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Biomedical subjects

P Moreau

Publications and source records attributed to P Moreau.

At least 163 records · Page 9Linked to original sources
PubMed1995

High dose radiochemotherapy followed by autologous stem cell transplantation in four patients with multiple lymphomatous polyposis.

BACKGROUND: Multiple lymphomatous polyposis (MLP) results from gastrointestinal involvement by a B-cell lymphoma that originates from the mantle zone of lymphoid follicles. This well described clinicopathologic entity has a poor prognosis: the rate of complete response after conventional chemotherapy is very low. High dose radiochemotherapy with autologous stem cell transplantation (ASCT), which is one of the most intensive treatments of lymphoma, to the authors' knowledge has not been evaluated in the treatment of MLP. METHODS: Four consecutive patients with MLP were treated with high dose radiochemotherapy and ASCT while they were in partial response after conventional chemotherapy. RESULTS: Three patients achieved a complete clinical and histologic response and one achieved a complete clinical resolution of symptoms, but with persistent histologic lesions. Progression free survival ranged from 11 to 35 months. CONCLUSIONS: Autologous stem cell transplantation for patients with MLP is feasible and may be more effective than conventional chemotherapy. However, further studies are needed to assess the actual place of this type of treatment in the management of MLP.

Adult↗
PubMed1995

Vascular protective effects of ACE inhibitors and calcium antagonists: theoretical basis for a combination therapy in hypertension and other cardiovascular diseases.

Hypertension is an important cardiovascular risk factor. High blood pressure per se is not a disease but a hemodynamic alteration associated with vascular disease. Two classes of drugs are especially effective in lowering blood pressure and preventing cardiovascular complications, angiotensin converting enzyme (ACE) inhibitors and calcium antagonists. The hemodynamic effects of ACE inhibitors and calcium antagonists are complementary. While ACE inhibitors inhibit the renin-angiotensin system and reduce sympathetic outflow, calcium antagonists dilate large conduit and resistance arteries. Certain calcium antagonists, such as verapamil, lower heart rate. In the blood vessel wall, the local vascular effects of ACE inhibitors and calcium antagonists are also complementary. While ACE inhibitors inhibit activation of angiotensin I into angiotensin II and prevent the breakdown of bradykinin (which stimulates nitric oxide and prostacyclin formation), calcium antagonists inhibit the effects of vasoconstrictor hormones such as angiotensin II at the level of vascular smooth muscle by reducing calcium inflow and facilitating the vasodilator effects of nitric oxide. Calcium antagonists reduce smooth muscle cell proliferation and atherosclerosis. In hypertensive animals, verapamil and trandolapril normalize endothelial dysfunction. In large angiographic trials, nifedipine and nicardipine reduced the development of new atherosclerotic plaques. After myocardial infarction, verapamil reduces mortality and cardiac events in patients without heart failure. In contrast, ACE inhibitors are effective after myocardial infarction in patients with impaired left ventricular function. Urinary albumin excretion rate decreases during ACE inhibitor therapy or with a calcium antagonist such as verapamil; combination of the two drugs has an additive effect. In resistance arteries, hypertension is associated with an increased media/lumen ratio. ACE inhibitors, but not beta-blockers, markedly improve these structural changes. In summary, ACE inhibitors and calcium antagonists have a complementary profile, both in their hemodynamic and local vascular action. Hence, combination therapy with these two classes of drugs appears particularly useful in patients with hypertension, not only to lower blood pressure, but hopefully to achieve improved cardiovascular protection.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1995

Evidence for the presence of the alternatively spliced HLA-G mRNA forms in human mononuclear cells from peripheral blood and umbilical cord blood.

