxylase and thus are able to accumulate SA and develop a SAR. Suppressed accumulation of tcI 7 transcripts in NahG 8+ tobacco plants after cryptogein or SA treatment correlated with the loss of SAR. H2O2 was also shown to up-regulate tcI 7 in tobacco plants. Using gene walking by PCR we cloned and sequenced the 5' flanking region of tcI 7 containing hypothetical regulatory sequences, especially myb and NF-kappaB boxes, that could be responsible for the regulation of tcI 7 by salicylic acid and H2O2 respectively.

Amino Acid Sequence↗
PubMed1999

Involvement of lipoxygenase-dependent production of fatty acid hydroperoxides in the development of the hypersensitive cell death induced by cryptogein on tobacco leaves.

Lipid peroxidation was investigated in relation with the hypersensitive reaction in cryptogein-elicited tobacco leaves. A massive production of free polyunsaturated fatty acid (PUFA) hydroperoxides dependent on a 9-lipoxygenase (LOX) activity was characterized during the development of leaf necrosis. The process occurred after a lag phase of 12 h, was accompanied by the concomitant increase of 9-LOX activity, and preceded by a transient accumulation of LOX transcripts. Free radical-mediated lipid peroxidation represented 10% of the process. Inhibition and activation of the LOX pathway was shown to inhibit or to activate cell death, and evidence was provided that fatty acid hydroperoxides are able to mimic leaf necrotic symptoms. Within 24 h, about 50% of leaf PUFAs were consumed, chloroplast lipids being the major source of PUFAs. The results minimize the direct participation of active oxygen species from the oxidative burst in membrane lipid peroxidation. They suggest, furthermore, the involvement of lipase activity to provide the free PUFA substrates for LOX. The LOX-dependent peroxidative pathway, responsible for tissue necrosis, appears as being one of the features of hypersensitive programmed cell death.

Algal Proteins↗
PubMed1999

Systematic use of total vascular exclusion in 14 elective hepatic resections.

Between March 1992 and May 1995, 14 hepatic resections under total vascular exclusion were performed (10 major resections and 4 minor resections involving central segments). Mean age was 64 years (SD +/- 12). During hepatic resection, 4 patients required blood transfusion. The reason was a too low level of haemoglobin (< 10 gr/100 ml) to undergo Hepatic Vascular Exclusion (HVE) (1 patient), an unacceptable decrease in blood pressure following HVE leading to insertion of venovenous bypass (1 patient), or an extensive bleeding following removal of the clamps (2 patients). The 10 remaining patients did not need peroperative blood transfusion. Two patients were transfused after the 6th postoperative day. Complications usually described during HVE were not encountered except for one pleural effusion needing thoracocentesis.

Adult↗
PubMed1998

Phenotype modulation in primary cultures of aortic smooth muscle cells from streptozotocin-diabetic rats.

Diabetes mellitus is a major risk factor for atherosclerosis. In atherosclerotic lesions, arterial smooth muscle cells (SMC) change from a contractile to a synthetic phenotype characterized by active proliferation. A similar phenotype modulation occurs in vitro when isolated arterial SMC are grown in culture and is characterized by both changes in cell morphology and a typical switch in actin isoform expression. In this study, we examined the influence of streptozotocin (STZ)-induced diabetes on the differentiation state and the phenotype modulation of cultured rat aortic SMC. We used transmission electron microscopy to study the fine structure of STZ-diabetic and non-diabetic SMC in primary culture and immunological methods for the determination of the proportions of alpha-smooth muscle actin (alpha-SM) and nonmuscle beta-actin (beta-NM) isoforms. Cultured STZ-diabetic SMC exhibited a large cytoplasmic volume, rich in rough endoplasmic reticulum, when compared with cultured non-diabetic SMC. alpha-SM, organized in stress fibers, was less homogeneously and abundantly distributed and by contrast, beta-NM was more abundant in STZ-diabetic than in non-diabetic SMC. Cytofluorimetric analyses demonstrated that the alpha-SM content was reduced in freshly STZ-diabetic SMC. Furthermore, during logarithmic growth of cultured SMC, the decrease of alpha-SM was more important in STZ-diabetic than in non-diabetic SMC. Immunoblotting of actin isoforms confirmed that expression of beta-NM was more important in STZ-diabetic than in non-diabetic SMC even in freshly isolated cells. The results suggest that SMC from STZ-diabetic rats express a more dedifferentiated state and undergo a more rapid phenotypic modulation in primary cultures than SMC from non-diabetic rats. Therefore, diabetes could induce changes in the phenotype of arterial SMC which might be associated with the onset or progression of the atherogenic process.

Actins↗
PubMed1996

Regulation of growth of cultured smooth muscle cells from diabetic rats by interleukin-1 beta: role of nitric oxide.