The HLA-G monomorphic, nonclassic HLA class I gene encodes the molecule that is the only major histocompatibility complex antigen expressed on cytotrophoblasts of placenta. This restricted expression on fetal tissue that is in contact with maternal tissue suggests that HLA-G products may play a role in maternofetal tolerance. We previously have demonstrated in first-trimester human trophoblasts a new alternatively spliced form of HLA-G mRNA lacking exon 4 (HLA-G4) and weak expression of HLA-G1 copy mRNA in adult peripheral blood lymphocytes. By using exon-specific HLA-G primers, we demonstrate in this work the presence of three additional alternatively spliced forms of HLA-G mRNA in human peripheral mononuclear cells (HLA-G2, HLA-G3, and HLA-G4). In umbilical cord blood, HLA-G transcription was observed at very low level and only three alternatively spliced forms were detected (HLA-G1, HLA-G2, and HLA-G3). In contrast, we did not revealed any HLA-G transcript in CD34+ fraction of cord blood cells.

Alternative Splicing↗
PubMed1995

Soluble HLA-G molecule. An alternatively spliced HLA-G mRNA form candidate to encode it in peripheral blood mononuclear cells and human trophoblasts.

The HLA-G nonclassic MHC class I gene expressed at the maternal-fetal interface may be involved in cell protection against NK cell lysis. HLA-G mRNA is observed in different adult or fetal human cells and exhibits four alternative forms: HLA-G1, HLA-G2, HLA-G3, and HLA-G4 lacking, respectively, exon 7; exons 7 and 3, exons 7, 3, and 4; exons 7 and 4. Because exon 5 encodes the transmembrane domain of the HLA-G antigen, none of these transcripts could give a soluble form as detected in supernatant of trophoblasts. In this report, we describe an additional alternatively spliced for of HLA-G transcript (HLA-G5) present in adult PBMCs and first-trimester trophoblasts that contains intron 4. Moreover, as with all other transcripts, HLA-G5, is devoid of exon 7. Its relative frequency is, respectively, approximately 1:8 and approximately 1:26 in adult PBMCs and first-trimester trophoblasts. The presence of intron 4 generates a stop codon that excludes transmembrane region (exon 5) of the HLA-G molecule and therefore might produce a soluble antigen. These results are discussed with regard to data on soluble forms of classic HLA antigens and the possible role of HLA-G.

Alternative Splicing↗
PubMed1995

Alteration of prejunctional alpha 2-adrenergic autoinhibition in DOCA-salt hypertension.

The possible involvement of prejunctional alpha 2-adrenergic autoinhibition in hypertension is still controversial. The aim of this study was to determine the functional integrity of this regulatory mechanism in conscious DOCA-salt hypertensive rats, a model characterized by an increased sympathetic tone and reactivity. Basal and hemorrhage-induced increases in catecholamine and immunoreactive neuropeptide Y (NPY) levels were compared between control and yohimbine (alpha 2-adrenergic receptor antagonist) pretreated normotensive and DOCA-salt hypertensive rats. DOCA-salt hypertensive rats had higher basal norepinephrine levels (NE), as well as increased NE and epinephrine (EPI) responses to a 15-mL/kg hemorrhage as compared to control normotensive rats. In normotensive animals, yohimbine (0.5 mg/kg, intravenous [iv]) doubled plasma NE, EPI, and NPY levels in basal conditions and in response to the hemorrhage. In contrast, the same treatment had smaller or no effect on basal NE levels and on the hemorrhage-induced responses in DOCA-salt hypertensive rats, although basal EPI levels were increased in this group. These results therefore suggest a decreased function of the prejunctional alpha 2-adrenergic autoinhibitory mechanism at the level of sympathetic nerve terminals and adrenal medulla during sympathetic hyperactivity in DOCA-salt hypertension. This dysfunction could in part explain the hyperactivity and hyperreactivity of the sympathetic nervous system observed in this model, and thus contribute to the elevation of blood pressure in DOCA-salt hypertension.

Adrenal Medulla↗
PubMed1995

Actin-based movement of Listeria monocytogenes: actin assembly results from the local maintenance of uncapped filament barbed ends at the bacterium surface.