We examined the influence of streptozotocin-induced diabetes on the growth of cultured rat aortic smooth muscle cells in the presence of interleukin-1 beta. Interleukin-1 beta induced a dose-dependent biphasic effect on proliferation of diabetic and control smooth muscle cells, consistent with the data on [3H]thymidine incorporation and cell counts. However, the major effect of interleukin-1 beta was to stimulate growth of diabetic cells and inhibit growth of control cells. Furthermore, interleukin-1 beta induced a dose-dependent increase in nitric oxide (NO) release and in intracellular cyclic GMP accumulation: nitrite release was similar in both smooth muscle cell models but cyclic GMP accumulation was greater in diabetic cells than in controls. These results suggest that the inhibitory loop involving NO is not effective enough to completely counterbalance the stimulatory effects of interleukin-1 beta on diabetic cells. Therefore, experimental diabetes may modify the interleukin-1 beta-regulated smooth muscle cell growth.

Animals↗
PubMed1996

Enhanced antiproliferative effect of nitric oxide in cultured smooth muscle cells from diabetic rats.

We examined the influence of experimental diabetes on the proliferation of cultured vascular smooth muscle cells (VSMCs) in presence of a nitric oxide (NO)-generating agent, sodium nitroprusside (SNP), and 8-bromo-cGMP. VSMC cultures were prepared from aortas of control and streptozotocin-diabetic rats. SNP induced a time- and dose-dependent inhibition of control and diabetic VSMC proliferation, consistent with the data on [3H]thymidine incorporation, cell counts, and index of culture mass. However, the responses to SNP were significantly enhanced in VSMCs from diabetic rats. SNP induced an increased dose-dependent accumulation of intracellular cGMP in diabetic VSMCs. In contrast, growth-inhibitory responses to 8-bromo-cGMP were not significantly different between the two VSMC models. Moreover, basal cGMP content in VSMCs was lower in diabetic rats than in controls, a result that can explain the enhanced proliferation observed in VSMCs from diabetic rats. These results suggest an enhanced antiproliferative effect of NO in VSMCs from diabetic rats through increased cGMP production. Therefore, experimental diabetes may impair and up-regulate soluble guanylate cyclase activity in VSMCs.

Animals↗
PubMed1996

Adenosine inhibitory effect on enhanced growth of aortic smooth muscle cells from streptozotocin-induced diabetic rats.

1. There is evidence to suggest that adenosine may regulate arterial smooth muscle cell (SMC) growth and proliferation, which is a key event in atherogenesis. This regulation may be mediated via adenylate cyclase. As diabetes is a known risk factor for atherosclerosis, we investigated the growth of aortic SMC from diabetic rats in primary culture and their sensitivity to adenosine and to adenylate cyclase activity. 2. Diabetes was induced with streptozotocin (STZ, 66 mg kg-1, i.p.) Aortic SMC primary cultures were prepared from STZ-diabetic and age-matched rats 5 weeks after the STZ injection. 3. SMC from STZ-diabetic rats grew faster and reached greater densities at confluence than those from non-diabetic animals. 4. Adenosine inhibited growth in both control and diabetic SMC. However, cells from STZ-diabetic rats were apparently more sensitive to adenosine. 5. Direct activation of adenylate cyclase by forskolin induced a dose-dependent growth inhibition, similar in both groups of cells. 6. Cholera toxin, an activator of stimulatory GTP-binding protein (Gs), induced a similar growth inhibitory response in non-diabetic and diabetic SMC. Pertussis toxin (PTX), an inactivator of inhibitory GTP-binding protein (Gi), did not itself affect SMC growth. However, PTX increased dose-dependently the growth inhibition induced by adenosine in SMC from non-diabetic rats but not in SMC from diabetic rats. 7. These findings suggest a functional abnormality in Gi activity in SMC from diabetic rats, that would explain the increased sensitivity to the nucleoside. This impaired inhibitory pathway may reflect changes in the growth regulation of SMC in experimental diabetic states.

Adenosine↗
PubMed1994

Elevated dopa decarboxylase activity in living brain of patients with psychosis.

The hypofrontality theory of the pathogenesis of schizophrenia predicts that cortical lesions cause psychosis. During a search for abnormalities of catecholaminergic neurotransmission in patients with complex partial seizures of the mesial temporal lobe, we discovered an increase of the rate of metabolism of an exogenous dopa tracer (6-[18F]fluoro-L-dopa) in the neostriatum of a subgroup of patients with a history of psychosis. When specifically assayed for this abnormality, patients with schizophrenia revealed the same significant increase of the rate of metabolism in the striatum. The finding is consistent with the theory that a state of psychosis arises when episodic dopamine excess is superimposed on a trait of basic dopamine deficiency in the striatum. The finding is explained by the hypothesis that cortical insufficiency, a proposed pathogenetic mechanism of both disorders, causes an up-regulation of the enzymes responsible for dopa turnover in the neostriatum as well as the receptors mediating dopaminergic neurotransmission.

Adult↗
PubMed1993

[Peritonitis caused by a purulent cyst of the urachus in a young woman].