The thermodynamic basis for actin-based motility of Listeria monocytogenes has been investigated using cytoplasmic extracts of Xenopus eggs, initially developed by Theriot et al. (Theriot, J. A., J. Rosenblatt, D. A. Portnoy, P. J. Goldschmidt-Clermont, and T. J. Mitchison. 1994. Cell. 76:505-517) as an in vitro cell-free system. A large proportion (75%) of actin was found unpolymerized in the extracts. The amount of unassembled actin (12 microM) is accounted for by the sequestering functions of T beta 4Xen (20 microM) and profilin (5 microM), the barbed ends being capped. Movement of Listeria was not abolished by depletion of over 99% of the endogenous profilin. The proline-rich sequences of ActA are unlikely to be the target of profilin. All data support the view that actin assembly at the rear of Listeria results from a local shift in steady state due to a factor, keeping filaments uncapped, bound to the surface of the bacterium, while barbed ends are capped in the bulk cytoplasm. Movement is controlled by the energetic difference (i.e., the difference in critical concentration) between the two ends of the filaments, hence a constant ATP supply and the presence of barbed end capped F-actin in the medium are required to buffer free G-actin at a high concentration. The role of membrane components is demonstrated by the facts that: (a) Listeria movement can be reconstituted in the resuspended pellets of high speed-centrifuged extracts that are enriched in membranes; (b) Actin-based motility of endogenous vesicles, exhibiting the same rocketing movement as Listeria, can be observed in the extracts.

Actins↗
PubMed1995

Comparative study of marbofloxacin and amoxicillin-clavulanic acid in the treatment of urinary tract infections in dogs.

One hundred and four dogs with clinical signs of urinary tract infection were selected by 15 practitioners in a multicentric, controlled and randomised study. The clinical diagnosis was confirmed by urinalysis and imaging. Each dog received either marbofloxacin (2 mg/kg orally once daily or 4 mg/kg by subcutaneous injection every four days) or amoxicillin-clavulanic acid tablets (12.5 mg/kg twice daily) for 10 or 28 days, depending on the clinical diagnosis. Rectal temperature, general condition, appetite, urinary signs, defecation disorders and pain on abdominal palpation were monitored at each visit, the timetable depending on diagnosis: three urinalyses and at least three examinations per case were performed. Side effects were also thoroughly sought at each examination. Marbofloxacin and amoxicillin-clavulanic acid both yielded good bacteriological cure rates (96.2 per cent versus 85.0 per cent, respectively) and clinical cure rates (83.3 per cent versus 69.7 per cent). Fewer relapses were observed in those dogs that received marbofloxacin. Few mild side effects were recorded with both products.

Administration, Oral↗
PubMed1995

Endothelin receptor subtypes in small arteries. Studies with FR139317 and bosentan.

We studied the effects of the selective endothelin A receptor antagonist FR139317 and the combined endothelin A/endothelin B receptor antagonist bosentan in rat mesenteric arteries by using a video dimension analyzer. In endothelium-denuded arteries, increasing concentrations of endothelin-1 evoked a biphasic vasoconstriction. The first phase was observed at low concentrations (10(-16) to 10(-11) mol/L) of endothelin-1 and was relatively weak. However, the contractions characterizing the second phase, which occurred at higher concentrations (10(-10) to 3 x 10(-8) mol/L) of endothelin-1, were much stronger. FR139317 concentration-dependently shifted the second phase of the endothelin-1-induced contraction curve to the right without affecting the first phase. In contrast, bosentan inhibited both the first and the second phase. Even after the blockade of endothelin A receptor, increasing concentrations of the endothelin B receptor agonists endothelin-3 and sarafotoxin S6c still induced small contractions. Maximal contractions induced by single-bolus extraluminal application of endothelin-3 (10(-9) mol/L) or sarafotoxin S6c (3 x 10(-8) mol/L) were markedly more pronounced than responses induced by cumulative concentrations, suggesting endothelin B receptor downregulation upon repeated and sustained activation. The response induced by a single bolus of endothelin-3 (10(-9) mol/L) was antagonized by bosentan but not by FR139317, confirming that endothelin B receptors were involved. In endothelium-intact arteries half-maximally precontracted with norepinephrine, bosentan but not FR139317 inhibited the relaxations induced by intraluminally applied endothelin-3. (ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

L-NAME hypertension alters endothelial and smooth muscle function in rat aorta. Prevention by trandolapril and verapamil.