Urachal cysts are not exceptional and are observed more often in children. In adults, they may become infected and cause clinical symptoms associating subumbilical midabdominal pain, fever, guarding and leukocytosis. Intraperitoneal rupture is exceptional (21 published cases) and only 7 cases have involved adult female patients. The authors report the case of a 27-year old woman with peritonitis caused by rupture of a suppurated urachal cyst, 6 cm in diameter, for which diagnosis was established by perioperative ultrasound. The surgical procedure used consisted of total excision of the urachus, the umbilico-prevesical fascia and partial excision of the dome of the urinary bladder. Indeed, total excision is imperative because of the risk of malignant degeneration of this mass into an adenocarcinoma.

Adult↗
PubMed1992

Acute tryptophan depletion blocks morphine analgesia in the cold-pressor test in humans.

The effects of depletion of the serotonin precursor, L-tryptophan, on the threshold and tolerance to cold pressor pain, and the analgesic effect of morphine (10 mg intramuscularly), were tested in a double blind trial on human volunteers. Effects on mood were also assessed using the Profile of Mood States and the Addiction Research Center Inventory (ARCI) Scales. To deplete tryptophan, subjects were fed a tryptophan-deficient amino acid mixture 4.5 h before morphine was administered. Controls received the mixture with tryptophan, which is equivalent to a nutritionally balanced protein. The tryptophan-deficient meal reduced plasma tryptophan more than 70% but had no effect on threshold or tolerance to cold pressor pain. After morphine, tolerance to cold pressor pain increased in controls. Tryptophan depletion abolished this analgesic effect. Pain threshold was not altered by morphine. In subjects with normal tryptophan, the analgesic effect of morphine was predicted by the level of plasma morphine-6-glucuronide, but not by the level of morphine. Morphine increased scores on the LSD scale of the ARCI, but had no effect on other measures of mood. Tryptophan depletion also failed to alter mood in these subjects, who had unusually low depression scores before tryptophan depletion.

Adolescent↗
PubMed1992

[Peritonitis due to a suppurating urachal cyst in a young woman. Review of the literature].

Peritonitis caused by a suppurating urachal cyst in a young woman. A review of the literature. Urachal cysts are not rare but occur much more often in children. In adults they may become infected and cause clinical symptoms including sub-umbilical mid-abdominal pain, fever, guarding and leukocytosis. Intraperitoneal rupture is rare (21 published cases) and only 7 cases have involved an adult female patient. The authors report the case of a 27 year old woman with peritonitis caused by rupture of a suppurating urachal cyst. 6 cm in diameter, for which the diagnosis had been established by pre-operative ultrasound. The surgical procedure carried out was total excision of the urachus, of the fascia between the umbilicus and the bladder, and partial excision of the dome of the bladder. Indeed total excision should have been carried out because of the risk of malignant degeneration of this mass to an adenocarcinoma.

Adolescent↗
PubMed1990

Role of excitatory amino acid neurotransmission in synaptic plasticity and pathology. An integrative hypothesis concerning the pathogenesis and evolutionary advantages of schizophrenia-related genes.

N-methyl-D-aspartate (NMDA) receptors are involved in long-term potentiation, burst firing and the generation of patterned activity in neuronal networks; in use-dependent stabilization of synaptic connectivity in developing animals; in some forms of learning in mature animals; and in pathologies as found in brain aging. A number of these characteristics are reminiscent of several manifestations of schizophrenia and therefore we present the hypothesis that one of the genes modified in schizophrenia is directly or indirectly linked to the control of excitatory neurotransmission; possibly the normal switching on of the expression of the adult form of the NMDA receptor is delayed. Alternatively the adult form of the NMDA receptor is altered, resulting in inappropriate functioning of this receptor. The delayed or faulty expression of the adult form of the NMDA receptor, in turn, should confer a series of evolutionary advantages including protection against aging-associated brain pathologies.

Amino Acids↗
PubMed1990

Nootropic effects of ACE inhibitors in mice.

The angiotensin converting enzyme (ACE) inhibitors captopril and enalapril and the nootropic piracetam reduced the amnesiogenic effects of cerebral electroshock treatment in mice. These compounds also directly improved passive-avoidance learning if administered before the learning trial. When given immediately after the learning trial, captopril and piracetam were active, but not enalapril. Captopril, but neither enalapril nor piracetam, facilitated memory retrieval after a 2-month retention interval. Unlike those of piracetam, the memory-improving effects of captopril and enalapril are not established by aldosterone-receptor blockade, suggesting that the two types of drug act via different mechanisms of action.

Adrenalectomy↗
PubMed1990

A pilot study of magnesium aspartate hydrochloride (Magnesiocard) as a mood stabilizer for rapid cycling bipolar affective disorder patients.

1. Nine severe rapid cycling manic-depressive patients were treated with a magnesium preparation, Magnesiocard 40 mEq/day in an open label study for a period up to 32 weeks. 2. Magnesiocard was found to have clinical results at least equivalent to those of lithium in about 50% of these patients. These results were obtained in an exploratory study and should be interpreted with caution. 3. The possibility that Magnesiocard could replace or improve the efficacy of lithium as a preventive treatment of manic-depressive illness merits further clinical investigation.

Aspartic Acid↗