Nitric oxide is an important regulator of vascular function and blood pressure. Chronic administration of nitric oxide inhibitors provides a new model of hypertension with pronounced target organ damage. We investigated the effects of oral treatment with N omega-nitro-L-arginine methyl ester (L-NAME) for 6 weeks on vascular reactivity of the aorta in Wistar-Kyoto rats. Certain rats received verapamil or trandolapril in addition to L-NAME. Systolic blood pressure increased in the L-NAME group (by approximately or equal to 80 mm Hg systolic) but not in controls or rats treated with verapamil or trandolapril. Isometric tension changes of aortic rings were recorded. Endothelium-dependent relaxations to acetylcholine were reduced in the L-NAME group (58 +/- 6% versus 104 +/- 1% in placebo, P < .05) but were normalized by treatment with verapamil or trandolapril. In contrast, endothelium-independent relaxations to sodium nitroprusside were not significantly reduced in L-NAME hypertension but were slightly enhanced by trandolapril therapy (P < .05) in the L-NAME group only. In quiescent rings, acetylcholine caused endothelium-dependent contractions in particular after in vitro incubation with L-NAME. These contractions tended to be enhanced in L-NAME hypertension (23 +/- 4% versus 14 +/- 3% in the placebo group; P = NS) and were significantly reduced after treatment with verapamil or trandolapril (P < .05). Concentrations to norepinephrine and angiotensin I and II were unaffected by L-NAME hypertension, whereas those to endothelin-1 were reduced (P < .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1995

Structure and function of the rat basilar artery during chronic nitric oxide synthase inhibition.

BACKGROUND AND PURPOSE: Nitric oxide is an important regulator of vascular tone and may also be implicated in the modulation of vascular growth and structure. This study presents the effects of chronic nitric oxide inhibition, with or without antihypertensive treatment, on the structure and function of the basilar artery in rats. METHODS: Rats were treated for 6 weeks with N omega-nitro-L-arginine methyl ester (50 mg/kg per day) alone or in combination with verapamil (100 mg/kg per day) or with trandolapril (1 mg/kg per day). Untreated rats served as controls. The structure and reactivity of perfused and pressurized basilar arteries were analyzed in vitro using a video dimension analyzer. RESULTS: Systolic arterial pressure increased only in the nitro-arginine-treated group, as did the media-to-lumen ratio of the basilar artery. This structural alteration, which was prevented by verapamil and trandolapril, was mainly due to remodeling and not to growth. Chronic inhibition of the L-arginine pathway increased the response of the basilar artery to serotonin, while the opposite was found for endothelin. Verapamil and trandolapril prevented these functional alterations that seemed related to the changes in the vascular structure. CONCLUSIONS: The remodeling and functional alterations of the basilar artery seem to depend mainly on the elevation of arterial pressure with little contribution of the L-arginine pathway. Furthermore, nitric oxide does not seem to be implicated in the modulation of normal cerebral vascular growth in vivo. However, hypertension-induced changes in vascular reactivity and structure could alter cerebral blood flow and eventually contribute to the development of stroke in this model of hypertension.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1995

[Invasive aspergillosis in intensive care].

Invasive pulmonary aspergilloses occur in patients with antineoplasic chemotherapy, mainly when associated with a prolonged neutropenia, in transplanted patients with continuous corticotherapy and less frequently in immunocompetent surgical patients. The clinical features are those of an acute infective pneumonia, not responding to antibiotherapy. Radiologic signs are often non specific. Diagnosis is obtained with bronchoalveolar lavage in which Aspergillus is found both at direct examination and in culture. Serological tests are of little interest for the diagnosis of invasive aspergillosis. Extrapulmonary locations such as sinusitis, cutaneous or brain abscesses occur in 20% of cases. The gold standard of treatment is intravenous amphotericin B which elicits an acute reaction often followed by a nephrotoxic effect which can be decreased by fluid loading with saline. Oral itraconazole administration can follow the initial treatment with amphotericin B. The mortality rate remains high and an early diagnosis and an appropriate treatment are essential.

Amphotericin B↗
PubMed1995

[Alternative transcripts of the MHC of the non-classical class I HLA-G gene in the in trophoblast during the first pregnancy trimester and in the placenta at term].

HLA-G, a non-classical class I gene, is located within the human major histocompatibility complex locus. It has a tissue-specific expression in trophoblast, where the products of HLA-A, -B and -C classical genes are absent. Therefore, the HLA-G gene may have a role during pregnancy in inducing protection of the semi-allogeneic fetus from recognition and destruction by maternal immune cells. The primary transcript of the HLA-G gene is alternatively spliced into 6 mRNA forms (HLA-G1 to HLA-G6), 2 of them may encode soluble forms of the HLA-G antigen (HLA-G5 and HLA-G6). In this work, by using reverse transcription polymerase chain reaction technique, we demonstrate that all transcripts are detected in similar amounts, both in the first and third trimester of gestation. These results are discussed in context of putative function of HLA-G antigen isoforms.

Alternative Splicing↗
PubMed1995

Chronic hyperinsulinaemia and hypertension: the role of the sympathetic nervous system.

OBJECTIVE: To determine the implication of the sympathetic nervous system in the relationship observed between insulin resistance and hypertension. DESIGN: Rats were chronically treated with insulin for 12 days by subcutaneously implanted osmotic pumps and given 10% glucose in their drinking water. A separate group of rats also received glucose only, and control rats received tap water. RESULTS: Physiological hyperinsulinaemia (1.5 and 4.5 mU/kg per min insulin) increased mean arterial pressure by approximately 10 mmHg and heart rate by 60 beats/min, and supraphysiological insulinaemia (9 mU/kg per min) did not produce additional haemodynamic effects. Insulin-treated rats developed insulin resistance, as shown by an intravenous glucose-tolerance test. Glucose treatment alone induced intermediate haemodynamic and metabolic responses. Plasma noradrenaline levels rose slightly in insulin-treated rats and were positively correlated with mean arterial pressure but not with insulinaemia, even though insulinaemia was also correlated with mean arterial pressure. The reflex sympathetic activation during hypotension revealed, in the presence of a noradrenaline uptake antagonist, that insulin increases noradrenaline release but also enhances noradrenaline uptake. Chronic hyperinsulinaemia did not alter the sympathetic vascular and cardiac responses, as assessed by the measurement of the second messengers produced by activation of alpha 1- or beta-adrenergic receptor pathways. CONCLUSION: Chronic euglycaemic hyperinsulinaemia seems to modify sympathetic activity through several mechanisms, and this action could participate in the elevation of blood pressure observed in this rat model.

Animals↗
PubMed1995

Clinical and practical value of human cytomegalovirus DNAemia detection by semi-nested PCR for follow-up of BMT recipients.

The aim of this prospective study of 162 recipients of bone marrow transplantation (BMT) was to evaluate the use of DNAemia detection by semi-nested PCR for the diagnosis of human cytomegalovirus (HCMV) infection and HCMV disease. We compared the results obtained for DNAemia with those obtained for viremia, using the shell vial assay. Patients were divided in three groups, according to BMT type (allogeneic or autologous) and date of transplant; 876 DNAemia/viremia pairs were analyzed and the overall concordance between the two tests was 97.5%. Discrepancies between the two tests were essentially due to the earlier positivity of DNAemia. Among the 10 patients with positive DNAemia episodes, 9 developed HCMV disease. DNAemia was more sensitive than viremia for HCMV disease diagnosis, while viremia had a higher positive predictive value. DNAemia appeared easily adaptable to routine laboratory use, less expensive and more informative than viremia. This study shows that DNAemia is a method that can replace viremia detection, allowing HCMV infection and disease follow-up of recipients of allogeneic BMT during the first year after BMT.

Adolescent↗
PubMed1995

[Cervical complications in dental infections. Causes--diagnosis--treatment].

Head and neck complications due to dental infections. Six cases of deep neck infection are reported. The odontogenic origin was confirmed in five patients. In one case, the aetiology remained unknown. All case reports are discussed emphasizing cervical space anatomy, mixed microbial flora and potential iatrogenic treatment.

Adolescent↗
PubMed1995

[Effect of chronic inhibition of nitric oxide synthesis on vascular structure: remodeling or growth?].

Nitric oxide is an important regulator of vascular tone, as evidenced by the marked increase in blood pressure produced by the inhibition of its synthesis. Furthermore, nitric oxide may be implicated in the modulation of vascular growth, although in vitro and in vivo studies have provided conflicting results. The aim of this study is to determine the effects of chronic nitric oxide synthase inhibition, with or without antihypertensive treatment, on the structure of the basilar artery in the rat. Rats were treated for 6 weeks with N omega-nitro-L-arginine methyl ester (L-NAME, 50 mg/kg/day) alone or in combination with verapamil (100 mg/kg/day) or with trandolapril (1 mg/kg/day). Untreated rats served as controls. The structure of perfused and pressurized basilar arteries were analyzed in vitro using a video dimension analyzer. Chronic L-NAME treatment increased systolic arterial pressure (229 +/- 5 vs 147 +/- 3 for controls; p < 0.05) and the media to lumen ratio of the basilar artery (0.22 +/- 0.02 vs 0.15 +/- 0.01 for controls; p < 0.05). This structural alteration was mainly due to remodeling (remodeling index: 76%), but not to growth (growth index: 8%, NS). The concomitant administration of verapamil and trandolapril prevented the increase in blood pressure (154 +/- 6 and 146 +/- 5 mmHg, respectively) and the structural changes produced by L-NAME (Media/lumen ratio: 0.15 +/- 0.01 and 0.14 +/- 0.01 mmHg, respectively). In fact, a positive correlation was observed between the media to lumen ratio and the systolic arterial pressure (r = 0.6; p < 0.001). The effect of the two antihypertensive treatments, as well as the correlation between the wall to lumen ratio and the arterial pressure, suggest that the remodeling of the basilar artery depends mainly on the elevation of arterial pressure with little contribution of the L-arginine pathway. Furthermore, the very small and non significant increase in the cross-sectional area of the basilar arteries from L-NAME-treated rats (growth index of 8%), suggest that nitric oxide does not play an important role in the modulation of normal cerebral vascular growth in vivo.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1995

Natural killer cells are the unique lymphocyte cell subset which do not express HLA-G.

In order to better understand the immunological functions of the HLA-G gene, expression of this gene has been studied with RT-PCR in human functional lymphocyte subpopulations. Only one population of cells has not shown any HLA-G mRNA expression, the BY55-mAb-defined natural killer cells in cord blood. This absence of transcription was not modulated by IL2, IFN-gamma or TNF-alpha. Several T clone lymphocytes isolated from human peripheral blood, bone marrow or thymus have shown a significant transcription of the HLA-G gene. Only one clone, with a natural killer phenotype, did not reveal full length or alternatively spliced transcripts of HLA-G. Intensity of HLA-G transcription was not affected by TNF-alpha, IL13 or IL4, but HLA-G transcripts appeared more abundant in the presence than in the absence of IL2.

Fetal Blood↗